📕

OMI Pocket Guide

Identify ischemia on the ECG like an expert
Learn to identify occlusion myocardial infarctions (OMIs) by reviewing angiographically confirmed cases from Dr. Smith's ECG Blog curated by Mark Hellerman, MD

⚠️Note:

  • 25-30% of NSTEMIs are found to have total thrombotic occlusion at the time of cardiac cath (PMID 29020244)
  • Mortality rates in these patients are ~2x higher than in those with non-occluded vessels (PMID 29020244)
  • The Occlusion Myocardial Infarction (OMI) / Non-Occlusion Myocardial Infarction (NOMI) paradigm provides a framework for identifying patients with “NSTEMIs” who are more likely to have acute total thrombotic occlusion of a coronary artery

📕 OMI Guide:

  • This guide is intended to provide a quick reference to remind you of the patterns associated with OMIs and their mimics
  • Swipe left/right (on mobile) or use left/right arrow keys to quickly compare ECGs corresponding to angiographically confirmed OMIs curated from Dr. Smith’s ECG Blog:

📚 Learn More:

Mimics of OMI with ST Elevation:

🚨 Suggestive of OMI:

  • Smith-Modified Sgarbossa’s Criteria
    • Concordant STE >1 mm any lead
    • Concordant STD >1 mm V1-V3
    • Discordant STE >25% preceding S-wave in any lead
    • Discordant STE or STD >30% preceding S- or R-wave in any lead

✅ Expected STE in LBBB or V-Pacing:

  • Discordant STE <1/4 S-Wave V1-V4

🚨 OMI (+) in LBBB or Paced Rhythm:

13 examples below. Swipe ↔️ or use arrow keys to view more.
ECG
  • HPI: 70M with acute chest pain
  • Cath: Culprit artery: LAD (100% stenosis, TIMI 0) requiring thrombectomy and stent. Impella placed for cardiogenic shock
  • Key ECG: There is concordant ST elevation in I, aVL with reciprocal concordant STD in inferior leads, as well as excessively discordant TE in V2-V4. 
  • Link to full case @ Dr. Smith’s ECG Blog: 2023-05-08
ECG
  • HPI: 60M w/ 2 days intermittent CP
  • Cath: 100% thrombotic RCA occlusion
  • Key ECG: concordant STE in II, proportionally excessively discordant STE in III (ST/S ratio = 2/4 = 0.5) and aVF with reciprocal depression in I and aVL, hyperacute T wave morphology in II, III, and aVF, and concordant STD with TWI in V1 and V2
  • Link to full case @ Dr. Smith’s ECG Blog: 2022-08-01
ECG
  • HPI: 50M w/ neck and jaw pain for 1 hour
  • Cath: 100% Thrombotic Occlusion of a Dominant Circumflex
  • Key ECG: Leads II, and V4-V6 have discordant ST Elevation with an ST/S ratio >25%
  • Link to full case @ Dr. Smith’s ECG Blog: 2021-06-21

ECG

ECG
  • HPI: Elderly woman w/ midsternal chest pain x 2 hr
  • Cath: 95% thrombotic lesion of the ostial RCA
  • Key ECG: excessively discordant STE in II, III, aVF, as well as V4-V6; Reciprocal excessively discordant STD in I and aVL; concordant STD in V2
  • Link to full case @ Dr. Smith’s ECG Blog: 2019-04-25
ECG
  • HPI: 60M w/ acute chest pain x hours
  • Cath: 95% ostial RCA in-stent thrombosis
  • Key ECG: Discordant STE >25% in inferior leads with reciprocal STD in I and aVL
  • Link to full case @ Dr. Smith’s ECG Blog: 2018-06-22

ECG
  • HPI: Middle aged woman with acute chest pain
  • Cath: 100% occlusion of the LCX OM2
  • Key ECG: Excessively discordant STE in III (33% of the preceding S-wave: 2mm/6mm)
  • Link to full case @ Dr. Smith’s ECG Blog: 2018-06-04
ECG
ECG
ECG
  • HPI: 70 something with history of CAD and pulmonary embolism presented with sudden onset chest pain, diaphoresis, and abdominal pain 2 hours prior. BP 70s/30s, acute shock (cold and clammy, hypotensive, abd pain)
  • Cath: Acute occlusion of the ostial ramus and culprit stenoses of the proximal and mid circumflex
  • Key ECG: Ventricularly paced rhythm with multiple leads confirming OMI by the Smith modified Sgarbossa Criteria: proportionally excessively discordant ST elevation in all inferior leads. Proportionally excessively reciprocal discordant ST depression in aVL. Concordant ST depression in V2
  • Link to full case @ Dr. Smith’s ECG blog: (date pending) view post
    https://drsmithsecgblog.com/acute-cardiogenic-shock-in-a-patient-with-ventricular-paced-rhythm/
  • Queen of Hearts: OMI with mid confidence
ECG
  • HPI: A man in his 80s presented with acute chest pain and normal vital signs
  • Cath: Culprit occlusion of the proximal left circumflex artery
  • Key ECG: Ventricular paced rhythm with findings very suspicious for posterior OMI, including inappropriately isoelectric ST segments in V2-V3. There is also excessively discordant STD in V4 (which is the transition lead in this case, but has a bigger component up than down). The ST/R ratio in V4 is 2/5.5 = 36%.
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/a-man-in-his-80s-with-chest-pain-and/
  • Queen of Hearts: Not OMI with mid confidence
ECG
  • HPI: A middle-aged male presented with chest pain, onset 1 hour prior.
  • Cath: 100% LAD occlusion
  • Key ECG: There is sinus with a wide complex that is left bundle branch block (LBBB). There is also proportionally excessively discordant ST Elevation in lead V2, and hyperacute T-waves in leads V1-V4. By the Smith Modified Sgarbossa criteria, one need have only 1 lead with proportionally excessively discordant STE [ST/S ratio of 25% (80% sensitive and 99% specific)]. [ST/S ratio, with ST measured at the J-point relative to the PQ junction/QRS onset]. An ST/S ratio of >/= 20% is 84% sensitive and 94% specific. I get worried about any ratio > 15%, as the normal maximal ratio of ST/S in V1-V4 is 11%. The ratio in V2 is 2.75/7.5 which is 37%.
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/chest-pain-and-lbbb/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: An 80 year-old female with a history of diabetes and CABG called paramedics for 2 hours of epigastric burning that did not resolve after nitro. Blood pressure was 130/60 and heart rate was 50. Paramedic ECG machine read ‘STEMI’ so the patient was transferred to the nearest cath lab. On arrival the ECG was noted to have LBBB.
  • Cath: 100% RCA occlusion
  • Key ECG: It is the shape of the ST-T waves in leads I, aVL and III that immediately tells me this is an acute OMI until proven otherwise. Even though the amount of ST elevation in lead III is not great — there should be no ST elevation at all in this lead given the LBBB. Similarly, the ST depression and obviously disproportionate ST-T wave depression in leads I and aVL have to be assumed acute in this elderly patient who presents with a potential “CP-equivalent” symptom
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/80-year-old-female-with-epigastric-burning-and-previously-diagnosed-lbbb/
  • Queen of Hearts: OMI high confidence

🔎 Specificity:

  • Specificity: 99% for excessively proportionally discordant STE >25%
  • Specificity: 94% for excessively proportionally discordant STE >20% (not part of official Modified-Sgarbossa criteria)
  • Specificity: 98% for excessively proportionally discordant STE or STD >30% in any lead (not part of official Modified-Sgarbossa criteria)
  • Sources: PMID 22939607, PMID 34172301

⚠️Note:

  • Acute OMI with preservation of LVH voltage criteria is rare
  • In most cases, acute LAD OMI causes diminution of S-wave voltage in V1-V3, which makes finding examples of OMI which preserve LVH voltage criteria unusual

🚨 Suggestive of OMI:

  • Discordant STE > 1/6 (17%) preceding S-wave
  • STE in V1-V3 > 25% of the preceding QRS
    • This is very insensitive: STE in LVH rarely exceeds 4 mm. If an S-wave is 30 mm in depth, STE would have to exceed 7 mm to meet criteria.
  • Symmetric TWI is more suggestive of ischemia (Figure from Dr. Ken Grauer )

✅ Expected ST changes in LVH:

  • STE in leads with deep S waves (usually V1-V3) may mimic STEMI. This may be seen in LVH
  • LVH usually has concave-upwards ST segments, but conVEX-upwards can also be seen
  • LV “strain”:
    • ST-T wave changes of LV “strain” in response to marked LVH are most commonly seen in one or more of the lateral leads (ie, leads I, aVL; V4,V5,V6).
      • In its most extreme form — these changes manifest as asymmetric ST depression (ie, the ST segment descends slower than it rises)
    • Instead of seeing ST-T wave changes of LV “strain” in lateral leads — some patients manifest a “mirror-image” of strain in anterior leads
      • Use of the Mirror Test (ie, inverting the QRST complex in lead V1) may facilitate recognizing what the shape of LV “strain” may look like in a right-sided lead (such as lead V1 or V2). Example from Dr. Ken Grauer
    • Some patients with LVH (especially if the frontal plane axis is vertical) — also manifest ST-T changes of LV “strain” in the inferior leads.
  • The increase in leftward and posterior forces may overshadow baseline anterior forces — with a “net result” that R wave progression is delayed (sometimes to the point of producing QS complexes in one or more anterior leads).
  • Inferior STE with reciprocal ST depression in aVL is frequently found in the following STEMI mimics: LVH, LBBB, inferior LV aneurysm, myocarditis

📝 LVH Criteria:

  • Sokolow-Lyon
    • [S wave V1 or V2] + [R wave V5 or V6] > 35 mm
    • Sensitivity: 14%
    • Specificity: 99%
  • Modified Cornell
    • [R wave aVL] > 11 mm
    • Sensitivity: 14%
    • Specificity: 92%
  • Cornell
    • [R wave in aVL] + [S wave in V3] > [28 mm for men] or [20 mm for women]
    • Sensitivity: 31%
    • Specificity: 93%
  • Peguero
    • [Deepest S wave in any precordial lead] + [S wave V4] > [28 mm for men ] or [23 mm women]; if deepest S wave is in V4, double this value
    • Sensitivity: 57%
    • Specificity: 90%
  • Summary Figure from Dr. Ken Grauer

🚨 OMI (+) with LVH:

2 examples below. Swipe ↔️ or use arrow keys to view more.
ECG
  • HPI: 40M with HTN presented with acute onset chest pain, diaphoresis and SOB
  • Cath: Thrombotically or embolically occluded RCA at bifurcation to the RPDA and RPLA.
  • Key ECG: It is tricky because it is in the setting of LVH. See V2: there is downsloping ST segment. The T wave in lead III Is too big for that small S wave. There is terminal QRS distortion in aVF. The STT in aVF is not discordant as you would expect with LVH, and there is a straight ST segment. The abnormal shape of the ST-T wave in lead V2 also constitutes a positive Mirror Test. Even without LVH — the taller-than-expected initial R wave in lead V2 and the ST-T wave appearance in this lead instantly suggested to me that posterior OMI was likely
  • Link to full case @ Dr. Smith’s ECG Blog: 2022-09-30

ECG
  • HPI:35F with 2 days progressive chest pain which worsened acutely
  • Cath: total thrombotic proximal LAD occlusion
  • Key ECG: There is large STE in V1-V3, as well as aVL. There is STD in V5-6, II, III, and aVF. None of this is diagnostic for OMI. The T waves are questionably hyperacute in V1-V4, but the QRS is also very tall and dramatic.
  • Link to full case @ Dr. Smith’s ECG Blog: 2022-08-15

✅ OMI Mimics due to LVH:

6 examples below. Swipe ↔️ or use arrow keys to view more.
ECG

  • Course: the patient ruled out for MI by serial troponin
  • Key ECG: It is a scary ECG, with a lot of ST Elevation and what appear to be hyperacute T-waves in inferior leads, and profound reciprocal ST Depression in aVL.  There are Q-waves in V4-V6, with what appear to be hyperacute T-waves.  Any objective, rule-based analysis of this ECG would scream “STEMI” or “OMI”.   The presence of deep, slender Q waves in so many leads — especially with the bizarre QrS morphology in leads V4,5,6 (with tiny r waves despite marked LVH in lead I) seems much more suggestive of some unusual form of underlying structural heart disease than of an acute MI pattern
  • Link to full case @ Dr. Smith’s ECG blog: 2023-07-05
ECG
  • HPI: 23M with no chest pain. Preseting s/p tased by police.
  • Key ECG: There is convex ST segment in V3 (STE convexity in any of leads V2-V6 is fairly specific sign of LAD occlusion), however in this case there is too much voltage in the QRS (deep S-wave in V3 especially). The T(volume)/QRS ratio is not large enough for the T-waves to be considered hyperacute. There is well formed J-point notching – a finding associated with benign repolarization changes.
  • Link to full case @ Dr. Smith’s ECG Blog: 2023-04-17
ECG
  • Key ECG: Whenever you see voltage like that, ST-T abnormalities which at first appear to be ischemic are probably simply secondary to the abnormal depolarization and due to LVH or some other baseline disease
ECG
  • HPI: 75 M w/ CAD, HFrEF presented for syncope without prodrome
  • Key ECG: High voltage on ECG correlates with abnormal ST segments. The S-wave in V2 is 50 mm; STE is 2.5; Ratio = 0.05, which is normal.
  • Link to full case @ Dr. Smith’s ECG Blog: 2020-06-02
ECG
  • HPI: 61M w/ epigastric pain followed by syncope
  • Key ECG: ST elevation in V1 and V2, with ST depression and T-wave inversion in V5, V6 should always make you think of LVH with chronic ST-T abnormalities, even if the voltage does not meet LVH criteria. STE in V1 and V2, with ST depression in V5 and V6 is a pattern that occurs in Septal OMI, but it looks different that this and does not have the deep lateral T-wave inversion (Typical subtle ECG of LAD occlusion, in which ST depression in V5, V6 make it far MORE likely to be OMI (whereas with deep T-wave inversion, it makes it less likely, and more likely to be LVH – see this example). The inferior ST depression is still worrisome for possible high lateral OMI however all troponins were undetectable
  • Link to full case @ Dr. Smith’s ECG Blog: 2020-02-06
ECG
  • HPI: Elderly woman with weakness. No chest pain
  • Key ECG: One could mistake this for an inferior-posterior STEMI, as there is ST elevation in lead III with reciprocal ST depression in aVL, and there is ST depression in V2 and V3 with a tall R-wave (the mirror image of a posterior Q-wave), however the high voltage in I, V2, V3 and aVL meet “criteria” for LVH. ST elevation in III is a scooped-out saddleback, and that is because the ST segment is long and flat, and thus the T-wave is not hyperacute; rather, it has a narrow base. Contrast it with this wide-based T-wave in a true inferior STEMI. But doesn’t all ST elevation with reciprocal ST depression in aVL mean Acute MI? No! Rciprocal STD in aVL is frequently found in these STEMI mimics: LVH, LBBB, inferior LV aneurysm, myocarditis.
  • Link to full case @ Dr. Smith’s ECG Blog: 2015-10-28

🔎 Specificity:

  • Specificity: 93% if 1-mm ST-segment elevation in any contiguous leads (2 mm if leads V1–V3), and ST-segment/R-wave ratio >25% for leads V1–V3
  • Source: PMID 22738872

⚠️ Note:

  • LV aneurysm should be suspected when there are QS-waves in any of leads V1-V4
  • A QS-wave means a single negative deflection, without any R-wave or with only a tiny r-wave.
  • Only about 70%-80% of patients with the ECG morphology of “LV aneurysm” actually have an LV aneurysm, as defined by echocardiographic dyskinesis.
  • “LV aneurysm” is far less common in this era of reperfusion, in which STEMI is not allowed to progress to full infarction
  • LV Aneurysm can be inferior, anterior, or posterior. Inferior aneurysm looks very much like acute MI because it does not get QS-waves, but rather QR-waves, which can also be present in acute MI.

🚨 Suggestive of OMI:

✅ Expected changes in LV Aneurysm:

  • In acute coronary occlusion, the T-wave is large, whereas in LV aneurysm, the T-wave is not so large. There are two pretty accurate formulas:
    • T/QRS ratio < 0.36 in any of leads V1 – V4
    • [TV1 + TV2 + TV3 + TV4] divided by [QRS V1 + QRS V2 + QRS V3 + QRS V4] < 0.22

🚨 OMI (+) with LV Aneurysm:

8 examples below. Swipe ↔️ or use arrow keys to view more.
ECG
  • HPI: Elderly woman p/w shortness of breath and recent stent placement
  • Echo: anterior and apical dyskinesis
  • Key ECG: There is sinus rhythm with RBBB. “Coved” ST in V3, V4, V5 with subtle ST elevation is highly suspicious for OMI but looking at the entire QRST, there ar eQR-waves in V1 and V2. LV Aneurysm has QS-waves. RBBB presence requires that there are R’-waves even in the presence of LV aneurysm. So, a patient with normal conduction and QS-waves who then develops RBBB will have QR-waves
  • Link to full case @ Dr. Smith’s ECG blog: (November 18, 2023)
    https://drsmithsecgblog.com/acute-dyspnea-and-right-bundle-branch/
ECG
  • HPI: Elderly male presented with chest pain. Was diagnosed with OMI and cath lab showed 100% occlusion of LAD. This EKG is one month post cath.
  • Echo: Mildly enlarged LV cavity size, normal wall thickness, severe LV systolic dysfunction. Regional wall motion abnormality-mid and apical septum, mid and apical anterior and true apex, thinned out and dyskinetic.
  • Key ECG: Anterior LV Aneurysm in the presence of RBBB
  • Link to full case @ Dr. Smith’s ECG blog: (October 6, 2023)
    https://drsmithsecgblog.com/what-is-infarct-artery-what-does-post/
ECG
  • HPI: 45M with chest pain x 6 hr
  • Cath: 100% proximal LAD occlusion
  • ECG: 1)There is a QS-wave in V2. That indicates old or subacute MI. But the patient has no previous cardiac history, so we must assume it is new, and so subacute, and that is consistent with the 6-hour duration of pain. 2) The T-wave is also large for old MI. My rule is that if any lead has a T/QRS ratio ＞0.36, then it is acute OMI; if ＜0.36, then either old MI (LV aneurysm) or subacute OMI. 3) There is ST depression in V3 and V4. Always abnormal. 4) There is coving of the ST segment in I and aVL, with large inverted T-waves and reciprocally upright large inferior T-waves (these actually suggest some reperfusion, but as the patient has persistent symptoms, one must assume there is continued ischemia). 5) The proximal LAD will affect the territory of the LAD and of the 1st diagonal, which supplies the high lateral wall, resulting in the findings in I and aVL, and the reciprocal findings in III and aVF.
  • Link to full case @ Dr. Smith’s ECG Blog: 2023-05-18
ECG

  • HPI: Middle aged man sent to ED for tachycardia
  • Cath: An occlusion of the proximal LAD was then found and intervened on.
  • Key ECG: The rhythm appeared to be atrial flutter, but also concerning were the ST segment elevations in I, aVL, V2, and V3, as well as ST depression in the reciprocal inferior leads. But atrial flutter can alter the baseline such that there is only apparent STE or STD. This pattern is concerning for anterior wall OMI, specifically a proximal LAD lesion. There are Q waves in V1-V3, suggesting an old anterior MI, but the T waves in V2 and V3 are fairly tall, suggesting some degree of acute ischemia. Also, there are no T wave inversions which would suggest a subacute, evolved, or reperfused MI. If there is one lead of V1-V4 with a T/QRS ratio greater than 0.36, it suggests acute MI. If less then 0.36, it suggests either subacute (over 6 hours) or old MI. In this case, the T/QRS ratio is largest in V3 at 5/9 = 0.55.
  • Link to full case @ Dr. Smith’s ECG Blog: 2018-09-24
ECG
  • HPI: middle aged woman presenting with pulmonary edeam, chest pain 2 wks earlier
  • Cath: 100% thrombotic mid-LAD occlusion was found; peak cTnT 8.7
  • Key ECG: This likely represents subacute STEMI. Dr. Smith’s rule for differentiating acute STEMI from LV aneurysm really only reliably distinguishes between: 1. acute STEMI on the one hand 2. subacute STEMI or LV aneurysm on the other. First, there must be ST Elevation. Second, the ECG differential diagnosis much be LV aneurysm vs. acute STEMI. When should LV aneurysm be on the ECG differential diagnosis? Primarily when there are well-formed Q-waves, with at least one QS-wave, in V1-V4. A QS-wave is defined by absence of any R-wave or r-wave of at least 1 mm. (If there is an R-wave or r-wave, we call the whole wave a QR-wave, Qr-wave, or qR-wave, depending on the relative size of the Q-wave vs. R-wave.) The rule: If there is one lead of V1-V4 in which the T/QRS ratio is greater than 0.36, then acute STEMI is the likely diagnosis, though subacute STEMI is also possible. Since both require the cath lab, if the ratio is greater than 0.36, and the clinical situation is right (i.e., unexplained chest discomfort), then cath lab activation is should be considered. If the formula were used here, then lead V4 would have a T/QRS ratio of 5/11.5 = 0.43. Only one lead is needed, so the criterion is met for acute STEMI. Really, however, LV aneurysm was never on Dr. Smith’s differential diagnosis when he glanced at this ECG. Why? It is true that there are QS-waves in all of V1-V4, which might lead you to believe it is LV aneurysm. However, this ECG has up to 4 mm of ST elevation (in V4, 4 mm STE is relative to an 11.5 mm S-wave), and Dr. Smith has never seen an LV aneurysm case with this much ST elevation.
  • Link to full case @ Dr. Smith’s ECG Blog: 2017-04-21

ECG
  • HPI: Middle aged man with chest pain x 48 hrs
  • Cath: 100% mid LAD occlusion which was stented.
  • Key ECG: There are QS-waves in leads V1-V3, and a QR in lead V4. It looks like anterior LV aneurysm, however the T/QRS ratio is greater than 0.36 in V4 (4mm/4mm = 1.0)
  • Link to full case @ Dr. Smith’s ECG Blog: 2012-05-12

ECG
  • HPI: 70 something patient started having chest pain about one hour prior to arrival. Had a “heart attack” about two weeks ago in a developing country and states that it feels like that same pain. There was some shortness of breath associated with. No recent sick symptoms. It had been managed medically in that country. BP 134/79
  • Cath: Culprit in the LAD spanning the first diagonal. Formal Echo showed LV aneurysm with thrombus
  • Key ECG: Reduced R wave progression between leads V3 with loss of R wave from V3-V4 and associated ST-T wave changes is diagnostic of anteroseptal infarction. Patient had a MI 2 weeks earlier. The limited amount of ST elevation of coved morphology, with associated T wave inversion in leads V2-V5 looks older rather than acute.
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/recurrent-and-refractory-chest-pain-after-infarct-in-a-developing-country
ECG
  • HPI: 66 yo M presented with chest pain, history of CAD
  • Cath: No culprit, all open arteries
  • Key ECG: T wave inversion in I and aVL is reciprocal to the old inferior aneurysm. Terminal S waves in lateral leads I and V6 consistent with incomplete RBBB. Shape of the ST segments in inferior leads is coved, of relatively long duration, and shows slight ST elevation. Inferior lead ST-T wave appearance is unlikely to be acute, further supported by lack of reciprocal ST depression in high lateral leads I and aVL.
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/what-do-you-think-of-these-2-ecgs-in/

🔎 Specificity:

⚠️ Note:

  • 30-60% of anterior OMIs do NOT have reciprocal STD in inferior leads (Sources: PMID 8213517, PMID 10440150, PMID 8682009, PMID 11195604)
  • The 🔢 4 Variable Formula can help distinguish subtle LAD occlusion from early repolarization
    • It is critical to use it only when the differential is subtle LAD occlusion vs. early repol
  • There must be ST Elevation of at least 1 mm in any of leads V2-V4.
    • If there is LVH, it may not apply. If there are features that make LAD occlusion obvious (inferior or anterior ST depression, convexity, terminal QRS distortion, Q-waves, or ST Elevation of 5 mm or more), then the formula MAY NOT apply. These kinds of cases were excluded from the study as they were recognized as obvious anterior STEMI.

🚨 Suggestive of OMI:

  • 4 variable formula value >18.2
  • Terminal QRS distortion

✅ Suggestive of “Benign” Early Repolarization:

  • Early repolarization always has prominent R-waves in V2-V4 (Source)

🚨 OMI (+) Subtle Anterior STE

8 examples below. Swipe ↔️ or use arrow keys to view more.
ECG
  • HPI: 60M with acute chest pain x 30 min, pale & diaphoretic
  • Cath: Large proximal LAD thrombus with TIMI-1 flow. It was a wraparound LAD, explaining the inferior ST elevation with reciprocal ST depression in aVL (the opposite of what you expect with a proximal LAD occlusion). It was stented.
  • 4V formula score: 18.38 (>18.2 is the most accurate cutoff suggestive of LAD OMI)
  • Key ECG: There is upward concavity. There is no STD. There are no Q-waves. There is no terminal QRS distortion. So early repolarization is a possibility, however, there is very suspicious STE in III and aVF, with STD in aVL. This makes the ECG nearly diagnostic of ischemia, though if it is LAD occlusion, there should be ST depression in III, so it is a bit confusing. Unless you consider a wraparound LAD.
  • Link to full case @ Dr. Smith’s ECG Blog: 2017-06-21
ECG
  • HPI: 35M with acute chest pain
  • Cath: Occlusion of the very distal LAD s/p thrombectomy 3V fomula score: 23.9 (>23.4 favors OMI)
  • Key ECG: This is highly suspicious for LAD occlusion, though not diagnostic. The 3V formula score is 23.9 (which is > 23.4 which is pretty specific for LAD occlusion). Consider frequent serial EKGs, every 15 minutes, for several hours, an emergent formal contrast echocardiogram and if still non diagnostic, consider immediate angiography. One might argue, with good rationale, that such a small MI can wait until the next day for angiogram.
  • Link to full case @ Dr. Smith’s ECG Blog: 2015-11-18

ECG
  • HPI: Acute onset chest pain x 20 min
  • Cath: 100% occlusion of the mid-LAD
  • Key ECG: On this ECG there is ST elevation in lead V2, and it must be explained. Is it benign? If it were benign, then there should be excellent R-wave progression. There is not. In fact, the R-wave gets smaller from V2 to V3. Furthermore, the T-waves are much more symmetric than the T-waves of early repolarization. If you plug these numbers into the 3V formula you get a value of 25 (Any value greater than 23.4 is suggestive of LAD OMI. Less than 4% of LAD occlusion have a value < 22.0.)
  • Link to full case @ Dr. Smith’s ECG Blog: 2014-12-12

ECG
  • HPI: 40M with 1.5 hr chest pain
  • Cath: 100% mid LAD occlusion after a large D1 3V formula score 22.6 (At a cutoff of 22.0, the sensitivity was 96% but with decreased specificity of 81%)
  • Key ECG: Note there is not enough ST elevation to meet the standard criteria, which require at least 2 mm ST elevation at the J-point, relative to the PQ jct., in leads V2 and V3 for a male over 40 years old. In this case, there is 1 mm in V2 and 2 mm in V3. The T-waves looked too fat to be normal. Even though the 3V formula was not greater than 23.4, at 22.6, it was close enough to be worried.
  • Link to full case @ Dr. Smith’s ECG Blog: 2014-11-22

ECG
  • HPI: 75F p/w “reflux”
  • Cath: culprit lesion of a large obtuse-marginal artery successfully stented
  • 3V formula score: 25.4 (>23.4 favors OMI)
  • Key ECG: There is a poor R-wave progression across the precordials (transition is between V4 and V5); subtle ST-elevation in V2-V4, I, and aVL; and reciprocal ST-depression in II, III, and aVF. Additionally, using the BER vs. anterior STEMI calculator on the right side of this page, the equation value of this tracing is 25.4, greater than 23.4 (using measurements of 2.7 mm, 400 ms, and 4.4 mm, respectively). This tracing is suggestive of anterior subepicardial ischemia, almost always due to LAD occlusion.
  • Link to full case @ Dr. Smith’s ECG Blog: 2014-04-18

ECG
  • HPI: 45M with CAD p/w 3 hr typical chest pain
  • 3V formula score: 23.9 (>23.4 favors OMI)
  • Key ECG: There is ST elevation and tall T-waves in precordial leads, with reasonably good R-wave progression. He is a 45 year old male, so this could be male pattern benign early repolarization (BER, or ER). But it could be anterior STEMI. 40% of anterior STEMI has upward concavity in all of leads V2-V6. How can one decide whether this is ER or MI? First, if an old ECG is available, then compare. Only rarely does early repolarization change from date to date, though it is possible.
  • Link to full case @ Dr. Smith’s ECG Blog: 2011-06-18

ECG
  • HPI: 46 yo male with acute onset of chest pain
  • 3V score: 24.1 (>21 favors OMI)
  • Cath: 100% proximal thrombotic LAD occlusion with TIMI-0 flow. It was opened and stented
  • Key ECG: When the DDx is Anterior MI vs BER, a simple rule is the R-wave rule: which depends on the fact that, in BER, the R-wave is always well developed
  • Link to full case @ Dr. Smith’s ECG Blog: 2009-06-10

ECG
  • HPI: A man in his 90s with a history of hypertension, chronic kidney disease, COPD, and OSA presented to ED after being found unresponsive at home
  • Cath: Preliminary findings documented in Cath lab were Anterior STEMI with no significant coronary artery disease
  • Key ECG: There is no T-QRS-D (terminal QRS distortion). There is loss of J wave and S wave (slur, J point equivalent) in lead V2
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/an-elderly-male-with-acute-altered/
  • Queen of Hearts: High confidence for NOT OMI

🔎 Specificity:

  • Specificity: 100% specific for LAD occlusion when there is terminal QRS distortion
  • Specificity: 94.7% specific for OMI when 4 variable formula value >18.2
  • Source: PMID 28460689
  • Source: PMID 27658331

🚨 Suggestive of OMI:

  • Any STD in AVL
  • Any reciprocal STD
  • STE in lead III > STE in lead II

✅ Suggestive of Pericarditis:

  • Diffuse STE without reciprocal STD (except in V1 or AVR)
  • STE in lead II > STE in lead III

🚨 OMI (+) Mimics of Pericarditis:

9 examples below. Swipe ↔️ or use arrow keys to view more.
ECG
  • HPI: 50M with acute chest pain x 1 hr
  • Cath: total thrombotic occlusion of the mid-LAD was opened and stented
  • Key ECG: There is sinus rhythm with normal QRS complex except slightly sluggish R wave progression (this is due to acute LAD OMI, diminishing the R wave voltage in its distribution). We see STE in V2-V4, and a hint of STE in II, III, and aVF. Hyperacute T waves are present in V2-V4, and II, III, and aVF. The T waves in V5 and V6 could also be increased in size and area compared to baseline, but no baseline was available. There is a small amount of reciprocal STD in aVL (reciprocal from lead III), as well as a reciprocally negative T wave which is inappropriate for that QRS. This is highly suggestive of acute transmural infarction of anterior, lateral, and apical LV areas.
  • Link to full case @ Dr. Smith’s ECG Blog: 2022-02-12
ECG
  • HPI: 24F with acute chest pain x 1 hr
  • Cath: the culprit was a proximal LAD lesion (open, with TIMI-3 flow)! It had embolized to the distal LAD, which was a “type III” or “wraparound” LAD supplying the inferor wall. So this was an antero-infero-lateral MI. The proximal lesion was stented and the distal was treated with antiplatelet and antithrombotic therapy.
  • Key ECG: Sinus rhythm. Inferior and lateral ST elevation with reciprocal ST depression in aVL. There is no significant PR segment depression. Some might suspect pericarditis in a young person with diffuse ST elevation.
  • Link to full case @ Dr. Smith’s ECG Blog: 2013-05-23
ECG
  • HPI: A woman in her 50s with no significant past medical history experienced acute anterior chest pain that woke her from sleep and radiated to her back. She described it as “stabbing”, 8/10, constant, and associated with nausea.
  • Cath: No significant coronary disease
  • Key ECG: Diffuse ST Elevation seen in leads I, II, III, aVF, and in leads V3-V6
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/a-woman-in-her-50s-with-acute-chest-pain-2/
  • Queen of Hearts: No signs of STEMI
ECG
  • HPI: 67 yo M with history of HTN presented with 3 days of chest pain radiating to his back. Also had nausea, vomiting, dyspnea
  • Cath: — not recorded in source —
  • Key ECG: Absence of large T waves or any STD in aVL (seen in inferior OMI). No reciprocal depression. STE spanning from lead I all the way to lead III (diffuse). PR depression in leads I, II, V4-V6. Downsloping TP segment (Spodick’s sign) in leads V3-V4. STE has a more concave morphology. End QRS slurring in II, aVF, V6. STE in lead II is greater than the STE in lead III. Rate is tachycardic.
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/acute-chest-pain-and-st-elevation/
  • Queen of Hearts: Mid Confidence this is NOT OMI
ECG
  • HPI: 82 yo M with a history of HTN presented to ED with chest pain at 1211. He described the chest pain as pleuritic and reported it started one day prior while swinging a gof club
  • Cath: — not recorded in source —
  • Key ECG: New ST elevations throughout the proximal LAD distribution. All leads with ST elevation have very concave ST-T complexes, with flat ST segments. The ST elevation is diffuse. Leads III and V1 are isoelectric, but all other leads have some ST elevation.
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/what-would-you-do-with-acute-chest-pain/
  • Queen of Hearts: Not OMI with high confidence
ECG
  • HPI: A woman in her 70s with a previous PMHx of HTN and HLD. Presented to an outside hospital after several days of malaise and feeling unwell. EKG on admission showed subacute completed inferior, lateral, and posterior transmural infarction. Patient awoke suddenly during the night before angiography and stated she felt “strange”
  • Cath: — not recorded in source —
  • Key ECG: This EKG is consistent with infero-postero-lateral infarction with persistent inferior STE and reciprocal high-lateral STD. STD in lead V2. Some terminal T wave inversion in inferior/lateral chest leads. Not significantly different from admission EKG. However, this EKG showed an increase in heart rate showing sinus tachycardia at 118 bpm. Admission heart rate was 80s bpm. There are still upright, not inverted, T waves. Persistent STE with upright T waves >48 hours after myocardial infarction is associated with post-infarction regional pericarditis
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/why-sudden-shock/
  • Queen of Hearts: Not listed
ECG
  • HPI: A man in his 40s presented to the ED with 1 day history of sudden onset chest pain. 2 weeks ago he had a significant MVC with many severe injuries, including aortic injury s/p endovascular repair
  • Cath: — not recorded in source —
  • Key ECG: Sinus rhythm with abnormal STE in V2-V6, and I, II, aVF. Reciprocal STD in aVR and V1. Most leads with STE have non-hyperacute, flat T waves. PR depression in II and reciprocal PR elevation in aVR. Terminal QRS distortion in V4-V6
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/what-does-this-ecg-show/
  • Queen of Hearts: High confidence NOT OMI
ECG
  • HPI: A man in his 30s presented for similar symptoms (acute substernal chest pain) twice, each visit one year apart. History includes acute substernal chest pain, shortness of breath, and diaphoresis, within 3 hours of onset. Obesity, but no other cardiac risk factors
  • Cath: — not recorded in source —
  • Key ECG: STE in lead II is far higher than III and there is no reciprocal STD in aVL. Diffuse ST elevation in 9/12 leads, PR depression in multiple leads and PR elevation in aVR. Normal R wave progression
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/acute-chest-pain-2-years-in-a-row/
  • Queen of Hearts: Not OMI
ECG
  • HPI: A man in his late 60s was convalescing in the hospital following bilateral lung transplantation for pulmonary fibrosis. Medical history is significant for rheumatoid arthritis and chronic steroid use (risk factor for CAD)
  • Cath: None
  • Key ECG: Extreme convexity of all leads with ST elevation preceded by a very flat ST segment that rapidly turns upward, creating a narrow base to the T wave. STE in I and aVL may indicate proximal LAD occlusion but it is not associated with inferior ST depression. STE in lead II however is unusual in proximal LAD OMI.
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/stemi-positive-by-conventional-algorithm-in-a-high-risk-post-operative-patient/
  • Queen of Hearts: No OMI with low confidence

🔎 Specificity:

  • Specificity: 100% specific for OMI if any STD in AVL
  • Source: PMID 26542793

⚠️ Note:

  • Pulse Tapping Artifact is caused by rhythmic tapping of an arterial pulse or cardiac pulsatation to an overlying electrode. If the culprit electrode is one of the extremity electrodes (as is frequently the case) the standard leads using this electrode show abnormal waves coinciding with ST-segment or T-waves. Notably, the remaining standard lead will be spared.

✅ Suggestive of Pulse Taping Artifiact:

  • Diffuse, bizarre ST-segments or T-waves in all but one lead (usually I, II or III)

🔎 Identifying the Culprit Electrode

For artifact arising from a limb electrode:

  • Look for the augmented limb lead (aVR, aVL, or aVF) with the greatest artifact – this points toward the culprit electrode.
  • Then look for the bipolar limb lead (I, II, or III) that is relatively spared – this provides a second clue to the culprit electrode.
  • RA electrode: maximal artifact in aVR, with lead III relatively spared
  • LA electrode: maximal artifact in aVL, with lead II relatively spared
  • LL electrode: maximal artifact in aVF, with lead I relatively spared
  • Repositioning or replacing the culprit electrode should eliminate the artifact.

✅ OMI (-) mimics from artifact:

10 examples below. Swipe ↔️ or use arrow keys to view more.
ECG
  • HPI: 60 yo diabetic with chest pain
  • Cath: No significant obstructive disease in the LAD, LCX, and RCA
  • Key ECG: Look at leads I, II, and III. If one of them does not look bizarre, while all other 11 leads do look bizarre, then it is arterial pulse tapping artifact where likely the LL electrode was placed over an artery
  • Link to full case @ Dr. Smith’s ECG blog: (September 15, 2023)
    https://drsmithsecgblog.com/a-60-year-old-diabetic-with-chest-pain/
  • Queen of Hearts: Not OMI with high confidence
ECG
  • HPI: 50F with chest pain and SOB
  • Key ECG: All other leads are very weird. In pulse tapping artifact, one of lead I, II, and III will be normal. When the ECG in front of you looks “funny” — Think of the possibility of artifact sooner rather than later. Repeat the ECG before you consider activating the cath lab.
  • Link to full case @ Dr. Smith’s ECG Blog: 2023-03-17

ECG
  • HPI: 60M with chest pain
  • Key ECG: Whenever you see a bizarre ECG, look at leads I, II, and III. See if one of them does NOT look bizarre. In this case, lead I does not look bizarre, but all other leads do. Since lead I looks relatively normal, that means that the right arm and left arm electrodes must be OK. It is the left leg electrode that is abnormal. The amplitude of the artifact from a single extremity source, is maximal in the unipolar augmented electrode of the “culprit” extremity. The amplitude of the artifact in the other 2 augmented leds (ie, leads aVR and aVL) — is about 1/2 the amplitude of the artifact in lead aVF.
  • Link to full case @ Dr. Smith’s ECG Blog: 2023-01-17

ECG
  • HPI: Elderly septic patient
  • Key ECG: If ever you see a bizarre appearance for 2 of the 3 standard limb leads (ie, leads I,II,III) — with the 3rd standard limb lead looking relatively (if not completely) appropriate — Think Artifact! Since lead II is the only normal lead in this ECG, the left arm electrode must be the affected electrode. Indeed, the patients dialysis fistula was on the left arm and was pulsating with each heart beat, moving the electrode and causing artifact. Since the cause of the Pulse-Tap Artifact is contact of one of the limb lead electrodes with a pulsating artery below it — the bizarre deflection that you suspect is artifact will have a fixed relationship to neighboring QRS complexes. You can prove the “culprit extremity” cause of artifact by demonstrating that artifact deflections are no longer present after repositioning the limb lead electrodes.
  • Link to full case @ Dr. Smith’s ECG Blog: 2022-12-05

ECG
  • Key ECG: Whenever you see a very bizarre EKG, you should think about pulse tapping artifact. When you suspect this, your next task is look for the one lead among leads I, II, and III which is NOT bizarre.
  • Link to full case @ Dr. Smith’s ECG Blog: 2022-11-08

ECG
  • HPI: Middle aged adult with acute chest pain
  • Key ECG: The 1st thing to notice is that there is a tremendous amount of baseline artifact. This is especially true in the limb leads — where none of the seemingly elevated and depressed ST segments look the same. In the long lead V1 rhythm strip — each of the 10 beats manifest a different variation on the shape of the ST segment. When there is much artifact elsewhere on a tracing — the chances increase greatly that artifact is also affecting the ST segments you are concerned about. CLUE #2: The shape of the elevated and depressed ST segments in the limb leads is bizarre. The ST segment is jagged in the 2 limb leads with ST elevation (ie, leads I, aVL) — and the deepest part of the depressed ST segments in leads III and aVF is almost pointed. CLUE #3: The shape of the depressed ST segments in all 6 chest leads looks very similar (ie, with a “rounded scoop”, showing approximately the same amount of ST depression in each of these 6 leads — as highlighted in GREEN). The presence of geometric shapes (in this case, the “rounded scooping”) — is also unlikely to be physiologic. CLUE #4: All of the above described unusual shapes (ie, the peak of the ST elevation in leads I,aVL — the negative peaking in leads III and aVF — and the lowest part of the rounded GREEN scoopings) — occur at a fixed interval with respect to the preceding QRS complex. This suggests us that whatever is producing these deflections must be related to cardiac contraction (and/or to arterial pulsation)! CLUE #5: The distribution in ECG #1 of the bizarre ST-T wave deflections precisely follows the location and relative amount of amplitude distortion predicted by Einthoven’s Triangle.
  • Link to full case @ Dr. Smith’s ECG Blog: 2022-08-26
ECG
  • HPI: A dialysis patient with dyspnea
  • Key ECG: The artifact manifests a FIXED relationship to the QRS complex — therefore, it has to be related to the heart beat (or to arterial pulsations); ii) Although in opposite directions, the AMPLITUDE of the artifactual deflection in limb leads I and III is equal — but there is no artifact at all in lead II.
  • Link to full case @ Dr. Smith’s ECG Blog: 2018-01-30
ECG
  • HPI: 66 yo M presented with chest pain, history of CAD
  • Cath: No culprit, all open arteries
  • Key ECG: T wave inversion in I and aVL is reciprocal to the old inferior aneurysm. Terminal S waves in lateral leads I and V6 consistent with incomplete RBBB. Shape of the ST segments in inferior leads is coved, of relatively long duration, and shows slight ST elevation. Inferior lead ST-T wave appearance is unlikely to be acute, further supported by lack of reciprocal ST depression in high lateral leads I and aVL.
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/what-do-you-think-of-these-2-ecgs-in/
ECG
  • HPI: An elderly woman presented with one day of chest and right arm pain, also abdominal pain. Associated with tingling and numbness in the right hand and generalized weakness, worse on the right side
  • Cath: 100% occluded ramus intermedius
  • Key ECG: Widespread artifact, except in lead III. Since lead III is not artifactual, one can deduce that the artifact is caused by movement of the right arm electrode, so the electrode should be moved and the EKG re-recorded. Repeat EKG showed STE in inferior leads, including lead III.
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/chest-or-abdominal-pain-and-ecg-artifact/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: A man in his 40s presented with acute chest pain
  • Cath: Activated, but repeat EKG showed resolved artifact so cath lab was deactivated.
  • Key ECG: EKG shows dramatic artifact originating from the left arm electrode. Lead II is the only normal/unaffected limb lead present, meaning that there is no significant artifact coming from the electrodes that compose it: RA and LL. All other leads are affected by the artifact which must be coming from the LA electrode
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/acute-chest-pain-activate-the-cath-lab/

🎥 Watch: How to identify the culprit electrode in ECG artifact

OMI not meeting STEMI criteria:

⚠️ Note:

  • Wellens’ syndrome is a syndrome of Transient OMI, in which the ECG was not recorded at the time of the anginal pain, but only after spontaneous resolution of the pain, at which time the ECG shows reperfusion T-waves in the LAD distribution. 
    • Pattern A = terminal T-wave inversion (biphasic)
    • Pattern B shows deep symmetric T-wave inversion. 
  • Wellens’ syndrome also requires preservation of R-waves

🚨 OMI (+) Wellens Examples:

18 examples below. Swipe ↔️ or use arrow keys to view more.
ECG
  • HPI: 50-something male with HTN and 20- to 40-year smoking history presented with 1 week of stuttering chest pain that is worse with exertion, which takes many minutes to resolve after resting and never occurs at rest. It was present on arrival at triage but then resolved before bed placement in the ED
  • Cath: Ruptured plaque in mid LAD
  • Key ECG: Biphasic, terminal T wave inversion with an initial upsloping ST segment, preserved R waves
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/chest-pain-resolved-does-it-need/
  • Queen of Hearts: Low confidence for OMI
ECG
  • HPI: 40 year old male with no cardiac history presented with acute substernal chest pain. He was given NTG sublingually. Original EKG showed HATW pattern consistent with LAD OMI. Pain eventually resolved and repeat EKG was done.
  • Cath: 95% stenosis of LAD
  • Key ECG: Subtle terminal T-wave inversion in V3-V6. This is diagnostic of full reperfusion
  • Link to full case @ Dr. Smith’s ECG blog: (September 22, 2023)
    https://drsmithsecgblog.com/this-ecg-was-texted-to-me-normal/
  • Queen of Hearts: Not reported for this EKG
ECG
  • HPI: 40F with intermittent chest pain
  • Cath: 99% acute proximal LAD thrombosis. It was opened and stented.
  • Key ECG: There is deep T-wave inversion in proximal LAD territory (V2-V4, I, aVL) that is all but diagnostic of Wellens’. This is acute ACS, but it almost always seen in a pain free state. Since the patient has active pain now, if this is indeed Wellens,’ she must be re-occluded at this moment.
  • Link to full case @ Dr. Smith’s ECG Blog: 2023-03-13

ECG
  • HPI: 60F with intermittent chest pain x 2 days. ECG recorded after nitro which relieved chest pain
  • Cath: Culprit is 90% stenosis in the proximal LAD
  • Key ECG: This is classic Wellens’ pattern B morphology, and fits with the entire presentation
  • Link to full case @ Dr. Smith’s ECG Blog: 2022-08-12

ECG
  • HPI: 70M with central chest pain, resolving at time of ECG
  • Cath: Proximal LAD had an ulcerated plaque with 90% stenosis, TIMI II-III flow s/p successful PCI
  • Key ECG: terminal T-wave inversion in V2. This is very subtle Wellens’
  • Link to full case @ Dr. Smith’s ECG Blog: 2022-02-29

ECG
  • HPI: 55M with exertional chest pain, worse on day of presentation
  • Cath: Moderate hazy Eccentric plaque in the ostial/proximal LAD assessed via intravascular ultrasound (IVUS), which showed that the lesion on the Proximal LAD had 50% stenosis but without evidence of ruptured plaque.
  • Key ECG: classic Wellens’ pattern A (biphasic, terminal T-wave inversion), and it is Wellens’ syndrome (Angina, resolved — pain free — with preserved R-waves and Wellens’ pattern A T-waves). The morphology of these T-waves is very distinct. The pattern manifests a rising ST segment with a sudden fall into the slightly negative T-wave
  • Link to full case @ Dr. Smith’s ECG Blog: 2021-01-28

ECG
  • HPI: 40M with squeezing chest pain, resolved at time of ECG
  • Cath:90% thrombotic proximal LAD lesion that was stented
  • Key ECG: terminal T-wave inversion in V2 and V3
  • Link to full case @ Dr. Smith’s ECG Blog: 2019-09-22

ECG
  • HPI: 50M with intermittent substernal chest pain, resolved at time of ECG
  • Cath: 80% thrombotic occlusion of the LAD with TIMI II flow
  • Key ECG: terminal T-wave inversion after resolution of chest pain
  • Link to full case @ Dr. Smith’s ECG Blog: 2017-07-23

ECG
  • HPI: 50M with intermittent squeezing chest pain, asymptomatic at time of ECG
  • Cath:80% mid-LAD active lesion which was stented
  • Key ECG: There is very subtle Wellens’ waves in V2, less subtle in V3, still less in V4. This is nearly diagnostic of Wellens’ syndrome: pain that resolves, biphasic T-waves with preservation of R-waves. It extends all the way out to V6, and there is some T flattening in I and aVL, so this is probably a proximal LAD lesion
  • Link to full case @ Dr. Smith’s ECG Blog: 2013-11-15
ECG
  • HPI: 40M with intermittent chest pain, resolved at time of ECG
  • Cath: 95% stenotic LAD with TIMI-3 flow. A stent was placed.
  • Key ECG: There are Wellens’ waves, type A (upsloping ST segment then inversion of the terminal part of the T-wave – terminal T-wave inversion, or biphasic T-waves) in V2-V4, and aVL. Type B waves are deeper and symmetric.
  • Link to full case @ Dr. Smith’s ECG Blog: 2013-03-19

ECG
  • HPI: 55M with 4 days intermittent chest pain,
  • Cath: no culprit, 50-60% narrowing of the proximal LAD with high plaque burden, the vessel reoccluded on hospital day 3 with clear ST elevation for which pt recieved stent
  • Key ECG: There is a suggestion of terminal T-wave inversion in V2, highly suggestive for early Wellens’ syndrome. There is T-wave inversion in I and aVL highly suggestive of ACS.
  • Link to full case @ Dr. Smith’s ECG Blog: 2011-10-29

ECG
  • HPI: 55M with 4 days intermittent chest pain,
  • Cath: no culprit, 50-60% narrowing of the proximal LAD with high plaque burden, the vessel reoccluded on hospital day 3 with clear ST elevation for which pt recieved stent
  • Key ECG: There is a suggestion of terminal T-wave inversion in V2, highly suggestive for early Wellens’ syndrome. There is T-wave inversion in I and aVL highly suggestive of ACS.
  • Link to full case @ Dr. Smith’s ECG Blog: 2011-10-29

ECG
  • HPI: 60 yo M who presented with apparent tonic clonic seizure, no history of seizures. First responders found him to be very tachycardic, confused, perserverating, and no memory of event. There was tongue biting, lightheadedness continued. Had been having chest pain on and off for 1 week.
  • Cath: Uncertain culprit, myocardial territory served by the apical LAD is disproportionately large compared to troponin elevation. Diagonal branch supplying collaterals to the apicalal LAD could also represent a culprit
  • Key ECG: Terminal T-wave inversion (Wellens morphology Pattern A) in lead V2, upsloping ST segment with sharp downturn into negative T wave. Slight ST elevation in aVL with terminal T wave inversion, and reciprocally upright large T waves in inferior leads
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/seizure-in-60-year-old-male/
  • Queen of Hearts: High confidence for OMI
ECG
  • HPI: 30 yo African American male presented to the ED with chest pain that occurred the day before. 6-7/10 in intensity and lasted for 10 minutes, associated with strenuous activity. It radiated to the left arm and was associated with SOB
  • Key ECG: Episode of anginal chest pain that is resolved, preserved R waves, terminal T wave inversion (biphasic T waves) which is pattern A
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/what-is-wellens-syndrome-and-what-2/
  • Queen of Hearts: Reperfused OMI
ECG
  • HPI: 60 year old M with no reported PMHx presented to the ED for evaluation of chest pain. He had been experiencing substernal, exertional chest pain that resolves with rest.
  • Cath: Found to have 100% RCA occlusion. This EKG is post PCI
  • Key ECG: Subtle biphasic terminal T wave inversion in the inferior and lateral territories, Wellens Pattern A
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/can-you-spot-this-subtle-but-important/
  • Queen of Hearts: Did not detect reperfusion or active OMI
ECG
  • HPI: 90 yo M with history of HTN, HLD, and stroke with mild memory difficulty who presented to his PCP complaining of left shoulder pain radiating down the arm. Pain is often produced by activity but sometimes comes on a rest.
  • Cath: Patient received overlapping stents covering the entire length of the RCA into the PDA
  • Key ECG: Biphasic T waves in II, III, aVF, and to some extent V5-V6
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/what-happens-when-clinic-does-not-have/
  • Queen of Hearts: Low confidence for reperfusion
ECG
  • HPI: 50-something woman with history significant for HTN presented to ED with 1 week of intermittent chest pain. Sudden onset of central chest pain described as sharp and rated 10/10 pain 6 days ago while at rest.
  • Cath: N/A
  • Key ECG: Lead V2 ST segment is straightened, and although there is no significant ST elevation, we see the biphasic T wave characteristic of Wellens’ syndrome. Consistent with recent LAD OMI, ST segment coving with terminal T wave inversion in neighboring leads V1 and V3. Subtle T wave inversion persists in V4-V6.
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/severe-chest-pain-serial-troponins-nearly-undetectable-at-3-ng-l/
  • Queen of Hearts: Reperfused OMI
ECG
  • HPI: 80-year-old man with a history of hypertension and paroxysmal atrial fibrillation contacted EMS due to episodes of chest pain. He stated he had been experiencing recurring episodes of chest pain over the last couple of days, lasting from a few minutes to half an hour. On the day of presentation, the CP became more intense, prompting him to seek medical attention. When EMS arrived, the pain had improved, and after administration of ASA and NTG, he reported complete symptom relief.
  • Cath: Critical LAD stenosis with TIMI III flow
  • Key ECG: There is sinus bradycardia at 50 bpm. QRS complexes are narrow. There is no ST-segment elevation. There are terminal T wave inversions in leads V3–V5. These slight TWI in the setting of resolved chest pain, is most consistent with early post-ischemic reperfusion changes. Pattern A requires resolution of chest pain and terminal T wave inversion which evolve into Pattern B with deep symmetric T wave inversion
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/an-80-year-old-with-intermittent-cp/
  • Queen of Hearts: NSTEMI low confidence

⚠️ OMI (-) Wellens Mimic | RH Strain:

6 examples below. Swipe ↔️ or use arrow keys to view more.
ECG
  • HPI:  80-something woman who presented with chest pain and dyspnea
  • Course: acute MI was ruled out by serial troponins
  • ECG: There are small Q waves in leads III and aVF. These are probably not significant. Regarding R wave progression — the QRS complex in lead V1 is not “normal”. Instead — there is what appears to be an rsR’ configuration, with essentially no negative deflection following the R’. In adults — it is not normal for the R wave in right-sided lead V1 to be taller than the S wave is deep. This is because of left ventricular predominance in adults. As a result — the finding of a Tall R Wave in Lead V1 (ie, R=S or R>S in V1) should prompt the following diagnostic considerations: i) WPW; ii) RBBB; iii) RVH; iv) Posterior MI; v) HCM (Hypertrophic CardioMyopathy); and, vi) Normal Variant (which is a diagnosis of exclusion!). As per Dr. Smith — there also appears to be RVH in ECG #1 — because there is a predominant R wave in lead V1 + a rightward axis + incomplete RBBB + low voltage + ST-T wave abnormalities in anterior leads potentially consistent with RV “strain” — with this making 4 ECG findings potentially consistent with RVH in this patient who presented with acute dyspnea
  • Link to full case @ Dr. Smith’s ECG Blog: 2023-07-7
ECG
  • Key ECG: Pathognomonic for acute severe R heart strain (the most common etiology by far being acute PE). V2-V3 have the most important pathognomonic morphology here, with the small R wave followed by large S wave, then slightly convex ST segment followed by terminal-to-whole T wave inversion. Paired with the classic simultaneous “inferior and anterior” T wave inversion
  • Note: Kosuge’s study found that ALL cases of PE with precordial T-wave inversion have an inverted T wave in lead III and ALL cases of MI have an upright T wave in lead III:
  • Source: Dr. Smith’s ECG Blog:
ECG
  • Key ECG: Pathognomonic for acute severe R heart strain (the most common etiology by far being acute PE). V2-V3 have the most important pathognomonic morphology here, with the small R wave followed by large S wave, then slightly convex ST segment followed by terminal-to-whole T wave inversion. Paired with the classic simultaneous “inferior and anterior” T wave inversion
  • Note: Kosuge’s study found that ALL cases of PE with precordial T-wave inversion have an inverted T wave in lead III and ALL cases of MI have an upright T wave in lead III:
  • Source: Dr. Smith’s ECG Blog: 2021-03-30
ECG
  • Key ECG: Pathognomonic for acute severe R heart strain (the most common etiology by far being acute PE). V2-V3 have the most important pathognomonic morphology here, with the small R wave followed by large S wave, then slightly convex ST segment followed by terminal-to-whole T wave inversion. Paired with the classic simultaneous “inferior and anterior” T wave inversion
  • Note: Kosuge’s study found that ALL cases of PE with precordial T-wave inversion have an inverted T wave in lead III and ALL cases of MI have an upright T wave in lead III:
  • Source: Dr. Smith’s ECG Blog: 2021-03-30
ECG
  • Key ECG: Pathognomonic for acute severe R heart strain (the most common etiology by far being acute PE). V2-V3 have the most important pathognomonic morphology here, with the small R wave followed by large S wave, then slightly convex ST segment followed by terminal-to-whole T wave inversion. Paired with the classic simultaneous “inferior and anterior” T wave inversion
  • Note: Kosuge’s study found that ALL cases of PE with precordial T-wave inversion have an inverted T wave in lead III and ALL cases of MI have an upright T wave in lead III:
  • Source: Dr. Smith’s ECG Blog: 2021-03-30
ECG
  • Key ECG: Pathognomonic for acute severe R heart strain (the most common etiology by far being acute PE). V2-V3 have the most important pathognomonic morphology here, with the small R wave followed by large S wave, then slightly convex ST segment followed by terminal-to-whole T wave inversion. Paired with the classic simultaneous “inferior and anterior” T wave inversion
  • Note: Kosuge’s study found that ALL cases of PE with precordial T-wave inversion have an inverted T wave in lead III and ALL cases of MI have an upright T wave in lead III:
  • Link to full case @ Dr. Smith’s ECG Blog: 2021-03-3

⚠️ OMI (-) Wellens Mimic | Takotsubo:

7 examples below. Swipe ↔️ or use arrow keys to view more.
ECG
  • HPI: 60F presenting with aggitation s/p benzodiazepine overdose
  • Key ECG: This is almost certainly takotsubo. The widespread bizarre T-wave inversion with very prolonged QT interval is classic for takotsubo cardiomyopathy. Most people will say “Wellens?” to this ECG, but the T wave inversions are too big, the QT too long and too bizarre for Wellens’ (which is due to spontaneous reperfusion of OMI). Moreover, Wellens’ would involve just one territory, and Wellens’ of the LAD would be V2-V4 with possible extension to V5-V6 and to I, aVL if it is a proximal LAD lesion; but it could exend to II, III, aVF if it is an LAD that “wraps around” to the inferior wall (“wraparound, or Type III, LAD).
  • Source: Dr. Smith’s ECG Blog: 2022-09-19
ECG
  • HPI: Abdominal pain, no chest pain
  • Key ECG: It is possible that it is due to ACS, but the bizarre diffuse T-wave inversions with a very long QT are nearly pathognomonic of takotsubo. (They can also be seen in apical hypertrophic cardiomyopathy, but this patient did not have any such history and previous ECGs were different)
  • ⚠️ Note: it is unclear if this case truely represents Takotsubo. Echo revealed no WMA. Cath revealed 3VD for which patient was scheduled for CABG. Link to full case below.
  • Source: Dr. Smith’s ECG Blog: 2021-07-31
ECG
  • HPI: 50 something with abominal pain, no chest pain
  • Key ECG: Bizarre T-waves, with T-wave inversion and extremely long QT. The computer measures the QT at 506 ms, but it really is more like 560-580 ms, with a QTc of 600-620 ms. This is not at all typical of ACS but very typical of takotsubo or stress cardiomyopathy. Takotsubo may manifest T-wave inversion, but also STE that mimics STEMI. Although earlier work had suggested that ECG criteria might distinguish this STE from anterior STEMI,(57) recent literature does not support this result.(58 59) Many anterior STEMI, especially due to wraparound LAD to the inferior wall, have similar ECG findings and also apical ballooning. Therefore, coronary angiography is often essential to rule out acute coronary occlusion, even when the STE pattern and cardiac ultrasound both suggest Takotsubo.
  • Source: Dr. Smith’s ECG Blog: 2020-03-25
ECG
  • HPI: 60M admitted for GIB c/b hemodynamic instability
  • Key ECG: There are bizarre inverted T-waves and also inverted U-waves (see the 2nd inverted bump?). The QT is incredibly long. There is some subtle STE in inferior leads but also STE in I, aVL. There is STE before the bizarre TU inversion in leads V3-V6.
  • Source: Dr. Smith’s ECG Blog: 2019-07-24
ECG
  • HPI: 60F with 3/10 chest pain
  • Key ECG: The inverted T-waves are too big, too broad, too bizarre to be reperfusion T-waves or pulmonary embolism pattern alone. These T-waves are very suggestive of Takotsubo cardiomyopathy.
  • Source: Dr. Smith’s ECG Blog: 2018-10-01
ECG
  • HPI: Elderly woman with chest pain
  • Key ECG: Very wide, rather bizarre inverted T-waves. These are very typical of takotsubo
  • Source: Dr. Smith’s ECG Blog: 2018-01-22
ECG
  • HPI: Elderly smoker with abdominal pain and syncope
  • Key ECG: There is bizarre T-wave inversion with very long QT in all these leads. These are typical of Takotsubo or CNS catastrophe.
  • Source: Dr. Smith’s ECG Blog: 2017-10-22

⚠️ Note:

  • In cases of limited inferior wall injury, the ST vector of inferior MI localizes the area of infarction and is typically directed inferiorly and rightwards (yellow arrow)
  • The ST vector of subendocardial ischaemia does not localize to the ischaemia and regardless of involved coronary region directs to lead aVR (blue arrow)
  • The resultant average ST vector directs rightwards, causing ST elevation only in lead III and aVR (red arrow)

🚨 Aslanger pattern:

The following pattern may indicated a limited inferior OMI with multivessel disease in the right clinical context:

  • STE only in lead III
  • ST segment in V1 > V2
  • ST-depression (STD) in V4-V6, with a positive/terminally positive T-wave

🚨 OMI (+) Aslanger Pattern:

4 examples below. Swipe ↔️ or use arrow keys to view more.
ECG
  • HPI: 40-something with abdominal upset x 1 week
  • Cath: Severe 3 vessel Coronary artery disease involving the LAD; 100% mid LCX occlusion; first troponin 3000 ng/L
  • Key ECG: This is Aslanger’s pattern. You’d better get an angiogram or at least a stat echo. There is single lead STE in III, with recipocal STD in aVL (inferior OMI). There is STD in V3-V6 diagnostic of subendocardial ischemia. Aslanger pattern, even if the STE is less than 1 mm (with reciprocal STD in aVL), is diagnostic of OMI in the right clinical situation. This presentation has a low pretest probability, so obtaining an echo is wise, UNLESS the troponin comes back diagnostic, as in this case
  • Link to full case @ Dr. Smith’s ECG Blog: 2021-08-10
ECG
  • HPI: A woman in her 50s presented with acute chest pain and shortness of breath
  • Cath: Ostial LAD occlusion
  • Key ECG: STE and/or HATW in V1-V2, with reciprocal STD and/or TWI in V5-V6. Septum is ischemic with corresponding ST elevation from left to right in the septum resulting in STE in V1. Evidence of inferior OMI in lead III, with STE and HATW, but with STD in I, II, aVF, V4-V6.
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/a-woman-in-her-50s-with-chest-pain-no-diagnostic-ste-that-worthless-diagnosis-nstemi-what-is-it-and-what-happened/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 63 yo M PMHx CAD and PAD from T1DM p/w DKA to the ED. In ED, pt developed acute dyspnea at rest and mild continuous crushing chest pain.
  • Cath: Severe 2 vessel CAD (90% proximal circumflex, 70% mid/distal RCA) in the setting of NSTEMI.
  • Key ECG: ST depression vector towards leads V5 and II, leads aVF and II cannot manifest STE or hyperacute T wave from the inferior OMI. STD vector includes these leads and cancels out the STE of inferior OMI. Only lead III can have STE.
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/infection-and-dka-then-sudden-dyspnea/
  • Queen of Hearts: OMI with high confidence
ECG
  • HPI: 70-year-old man presented to the emergency department at time zero with persistent retrosternal chest pain of approximately 6 hours’ duration, accompanied by shortness of breath. He was an active cigarette smoker. His past medical history was significant for hypertension, ischemic heart disease, and heart failure. He had experienced a similar episode of chest pain approximately 2 months earlier
  • Cath: Not able to reach the cath table
  • Key ECG: Aslanger’s pattern (which is inferior OMI, with STE in single limb lead III, simultaneous with subendocardial ischemia (profound ST depression in V5-6). Posterior OMI – profound ST depression in V2.
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/if-you-cant-listen-to-a-good-student-your-patient-might-be-in-trouble/
  • Queen of Hearts: OMI high confidence

⚠️ Note:

  • High lateral STEMI is associated with a pattern of ST elevation caused by acute occlusion of the first diagonal branch of the left anterior descending coronary artery (LAD-D1).
  • With the 4×3 display of the 12-lead ECG, the location of the most impressive ST deviations resemble the shape of the South African flag

🚨 South African Flag :

  • STE in I, aVL, (+/-) V2
  • STD or TWI in III (or other inferior leads)

🚨 OMI (+) South African Flag Pattern:

12 examples below. Swipe ↔️ or use arrow keys to view more.
ECG
  • HPI: 50 yo M presenting with chest pain for 1 hour radiating to the back and jaw
  • Cath: 80% mid LAD stenosis, first diagonal artery with 95% stenosis
  • Key ECG: There’s normal sinus rhythm, normal conduction, normal axis, normal R wave progression and normal voltages. There’s clear T wave inversion in III/aVF, which is reciprocal to subtle ST elevation and hyperacute T waves in I/aVL (broad, symmetric, and larger than the entire QRS in aVL). There is also straightening of the ST segments in I/aVL, and some ST depression in V3.This is diagnostic of Occlusion MI of the high lateral wall, either from circumflex or first diagonal.
  • Link to full case @ Dr. Smith’s ECG blog: (September 8, 2023)
    https://drsmithsecgblog.com/50-year-old-in-remote-rural-community/
  • Queen of Hearts: High confidence OMI
ECG
  • HPI: A woman in her 70s presented with acute chest pain. It started 10 hours prior to arrival, then had improved, then recently returned.
  • Cath: Acute proximal LAD occlusion
  • Key ECG: V1 and V2 have abnormal STE, and V2 has a hyperacute T wave. There is reciprocal STD in II, III, and aVF. Since there are only Q waves from V1 to V3, it is possible that there was an old anterior wall MI, or that the current event is subacute, or acute on top of an old Q wave. Regardless, V2 with a hyperacute T wave and abnormal T/S ratio means there must be acute OMI, regardless of prior events.
  • Link to full case @ Dr. Smith’s ECG blog: (August 30, 2023)
    https://drsmithsecgblog.com/a-woman-in-her-70s-with-chest-pain/
  • Queen of Hearts: High confidence OMI
ECG
  • HPI: 60F with intermittent chest pain x 10 days
  • Cath: Culprit lesion mid-LAD, 99% stenosis
  • Key ECG: Sinus rhythm, normal QRS (except poor R wave progression), perhaps the tiniest possible STE in aVL, tiny STE in V2, awkwardly straight ST segment morphology in I and aVL and V2, concern for increased area under the T waves in aVL, V2, with reciprocal STD and negative hyperacute T waves in III and aVF. All very very subtle.
  • Link to full case @ Dr. Smith’s ECG Blog: 2023-01-12
ECG
  • HPI: 70M with chest pain x 1 hr
  • Cath: 100% thrombotic acute D1 occlusion, stented.
  • Key ECG: The lead that caught my eye was lead aVL. The shape of the subtle-but-real ST elevation in this lead is not normal. Adding to my concern is the small q wave, and hint of beginning T wave inversion. This is not the appearance of a repolarization change. In view of the abnormal appearance in lead aVL — the subtle ST elevation in lead I (the dotted RED line in this lead) suggests a similar ongoing process in this other high-lateral lead. Confirmation that the lead aVL appearance is likely to be acute — is forthcoming from reciprocal changes in all 3 inferior leads (II,III,aVF). The ST segment straightening that we see in these leads (as per the RED lines) — that then leads up into clearly disproportionately tall T waves (considering the modest R wave amplitude) is not normal.
  • Link to full case @ Dr. Smith’s ECG Blog: 2022-05-11
ECG
  • HPI: Patient with abdominal pain. No chest pain.
  • Cath: Occlusion of Large Diagonal
  • Key ECG: Hyperacute T wave in V1, I, aVL and reciprocal STD in lead III
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/abdominal-pain-in-middle-aged-patient/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: A man in his 70s with hypertension and type 2 diabetes mellitus presented with chest pain which awoke him from sleep around midnight. He described it as substernal, non-radiating, 7/10 intensity.
  • Cath: LAD occlusion involving the septal perforators and major diagonal vessel
  • Key ECG: STE and HATW in aVL and V2 (less apparent in lead I). Reciprocal STD in III. Precordial swirl as well with STE and HATW in V1, V2 and reciprocal STD in lateral precordium V4-V6
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/everyone-sees-st-depression-but-what-2/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 80 year old patient with HTN and HLD presented at 1:50 PM for midsternal chest pain since noon
  • Cath: Culprit lesion was mid LAD-1 lesion, 70% stenosed
  • Key ECG: Lead aVR and aVL reversal, V1 and V2 have HATW, ST elevation in aVR with diffuse STD concerning for left main OMI, LBBB with discordance.
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/five-lessons-from-a-misleading-ecg/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 69 yo woman with a 50 year history of smoking contacted EMS due to sudden onset chest pain. The chest pain was substernal and described as dull with an intensity of 8/10. The pain was accompanied by nausea, vomiting, and diaphoresis
  • Cath: Proximal LAD occlusion
  • Key ECG: Precordial swirl pattern with minimal ST elevation in the right precordial leads and ST depression in V4-V6. Reciprocal inferior ST depressions with a slight upward-convex ST segment in aVL. Diagnostic of LAD occlusion. EKG also manifests south african flag sign: STE in V2, aVL and I, with reciprocal inferior STD depression
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/chest-pain-with-non-diagnostic-ecg-what-is-the-finding-what-do-you-think-happened/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: Man in his 60s presented with acute pain of the shoulders, neck, throat, and jaw following rigorous physical activity without trauma. He adamantly denied any “chest” pain or discomfort. His triage vital signs were within normal limits
  • Cath: D1 99% culprit lesion
  • Key ECG: There is sinus rhythm with a reasonably normal QRS complex. There is no diagnostic ST elevation, but there is a hint of ST depression in V3 and V6. There are abnormally large T waves in I, aVL, and V2, with likely abnormal T wave inversion in III and aVF. If these findings are due to OMI, then the question is whether they represent inferior reperfusion, or high lateral active coronary occlusion. Of course, we know that the patient has active chest pain, so that greatly favors high lateral active OMI rather than reperfusion
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/a-60s-year-old-man-with-neck-and-shoulder-pain-no-chest-pain/
  • Queen of Hearts: OMI indeterminate
ECG
  • HPI: Man in his 50s was walking his dog early in the morning when he suddenly experienced acute chest pain.
  • Cath: Proximally occluded LAD above
  • Key ECG: Sinus rhythm, grossly normal QRS, with diagnostic findings of acute LAD occlusion: precordial swirl pattern (STE in V1-V2, hyperacute T wave in V2, ST depression in lateral precordial leads V5-6), and also aVL HATW with inferior reciprocal depression. It is a mix of South African Flag sign and Precordial swirl, both of which indicate proximal LAD Occlusion. You could also describe it as a mix of LAD occlusion pattern superimposed on a subendocardial ischemia pattern
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/a-man-in-his-50s-with-acute-chest-pain-see-what-happens-when-it-is-not-a-stemi/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 50 something male with history of Type 1 DM and HTn presented to ED with complaints of Chest Pain
  • Cath: Occlusion of the 1st diagonal branch of LAD
  • Key ECG: Lead I does not show frank ST elevation but does show hyperacute appearing T waves. aVL also has minimal upward concave ST segment elevation and bulky, hyperacute T waves. Lead III has slight ST depression and an inverted T wave which is reciprocal to the high lateral hyperacute T wave and ST change in aVL. Lead V2 shows a symmetric ischemic looking T wave – and the remaining precordial leads have ischemic looking minimal ST depression
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/the-diagnosis-is-nstemi-worthless-2/
  • Queen of Hearts: High confidence OMI
ECG
  • HPI: A 60-year-old woman presented to a rural emergency department with sudden-onset, crushing chest pain that began 20 minutes prior to arrival. She described it as a 10/10 heaviness in the center of her chest, without radiation or shortness of breath. Past medical history: hypertension on perindopril. She took two aspirin tablets at home before coming to the ED.
  • Cath: Tight proximal LAD lesion
  • Key ECG: Sinus tachycardia, borderline left axis, early R wave progression in V2, normal voltages, subtle ST elevation in leads I/aVL with reciprocal ST depression in lead III, and ST elevation with HATW in V2 with a small Q wave
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/chest-pain-in-a-rural-hospital-is-this-pericarditis-or-does-the-patient-need-thrombolytics/
  • Queen of Hearts: OMI high confidence

🚨 Suggestive of OMI:

  • Terminal QRS Distortion:
    • Terminal QRS (TQRSD) distortion in V2 or V3 is a specific finding for LAD occlusion when trying to differentiate from early repolarization
    • When the differential is LAD occlusion vs early repolarization, TQRSD was 100% specific for LAD occlusion in 171 cases
    • TQRSD is defined by ABSENCE of BOTH S-wave (reaching below isoelectric/PR) and J-wave (elevation of J-point above ST segment) in V2 or V3
  • Any STE or hyperacute T wave in inferior leads (especially lead III) associated with any STD in aVL
  • Any STD depression in inferior leads with associated STE in aVL

🚨 OMI (+) Terminal QRS Distortion:

8 examples below. Swipe ↔️ or use arrow keys to view more.
ECG
  • HPI: 60M presenting with acute chest tightness
  • Cath: 100% mid-thrombotic occlusion – stented
  • Key ECG: Terminal QRS distortion (TQRSD) in V3 and perhaps almost also V4. TQRSD means absence of BOTH S-wave and J-wave in EITHER of leads V2 or V3 — this is never seen in normal ST Elevation
  • Link to full case @ Dr. Smith’s ECG Blog: 2021-08-19
ECG
  • HPI: 40M with squeezing chest pain
  • Cath: 90% thrombotic proximal LAD lesion that was stented
  • Key ECG: This is very suggestive of LAD OMI. There is STE that does not meet STEMI criteria in V1-V6. There are normal size T-waves in V1-V3, but these T-waves are enormous relative to the QRS amplitude. These are hyperacute T-waves. Moreover, any time there is ST Elevation of any amount, it must be explained: is it normal STE? Or ischemic? One sign that eliminates the possibility of normal STE is “Terminal QRS distortion.” That is the absence of both an S-wave and a J-wave in EITHER V2 or V3. Here there is no S-wave in V3 and also no J-wave. This is very suggestive of ischemic STE and of LAD OMI.
  • Link to full case @ Dr. Smith’s ECG Blog: 2019-09-22
ECG
  • HPI: 65F with chest pain
  • Cath: Subtotal occlusion of mid-LAD. Wire passed through soft clot.
  • Key ECG: The T-wave in V3 may not be hyperacute when considered in isolation; however, when considered in the context of V4, I would consider this also suspicious for being a hyperacute T-wave. V2 has a small amount of STE which is inappropriate for its QRS, as well as a possible very small Q-wave which must be assumed to be new in this scenario without a prior ECG for review. Additionally, lead V2 technically has terminal QRS distortion, because there is no S-wave (never goes back below baseline) and there is also no J-wave. Because of the possible reciprocal changes, the Q-wave, and the terminal QRS distortion in V2, the formulas (for Subtle LAD-STEMI vs BER) would be formally contraindicated. Additionally, the formula technically requires at least 1mm STE in V2-V4 to consider using the formula.
  • Link to full case @ Dr. Smith’s ECG Blog
ECG
  • HPI: 35F with chest pain, nausea, vomiting
  • Cath: 95% LAD thrombotic culprit
  • Key ECG: There is terminal QRS distortion in lead V3 (meaning there is neither a J-wave nor an S-wave). The QTc is 462 ms. Terminal QRS distortion is never seen in normal variant ST Elevation in anterior leads (so-called early repolarization). These are suspicious for hyperacute T-waves and anterior injury.
  • Link to full case @ Dr. Smith’s ECG Blog: 2017-06-17
ECG
  • HPI: 20-something man with chest pain after extacy/ETOH use
  • Case: Pt went into VF arrest and was unable to be recussitated. Autopsy showed proximal LAD thrombus with 100% occlusion
  • Key ECG: Terminal QRS Distortion: no S-wave or J-wave in one of leads V2 and V3 (in this case, V3)
  • Link to full case @ Dr. Smith’s ECG Blog: 2017-05-13
ECG
  • HPI: 40M with chest pain
  • Cath: 100% acute thrombotic LAD occlusion
  • Key ECG: QRS distortion, which does not happen in early repol or in pericarditis. This is when there is an absence of BOTH and S-wave AND a J-wave in EITHER V2 or V3. This ECG only barely has an S-wave in V3 (the S-wave only goes 0.5 mm below the PQ jct.) There is ST elevation in V1-V3, maximal in V2 at barely more than 1 mm (measured at J-point, relative to PQ junction). The T-wave in V2 is nearly peaked. It does not have the typical wide and fat appearance of an ischemic hyperacute T-wave. Look at inferior leads: there is downsloping ST depression with a down-up T-wave in III and aVF. These are highly suspicious for reciprocal changes of LAD occlusion
  • Link to full case @ Dr. Smith’s ECG Blog: 2016-06-24
ECG
  • HPI: young adult with acute chest pain
  • Cath: A 100% acute occlusion of the proximal LAD was found, and stented
  • Key ECG: There is ST segment elevation in multiple leads, most of which have an associated J-wave (slurring of the J-point); e.g. in V4-V6, I, II, and aVF. There is no reciprocal depression, the QTc is not significantly lengthened, and the ST segments in V2 – V4, although elevated, are concave upwards. All of these elements point to benign early repolarization. If you used the LAD occlusion vs. Early Repol formula you get 21.9 (which effectively excludes LAD occlusion). But you should not have used the formula for this case. Why not? Look at V3: There is no S-wave in this lead, and neither is there a J-wave. This loss of the S-wave is called terminal QRS distortion, and multiple studies suggest that, with an anterior MI, this predicts a larger infarct, with higher mortality, and even a worse response to fibrinolytics or PCI.
  • Link to full case @ Dr. Smith’s ECG Blog: 2015-10-06
ECG
  • HPI: 60-something male presented with one hour of “oppressive” chest pain radiating to the back and to the left arm. Has a history of diabetes and COPD
  • Cath: 99% culprit lesion of proximal LAD
  • Key ECG: 0.5 mm ST elevation in V2 and V3, HATW in V2-V4. Terminal QRS distortion, meaning there are no S- or J- waves in either V2 or V3. Lead II has ST depression. Lead III has STD with down-up T-wave, as does aVF. There is minimal STE in aVL
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/this-is-excellent-omi-care/
  • Queen of Hearts: OMI high confidence

🚨 OMI (+) Subtle Anterior STE:

11 examples below. Swipe ↔️ or use arrow keys to view more.
ECG
  • HPI: 60M with acute chest pain x 30 min, pale & diaphoretic
  • Cath: Large proximal LAD thrombus with TIMI-1 flow. It was a wraparound LAD, explaining the inferior ST elevation with reciprocal ST depression in aVL (the opposite of what you expect with a proximal LAD occlusion). It was stented.
  • 4V formula score: 18.38 (>18.2 is the most accurate cutoff suggestive of LAD OMI)
  • Key ECG: There is upward concavity. There is no STD. There are no Q-waves. There is no terminal QRS distortion. So early repolarization is a possibility, however, there is very suspicious STE in III and aVF, with STD in aVL. This makes the ECG nearly diagnostic of ischemia, though if it is LAD occlusion, there should be ST depression in III, so it is a bit confusing. Unless you consider a wraparound LAD.
  • Link to full case @ Dr. Smith’s ECG Blog: 2017-06-21
ECG
  • HPI: 35M with acute chest pain
  • Cath: Occlusion of the very distal LAD s/p thrombectomy 3V fomula score: 23.9 (>23.4 favors OMI)
  • Key ECG: This is highly suspicious for LAD occlusion, though not diagnostic. The 3V formula score is 23.9 (which is > 23.4 which is pretty specific for LAD occlusion). Consider frequent serial EKGs, every 15 minutes, for several hours, an emergent formal contrast echocardiogram and if still non diagnostic, consider immediate angiography. One might argue, with good rationale, that such a small MI can wait until the next day for angiogram.
  • Link to full case @ Dr. Smith’s ECG Blog: 2015-11-18
ECG
  • HPI: Acute onset chest pain x 20 min
  • Cath: 100% occlusion of the mid-LAD
  • Key ECG: On this ECG there is ST elevation in lead V2, and it must be explained. Is it benign? If it were benign, then there should be excellent R-wave progression. There is not. In fact, the R-wave gets smaller from V2 to V3. Furthermore, the T-waves are much more symmetric than the T-waves of early repolarization. If you plug these numbers into the 3V formula you get a value of 25 (Any value greater than 23.4 is suggestive of LAD OMI. Less than 4% of LAD occlusion have a value < 22.0.)
  • Link to full case @ Dr. Smith’s ECG Blog: 2014-12-12
ECG
  • HPI: 40M with 1.5 hr chest pain
  • Cath: 100% mid LAD occlusion after a large D1 3V formula score 22.6 (At a cutoff of 22.0, the sensitivity was 96% but with decreased specificity of 81%)
  • Key ECG: Note there is not enough ST elevation to meet the standard criteria, which require at least 2 mm ST elevation at the J-point, relative to the PQ jct., in leads V2 and V3 for a male over 40 years old. In this case, there is 1 mm in V2 and 2 mm in V3. The T-waves looked too fat to be normal. Even though the 3V formula was not greater than 23.4, at 22.6, it was close enough to be worried.
  • Link to full case @ Dr. Smith’s ECG Blog: 2014-11-22
ECG
  • HPI: 75F p/w “reflux”
  • Cath: culprit lesion of a large obtuse-marginal artery successfully stented
  • 3V formula score: 25.4 (>23.4 favors OMI)
  • Key ECG: There is a poor R-wave progression across the precordials (transition is between V4 and V5); subtle ST-elevation in V2-V4, I, and aVL; and reciprocal ST-depression in II, III, and aVF. Additionally, using the BER vs. anterior STEMI calculator on the right side of this page, the equation value of this tracing is 25.4, greater than 23.4 (using measurements of 2.7 mm, 400 ms, and 4.4 mm, respectively). This tracing is suggestive of anterior subepicardial ischemia, almost always due to LAD occlusion.
  • Link to full case @ Dr. Smith’s ECG Blog: 2014-04-18
ECG
  • HPI: 45M with CAD p/w 3 hr typical chest pain
  • 3V formula score: 23.9 (>23.4 favors OMI)
  • Key ECG: There is ST elevation and tall T-waves in precordial leads, with reasonably good R-wave progression. He is a 45 year old male, so this could be male pattern benign early repolarization (BER, or ER). But it could be anterior STEMI. 40% of anterior STEMI has upward concavity in all of leads V2-V6. How can one decide whether this is ER or MI? First, if an old ECG is available, then compare. Only rarely does early repolarization change from date to date, though it is possible.
  • Link to full case @ Dr. Smith’s ECG Blog: 2011-06-18
ECG
  • HPI: 46 yo male with acute onset of chest pain
  • 3V score: 24.1 (>21 favors OMI)
  • Cath: 100% proximal thrombotic LAD occlusion with TIMI-0 flow. It was opened and stented
  • Key ECG: When the DDx is Anterior MI vs BER, a simple rule is the R-wave rule: which depends on the fact that, in BER, the R-wave is always well developed
  • Link to full case @ Dr. Smith’s ECG Blog: 2009-06-10
ECG
  • HPI: A woman in her 40s with no known comorbid conditions presented with acute chest pain radiating to left arm and neck, started approximately 4 hours prior to arrival
  • Cath: 100% LAD thrombotic occlusion
  • Key ECG: Right arm/right leg lead reversal (lead I resembles aVL, lead aVF resembles aVR). RBBB and concordant STE in V1-V3, reciprocal STD in v5-V6, HATW in I and aVL with reciprocally negative HATW in III and aVF
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/would-you-like-to-see-this-ecg-without/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: A woman in her 60s had acute chest pain and shortness of breath
  • Cath: Proximal total LAD occlusion
  • Key ECG: Sinus rhythm, RBBB, and anterolateral OMI pattern with concordant STE in V2, inappropriate STD and negative HATW in III and aVF
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/a-woman-in-her-60s-with-acute-chest/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: A 60-year-old woman presented to a rural emergency department with sudden-onset, crushing chest pain that began 20 minutes prior to arrival. She described it as a 10/10 heaviness in the center of her chest, without radiation or shortness of breath. Past medical history: hypertension on perindopril. She took two aspirin tablets at home before coming to the ED.
  • Cath: Tight proximal LAD lesion
  • Key ECG: Sinus tachycardia, borderline left axis, early R wave progression in V2, normal voltages, subtle ST elevation in leads I/aVL with reciprocal ST depression in lead III, and ST elevation with HATW in V2 with a small Q wave
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/chest-pain-in-a-rural-hospital-is-this-pericarditis-or-does-the-patient-need-thrombolytics/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: A woman in her 50s presented with acute chest pain and shortness of breath
  • Cath: Ostial LAD occlusion
  • Key ECG: STE and/or HATW in V1-V2, with reciprocal STD and/or TWI in V5-V6. Septum is ischemic with corresponding ST elevation from left to right in the septum resulting in STE in V1. Evidence of inferior OMI in lead III, with STE and HATW, but with STD in I, II, aVF, V4-V6.
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/a-woman-in-her-50s-with-chest-pain-no-diagnostic-ste-that-worthless-diagnosis-nstemi-what-is-it-and-what-happened/
  • Queen of Hearts: OMI high confidence

🚨 OMI (+) Subtle Inferior STE:

25 examples below. Swipe ↔️ or use arrow keys to view more.
ECG
  • HPI: Woman in her late 70s p/w left arm pain for 1 day, BP over 200 mmHg systolic 1 day prior. Given nitroglycerin which improved BP and arm pain but pain returned same evening and woke her from sleep. Pain was dull, achy, worse with exertion.
  • Cath: Complete occlusion of mid left circumflex artery
  • Key ECG: Subtle inferior STE with subtle reciprocal STD in I and aVL is highly suspicious for inferior OMI. Look at V2 for evidence of posterior OMI (STD, loss or inversion of T wave, downsloping ST segment) and V6 for STE.
  • Link to full case @ Dr. Smith’s ECG blog: (December 11, 2023)
    https://drsmithsecgblog.com/occlusion-myocardial-infarction-is/
  • Queen of Hearts: No OMI with high confidence
ECG
  • HPI:50M with 24 hr worsening L-sided chest pain
  • Cath: 3VD with 99% distal RCA (culprit) for which CABG was arranged
  • Key ECG: Minimal STE in III, some STD in I and aVL, and terminal T wave inversion in III, suggesting some reperfusion. This is not specific for OMI, however if the patient has resolving chest pain this could be consistent with recent OMI, now with reperfusion ST-T. ECG findings suggests that *at some point in time* — the patient has had an inferior infarction: The Q wave in lead III is huge. There is also a significant Q wave in lead aVF — that is equal in depth to the height of the tiny R wave in this lead. These findings could represent multi-vessel disease, on top of which there may (or may not be) ECG changes of another new event.
  • Link to full case @ Dr. Smith’s ECG Blog: 2023-04-09
ECG
  • HPI: 50s M p/w exertional chest pain & dyspnea
  • Cath: complete acute occlusion (TIMI 0) of the RPL (right posterolateral artery), requiring 3 stents to restore TIMI 3 flow.
  • Key ECG: subtle inferior (and likely also posterior) OMI. There is a small and narrow QRS complex with reasonable axis and R wave progression, therefore the QRS cannot explain any abnormalities of the ST segment and/or T waves. The T waves in II, III, and aVF are subtly too large for their QRS, and the most important finding is that, in aVL, there is reciprocal STD and proportionally-large-volume T wave inversion (a “reciprocal negative hyperacute T wave”). There is also slight STD in I.
  • Link to full case @ Dr. Smith’s ECG Blog: 2021-06-06
ECG
  • HPI: 60F with chest pain started 1 day PTA
  • Cath: RCA culprit lesion with subtotal approximately “99%” lesion
  • Key ECG: STE in leads II, III, and aVF, reaching at least 1.0 mm in III and aVF; Large Q wave in lead III; STD in aVL and I; Subtle STD in V2. Highly suggestive of inferoposterior transmural injury, with the most common etiology being Occlusion MI of the RCA until proven otherwise. The normal QRS complex followed by focal inferior STE and reciprocal STD in I and aVL is suggestive of inferior involvement, while the subtle STD maximal in V2 is highly suggestive of the posterior involvement.
  • Link to full case @ Dr. Smith’s ECG Blog: 2021-04-30
ECG
  • HPI: 30s M p/w 12 hr chest pain radiating to jaw
  • Cath: Culprit lesions of the mid and distal RCA each with 95% stenosis
  • Key ECG: Inferior hyperacute T-waves, with negative hyperacute T-wave in aVL. The lateral leads also have minimal STE and hyperacute T-waves.
  • Link to full case @ Dr. Smith’s ECG Blog: 2019-11-20

ECG
  • HPI: 40M with chest pain x 1 hr
  • Cath: 100% mRCA occlusion with TIMI 0 flow
  • Key ECG: STE in II, III, and aVF (which probably barely does meet STEMI critiera) with hyperacute T waves in II, IIII, aVF and reciprocal negative hyperacute T-wave in aVL, with STD in V1-V2. Small R waves in II, III, aVF. This is suggestive of inferoposterior OMI. The most likely culprit vessel would be the RCA.
  • Link to full case @ Dr. Smith’s ECG Blog: 2019-10-10
ECG
  • HPI: 40M with chest pain x 1hr
  • Cath: 100% RCA occlusion
  • Key ECG: STE in inferior leads and STD in I and aVL which do not meet STEMI criteria, but suggest OMI. The principal ST-T wave abnormality in this tracing is ST segment straightening and slight ST depression in leads I and aVL. Although isolated T wave inversion in lead aVL would not necessarily be abnormal (especially given the predominantly negative QRS complex in this lead) — there should not be ST flattening with ST depression in both of these high lateral leads. Given the history of new-onset chest pain — this ECG finding is ischemic until proven otherwise.
  • Link to full case @ Dr. Smith’s ECG Blog: 2019-04-22
ECG
  • HPI: 77F acute chest pain and SOB
  • Cath: LCx large codominant, normal appearing until point of occlusion in mid-vessel
  • Key ECG: There is ST elevation in inferior leads, with reciprocal ST depression in aVL, so one must strongly suspect acute inferior MI. However, 3 features should provide pause for poassible false positive (pseudoOMI): 1) There is LVH, 2) There is an intraventricular conduction defect, with QRS duration of 125 ms, 3) There is an RSR’ (saddleback) in lead III. This patient clearly has underlying structural heart disease (based on the intraventricular conduction delay) — and that can affect ST-T wave appearance appearance in a way that is hard to determine without seeing a baseline ECG
  • Link to full case @ Dr. Smith’s ECG Blog: 2019-03-18
ECG
  • HPI: 60F with acute chrushing chest pain x 1hr
  • Cath: 100% occluded RCA with TIMI 0 flow
  • Key ECG: Hyperacute T-waves in leads II, III, and aVF, inverted T-wave with slight STD in aVL.
  • Link to full case @ Dr. Smith’s ECG Blog: 2018-02-15
ECG
  • HPI: Acute chest pain
  • Cath: 100% thrombotic occlusion of the (very large) proximal segment of OM1
  • Key ECG: There is a tiny amount of STE in the inferior leads, with lead III having possibly a large T-wave compared to its QRS complex. Lead aVL clinches the diagnosis with a very small normal QRS complex followed by minimal ST depression and a proportionally massively inverted T-wave.Lead I also shows reciprocal STD. There is STD in V2-V4 which suggests posterior involvement. This ECG is suggestive of acute coronary occlusion affecting the inferior and posterior walls.
  • Link to full case @ Dr. Smith’s ECG Blog: 2018-02-01
ECG
  • HPI: 60s M woke up from sleep with chest pain radiating to the back with nausea x 1 hr
  • Cath: 100% in-stent thrombosis of his prior RCA stent
  • Key ECG: No pathologic Q-waves. Without the prior ECG for comaparison, the T-waves are not clearly hyperacute. There is slight STE in V3-V5. There is 1-2mm STE in II, III, and aVF with slight J-point depression in aVL and marked, large T-wave inversion in aVL. If you consider only the ST elevation in the inferior leads out of context, this amount and morphology would not be incompatible with a baseline ECG of a young man with high voltage and diffuse baseline ST elevation. The ST depression and T-wave inversion in aVL, however, is NOT compatible with a baseline abnormality, and makes the ECG highly suspicious for acute coronary occlusion. As has been shown through many prior cases and publications by Dr. Smith, lead aVL holds the key to understanding inferior ST elevation. ST depression in aVL should always be assumed to be due to inferior MI, unless there is: limb lead LVH, WPW, LBBB, paced rhythm, etc. If there are well-formed Q-waves, it could be due to inferior LV aneurysm as well.
  • Link to full case @ Dr. Smith’s ECG Blog: 2017-10-31
ECG
  • HPI: 30M with acute chest pain
  • Cath: 100% circumflex lesion
  • Key ECG: Inferior ST elevation, with reciprocal ST depression in aVL. This is highly suggestive of inferior MI, though does not meet millimeter criteria for “STEMI.” There is also ST elevation in lateral precordial leads V5 and V6
  • Link to full case @ Dr. Smith’s ECG Blog: 2017-06-12
ECG
  • HPI: Mid-30s man p/w acute chest pain x 30 min
  • Cath: 100% occlusion of the mid RCA
  • Key ECG: There is subtle ST elevation in III, but also in II and aVF. Most importantly, there is clear reciprocal ST depression in aVL. This is all but diagnostic of inferior MI (but not STEMI because there is not enough ST elevation for STEMI)
  • Link to full case @ Dr. Smith’s ECG Blog: 2015-01-28
ECG
  • HPI: 68 yo M with PMHx HTN, HLD, CAD with stent deployment in the RCA who presented to the ED with chest pain for 20 minutes
  • Cath: 99% occlusion of proximal segment of RCA
  • Key ECG: Minimal STE in inferior leads, but also with terminal QRS distortion and some reciprocal ST depression in aVL. Terminal QRS distortion is always abnormal in leads V2 and V3, but can be useful in other leads.
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/normal-ecg-by-many-measures-is-it-normal/
  • Queen of Hearts: Not OMI high confidence
ECG
  • HPI: 84 yo M with notable cardiac history (CABG, multiple stents) woke at 0500 hrs with pressure in his chest, diaphoresis, and light-headedness. He presented to a rural ED 1.5 hours later. He was recovering from a recent bout of influenza-like illness. His symptoms are associated with chest tightness and diaphoresis
  • Cath: 100% RCA occlusion
  • Key ECG: Sinus bradycardia, convex ST elevation in III, reciprocal ST depression in aVL and possible anterior ST depression – indicating inferoposterior OMI
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/is-it-possible-that-this-patient-with/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 75 yo with history of CABG who presented after 24 hr Chest pain. HR 40, BP 135/70, RR16, O2 100%.
  • Cath: 100% Occlusion of RCA Graft
  • Key ECG: There’s sinus bradycardia, normal conduction, normal axis, delayed R wave progression, and normal voltages. There are inferior Q waves and lead III had mild concave ST elevation, with subtle reciprocal depression in I & aVL. This is diagnostic of inferior OMI, likely from RCA.
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/75-year-old-with-24-hours-of-chest-pain/
  • Queen of Hearts: High confidence OMI
ECG
  • HPI: 56 yo M with history of HTN who presented with chest pain for several hours located in the mid to left chest after riding his bike. Associated with fatigue and mild shortness of breath at symptom onset, resolved by the time he presented to ED.
  • Cath: Thrombotic occlusion of proximal RCA.
  • Key ECG: Sinus bradycardia with RBBB. Minimal STE in I and aVL (which can be normal in RBBB). Some minimal reciprocal STD in inferior leads. Some STD in V1-V3, but this is normal discordant STD in RBBB. Minimal STD in V4-V6, not ischemic in appearance. Some non-specific new T wave inversion in inferior leads (compared to prior EKGs). Also new Q waves, strongly suggestive of new infarction
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/56-year-old-male-had-510-chest-pain-for/
  • Queen of Hearts: Low confidence – not OMI
ECG
  • HPI: Middle aged man who developed sudden onset lightheadedness with diaphoresis, nausea, and had multiple episodes of emesis.
  • Cath: Proximal thrombotic or embolic occlusion of RCA
  • Key ECG: Subtle STE in III and aVF. Terminal QRS distortion in aVF. STD in aVL. STD in V2-V4 characteristic of posterior OMI. Terminal T wave inversion in lead III with terminal upright T-wave in aVL
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/why-is-this-patient-in-shock/
  • Queen of Hearts: OMI with high confidence
ECG
  • HPI: A man is his late 30s with a 10 pack year smoking history presented with acute substernal “crushing” chest pressure radiating into his left shoulder with associated nausea, vomiting, diaphoresis which began suddenly while he was getting ready for work
  • Cath: Mid left circumflex occlusion with no flow beyond the occlusion
  • Key ECG: Slight STE in III. Subtle STD in aVL, has inverted/coved appearance which is highly concerning for ischemia. Lead I is beginning to show reciprocal depression. J point in V3 is abnormally isoelectric when it was previously 1.5 mm elevation. Because it is now relativel depressed, it is susggestive of posterior extension
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/crushing-chest-pain-and-cant-see-omi-on/
  • Queen of Hearts: Not OMI with high confidence
ECG
  • HPI: 60 year old presented with chest pain
  • Cath: 99% mid RCA occlusion
  • Key ECG: AV block which can be a transient complication of RCA occlusion since it perfused the AV node. Inferior hyperacute T waves. Reciprocal STD and T wave inversion in aVL. Ischemic ST depression in V2-V4
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/chest-pain-are-these-really-nonspecific/
  • Queen of Hearts: High confidence – OMI
ECG
  • HPI: 69 yo F with chest pain
  • Cath: RCA Occlusion (SVG graft to RCA in patient with previous CABG)
  • Key ECG: Incomplete RBBB. There is minimal STE in lead III with an inverted T wave, suggesting acute MI with some degree of reperfusion. Same in aVF. There is minimal reciprocal STD in aVL. Normal amount od discordant STD in V2
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/a-69-year-old-with-acute-chest-pain/
  • Queen of Hearts: OMI with LOW confidence
ECG
  • HPI: 69 yo F with history of HTN presented to the ED by EMS for evaluation of chest pain and shortness of breath. She awoke in the morning with sharp chest pain, which worsened throughout the morning. As her pain worsened, so did her dyspnea and she was found with O2 sat 64%
  • Cath: Total occlusion of the middle segment of the RCA
  • Key ECG: ST segments in leads III and aVF are elevated. T waves are concave and terminally inverted, suggesting the possibility of reperfusion. Leads I and aVL show ST depression with terminally upright T wave, morphology typically reciprocal to inferior ST elevation representing transmural ischemia of the inferior wall
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/pulmonary-edema-with-tachycardia-and/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 50-something male with HTN, past smoker,, no history of CAD presented with chest pain
  • Cath: RCA was the culprit
  • Key ECG: ST depression in V2-V6, maximal in V3. Diagnostic for posterior OMI. There is also T wave inversion with ST depression in aVL. The inferior T waves are suspiciously large. The inferior leads alone plus aVL are extremely suspicious for an inferior OMI
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/should-you-record-posterior-leads/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 50 something with no previous cardiac history, but with history of seizures, presented to triage with a few hours of chest tightness and pressure, 5/10, radiating to the left arm. He was from out of town and had forgotten to bring his seizure medications. He thought maybe he had had a seizure as cause of his symptoms
  • Cath: Ostial/proximal LAD thrombus
  • Key ECG: There is < 1 mm STE in inferior leads, most in lead III. There is minimal reciprocal ST depression in aVL. The absence of an S-wave in leads III and aVF is very supportive (this finding in V2-3 is called “terminal QRS distortion” and is diagnostic for LAD occlusion in those leads; it is highly suggestive in other leads)
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/lookssmallbutcouldhavebeendisaster/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: A woman in her 40s presented with acute chest pain. Vitals were within normal limits.
  • Cath: Total mid-LAD thrombotic occlusion
  • Key ECG: HATW in V2-V5, and some STE in V3, V4, II, III, aVF. Reciprocal STD in aVL from lead III
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/will-this-patient-get-care-of-the-past-or-care-of-the-future-nstemi-is-a-worthless-diagnosis/
  • Queen of Hearts: OMI high confidence

🚨 OMI (+) Subtle STE in aVL:

5 examples below. Swipe ↔️ or use arrow keys to view more.
ECG
  • HPI: 60M with acute 10/10 chest pain
  • Cath: LCX proximal 99% stenosis with thrombus
  • Key ECG: Slight STE in aVL, with upright hyperacute T wave, with reciprocal STD in the inferior leads and negative hyperacute T waves. Posterior involvement is suggested by STD in V3-V4, which is highly specific for posterior OMI in the setting of ACS and no QRS explanation (RVH, RBBB, etc.) for such STD.
  • Link to full case @ Dr. Smith’s ECG Blog: 2021-12-01
ECG
  • HPI: Intermittent substernal chest pain x 1 day with radiation to jaw
  • Cath: 100% thrombotic mid-LAD occlusion
  • Key ECG: There is less than 1 mm of ST depression in II, III, aVF, and in V3-V6. The STD is nearly 1 mm in III and V6. There is a tiny amount of ST Elevation in aVL. The ST vector is around -60 degrees, so that there is some STE in aVL and a bit in I, and zero in aVR
  • Link to full case @ Dr. Smith’s ECG Blog: 2017-05-29
ECG
  • HPI: 60F with 3hr acute chest pain
  • Cath: D3 has a 95% tubular ostial stenosis. (Culprit, stented)
  • Key ECG: There is ST elevation in I and aVL, with inferior reciprocal ST depression in all of II, III, and aVF, and a down-up T-wave in aVF (a sign that is very specific for ischemia). There is also ST depression in V3-V6. This ECG is highly suggestive of ischemia.
  • Link to full case @ Dr. Smith’s ECG Blog: 2014-05-12
ECG
  • HPI: 60F awoke with substernal chest pressure x 1/2 hour
  • Cath: 99% thrombotic lesion in the proximal segment of a large obtuse marginal, with TIMI-2 flow
  • Key ECG:There is sinus rhythm with one PVC. There is subtle ST elevation in aVL and I, with reciprocal ST depression in III and aVF, indicative of a circuflex (or obtuse marginal – OM – branch), or possibly and first diagonal, occlusion. There are also hyperacute T-waves in V4-V6, with some ST elevation, suggesting more widespread STEMI, such as LAD or very large OM or diagonal. The ST elevation is even easier to see in the PVC in lead aVL: it is discordant, as it should be, but out of proportion.
  • Link to full case @ Dr. Smith’s ECG Blog: 2012-08-01
ECG
  • HPI: 47M with chet pain
  • Cath: culprit was a 99% proximal RCA
  • Key ECG: There is T-wave inversion in lead III and a very large T-wave in aVL (very large only compared to the small size of the QRS, and it is proportional ST elevation and T-wave size that is important, not absolute size!) One would predict high lateral MI from this ECG.
  • Link to full case @ Dr. Smith’s ECG Blog: 2011-02-22

🔎 Specificity:

  • Specificity: 100% specific for LAD occlusion when there is terminal QRS distortion (PMID 27658331)
  • Specificity: 94.7% specific for OMI when 4 variable formula value >18.2 (PMID 28460689)

🚨 Suggestive of OMI:

  • STD maximal in leads V1-V4
    • This is in contrast to if STD is maximal out to V5 and V6 which may indicate severe supply-demand imbalance due to critical multivessel or left main acute coronary syndrome, hypovolemia or severe anemia which may not indicate acute coronary occlusion
  • STE in posterior leads V7-V9

🚨 OMI (+) Posterior OMI:

35 examples below. Swipe ↔️ or use arrow keys to view more.
ECG
  • HPI: 40-something year old patient with severe diabetes, renal failure, and known coronary disease who presented with acute “crushing” chest pain.
  • Cath: Occluded LCx
  • Key ECG: Flat, downsloping ST segment in V2 and V3
  • Link to full case @ Dr. Smith’s ECG blog: (January 25, 2024)
    https://drsmithsecgblog.com/acute-chest-pain-in-patient-with-lvh/
  • Queen of Hearts: Low Confidence OMI
ECG
  • HPI: 50 something male was seen in the emergency room due to typical chest pain. Original EKG showed atrial fibrillation. He was given morphine for pain which converted him to sinus rhythm
  • Cath: 99% stenosis of proximal RCA
  • Key ECG: Hyperacute T-waves leads II, III, and aVF. Already forming Q-waves inferiorly. Reciprocal change in lead I and aVL with ST-depression and T wave inversion
  • Link to full case @ Dr. Smith’s ECG blog: (September 24, 2023)
    https://drsmithsecgblog.com/morphine-omi-is-bad-combination/
  • Queen of Hearts: High confidence OMI
ECG
  • HPI: 75 year-old patient with diabetes and end stage renal disease was sent to the ED after dialysis for three days of nausea, vomiting, loose stool, lightheadedness and fatigue. RR18 sat 99% HR 90 BP 90/60, afebrile
  • Cath: 99% Proximal RCA Occlusion
  • Key ECG: There’s normal sinus rhythm, normal conduction, normal axis, normal R wave progression and normal voltages. There’s subtle inferior ST elevation with straightening of the ST segment, reciprocal ST depression and T wave inversion in aVL, and ST depression in V2. This is diagnostic of infero-posterior OMI, but it is falsely negative by STEMI criteria and with falsely negative posterior leads (though they do show mild ST elevation in V4R)
  • Link to full case @ Dr. Smith’s ECG blog: (August 19, 2023)
    https://drsmithsecgblog.com/75-year-old-dialysis-patient-with/
  • Queen of Hearts: OMI High confidence
ECG
  • HPI: 50M with acute chest pain
  • Cath: PCI after cardiac arrest – LCX “subtotally stenosed” – peak hscTnT 2,696 ng/L
  • ECG: Findings are specific for posterior (and also likely inferior) wall transmural acute infarction, most likely due to acute coronary occlusion (OMI). There is a relatively normal QRS yet there is STD maximal in V2-V4, which resolves from V4 to V6. The inferior leads may have a slightly full T wave (possibly hyperacute if compared to baseline which is unavailable), but there is no clear TWI in aVL
  • Link to full case @ Dr. Smith’s ECG blog: 2023-06-21

ECG
  • HPI:50M on medical ward developed acute chest pain
  • Cath: 100% RCA occlusion, with peak troponin I over 10,000 ng/L
  • Key ECG:Lead aVL jumps out as abnormal because there is a discordant T wave inversion and mild ST depression. This is reciprocal to inferior mild ST elevation and hyperacute T waves (wide based, bulky, and symmetric, and in III taller than the QRS complex), and adjacent to ST depression in V2. This is highly suggestive of inferoposterior OMI.
  • Link to full case @ Dr. Smith’s ECG Blog: 2023-04-21

ECG
  • HPI: 39M with 2hr substernal chest pain
  • Cath: ostial left circumflex occlusion
  • Key ECG: Although not striking, this is clearly a diagnostic ECG for infero”posterior” myocardial infarction due to coronary occlusion (OMI), most likely due to left circumflex (LCx) artery occlusion. There is clear ST-segment depression in V2-5, which peaks around V4. The morphology in V2 is especially concerning for a reciprocal change to “posterior” ST-segment elevation (STE). There is also subtle STE in inferior leads, with hyperacute T-waves and accompanying Q waves in lead II and aVF. Lead III has a fractioned QRS complex. These all are highly unlikely to be seen in a 39-year-old man without previous cardiac history.
  • Link to full case @ Dr. Smith’s ECG Blog: 2022-12-18

ECG
  • HPI:40F with sudden chest pain
  • Cath: 100% Obtuse Marginal Occlusion (supplying the lateral and posterior wall) with TIMI-0 flow.
  • Key ECG: very subtle ST depression in V3 and V4, and new subtle ST Elevation in V5 and V6.
  • Link to full case @ Dr. Smith’s ECG Blog: 2022-09-21

ECG
  • HPI: middle aged man with 1hr substernal chest pain
  • Cath: Thrombotic D1 occlusion 100%
  • Key ECG: There is downsloping minimal STD in V2 and V3. The T-wave in lead II is somewhat suspicious, but is not a diagnostic OMI finding. This is highly suspicious for isolated posterior OMI
  • Link to full case @ Dr. Smith’s ECG Blog: 2021-11-25
ECG
  • HPI: 60F with chest pain
  • Cath: 100% thrombosis of the LCX with TIMI 0 flow
  • Key ECG: Sinus rhythm with ST depression (STD) in V2-V5, with maximal STD of less than 1mm in lead V3-V4
  • Link to full case @ Dr. Smith’s ECG Blog: 2021-02-27

ECG
  • HPI: 45M with acute chest pain
  • Cath: A proximal LCX occlusion (100%, TIMI 0) was found and stented.
  • Key ECG: There is STD in precordial leads, maximal in V2-V4. There is zero STE anywhere on the ECG. It is yet another ECG diagnostic of posterior OMI, with STD present from V1-V5 and maximal in V2-V4
  • Link to full case @ Dr. Smith’s ECG Blog: 2021-02-14

ECG
  • HPI: Elderly woman wiht acute epigastric pain
  • Cath: 100% (TIMI 0) LCX occlusion was found and stented.
  • Key ECG: There is an absence of sinus activity, including an absence of retrograde P waves. The rhythm is probably a junctional escape at a rate of approximately 45, with RBBB and likely also LAFB (given the leftward axis despite RBBB). Alternatively, it could be a posterior fascicular escape. There is STD in V2-V5 that is maximal in V2 and V3. This STD is excessively discordant in V2, and concordant in V3. The inferior leads show Q waves with STE in lead III, and there is some slight reciprocal STD in I and aVL. Interestingly, many of the T waves have a slightly peaked appearance. Along with bradycardia and conduction block, this would be alarming for potential hyperkalemia, which of course can also cause OMI mimics.
  • Link to full case @ Dr. Smith’s ECG Blog: 2020-09-28

ECG
  • HPI: 50M with 2hr chest pain
  • Cath: total thrombotic occlusion (100%, TIMI 0 flow) of the First Obtuse Marginal (OM1)
  • Key ECG: Sinus rhythm, Normal QRS complex, Hyperacute T waves in leads II, III, and aVF, reciprocal STD and T wave inversion in aVL, STD in V2-V4 (max in V3), Likely hyperacute T waves in V5 and V6 as well. This is highly suggestive for inferoposterolateral STEMI(-) OMI. There is always a small possibility of takotsubo or myocarditis, but this ECG is OMI until proven otherwise.
  • Link to full case @ Dr. Smith’s ECG Blog: 2020-09-13

ECG
  • HPI: 60M with acute chest pain
  • Cath: 100% thrombotic lesion of the proximal left circumflex (TIMI 0 flow)
  • Key ECG: There is sinus rhythm with normal QRS complex and ST depression in V2-V5, maximal in V3-V4. There is no ST depression in V6, II, III, or aVF, and no significant ST elevation in aVR, all confirming that the ST vector is not consistent with diffuse subendocardial ischemia, but rather a focal ST vector pointed at the posterior wall. It is posterior OMI until proven otherwise
  • Link to full case @ Dr. Smith’s ECG Blog: 2019-02-16

ECG
  • HPI: 50M with 1hr chest pain
  • Cath: 100% occlusion on of the circumflex, proximal to the first obtuse marginal, was found, opened, and stented
  • Key ECG: There is ST Elevation (STE) in II, III, aVF, with reciprocal ST depression in aVL. There is also ST depression in V2 and V3. V2 and V3 almost always have some amount of normal ST elevation, and since posterior MI is associated with inferior MI, you must make notice of this and think it is probably an inferior posterior MI. However, II, III, and aVF have what appear to be J-waves at the end of the QRS. If these are J-waves, then couldn’t the inferior ST elevation be due to early repol? 1) When there is ST depression in aVL, early repol as a cause of inferior STE is VERY unlikely. 2) These do NOT appear to be J-waves.
  • Link to full case @ Dr. Smith’s ECG Blog: 2018-05-06
ECG
  • HPI: 65 yo with history of atrial flutter, CABG, and end-stage renal disease on dialysis presented with 3 days of fluctuating chest pain
  • Cath: 95% circumflex occlusion (not fully occluded due to some spontaneous reperfusion)
  • Key ECG: Atrial flutter with controlled ventricular response, a non-specific intra-ventricular conduction delay, borderline right axis, normal R wave progression and normal voltages. The abnormal repolarization from the IVCD can produce secondary repolarization abnormalities, but here there appears to be superimposed primary ST depression V2-V4 indicating posterior OMI
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/chest-pain-with-anterior-st-depression/
  • Queen of Hearts: High Confidence OMI
ECG
  • HPI: Middle aged female who presented with acute chest pain for approximately 6 hours
  • Cath: Acute thrombotic occlusion of first obtuse marginal
  • Key ECG: ST depression in V2 and V3
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/what-happened-after-cath-lab-was/
  • Queen of Hearts: High confidence for OMI
ECG
  • HPI: Middle aged man who presented with chest pain
  • Cath: 100% RCA occlusion
  • Key ECG: Sinus rhythm, normal QRS. Inferior T waves are hyperacute, with reciprocal negative hyperacute T waves in aVL. Posterior OMI is indicated by the inappropriate STD maximal in V2.
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/two-prehospital-ecgs-of-patients-with/
  • Queen of Hearts: High confidence OMI
ECG
  • HPI: 50-something woman with CP of a couple hours duration
  • Cath: 100% distal RCA occlusion
  • Key ECG: Minimal ST elevation in II, III, and an inverted T-wave in aVL. Very flat ST segment in V2, highly suspicious for posterior OMI
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/omi-can-be-very-subtle-and-easy-to-miss/
  • Queen of Hearts: High confidence for OMI
ECG
  • HPI: Patient had onset of chest pain 24 hours before arrival to ED
  • Cath: 100% circumflex occlusion
  • Key ECG: STD maximal in V1-V4, which is diagnostic of posterior OMI. There is some ST elevation and slightly hyperacute T wave in V6. This is a common finding in posterior OMI because V6 is “almost” around to the back where posterior leads would be placed
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/this-is-what-happened-when-hospital-2/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: A man in his early 60s with no significant medical history who presented with acute chest paint or 5 hours
  • Cath: Proximal RCA with 99% stenosis
  • Key ECG: There are hyperacute T waves in inferior leads, with a reciprocally inverted hyperacute T wave in aVL. There is a negative T wave in V2, suggesting posterior OMI, and minimal ST depression in V3 with a down-up T wave, all diagnostic of posterior OMI
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/if-you-were-this-patient-would-you/
  • Queen of Hearts: OMI low confidence
ECG
  • HPI: 62 yo M with history of diabetes, hypertension, and smoker. Reported typical chest pain since 4 AM, arrived at ED with 10 hours of ongoing chest pain
  • Cath: 100% ostial main (obtuse) marginal occlusion
  • Key ECG: T wave inversion in inferior leads, STD in V2-V4
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/why-you-should-use-queen-of-hearts-and/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 62 yo M with history of hyperlipidemia presented to a rural ED with 7 hours of 3/10 chest pain
  • Cath: 100% first obtuse marginal, 95% mid LAD, 80% ostial LAD
  • Key ECG: ST depression maximal in V2-V4 and resolved by V5-V6. With inferior ST depression and possible ST segment straightening in aVL suggests high lateral involvement, meaning the likely culprit artery is the left circumflex or one of its branches
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/anterior-st-depression-which-lesion-is/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 84 yo M with notable cardiac history (CABG, multiple stents) woke at 0500 hrs with pressure in his chest, diaphoresis, and light-headedness. He presented to a rural ED 1.5 hours later. He was recovering from a recent bout of influenza-like illness. His symptoms are associated with chest tightness and diaphoresis
  • Cath: 100% RCA occlusion
  • Key ECG: Sinus bradycardia, convex ST elevation in III, reciprocal ST depression in aVL and possible anterior ST depression – indicating inferoposterior OMI
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/is-it-possible-that-this-patient-with/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: A man in his 60s presented to a community hospital with 2 days of oppressive chest pain radiating to the throat, lasting under 10 minutes and then spontaneously resolving. The next day, symptom free. Towards evening of Day 2, pt experienced the same pressure and radiation coming in waves and not improving. Not provoked.
  • Cath: Mid RCA: 100% occlusion
  • Key ECG: T-waves in the inferior leads are enormous, almost the same size relative to the QRS complex. Broad, bulky, symmetric — what we would call hyperacute T-waves. There is almost no ST-elevation. Yet there is clear reciprocal STD in leads I and aVL, along with an inverted T-wave in aVL and also ST depression maximal in V2–V3, where slight ST elevation would normally be expected and thus there is probably > 1 mm of relative ST depression (relative to the normal position of ST Elevation). There is also a reciprocally inverted hyperacute T-wave in aVL.
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/reciprocally-inverted-hyperacute-t-wave-what-is-that/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 50-something male with HTN, past smoker,, no history of CAD presented with chest pain
  • Cath: RCA was the culprit
  • Key ECG: ST depression in V2-V6, maximal in V3. Diagnostic for posterior OMI. There is also T wave inversion with ST depression in aVL. The inferior T waves are suspiciously large. The inferior leads alone plus aVL are extremely suspicious for an inferior OMI
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/should-you-record-posterior-leads/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: Very elderly patient with previous EF of 60% complained of shortness of breath for 2 weeks, with pleuritic chest pain.
  • Cath: 90% proximal RCA culprit
  • Key ECG: Inferior STE and hyperacute T-waves, with reciprocally inverted hyperacute T-wave in aVL. There is minimal ST depression in lead V2 (where there should be some STE!), thus highly suggestive of posterior OMI.
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/atypical-symptoms-should-we-give-thrombolytics/
  • Queen of Hearts: High confidence OMI
ECG
  • HPI: 50 something male presented in the evening to ED for evaluation of chest pain that started at 1600. He states that it felt like burning and pressure, like GERD. Reported it felt similar to how he felt when he had his heart attack 4 years prior, now s/p 4 stents
  • Cath: Ruptured plaque in the distal circumflex with local embolic occlusion of the distal OM3
  • Key ECG: STD V4-V6, hyperacute T wave in aVL and reciprocal STD in inferior leads
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/pay-now-in-evening-or-pay-later-with/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: A man in his 60s with a history of hypertension and 40 pack year smokin history presented to the ER with 1 day of intermittent, burning substernal chest pain radiating into both arms as well as his back and jaw. It has been stuttering, lasting 10 minutes at a time with associated diaphoresis.
  • Cath: 60-70% RCA
  • Key ECG: STE and HATW in II, III, aVF. Reciprocal STD in aVL > . STD in V2 and V3.
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/normal-acs-care-everything-by-book-but/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 40 something patient called 911 for 30 minutes of left sided chest pain radiating to right arm/shoulder
  • Cath: “Very tight” RCA stenosis
  • Key ECG: HATW in III and aVF, reciprocally inverted HATW in aVL. There is also a flattened ST segment in V2
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/do-we-need-serial-ecgs-for-this-case-of/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: A man in his 60s developed sudden chest pain, dizziness, diaphoresis, and shortness of breath shortly before ED arrival
  • Cath: RCA occlusion and concomitant severe LCx stenosis
  • Key ECG: STE in III and aVF with reciprocal STD in aVL, disproportionally large broad HATW in III and aVF, and flattening ST segment in V2-V3 concerning for inferior and posterior OMI
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/a-man-in-his-60s-with-chest-pain-are-these-very-small-t-waves-hyperacute/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: An elderly female called EMS with acute chest pain
  • Cath: 99% of mid-RCA
  • Key ECG: Subtle RBBB and LAFB. While some STE could be expected by the large wide S wave in inferior leads, there is STE and possibly HATW in II, III, aVF with reciprocal findings in aVL. While STD could be expected after a large R’ of a RBBB in V2, that is not the case here. The STD in V2 is not explained, and is very large in proportion to its QRS complex, concerning for posterior OMI. The T waves in V4-V6 are also suspicious for hyperacute T waves
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/an-elderly-woman-with-acute-chest-pain/
  • Queen of Hearts: OMI high confiendece
ECG
  • HPI: 60ish-year old complaining of vomiting, diarrhea, and “bubbles in my chest”
  • Cath: Severe 95% hazy distal LM, Severe 80% ostial LAD, 100% occluded distal LAD thought to be due to distal embolization from lesion in prox LAD, Mild CAD in LCx, 70% eccentric proximal RCA
  • Key ECG: Hyperacute T waves in III and aVF, reciprocal STD in aVL with a reciprocally inverted T wave in aVL. Hyperacute T waves in V3 and V4. ST depression in V1 and V2
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/vomiting-diarrhea-and-bubbles-in-my/
  • Queen of Hearts: High confidence OMI
ECG
  • HPI: 61 yo F with history of hypertension presented with 30 minutes of fluctuating non-radiating heaviness in chest, with diaphoresis and nausea.
  • Cath: Tight stenosis in circumflex
  • Key ECG: Inferior hyperacute T waves (diagnostic of inferior OMI) with reciprocal STD in aVL, reciprocally inverted hyperacute T wave in aVL, STD in V2 (diagnostic of posterior OMI), and large lateral T waves which are probably hyperacute
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/can-you-treat-non-stemi-with-2/
  • Queen of Hearts: OMI with high confidence
ECG
  • HPI: A woman in her 70s was woken from sleep by midsternal chest pain radiating to left arm with nausea
  • Cath: Mid LCX 90%
  • Key ECG: EKG shows sinus rhythm, normal QRS, and signs of inferoposterolateral OMI. There is very small STE in III and aVF which do not meet STEMI criteria, hyperacute T waves, reciprocal T wave inversion in aVL, and maximal STD in V2-V3 showing posterior OMI. The T waves in V5-V6 are likely also hyperacute.
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/what-does-final-diagnosis-of-stemi-vs/
  • Queen of Hearts: OMI with high confidence
ECG
  • HPI: Man in his 30s with type 1 DM presented with 2 days of midsternal and epigastric pain, described as both “sharp” and “squeezing”. Associated with nausea, vomiting, and dyspnea. Pain worse with supination and improved with upright posture.
  • Cath: Thrombotic subtotal occlusion of LCx/OM1
  • Key ECG: Subtle hyperacute T waves in lead I, STE and HATW in II > aVF, Subtle STD in V1 and V2, STE and HATW in V5 and V6
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/what-factor-determines-final-diagnosis/
  • Queen of Hearts: High confidence for OMI

🔎 Specificity:

  • Specificity: 97% specific for OMI when STD maximal in V1-V4
    • Of the 99 OMIs detected by STDmaxV1-4, 34% had <1mm STD, and 47 (47%) had accompanying STEMI criteria
    • Source: PMID 34775811
  • Specificity: 84% specific for posterior OMI when STE in V7-V9 and STD in V1-V3
    • Sensitivity: 80% (with respect to diagnostic accuracy of posterior involvement (at least severe hypokinesia on TTE)
    • 46 of 87 inferior MIs with posterior leads had posterior ST elevation of at least 0.5 mm in 2 consecutive leads of V7-V9
    • Significant STD in V1-V3 was noted in 52 patients (60%)
    • Source: PMID 9502627

🚨 Suggestive of OMI:

  • STD (especially with J-point depression) preceding large, hyperacute T waves in the precordial leads
    • The presence of de Winter’s T-waves indicates a complete or near complete occlusion of a proximal LAD
  • To illustrate the spectrum of ECG findings in deWinter pattern — the authors of the original 2008 NEJM manuscript included a composite picture taken from 8 representative tracings of patients in their study who manifested deWinter T waves.

🚨 OMI (+) de Winter's Examples:

18 examples below. Swipe ↔️ or use arrow keys to view more.
ECG

ECG
  • HPI: A man in his 50s experienced acute chest pain and shortness of breath
  • Cath: Total occlusion of the proximal LAD with thrombus
  • Key ECG: HATW in V2-V6, I, and aVL. Leads V3-V6 also have STD making them the de Winter subtype of HATW. Reciprocal STD in inferior leads
  • Link to full case @ Dr. Smith’s ECG blog: (12/20/25) view post
    https://drsmithsecgblog.com/a-man-in-his-50s-with-chest-pain-you-must-strongly-advocate-for-your-patient-who-has-an-nstemi-omi-ecg-pattern/
  • Queen’s Verdict: OMI high confidence
ECG
  • HPI: 50-something male with a history of hypertension and tobacco use. Patient cnotacted the ambulance service after he experienced sudden onset chest pain ad diaphoresis that had started 20 minutes prior
  • Cath: 100% proximal LAD occlusion
  • Key ECG: EKG shows sinus rhythm and narrow QRS complex. Significant and widespread ST-segment and T wave changes. The ST-segment in lead V1 has upward convexity. Throughout the precordium (V2-V6) there is ST depression followed by bulky, hyperacute T waves. This is diagnostic of LAD occlusion. The de Winter ECG pattern consists of an ST-segment upsloping depression at the J point of 1 to 3 mm in leads V1 to V6, associated with tall, bulky or “hyperacute” T waves.
  • Link to full case @ Dr. Smith’s ECG blog: (01/31/25) view post
    https://drsmithsecgblog.com/another-must-know-ecg-and-why-its/
  • Queen’s Verdict: OMI with High confidence
ECG
  • HPI: 60 year old developed exertional chest pain with diaphoresis and called EMS.
  • Cath: 100% proximal LAD occlusion
  • Key ECG: Loss of R waves in V2-V3 with hyperacute waves V1-V5. No significant ST elevation but there are two forms of ST depression: deWinter T wave V3-V5 and precordial swirl with ST depression V6 reciprocal to subtle STE in V1. Hyperacute T waves in I/aVL with reciprocal inferior ST depression
  • Link to full case @ Dr. Smith’s ECG blog: (July 7, 2024)
    https://drsmithsecgblog.com/60-year-old-with-chest-pain-stemi/
  • Queen’s Verdict: OMI with high confidence
ECG
  • HPI: 72 yo M with hx of CAD with stent placement presented to a rural hospital with chest pain for 2 hours
  • Cath: 99% in stent-restenosis of the proximal LAD
  • Key ECG: T waves in V2-V5 are hyperacute T waves. They have a large area under the curve relative to the QRS size. They are bulky, not just tall. The T waves are more than twice the height of the R waves in leads V2 and V3,
  • Link to full case @ Dr. Smith’s ECG blog: (June 3, 2024)
    https://drsmithsecgblog.com/every-rural-hospital-needs-queen-of/
  • Queen’s Verdict: High confidence OMI
ECG
  • HPI: Patient presented with acute chest pain
  • Cath: — not recorded in source —
  • Key ECG: DeWinter T waves in V3-V4
  • Link to full case @ Dr. Smith’s ECG blog: (March 14, 2024)
    https://drsmithsecgblog.com/three-patients-with-chest-pain-and/
  •  Queen’s Verdict: OMI with high confidence
ECG
  • HPI: A man in his late 30s with history of HTN, tobacco use, and obesity presented with acute chest pain for 3 hours with pain radiating down both arms, 10/10 in severity
  • Cath: Mid LAD 100% stenosis
  • Key ECG: Loss of R wave from Lead V1 with initial fragmentation of QRS complex. R wave progression is limited throughout remainder of chest leads, with R waves remaining small and transition delayed until leads V5-V6. T wave in lead V2 is hyperacute.
  • Link to full case @ Dr. Smith’s ECG blog: (January 20, 2024)
ECG
  • HPI: An elderly patient had onset of chest pain one hour prior.
  • Cath: 100% occlusion of LAD
  • Key ECG: Precordial hyperacute T waves with depressed ST Takeoff (de Winter’s). ST depression indicates proximal LAD occlusion.
  • Link to full case @ Dr. Smith’s ECG blog: (October 6, 2023)
ECG
  • HPI: 50M with acute chest pain x hours
  • Cath: 100% thrombotic occlusion of LAD
  • Key ECG: There are hyperacute T waves in V2-V5, I, II, aVL. The STD also present in V2 completes the description of de Winter T waves (hyperacute T wave with depressed ST takeoff)
  • Link to full case @ Dr. Smith’s ECG Blog: 2023-04-17
ECG
  • HPI: 50M with substernal chest pain x 1 hr
  • Cath: Prox LAD 99% s/p thrombectomy
  • Key ECG: It is very suggestive of OMI, but difficult to tell whether it is 1) anterolateral with de Winter morphology, or instead 2) A combination of Aslanger’s pattern (inferior OMI with single lead STE in III and reciprocal STD in I, aVL, plus widespread STD of subendocardial ischemia) with posterior (V2 STD) and RV extension (V1 STE). In other words, does V2 indicate ST depression of posterior OMI? or is the ST depression and hyperacute T wave indicative of de Winter hyperacute OMI morphology of the anterior wall? It is difficult to tell, but either way: OMI needing reperfusion
  • Link to full case @ Dr. Smith’s ECG Blog: 2022-09-22

ECG
  • HPI: 60M with chest pain x 1 hr
  • Cath: 100% (TIMI-0) thrombotic occlusion of the mid LAD, stented
  • Key ECG: The ECG is a classic, pathognomonic ECG for acute LAD OMI. There is STE in V1 and de Winter morphology (hyperacute T wave with depressed ST takeoff / ST depression) in V2-V4. In the lateral leads V5-V6 and I and aVL there is STD that is likely in part reciprocal to the STE in V1. Also reciprocal STD in II and aVF, or potentially also de Winter morphology in inferior leads as well. With hyperacute T wave and STE in V1 and STD in V5-6, this constitutes an LAD OMI pattern that Dr. Smith is currently studying
  • Link to full case @ Dr. Smith’s ECG Blog:
ECG
  • Key ECG: Hyperacute T-waves in V2-V5, very suggestive of Proximal LAD occlusion, but without ANY ST Elevation except for less than 1 mm in aVL, and 0.25 mm in lead I. There is also minimal STE in aVL with reciprocal STD in II, III, aVF. Notice that there is plenty of R-wave in V2 and V3. This should be an obvious case of acute proximal LAD Occlusion. In this, case the Hyperacute T-waves are preceded by subtle ST Depression in V2 and V3. Thus, they are specifically the hyperacute T-waves called “de Winter’s T-waves.”
  • Link to full case @ Dr. Smith’s ECG Blog:
ECG
  • HPI: 50M awoke from sleep with “gas” pain
  • Cath: complete proximal LAD occlusion
  • Key ECG: This is classic de Winter pattern in V3 and V4 (depressed ST takeoff with hyperacute T-wave). V1-V4 have hyperacute T-waves. Reciprocal STD in inferior leads.
  • Link to full case @ Dr. Smith’s ECG Blog:

ECG
  • HPI: 50M with chest pain
  • Cath: 100% proximal thrombotic occlusion of the LAD.
  • Key ECG: There is sinus rhythm with perhaps 1mm STE in aVL, and also in V2 with hyperacute T-wave. There is STD in V3-V5, as well as II, III, and aVF, with hyperacute T-waves in all these leads as well, thus de Winter’s pattern in the anterior and inferior leads. This is essentially pathognomonic for Occlusion MI of the anterior and apical walls (de Winter pattern more likely represents ~99% thrombotic stenosis with just a trickle of flow, but essentially the same overall event, with progression to full occlusion extremely likely). The OMI is therefore occurring in the LAD, and the LAD is likely a type III “wraparound” which supplies the apical and distal inferior wall in addition to the anterior wall. Aside: This case proves that de Winter’s waves are not limited to anterior leads, but may be seen in any location. This is similar to Wellens’ waves, which were first described in the LAD distribution, but may occur in inferior and/or lateral leads as well.
  • Link to full case @ Dr. Smith’s ECG Blog:
ECG
ECG
  • HPI: 50M with chest pain x hours
  • Cath: LAD D1 thrombus
  • Key ECG: There is approximately 1mm STE in aVL with reciprocal STD in II, III, and aVF. There is STD in V3-V6, with hyperacute T waves (de Winter’s morphology) in V3-V6 and also hyperacute T waves in leads V5, V6, and I. This is highly suggestive of acute transmural injury to the anterior and lateral walls, with the most likely etiology being acute occlusion (or near occlusion) of a coronary artery supplying these walls, such as the LAD, large diagonal, ramus intermedius, or sometimes the LCX or its branches. This morphology is distinctly de Winter’s T-waves. The de Winter pattern is characterized by ST depression and hyperacute (large) T-waves in the distribution of the ischemia. This is in contrast to upright T-waves from posterior MI, and also in contrast to the inferior ST depression in this case, which is reciprocal to the STE in aVL. In de Winter’s T-waves, if the ischemia worsens before reperfusion, the ST depression may evolve into ST elevation with or without hyperacute T-waves.
  • Link to full case @ Dr. Smith’s ECG Blog:
ECG
  • HPI: middle aged man with acute typical chest pain
  • Cath: 100% ostial LAD occlusion
  • Key ECG: There are subtle de Winter’s hyperacute T-waves; see the subtle ST depression in V3
  • Link to full case @ Dr. Smith’s ECG Blog:
ECG
  • HPI: 51M playing cards with friends and developed L-hand numbness
  • Cath: LAD occlusion, unfortunately he died before it could be opened
  • Key ECG: there are de Winter’s T-waves in V2 and V3 (hyperacute T-wave with depressed ST takeoff)
  • Link to full case @ Dr. Smith’s ECG Blog:

🔎 Specificity:

  • PPV: 95.2% (95% confidence interval: 76.2-99.9%), 100% (69.2-100.0%) and 100% (51.7-100%) in the three respective diagnostic studies with primary outcome was defined as at least 70% angiographic stenosis of a major epicardial vessel.(PMID 28362646)

⚠️ Note:

Precordial swirl is an ECG pattern associated with LAD occlusion, often without meeting traditional STEMI criteria. It reflects an anterior/rightward injury vector, producing ST-T changes that appear to “swirl” clockwise across the precordial leads.

🚨 Suggestive of Precordial Swirl:

  • STE and/or hyperacute T-waves in V1-V2
  • Reciprocal STD and/or T-wave inversion in V5-V6
  • Usually occurs with a narrow QRS without LVH
  • Think LAD OMI, particularly when the right-precordial ST-T abnormalities appear disproportionate to the preceding QRS.

🧠 Why does it happen?

Precordial swirl likely reflects a rightward/anterior ST injury vector, classically described with LAD occlusion proximal to the first septal perforator. The vector points toward V1-V2 and away from the lateral precordial leads, producing STE/hyperacute T-waves in V1-V2 with reciprocal STD/TWI in V5-V6.

⚠️ Important Mimics:

The big one is LVH, which can naturally produce STE in V1-V3 with lateral STD/strain. LBBB and other abnormal QRS complexes can produce similar secondary ST-T changes, which is why the validated definition emphasizes a narrow QRS without LVH. Diffuse subendocardial ischemia can also produce lateral STD with STE in aVR/V1 and should be distinguished from true precordial swirl.

🚨 OMI (+) Precordial Swirl Examples:

12 examples below. Swipe ↔️ or use arrow keys to view more.
ECG
  • HPI: 60-something male presented with 2 hours of chest pain
  • Cath: Total proximal LAD occlusion
  • Key ECG: This is diagnostic of proximal LAD Occlusion (LAD OMI). There is STE and Hyperacute T-wave (HATW) in V1, HATW in V2-V4 (with some STE), STD in V6 (precordial swirl pattern). There is a reciprocally inverted T-wave in lead III, and reciprocal STD in II and aVF.
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/60-something-male-with-2-hours-of-chest-pain/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: A man in his 70s with hypertension and type 2 diabetes mellitus presented with chest pain which awoke him from sleep around midnight. He described it as substernal, non-radiating, 7/10 intensity.
  • Cath: LAD occlusion involving the septal perforators and major diagonal vessel
  • Key ECG: STE and HATW in aVL and V2 (less apparent in lead I). Reciprocal STD in III. Precordial swirl as well with STE and HATW in V1, V2 and reciprocal STD in lateral precordium V4-V6
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/everyone-sees-st-depression-but-what-2/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 80 year old patient with HTN and HLD presented at 1:50 PM for midsternal chest pain since noon
  • Cath: Culprit lesion was mid LAD-1 lesion, 70% stenosed
  • Key ECG: Lead aVR and aVL reversal, V1 and V2 have HATW, ST elevation in aVR with diffuse STD concerning for left main OMI, LBBB with discordance.
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/five-lessons-from-a-misleading-ecg/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 69 yo woman with a 50 year history of smoking contacted EMS due to sudden onset chest pain. The chest pain was substernal and described as dull with an intensity of 8/10. The pain was accompanied by nausea, vomiting, and diaphoresis
  • Cath: Proximal LAD occlusion
  • Key ECG: Precordial swirl pattern with minimal ST elevation in the right precordial leads and ST depression in V4-V6. Reciprocal inferior ST depressions with a slight upward-convex ST segment in aVL. Diagnostic of LAD occlusion. EKG also manifests south african flag sign: STE in V2, aVL and I, with reciprocal inferior STD depression
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/chest-pain-with-non-diagnostic-ecg-what-is-the-finding-what-do-you-think-happened/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: Man in his 50s was walking his dog early in the morning when he suddenly experienced acute chest pain.
  • Cath: Proximally occluded LAD above
  • Key ECG: Sinus rhythm, grossly normal QRS, with diagnostic findings of acute LAD occlusion: precordial swirl pattern (STE in V1-V2, hyperacute T wave in V2, ST depression in lateral precordial leads V5-6), and also aVL HATW with inferior reciprocal depression. It is a mix of South African Flag sign and Precordial swirl, both of which indicate proximal LAD Occlusion. You could also describe it as a mix of LAD occlusion pattern superimposed on a subendocardial ischemia pattern
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/a-man-in-his-50s-with-acute-chest-pain-see-what-happens-when-it-is-not-a-stemi/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: A woman in her 40s with no known comorbid conditions presented with acute chest pain radiating to left arm and neck, started approximately 4 hours prior to arrival
  • Cath: 100% LAD thrombotic occlusion
  • Key ECG: Right arm/right leg lead reversal (lead I resembles aVL, lead aVF resembles aVR). RBBB and concordant STE in V1-V3, reciprocal STD in v5-V6, HATW in I and aVL with reciprocally negative HATW in III and aVF
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/would-you-like-to-see-this-ecg-without/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: A woman in her 60s had acute chest pain and shortness of breath
  • Cath: Proximal total LAD occlusion
  • Key ECG: Sinus rhythm, RBBB, and anterolateral OMI pattern with concordant STE in V2, inappropriate STD and negative HATW in III and aVF
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/a-woman-in-her-60s-with-acute-chest/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 30-something reports gradual onset of reproducible, persistent, substernal chest wall discomfort that radiates to both arms and described as a muscle contraction since waking up, associated with nausea and vomiting. There is a history of HTN with medication compliance.
  • Cath: 100% proximal LAD occlusion
  • Key ECG: HATW in V2 and aVL, STE in V1, and ST depression in I, inferior leads, and V3-V6.
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/the-worst-thing-you-can-be-when-you/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: Middle aged man presented with acute chest pain
  • Cath: 100% proximal LAD occlusion
  • Key ECG: Subtle STE in V1, very HATW in V2, and subtle HATWs in V3-V6. There is ST depression in V5 and V6. Any ST depression (except for in aVR( makes it impossible for any STE to be a normal variant. There is inferior ST depression and “down-up” T-waves
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/what_is_this_pattern_ps/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: A woman in her 60s presented with acute chest pain and normal vital signs
  • Cath: mid-LAD occlusion
  • Key ECG: HATW in V2-V3, down-up T waves in III, aVF, and V6. There are all highly specific for LAD Occlusion MI
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/a-woman-in-her-60s-with-chest-pain-and-no-stemi/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 60-something male with history of HTN and hyperlipidemia was driving when he had acute onset of chest pain
  • Cath: 100% ostial (very proximal) LAD occlusion
  • Key ECG: There is ST Elevation and Hyperacute T-wave in V1-V3. There is a touch of ST depression in V6. There is also minimal STD in inferior leads. So this is Precordial Swirl pattern of LAD occlusion proximal to the septal perforator, indicating septal OMI.
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/do-not-interrupt-the-physician-to-show-him-her-this-normal-ecg-unless-he-she-uses-the-queen-of-hearts/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: A woman in her 50s presented with acute chest pain and shortness of breath
  • Cath: Ostial LAD occlusion
  • Key ECG: STE and/or HATW in V1-V2, with reciprocal STD and/or TWI in V5-V6. Septum is ischemic with corresponding ST elevation from left to right in the septum resulting in STE in V1. Evidence of inferior OMI in lead III, with STE and HATW, but with STD in I, II, aVF, V4-V6.
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/a-woman-in-her-50s-with-chest-pain-no-diagnostic-ste-that-worthless-diagnosis-nstemi-what-is-it-and-what-happened/
  • Queen of Hearts: OMI high confidence

🔎 Evidence:

In the 2025 validation study of 808 high-risk ACS patients:

  • STD in V5/V6 + any STE in V1/V2, with a narrow QRS and no LVH:
    • Specificity 92%
    • Sensitivity 11%
    • PPV 42%
  • Adding T-wave/S-wave amplitude ratio >0.40 in V2:
    • Specificity 98%
    • Sensitivity 9%
    • PPV 70%
  • Among OMI patients identified by the precordial swirl sign, 83% had an LAD culprit, and 70% did not meet STEMI criteria
  • Source: PMID 40319770

🚨 Suggestive of OMI:

✅ Mimics of hyperacute T wave:

  • Reciprocal reperfusion T-waves (see example):
    • How can you tell if a large upright wave is hyperacute or if it is reciprocal to an inverted wave? Answer: You can tell mostly based on the state of the patient. If the patient is symptomatic (should usually be chest pain), then the large fat T-wave is hyperacute. Serial ECGs should show evolution to STEMI in that lead. If, on the other hand, the patient is now pain free, then the ischemia is in the territory of the inverted T-wave and that is a reperfusion T-wave. The hyperacute T-wave is only a reciprocal view.
    • How can you tell if a large upright wave is hyperacute or if it is reciprocal to an inverted wave? Answer: You can tell mostly based on the state of the patient. If the patient is symptomatic (should usually be chest pain), then the large fat T-wave is hyperacute. Serial ECGs should show evolution to STEMI in that lead. If, on the other hand, the patient is now pain free, then the ischemia is in the territory of the inverted T-wave and that is a reperfusion T-wave. The hyperacute T-wave is only a reciprocal view.

🚨 OMI (+) Inferior Hyperacute T-waves:

24 examples below. Swipe ↔️ or use arrow keys to view more.
ECG
  • HPI: 55 yo with history of NSTEMI presented with 2 hours of exertional chest pain with normal vitals
  • Cath: 90% RCA in-stent thrombus
  • Key ECG: ST depression in aVL, which is reciprocal to subtle inferior ST elevation and bulky T waves. There is also a down-up T wave in aVL, which makes aVL even more diagnostic. This is diagnostic of inferior OMI, accompanied by inferior Q waves, and with a flat ST segment in V2 that could indicated posterior extension
  • Link to full case @ Dr. Smith’s ECG blog: (January 27, 2024)
    https://drsmithsecgblog.com/chest-pain-and-computer-normal-ecg/
  • Queen of Hearts: High confidence
ECG
  • HPI: 50 something male was seen in the emergency room due to typical chest pain. Original EKG showed atrial fibrillation. He was given morphine for pain which converted him to sinus rhythm
  • Cath: 99% stenosis of proximal RCA
  • Key ECG: Hyperacute T-waves leads II, III, and aVF. Already forming Q-waves inferiorly. Reciprocal change in lead I and aVL with ST-depression and T wave inversion
  • Link to full case @ Dr. Smith’s ECG blog: (September 24, 2023)
    https://drsmithsecgblog.com/morphine-omi-is-bad-combination/
  • Queen of Hearts: High confidence OMI
ECG
  • HPI: 85M with CAD p/w 3hr chest pain radiating to L-arm
  • Cath: 90% RCA occlusion. Troponin rose from 600 to 17,000 ng/L
  • Key ECG: Inferior hyperacute T waves (broad based, symmetric, tall relative to the QRS). Reciprocal ST depression and T wave inversion in aVL (and I), which is highly specific for inferior OMI. Primary anterior ST depression, which is posterior OMI until proven otherwise
  • Link to full case @ Dr. Smith’s ECG Blog: 2023-03-24
ECG
  • HPI: 36F with 30 minutes central chest pressure
  • Cath: OM1 occlusion successfully stentent Troponin: initial <4ng/L, peak >8000 ng/L
  • Key ECG: T waves in each of the inferior leads (II,III,aVF) are “hypervoluminous” with respect to QRS amplitudes in these leads (ie, These T waves are taller — “fatter” at their peak — and wider at their base than they should be)
  • Link to full case @ Dr. Smith’s ECG Blog: 2022-12-23
ECG
  • HPI: Elderly man with chest pain & diaphoresis x 30 min
  • Cath: prox-mid RCA occlusion, stented
  • Key ECG: There is approximately 1.0 mm of STE in lead III, but only ~0.5 mm in II and aVF. There are very hyperacute T waves in II, III, and aVF. Reciprocal negative hyperacute T wave in aVL. Clear posterior OMI seen by the very specific ST depression maximal in V2.
  • Link to full case @ Dr. Smith’s ECG Blog: 2013-08-21
ECG
  • HPI: 20-something man with chest pain x 2.5 hr “Tight and pressure, radiates to right arm, + nausea, + SOB”
  • Cath: 99% stenosis in the RCA, and proximal to a posterolateral branch. A coronary aneurysm was found.
  • Key ECG: Reciprocal STD in aVL (this occurred in 0 of 66 cases of early repolarization and 99% of patients with inferior STEMI). T-waves in inferior leads are hyperacute, out of proportion to those in early repol. T-wave inversion in V2 is inconsistent with early repol, and is typical of posterior ischemia. Also, when there is normal variant STE in inferior leads, there is usually also normal variant ST elevation in V5 and V6 (which is not present in this case)
  • Link to full case @ Dr. Smith’s ECG Blog: 2013-08-31
ECG
  • HPI: 61M hx CABG p/w 1 hr chest pain
  • Cath: 100% occluded prox RCA opened and stented
  • Key ECG: There is an inverted T-wave in I and aVL with very minimal ST depression. T-waves in lead III looks hyperacute, but still without ST elevation. Also, there is ST elevation in V1, a common sign of right ventricular STEMI
  • Link to full case @ Dr. Smith’s ECG Blog: 2013-08-21
ECG
  • HPI: 65F with upper back pain and mild chest pressure
  • Cath: The proximal RCA was 100% occluded
  • Key ECG: There are hyperacute T-waves in II, III, and aVF.  Note T-wave inversion in aVL, which is the earliest finding in acute inferior STEMI, as well as in V2, suggesting posterior wall involvement
  • Link to full case @ Dr. Smith’s ECG blog: 2011-06-16
ECG
  • HPI: 66M with severe substernal chest pain
  • Cath: 95% thrombotic occlusion of the RCA s/p successful PCI
  • Key ECG: The T-waves in inferior leads have high voltage proportional to the QRS, very suspicious for inferior MI. aVL has T-wave inversion, which raises suspicion even higher
  • Link to full case @ Dr. Smith’s ECG Blog: 2011-02-08
ECG
  • HPI: A man in his early 60s with no significant medical history who presented with acute chest paint or 5 hours
  • Cath: Proximal RCA with 99% stenosis
  • Key ECG: There are hyperacute T waves in inferior leads, with a reciprocally inverted hyperacute T wave in aVL. There is a negative T wave in V2, suggesting posterior OMI, and minimal ST depression in V3 with a down-up T wave, all diagnostic of posterior OMI
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/if-you-were-this-patient-would-you/
  • Queen of Hearts: OMI low confidence
ECG
  • HPI: A middle aged man with a history of HOCM presented with 24 hours of chest pain, still active. Localized to left sternal border, without radiation. Patient was in no distress, had normal vital signs, but stated he had been dehydrated for a day as well
  • Cath: 100% distal circumflex occlusion
  • Key ECG: T wave in lead III is far larger in his presentation EKG compared to his historical EKG. In aVL, the inverted T wave is similar between presentation EKG and his historical EKG but the QRS is far larger in the historical EKG
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/hypertrophic-cardiomyopathy-with/
  • Queen of Hearts: Did not detect OMI
ECG
  • HPI: Very elderly patient with previous EF of 60% complained of shortness of breath for 2 weeks, with pleuritic chest pain.
  • Cath: 90% proximal RCA culprit
  • Key ECG: Inferior STE and hyperacute T-waves, with reciprocally inverted hyperacute T-wave in aVL. There is minimal ST depression in lead V2 (where there should be some STE!), thus highly suggestive of posterior OMI.
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/atypical-symptoms-should-we-give-thrombolytics/
  • Queen of Hearts: High confidence OMI
ECG
  • HPI: A man in his 60s with a history of hypertension and 40 pack year smokin history presented to the ER with 1 day of intermittent, burning substernal chest pain radiating into both arms as well as his back and jaw. It has been stuttering, lasting 10 minutes at a time with associated diaphoresis.
  • Cath: 60-70% RCA
  • Key ECG: STE and HATW in II, III, aVF. Reciprocal STD in aVL > . STD in V2 and V3.
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/normal-acs-care-everything-by-book-but/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 40 something patient called 911 for 30 minutes of left sided chest pain radiating to right arm/shoulder
  • Cath: “Very tight” RCA stenosis
  • Key ECG: HATW in III and aVF, reciprocally inverted HATW in aVL. There is also a flattened ST segment in V2
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/do-we-need-serial-ecgs-for-this-case-of/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: A man in his 60s developed sudden chest pain, dizziness, diaphoresis, and shortness of breath shortly before ED arrival
  • Cath: RCA occlusion and concomitant severe LCx stenosis
  • Key ECG: STE in III and aVF with reciprocal STD in aVL, disproportionally large broad HATW in III and aVF, and flattening ST segment in V2-V3 concerning for inferior and posterior OMI
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/a-man-in-his-60s-with-chest-pain-are-these-very-small-t-waves-hyperacute/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 60 something previously healthy female smoker presenting with 2-3 days of sharp intermittent chest discomfort
  • Cath: 100% proximal RCA occlusion
  • Key ECG: SR with narrow QRS complexes. There is normal R-wave progression in the precordial leads with no evidence of ischemia. In the limb leads there is T-wave inversion in lead aVL with a low amplitude QRS preceding the T-wave. There is some upwards concave ST segment elevation in the inferior leads with what seems to be well formed J-waves. T wave inversion in aVL must represent reciprocal change from inferior wall hyperacute T waves. The isoelectric ST segment in lead V2 on the presentation ECG becomes quite suspicious for posterior wall involvement
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/vague-symptoms-and-dilated-ventricle/
  • Queen of Hearts: Not reported
ECG
  • HPI: 54 yo M with chest pain. History of diabetes type II and stent placement in 2018.
  • Cath: 100% occlusion of mid-RCA (in-stent thrombosis)
  • Key ECG: STE in V1 is large suggestive of RV MI, large hyperacute T waves. Minimal STD in V2 suggestive of posterior OMI.
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/prehospital-cath-lab-activation-kg-done-2/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 45 year old man presented with chest pain
  • Cath: Proximal RCA occlusion
  • Key ECG: III and aVF, with reciprocal STD in aVL. There are also hyperacute T waves in V1-V3 so this is likely a proximal RCA occlusion with RV infarct
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/non-diagnostic-even-in-retrospect-according-to-an-entire-conference-full-of-ed-docs-and-cardiologists/
  • Queen of Hearts: OMI with mid confidence
ECG
  • HPI: 50-something woman with history of NICM with EF 20-25% on GDMT complained of vomiting, upper back pain, chest tightness on day of presentation. Also complained of bilateral heaviness and weakness of the arms.
  • Cath: Culprit is 100% stenosis in the distal LCX
  • Key ECG: There is an RBBB-like intraventricular conduction delay, with a wide S-wave in inferior leads and V2-V6. There is subtle STE in lead III with subtle reciprocal STD in aVL. The T-wave in III is very inflated (Hyperacute T-wave-HATW), with a large area under the curve, and the reciprocally inverted T-wave in aVL is equally hyperacute (inverted reciprocal HATW). There is ischemic ST depression in V4-6.
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/this-was-interpreted-as-no-ischemia-kg/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: An elderly female called EMS with acute chest pain
  • Cath: 99% of mid-RCA
  • Key ECG: Subtle RBBB and LAFB. While some STE could be expected by the large wide S wave in inferior leads, there is STE and possibly HATW in II, III, aVF with reciprocal findings in aVL. While STD could be expected after a large R’ of a RBBB in V2, that is not the case here. The STD in V2 is not explained, and is very large in proportion to its QRS complex, concerning for posterior OMI. The T waves in V4-V6 are also suspicious for hyperacute T waves
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/an-elderly-woman-with-acute-chest-pain/
  • Queen of Hearts: OMI high confiendece
ECG
  • HPI: 60ish-year old complaining of vomiting, diarrhea, and “bubbles in my chest”
  • Cath: Severe 95% hazy distal LM, Severe 80% ostial LAD, 100% occluded distal LAD thought to be due to distal embolization from lesion in prox LAD, Mild CAD in LCx, 70% eccentric proximal RCA
  • Key ECG: Hyperacute T waves in III and aVF, reciprocal STD in aVL with a reciprocally inverted T wave in aVL. Hyperacute T waves in V3 and V4. ST depression in V1 and V2
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/vomiting-diarrhea-and-bubbles-in-my/
  • Queen of Hearts: High confidence OMI
ECG
  • HPI: 61 yo F with history of hypertension presented with 30 minutes of fluctuating non-radiating heaviness in chest, with diaphoresis and nausea.
  • Cath: Tight stenosis in circumflex
  • Key ECG: Inferior hyperacute T waves (diagnostic of inferior OMI) with reciprocal STD in aVL, reciprocally inverted hyperacute T wave in aVL, STD in V2 (diagnostic of posterior OMI), and large lateral T waves which are probably hyperacute
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/can-you-treat-non-stemi-with-2/
  • Queen of Hearts: OMI with high confidence
ECG
  • HPI: A woman in her 70s was woken from sleep by midsternal chest pain radiating to left arm with nausea
  • Cath: Mid LCX 90%
  • Key ECG: EKG shows sinus rhythm, normal QRS, and signs of inferoposterolateral OMI. There is very small STE in III and aVF which do not meet STEMI criteria, hyperacute T waves, reciprocal T wave inversion in aVL, and maximal STD in V2-V3 showing posterior OMI. The T waves in V5-V6 are likely also hyperacute.
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/what-does-final-diagnosis-of-stemi-vs/
  • Queen of Hearts: OMI with high confidence
ECG
  • HPI: Man in his 30s with type 1 DM presented with 2 days of midsternal and epigastric pain, described as both “sharp” and “squeezing”. Associated with nausea, vomiting, and dyspnea. Pain worse with supination and improved with upright posture.
  • Cath: Thrombotic subtotal occlusion of LCx/OM1
  • Key ECG: Subtle hyperacute T waves in lead I, STE and HATW in II > aVF, Subtle STD in V1 and V2, STE and HATW in V5 and V6
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/what-factor-determines-final-diagnosis/
  • Queen of Hearts: High confidence for OMI

🚨 OMI (+) Anterior Hyperacute T-waves:

46 examples below. Swipe ↔️ or use arrow keys to view more.
ECG
  • HPI: middle aged man had sudden chest pain
  • Cath: 100% acute thrombotic LAD occlusion was opened and stented
  • Key ECG: The concern without context would be possible LAD OMI signs. There is poor R wave progression, slight STE, hyperacute T waves in V2-V5, reciprocal STD in inferior leads. By itself — The poor R wave progression we see in Figure-1 would not be diagnostic of acute OMI. But in association with the ST-T wave changes seen on this tracing — this clearly adds further support of an acute event in progress
  • Link to full case @ Dr. Smith’s ECG Blog:
ECG
  • HPI: 60-something male presented with 2 hours of chest pain
  • Cath: Total proximal LAD occlusion
  • Key ECG: This is diagnostic of proximal LAD Occlusion (LAD OMI). There is STE and Hyperacute T-wave (HATW) in V1, HATW in V2-V4 (with some STE), STD in V6 (precordial swirl pattern). There is a reciprocally inverted T-wave in lead III, and reciprocal STD in II and aVF.
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/60-something-male-with-2-hours-of-chest-pain/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 60 year old developed exertional chest pain with diaphoresis and called EMS.
  • Cath: 100% proximal LAD occlusion
  • Key ECG: Loss of R waves in V2-V3 with hyperacute waves V1-V5. No significant ST elevation but there are two forms of ST depression: deWinter T wave V3-V5 and precordial swirl with ST depression V6 reciprocal to subtle STE in V1. Hyperacute T waves in I/aVL with reciprocal inferior ST depression
  • Link to full case @ Dr. Smith’s ECG blog: (July 7, 2024)
    https://drsmithsecgblog.com/60-year-old-with-chest-pain-stemi/
  • Queen’s Verdict: OMI with high confidence
ECG
  • HPI: 72 yo M with hx of CAD with stent placement presented to a rural hospital with chest pain for 2 hours
  • Cath: 99% in stent-restenosis of the proximal LAD
  • Key ECG: T waves in V2-V5 are hyperacute T waves. They have a large area under the curve relative to the QRS size. They are bulky, not just tall. The T waves are more than twice the height of the R waves in leads V2 and V3,
  • Link to full case @ Dr. Smith’s ECG blog: (June 3, 2024)
    https://drsmithsecgblog.com/every-rural-hospital-needs-queen-of/
  • Queen’s Verdict: High confidence OMI
ECG
  • HPI: 62 yo M with 2 days of intermittent chest pain, now constant
  • Cath: 100% Mid LAD Occlusion
  • Key ECG: Some hyperacute T waves are tall in proportion to the QRS. T wave inversion in inferior leads also clues to LAD occlusion
  • Link to full case @ Dr. Smith’s ECG blog: (October 14, 2023)
    https://drsmithsecgblog.com/this-ecg-was-texted-to-me-after-fact/
  • Queen of Hearts: Not OMI, Mid-confidence
ECG
  • HPI: 40 year old male with no cardiac history presented with acute substernal chest pain. He reported associated diaphoresis, radiation to the bilateral upper extremities and mild shortness of breath.
  • Cath: 95% stenosis of distal LAD
  • Key ECG: Hyperacute T waves in V2-V6 are diagnostic. STE meet STEMI criteria as well since there is 1 mm of increase in V4 and V5. There is no reciprocal ST depression, but only 50% of LAD OMI have reciprocal ST depression.
  • Link to full case @ Dr. Smith’s ECG blog: (September 22, 2023)
    https://drsmithsecgblog.com/this-ecg-was-texted-to-me-normal/
  • Queen of Hearts: High Confidence
ECG
  • HPI: 50-something male had onset of chest pain. It is constant, 9/10, left-sided CP that radiates into left arm and jaw. Endorses some associated SOB, but denies back pain, fever, cough, chills, leg swelling, or other new symptoms. Has never had this before. Takes metoprolol for HTN.
  • Cath: 99% stenosis of distal LAD
  • Key ECG: Hyperacute T waves present in leads V1-V4. There is also diminution of the S-wave in V3, and increase in STE with more bulk to the T-wave also in V3.
  • Link to full case @ Dr. Smith’s ECG blog: (September 1, 2023)
    https://drsmithsecgblog.com/a-middle-aged-man-with-acute-chest-pain/
  • Queen of Hearts: High confidence OMI
ECG
  • HPI: 50M chest pain x hours
  • Cath: prox LAD 99-100% thrombus filled occlusion
  • Key ECG: There are hyperacute T waves in V2-V5, I, II, aVL. The STD also present in V2 completes the description of de Winter T waves (hyperacute T wave with depressed ST takeoff).
  • Link to full case @ Dr. Smith’s ECG Blog: 2023-04-17
ECG
  • HPI: 50M with intermittent chest pain, constant for past hour
  • Cath: 95% mid-LAD culprit
  • Key ECG: Suggestive of LAD OMI, with hyperacute T waves in a large LAD distribution including precordial leads, high lateral leads, and inferior leads. Barely any STE, and thus not meeting STEMI criteria 
  • Link to full case @ Dr. Smith’s ECG Blog: 2023-03-09
ECG
  • HPI: middle aged woman with acute chest pain & SOB
  • Cath: Mid-LAD culprit lesion, 99% stenosis stented with TIMI 3 flow
  • Key ECG: Very clear and specific for acute LAD OMI, with hyperacute T waves in the LAD distribution including leads V2-V6, II, III and aVF
  • Link to full case @ Dr. Smith’s ECG Blog: 2023-01-28
ECG
  • HPI:60F w/ CAD s/p PCI presenting with chest pain x 3 hr.
  • Cath: LAD thrombus
  • Key ECG:There are hyperacute T-waves in I, aVL, V2-V6. These are wide, bulky, with large area under the curve relative to the QRS size. Furthermore, there is a QS-wave in V3 and qrS in V4, both suggestive of MI at some time (past or present). Dr. Smith has shown here and validated here that old MI has relatively small T-wave (by amplitude). In this situation (QS-waves), a T/QRS ratio ＞0.36 in any of V1-V4 is highly specific for ACUTE MI.
  • Link to full case @ Dr. Smith’s ECG Blog: 2023-01-02
ECG
  • HPI: 50M with acute chest pain and dyspnea x 45 min
  • Cath: total thrombotic occlusion of the mid-LAD was opened and stented
  • Key ECG: There is sinus rhythm with normal QRS complex except slightly sluggish R wave progression (this is due to acute LAD OMI, diminishing the R wave voltage in its distribution). We see STE in V2-V4, and a hint of STE in II, III, and aVF. Hyperacute T waves are present in V2-V4, and II, III, and aVF.
  • Link to full case @ Dr. Smith’s ECG Blog: 2022-02-12
ECG
  • HPI: 40 M p/w substernal chest pain
  • Cath: 99% LAD thrombus s/p successful stent
  • Key ECG: The T-waves are hyperacute, but most important, the minimal ST Elevation is accompanied by Terminal QRS Distortion, or at least nearly so. The ST Elevation in V2 and V3 is NEVER normal if it is accompanied by terminal QRS distortion, as defined by absence of S-wave and J-wave in EITHER V2 or V3. There is absence of both in V3 here (although one of the complexes in V3 has a tiny S-wave).
  • Link to full case @ Dr. Smith’s ECG Blog: 2022-02-04
ECG
  • HPI: 60M with CAD awoken from sleep by severe epigastric/substernal pain
  • Cath: 100% thrombotic occlusion of the mid LAD, at the site of his prior LAD stent
  • Key ECG: There is sinus rhythm with overall normal QRS complexes, normal R wave progression. There is STE in V2-V4, maximal in V3. The T wave in V3 and V4 is likely hyperacute, as it is fat, broad, full, and nearly symmetric in V4. A prior ECG, if available as in this case, would help to confirm or deny whether these are truly hyperacute.
  • Link to full case @ Dr. Smith’s ECG Blog: 2021-10-05
ECG
  • HPI: 37F with chest pain for 5 hours
  • Outcome: patient was discharged but 12 hours later was found collapsed at home with no signs of life
  • Key ECG: The T-waves are huge in proportion to the QRS, the QRS amplitude is very small, the T-waves are symmetric and fat, there are sagging ST segments in I, II, V3 and V4.  V3 should have some ST elevation, but it actually has a bit of ST depression
  • Link to case @ Dr. Smith’s ECG blog: 2016-04-20
ECG
  • HPI: Patient with chest pain
  • Cath: 100% occlusion of the mid-LAD
  • Key ECG:  There is ST elevation in lead V2, and it must be explained.  Is it benign?  If it were benign, then there should be excellent R-wave progression.  There is not.  In fact, the R-wave gets smaller from V2 to V3.  Furthermore, the T-waves are much more symmetric than the T-waves of early repolarization
  • Link to full case @ Dr. Smith’s ECG blog: 2014-12-12
ECG
  • HPI: 50F with severe substernal chest pain x 30 min
  • Cath: complete occlusion of the proximal LAD which was opened and revealed a very large first diagonal (this explains the predominance of V4-V6 on the ECG)
  • Key ECG: There are hyperacute T-waves in V4-V6, I and aVL, with reciprocal ST depression and T-wave in version in III and aVF. V4 shows a de Winter’s T-wave, with some ST depression. This is suggestive of proximal LAD occlusion
  • Link to full case @ Dr. Smith’s ECG Blog: 2014-08-09
ECG
ECG
  • HPI: 60M with CAD presenting with 1 hr substernal chest pain
  • Cath: LAD occlusion was opened
  • Key ECG: There are symmetric T-waves and poor R-wave progression.  There is 1 mm of ST elevation at the J-point in leads V2 and V3.  This formerly met “criteria” for thrombolytics in the ACC/AHA guidelines of 2004, though of course this amount of ST elevation is very nonspecific.  It is nonspecific because normal variant ST elevation can be even much greater.  However, normal variant ST elevation always has better R-wave progression and asymmetric T-waves which have a slow upstroke and a rapid downstroke.
  • Link to full case @ Dr. Smith’s ECG blog: 2013-06-18
ECG
  • HPI:40F with CAD s/p LAD p/w chest pain
  • Cath: 100% in stent thrombotic re-occlusion of LAD
  • Key ECG: There are hyperacute T-waves in V1-V4, ST elevation in V1 and V2, and ST depression in II, III, aVF, V5 and V6. This is suggestive of LAD occlusion.
  • Link to full case @ Dr. Smith’s ECG Blog: 2011-06-06
ECG
  • HPI: 35F with sudden onset epigastric pain
  • Cath: ostial LAD occlusion, opened and stented; EF 35% post-cath
  • Key ECG: T-waves in V2 and V3 tower over the entire QRS. Early repolarization always has prominent R-waves in V2-V4. This is not early repol.
  • Link to full case @ Dr. Smith’s ECG Blog: 2010-08-12
ECG
  • HPI: A patient had cardiac arrest with ventricular fibrillation and was successfully defibrillated
  • Cath: 100% stenosis in proximal ostial LAD
  • Key ECG: ST elevation in V2-V4 and aVL. Hyperacute T waves
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/guidelines-would-erroneously-say-that/
  • Queen of Hearts: OMI with high confidence
ECG
  • HPI: 70 yo M who presented with acute chest pain
  • Cath: 100% LAD occlusion
  • Key ECG: Small Q waves in V2-V3 and loss of R wave in V3. QRS amplitude in V2 and R wave in V4 are smaller, making the anterior ST elevation more concerning. Relative to the QRS in V2-V3, the T waves are large. Also see down/up ST segment in III reciprocal to a hint of ST elevation in aVL, which localizes occlusion to the proximal LAD.
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/two-patients-with-chest-pain-with-qrs/
  • Queen of Hearts: High Confidence OMI
ECG
  • HPI: 77 yo F with history of HTN and hyperlipidemia presented to the ED at around 0520 after waking up at 0400 with 10/10 chest heaviness radiating to both arms
  • Cath: 100% proximal LAD occlusion
  • Key ECG: RBBB and transmural ischemia of the anterior wall, most likely from an occlusion of the proximal LAD. There is a hyperacute distribution of T waves from V1-V4. V1 has inappropriate ST elevation with a terminally negative T wave. The T waves in V2, V3, V4 are symmetrical, upright, and too large for their preceding QRS complexes. Leads I and aVL have hyperacute T waves as well. There are reciprocal changes inferiorly, most pronounced in lead III with downsloping ST segment followed by a terminally upright T wave
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/do-you-need-to-be-trained-health-care/
  • Queen of Hearts: High confidence for OMI
ECG
  • HPI: 60ish yo M with hx CAD and stents p/w sudden onset epigastric abdominal pain radiating up into his chest at home, waking him from sleep. He had active chest pain in this triage EKG
  • Cath: 100% Thrombotic occlusion of LAD
  • Key ECG: There is sinus rhythm with overall normal QRS complexes, normal R wave progression. There is STE in V2-V4, maximal in V3. The T wave in V3 and V4 is likely hyperacute, as it is fat, broad, full, and nearly symmetric in V4.
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/expert-human-ecg-interpretation-andor/
  • Queen of Hearts: OMI with high confidence
ECG
  • HPI: A woman in her 70s who presented with acute chest pain
  • Cath: Mid LAD lesion 95% occluded
  • Key ECG: Acute anterior OMI with STE less than STEMI criteria in V1-V4, hyperacute T waves in V2-V4, and suspiciously flat isoelectric ST segments in III and aVF suspicious for reciprocal findings. Because the reciprocal area from Vs-V4 is the posterior wall, many anterior OMIs do not have clear reciprocal findings on the standard 12 leads
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/ems-told-not-stemi-what-do-you-think/
  • Queen of Hearts: High confidence
ECG
  • HPI: 60ish-year old complaining of vomiting, diarrhea, and “bubbles in my chest”
  • Cath: Severe 95% hazy distal LM, Severe 80% ostial LAD, 100% occluded distal LAD thought to be due to distal embolization from lesion in prox LAD, Mild CAD in LCx, 70% eccentric proximal RCA
  • Key ECG: Hyperacute T waves in III and aVF, reciprocal STD in aVL with a reciprocally inverted T wave in aVL. Hyperacute T waves in V3 and V4. ST depression in V1 and V2
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/vomiting-diarrhea-and-bubbles-in-my/
  • Queen of Hearts: High confidence OMI
ECG
  • HPI: 43 yo M with history of DM II, hyperlipidemia, and a FMHx MI who presented to a family clinic with 2 days of epigastric pain that started after consuming a meal
  • Cath: 80% stenosis of proximal LAD. 99% stenosis of LAD distal to the first diagonal branch. 95% stenosis of the ostium of the first diagonal branch
  • Key ECG: T waves in V1-V4 are hyperacute. There is positively sloped ST segment straightening in V2 and V3. There is a fragmented QS complex in V2. Lead aVL has a very subtly convex T wave with terminal T wave inversion. There is very slight horizontal ST segment straightening in leads III and aVF. These inferior leads could be normal, however, in combination with the hyperacute anterior T waves, they should be interpreted as showing reciprocal changes. V6 also has very slight ST depression. There is also Q wave in V2 and a small amount of STE. STD in V5 – V6.
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/see-how-bad-outcome-can-be-if-you-dont/
  • Queen of Hearts: OMI with high confidence
ECG
  • HPI: 46 yo M presented to the ED with 2 days of heavy substernal chest pain and nausea. History of Wolff-Parkinson-White and “heart attack” but said neither had been treated
  • Cath: Complete occlusion of LAD at the ostium
  • Key ECG: STE and HATW across the precordium, Q waves in V1-V4, Subtle STE and HATW in I and aVL. Terminal TWI suggestive of early reperfusion most pronounced in I, aVL, V5, V6. Reciprocal STD with ischemic down-up T waves in II, III, aVF
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/46-year-old-with-chest-pain-develops/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: A man in his 60s presented with acute chest pain and normal vital signs
  • Cath: Acute total mid-LAD occlusion
  • Key ECG: HATW with massive and symmetric inflated area under the T wave compared to the QRS. They are symmetric, fat, convex on both sides. V3-V5 also have depressed HATW takeoff which qualifies them as rare deWinter subtype of HATW
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/60-yo-with-chest-pain-why-abnormal-qrs/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: A man in his 40s called EMS for acute chest pain that awoke him from sleep along with nausea and shortness of breath. His history is notable for heart failure with EF 18%, insulin dependent diabetes, and polysubstance use
  • Cath: Acute proximal LAD culprit, 100% stenosis, thrombotic occlusion
  • Key ECG: EKG shows new RBBB and LAFB, with small but important concordant STE in V2. The T waves in V5 are possibly hyperacute. Because the most severe LAD OMIs can cause ischemic failure of the RBB and LAF, any patient with ACS symptoms and new RBBB and LAFB with any concordant STE has LAD OMI until proven otherwise
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/acute-chest-pain-right-bundle-branch/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 56 yo M with a history of diabetes, dyslipidemia, hypertension, and coronary artery disease presented to the ED with sudden onset weakness, fatigue, lethargy, confusion. Developed 10/10 chest pain and some diaphoresis on day 2 of his admission.
  • Cath: 90% stenosis in the proximal segment of the LAD
  • Key ECG: The T waves in the anterior leads, especially in V2 and V3, are hyperacute. While they only show 0.5 mm of STE, the T waves are symmetrical, have a straightened upstroke, and are bulky in proportion to their QRS complexes. Though there is not reciprocal change here, it is important to remember that the reciprocal territory to the anterior wall is the posterior wall.
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/the-computer-and-overreading/
  • Queen of Hearts: Not OMI with high confidence
ECG
  • HPI: A woman in her 60s came to the ER with chest discomfort and shortness of breath. Had a history of previous anterior MI treated by primary PCI to the proximal EKG
  • Cath: 100% in-stent restenosis of proximal LAD
  • Key ECG: Massive hyperacute T waves in V2 and V3. There is ST Elevation that does not meet criteria in V2 and V3
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/how-terrible-can-it-be-to-fail-to/
  • Queen of Hearts: OMI with high confidence
ECG
  • HPI: 40 year old presented with 90 minutes of midsternal chest pressure, radiating to bilateral arms, with shortness of breath
  • Cath: 100% LAD occlusion
  • Key ECG: ST elevation in V3-V4 which meets STEMI criteria, which could be present in either early repolarization, pericarditis, or injury. There are also hyperacute T waves in V4-V5 (excluding early repolarization and pericarditis), leaving only LAD occlusion for this patient presenting with classic symptoms of ACS. The T waves in V3 are proportional to its large QRS whereas in V4 they tower over its small QRS. The T wave in V5 is much smaller, but relative to its QRS it is large and bulky
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/will-this-case-be-flagged-for-quality/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 30-something reports gradual onset of reproducible, persistent, substernal chest wall discomfort that radiates to both arms and described as a muscle contraction since waking up, associated with nausea and vomiting. There is a history of HTN with medication compliance.
  • Cath: 100% proximal LAD occlusion
  • Key ECG: HATW in V2 and aVL, STE in V1, and ST depression in I, inferior leads, and V3-V6.
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/the-worst-thing-you-can-be-when-you/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 60-something male presented with one hour of “oppressive” chest pain radiating to the back and to the left arm. Has a history of diabetes and COPD
  • Cath: 99% culprit lesion of proximal LAD
  • Key ECG: 0.5 mm ST elevation in V2 and V3, HATW in V2-V4. Terminal QRS distortion, meaning there are no S- or J- waves in either V2 or V3. Lead II has ST depression. Lead III has STD with down-up T-wave, as does aVF. There is minimal STE in aVL
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/this-is-excellent-omi-care/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: Middle aged man presented with acute chest pain
  • Cath: 100% proximal LAD occlusion
  • Key ECG: Subtle STE in V1, very HATW in V2, and subtle HATWs in V3-V6. There is ST depression in V5 and V6. Any ST depression (except for in aVR( makes it impossible for any STE to be a normal variant. There is inferior ST depression and “down-up” T-waves
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/what_is_this_pattern_ps/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 75 yo without cardiac history presented to the ED with 3 hours of acute chest pain which radiated to the jaw and bilateral shoulders
  • Cath: 100% proximal LAD occlusion
  • Key ECG: Sinus bradycardia, normal conduction, normal axis, normal R wave progression, and voltages. The minimal ST Elevation in the anterior leads is normal. T waves in V2-V4 are wide based, bulky, and large related to their QRS. ST depression in V6
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/75-year-old-with-acute-chest-pain-6-bad-reasons-not-to-cath/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: Elderly male with new onset chest pain. Substernal, 7/10 pain, crushing in nature, and radiating to the neck. History of T2DM treated with insulin, DVT, and abdominal surgery.
  • Cath: 100% occlusion of the first diagonal branch
  • Key ECG: Lead I QRS morphology along with absent significant R waves in V1-V2 is consistent with incomplete left bundle branch block. There is minimal J-point elevation noted in the anterolateral and high-lateral leads. T waves in leads V3-V6 are notably hyperacute with the most pronounced T wave changes seen in lead V5.
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/87-year-old-with-chest-pain/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: Middle aged man complaining of chest pain
  • Cath: 80% stenosis in LAD, acute culprit
  • Key ECG: HATW in V4-V5
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/chest-pain-this-ecg-and-an-undetectable-troponin-after-6-hours-of-pain/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: A woman in her 60s with multiple comorbidities presented to the ED with acute chest pain. Vitals were within normal limis. She described “burning” pain in the center of her chest, no radiation, and lightheadedness.
  • Cath: mid LAD was the culprit, TIMI 1 flow
  • Key ECG: Deep but narrow Q wave seen in lead III, with a smaller Q wave in lead aVF. ST depression with shallow T wave inversion in leads I and aVL. QS complexes present in leads V1 – V4. HATW in leads V3-V5
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/what-do-you-think-happened-to-this-woman-with-chest-pain/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: A woman in her 60s presented with acute chest pain and normal vital signs
  • Cath: mid-LAD occlusion
  • Key ECG: HATW in V2-V3, down-up T waves in III, aVF, and V6. There are all highly specific for LAD Occlusion MI
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/a-woman-in-her-60s-with-chest-pain-and-no-stemi/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: A woman in her 40s presented with acute chest pain. Vitals were within normal limits.
  • Cath: Total mid-LAD thrombotic occlusion
  • Key ECG: HATW in V2-V5, and some STE in V3, V4, II, III, aVF. Reciprocal STD in aVL from lead III
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/will-this-patient-get-care-of-the-past-or-care-of-the-future-nstemi-is-a-worthless-diagnosis/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 62 yo M with h/o CAD and stent in 1st OM presented with chest pain while biking
  • Cath: Cath results were complex, there was TIMI-2 flow in the LAD by the time of cath.
  • Key ECG: RBBB with large R wave in V1 and wide S-wave in lateral leads I, aVL, V5, and V6. There is a slight amount of ST elevation in lead V3. RBBB usually has inverted T wave with up to 1 mm ST depression in leads V2 and V3, so these upright T’s with slight ST elevation is highly suspicious for anterior STEMI. HATW in V5-V6.
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/chest-pain-and-right-bundle-branch-block-2/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 60-something male with history of HTN and hyperlipidemia was driving when he had acute onset of chest pain
  • Cath: 100% ostial (very proximal) LAD occlusion
  • Key ECG: There is ST Elevation and Hyperacute T-wave in V1-V3. There is a touch of ST depression in V6. There is also minimal STD in inferior leads. So this is Precordial Swirl pattern of LAD occlusion proximal to the septal perforator, indicating septal OMI.
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/do-not-interrupt-the-physician-to-show-him-her-this-normal-ecg-unless-he-she-uses-the-queen-of-hearts/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: 28 year old with 8 hours of chest pain
  • Cath: LAD: type III-IV vessel with a proximal thrombotic or embolic occlusion
  • Key ECG: Sinus rhythm with RBBB and likely LAD occlusion: HATW in I, aVL, and minimal STE in V1, V2
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/anterior-stemi-with-rbbb-has-vf-x-3-how/
  • Queen of Hearts: OMI high confidence

🚨 OMI (+) Lateral Hyperacute T-waves:

11 examples below. Swipe ↔️ or use arrow keys to view more.
ECG
  • HPI: 60 year old developed exertional chest pain with diaphoresis and called EMS.
  • Cath: 100% proximal LAD occlusion
  • Key ECG: Loss of R waves in V2-V3 with hyperacute waves V1-V5. No significant ST elevation but there are two forms of ST depression: deWinter T wave V3-V5 and precordial swirl with ST depression V6 reciprocal to subtle STE in V1. Hyperacute T waves in I/aVL with reciprocal inferior ST depression
  • Link to full case @ Dr. Smith’s ECG blog: (July 7, 2024)
    https://drsmithsecgblog.com/60-year-old-with-chest-pain-stemi/
  • Queen’s Verdict: OMI with high confidence
ECG
  • HPI: 50 yo M presenting with chest pain for 1 hour radiating to the back and jaw
  • Cath: 80% mid LAD stenosis, first diagonal artery with 95% stenosis
  • Key ECG: There’s normal sinus rhythm, normal conduction, normal axis, normal R wave progression and normal voltages. There’s clear T wave inversion in III/aVF, which is reciprocal to subtle ST elevation and hyperacute T waves in I/aVL (broad, symmetric, and larger than the entire QRS in aVL). There is also straightening of the ST segments in I/aVL, and some ST depression in V3.This is diagnostic of Occlusion MI of the high lateral wall, either from circumflex or first diagonal.
  • Link to full case @ Dr. Smith’s ECG blog: (September 8, 2023)
    https://drsmithsecgblog.com/50-year-old-in-remote-rural-community/
  • Queen of Hearts: High confidence OMI
ECG
  • HPI: 67F awoke from sleep at 2:00 AM with L-sided chest pain
  • Cath: Large D1 100% occluded
  • Key ECG: There are large, symmetric T-waves in I, aVL, V2-V5 suggestive of proximal LAD occlusion. There are also down-up T-waves in III and aVF (these are very specific RECIPROCAL findings and clinch the diagnosis.)
  • Link to full case @ Dr. Smith’s ECG Blog: 2016-03-03
ECG
  • HPI: Middle aged man with chest pain for hours
  • Cath: nearly occluded D1
  • Key ECG: The STE in aVL, with minimal reciprocal ST depression in inferior leads, in the setting of well-formed Q-waves, is of unknown age, but very likely to represent old lateral MI with persistent ST elevation. There is less than 1 mm of STE in I, aVL, V5 and V6, but these leads are notoriously insensitive for coronary occlusion. Only about 50% of occlusion of arteries supplying this area of myocardium have ST elevation that meets “criteria” of 1mm or more. The T-waves in V5 and V6 make this suggestive of coronary occlusion. They are far too tall and fat to be normal. They are hyperacute.
  • Link to full case @ Dr. Smith’s ECG Blog: 2015-07-10
ECG
  • HPI: 77M with acute chest pain a/w nausea, vomiting, diaphoresis x 2 hours
  • Cath: 100% distal LAD occlusion
  • Key ECG: It is clear that the T-waves in V4-V6 are hyperacute. They are far too large for the QRS. T-waves should be proportional to the QRS. If they are too large, you must suspect hyperacute T-waves and aggressively evaluate the patient with at least a high quality emergent echocardiogram
  • Link to full case @ Dr. Smith’s ECG Blog: 2014-11-26
ECG
  • HPI: Patient who originally was admitted for pneumonia and had been transferred out of the ICU a day prior. He had a history of HFrEF, HTN, and AML
  • Cath: Thrombotic occlusion of the proximal LAD
  • Key ECG: RBBB. There is <1 mm of STE in I, aVL, V5, V6. Hyperacute T waves in I, aVL, V5, V6.
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/the-current-stemi-paradigm-because/
  • Queen of Hearts: High confidence for OMI
ECG
  • HPI: 46 yo M presented to the ED with 2 days of heavy substernal chest pain and nausea. History of Wolff-Parkinson-White and “heart attack” but said neither had been treated
  • Cath: Complete occlusion of LAD at the ostium
  • Key ECG: STE and HATW across the precordium, Q waves in V1-V4, Subtle STE and HATW in I and aVL. Terminal TWI suggestive of early reperfusion most pronounced in I, aVL, V5, V6. Reciprocal STD with ischemic down-up T waves in II, III, aVF
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/46-year-old-with-chest-pain-develops/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: A woman in her 70s was woken from sleep by midsternal chest pain radiating to left arm with nausea
  • Cath: Mid LCX 90%
  • Key ECG: EKG shows sinus rhythm, normal QRS, and signs of inferoposterolateral OMI. There is very small STE in III and aVF which do not meet STEMI criteria, hyperacute T waves, reciprocal T wave inversion in aVL, and maximal STD in V2-V3 showing posterior OMI. The T waves in V5-V6 are likely also hyperacute.
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/what-does-final-diagnosis-of-stemi-vs/
  • Queen of Hearts: OMI with high confidence
ECG
  • HPI: Man in his 30s with type 1 DM presented with 2 days of midsternal and epigastric pain, described as both “sharp” and “squeezing”. Associated with nausea, vomiting, and dyspnea. Pain worse with supination and improved with upright posture.
  • Cath: Thrombotic subtotal occlusion of LCx/OM1
  • Key ECG: Subtle hyperacute T waves in lead I, STE and HATW in II > aVF, Subtle STD in V1 and V2, STE and HATW in V5 and V6
  • Link to full case @ Dr. Smith’s ECG blog: view post
    https://drsmithsecgblog.com/what-factor-determines-final-diagnosis/
  • Queen of Hearts: High confidence for OMI
ECG
  • HPI: A woman in her 40s with no known comorbid conditions presented with acute chest pain radiating to left arm and neck, started approximately 4 hours prior to arrival
  • Cath: 100% LAD thrombotic occlusion
  • Key ECG: Right arm/right leg lead reversal (lead I resembles aVL, lead aVF resembles aVR). RBBB and concordant STE in V1-V3, reciprocal STD in v5-V6, HATW in I and aVL with reciprocally negative HATW in III and aVF
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/would-you-like-to-see-this-ecg-without/
  • Queen of Hearts: OMI high confidence
ECG
  • HPI: A woman in her 60s had acute chest pain and shortness of breath
  • Cath: Proximal total LAD occlusion
  • Key ECG: Sinus rhythm, RBBB, and anterolateral OMI pattern with concordant STE in V2, inappropriate STD and negative HATW in III and aVF
  • Link to full case @ Dr. Smith’s ECG blog:  view post
    https://drsmithsecgblog.com/a-woman-in-her-60s-with-acute-chest/
  • Queen of Hearts: OMI high confidence

Additional Info

🔎 Where to measure ST Elevation:

  • At the J-point
    • According to the Fourth Universal Definition of Myocardial Infarction (2018) the magnitude of ST elevation should be determined using the J-point (junction between QRS termination and ST-segment onset)

🔎 Where to measure ST Baseline:

  • At the QRS onset
    • According to the Fourth Universal Definition of Myocardial Infarction (2018) the QRS onset should be used as the reference point.
    • They note that in patients with a stable baseline, the TP segment (isoelectric interval) is a more accurate method to assess the magnitude of ST-segment shift.
    • Tachycardia and baseline shift are common in the acute setting and can make this determination difficult. Therefore, QRS onset is recommended as the reference point for J-point determination
  • No clinical trial of reperfusion therapy has designated a method of measurement of ST elevation.
    • Because the PR segment may be normally depressed as part of the atrial repolarization wave, and that wave extends to the J-point, then if measured at the J-point, the ST segment should be measured relative to the PR segment.
    • If the ST segment is measured at 60 to 80 ms after the J-point (a point used in prior trials), it should be measured relative to the TP segment.
    • Measuring at 60-80 ms after the J-point, results in dramatically higher values (Source: PMID 16531592)

📺 MEDIA RESOURCES

📚 TEXT RESOURCES

👨‍🏫 TEST YOURSELF

  • The OMI Quizzes via Get The Gas
  • James McCabe’s 36 ECG challenge
    • Evaluate your ability to use the 12-Lead ECG to make the diagnosis of a coronary artery occlusion using a standardized list of 36 ECG’s from McCabe James McCabe’s paper below:
    • Source: McCabe, James M., et al. “Physician accuracy in interpreting potential ST‐segment elevation myocardial infarction electrocardiograms.” Journal of the American Heart Association 2.5 (2013): e000268. PMID 24096575

📱 MOBILE APPS

👸 QUEEN OF HEARTS ❤️

  • Queen of Hearts
    • Get an app that leverages an artificial intelligence model trained to detect acute coronary occlusion on any 12-lead ECG image with high precision

Q-wave / Non-Q-wave Dichotomy

  • 1941: Q-waves noted as a distinguishing feature of “acute coronary occlusion” compared to “acute coronary insufficiency with infarction”
    • Master, Arthur M., et al. “Differentiation of acute coronary insufficiency with myocardial infarction from coronary occlusion.” Archives of Internal Medicine 67.3 (1941): 647-657.
  • 1980: The terms “Q-wave” and “Non-Q-wave” infarctions were reportedly first coined
    • PMID 8421361: Spodick, David H. “Q-Wave vs Non—Q-Wave Infarction: An Oversimplified Dichotomy.” JAMA 269.5 (1993): 590-590.
      • “The terms ‘Q-wave’ and ‘non-Q-wave’ infarctions were first coined in a letter by respected cardiologists. Unfortunately, this terminology, probably due to its distinguished provenance, was rapidly taken up by clinicians and investigators.”
  • 1983: Q-wave vs Non-Q-wave recognized as an oversimplified dichotomy
    • PMID 6829457: Spodick, David H. “Q-wave infarction versus ST infarction. Nonspecificity of electrocardiographic criteria for differentiating transmural and nontransmural lesions.” Am J Cardiol 51 (1983): 913-915.
      • “Whatever the reason for continued confusion regarding their anatomic extent, the pseudospecificty of Q and S-T myocardial infarctions remains a lasting myth … False terminology does more than semantic damage: it does conceptual damage. If we continue to accept a Q infarct as dependably indicating a transmural lesion, we can inhibit consideration of what it really does mean … Given the ultimate nonspecificity of many electrocardiographic findings it should not be surprising that they overlap to such a a degree that “transmural” and “nontransmural” are gross misnomers.”
  • 1988: Q-Wave vs Non-Q-Wave recognized as an oversimplified dichotomy
    • PMID: 3414524: Spodick, David H. “Comprehensive electrocardiographic analysis of acute myocardial infarction by individual and combined waveforms.” The American Journal of Cardiology 62.7 (1988): 465-467.
      • “The ‘Q’ versus ‘non-Q’ dichotomy is inadequate for clinicopatholologic and prognostic electrocardiographic classification of acute myocardial infarction. All individual and appropriate combinations of waveforms, their distributions and temporal behavior must be characterized with due regard for the many confounding factors outlined”
  • 1992: Q-Wave vs Non-Q-Wave recognized as an oversimplified dichotomy
    • PMID 1518115: Moss, Arthur J. “Q-Wave vs Non—Q-Wave Myocardial Infarction: An Oversimplified Dichotomy.” JAMA 268.12 (1992): 1595-1596.
      • “The Q-wave vs non-Q-wave categorization does not provide sufficiently sensitivity, specificity, or predictive accuracy about the subsequent clinical course of patients with a first myocardial infarction to use it as reliable data in the clinical decision making process.”

STEMI / NSTEMI Dichotomy

Evolution of STEMI criteria:

  • 1994: 1mm in all leads – STEMI “millimeter criteria” are born
  • 2000: Increased to 2mm in V1-V3
  • 2004: Back to 1mm everywhere
  • 2007: V2 and V2 now have ♂ / ♀ difference
  • 2009: V2 and V3 now have ♂ / ♀ and age difference
    • PMID 01928193: 📕 AHA/ACCF/HRS Standardization and Interpretation of Electrocardiogram (Wagner and Macfarlane)
  • 2012: No changes to STEMI criteria
  • 2018: No changes to STEMI criteria
    • PMID 30571511: 📕 4th Universal Definition of MI
    • Introduce guidance on points from which to measure ST segment

OMI / NOMI Dichotomy

  • 2014: “The False STEMI – NonSTEMI Dichotomy” term is coined
  • 2018: “OMI / NOMI” term coined via Twitter poll
  • 2018: “The OMI Manifestos” is published
  • 2019: Prospective, real-world evidence showing the gap between ST elevation myocardial infarction (STEMI) and occlusion MI (OMI)
    • PMID 31331673: Meyers, H. Pendell, and Stephen W. Smith. “Prospective, real-world evidence showing the gap between ST elevation myocardial infarction (STEMI) and occlusion MI (OMI).” International Journal of Cardiology 293 (2019): 48-49.
  • 2021: STEMI(-) OMI patients noted with significant delays to catheterization but adverse outcomes more similar to STEMI(+) OMI than those with no occlusion.
    • PMID 33308915: Meyers, H. Pendell, et al. “Comparison of the ST-elevation myocardial infarction (STEMI) vs. NSTEMI and occlusion MI (OMI) vs. NOMI paradigms of acute MI.” The Journal of emergency medicine 60.3 (2021): 273-284.
  • 2021: Blinded interpretation using predefined OMI ECG findings found to be superior to STEMI criteria for the ECG diagnosis of Occlusion MI
    • PMID 33912650: Meyers, H. Pendell, et al. “Accuracy of OMI ECG findings versus STEMI criteria for diagnosis of acute coronary occlusion myocardial infarction.” IJC Heart & Vasculature 33 (2021): 100767.
  • 2021: Step-by-step approach to OMI diagnosis proposed by Drs. Aslanger, Meyers and Smith
    • PMID 34523597: Aslanger, Emre K., H. Pendell Meyers, and Stephen W. Smith. “Recognizing electrocardiographically subtle occlusion myocardial infarction and differentiating it from mimics: Ten steps to or away from cath lab.” Turk Kardiyoloji Dernegi Arsivi 49.6 (2021): 488.
  • 2022: The ACC endorses the following “STEMI Equivalents”: 1) LBBB or VP-rhythm with Sgarbossa or Smith-modified Sgarbossa Criteria; 2) Hyperacute T Waves; 3) Posterior STEMI; 4) De Winter Sign
    • PMID 36241466: 📕 Writing Committee, et al. “2022 ACC expert consensus decision pathway on the evaluation and disposition of acute chest pain in the emergency department: a report of the American College of Cardiology solution set oversight committee.” Journal of the American College of Cardiology 80.20 (2022): 1925-1960.
  • 2023:
    • PMID 37061867: Zoni, Cesar R., Debabrata Mukherjee, and Martha Gulati. “Proposed new classification for acute coronary syndrome: Acute coronary syndrome requiring immediate reperfusion.” Catheterization and Cardiovascular Interventions (2023).
  • 2023: A machine learning model demonstrated superiority in detecting subtle ischemic ECG changes indicative of OMI in an observer-independent approach
    • PMID 36778371: Al-Zaiti, Salah, et al. “Machine Learning for the ECG Diagnosis and Risk Stratification of Occlusion Myocardial Infarction at First Medical Contact.” (2023).
  • 2023: STEMI criteria found to miss the majority of OMI
    • PMID 34967919: McLaren, Jesse TT, et al. “Missing occlusions: Quality gaps for ED patients with occlusion MI.” The American Journal of Emergency Medicine (2023).

Created by

Mark Hellerman, MD
Mark Hellerman, MD

Mastering occlusion myocardial infarction (OMI) is no easy task. Recognizing the often-subtle ECG patterns of OMI and distinguishing them from their mimics requires an appreciation of numerous nuances and extensive exposure to real-world cases.

OMI Guide was created to make this learning process more efficient by helping clinicians train their own neural networks through deliberate visual pattern recognition. By organizing ECGs into discrete, thematic categories, the platform enables users to rapidly scroll through and compare related patterns while reinforcing the key features that distinguish OMI from its mimics.

Each case includes a concise summary of the clinical presentation, a quick reference to the defining ECG features, a link to the full case discussion on Dr. Smith’s ECG Blog, and links to relevant literature.

Building upon the educational foundation established by Dr. Smith’s ECG Blog and his tireless efforts to advance OMI education, OMI Guide was launched in August 2023  as a complementary resource designed to make this extensive collection of real-world cases more accessible for deliberate pattern-recognition training.

Currently curated by

Mriganka Nerkar (MS4)
Mriganka Nerkar (MS4)

In 2026, Mriganka Nerkar, MS4, led a major expansion of the OMI Guide, adding more than 100 new cases from Dr. Smith’s ECG Blog that had accumulated since the guide’s initial launch in August 2023

Mriganka has had an interest in Cardiology from a young age, working in a research laboratory where she was able to see cardiomyocytes beat in a petri dish for the first time. As a medical student, she had the opportunity to work with Dr. Hellerman and was introduced to OMI Guide at that time! She enjoyed learning about the nuances of ECG reading and especially about OMIs. She is currently applying for Internal Medicine this residency application cycle, with goals to pursue cardiology critical care.

Created by Mark Hellerman, MD, currently curated by Mriganka Nerkar, MS4