Learn to identify occlusion myocardial infarctions (OMIs) by reviewing angiographically confirmed cases from Dr. Smith's ECG Blog curated by Mark Hellerman, MD
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:
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
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.
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
2 examples below. Swipe ↔️ or use arrow keys to veiw more.
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
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.
6 examples below. Swipe ↔️ or use arrow keys to veiw more.
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
Queen's verdict: OMI (Confidence = High) This one stumped the Queen but she's still learning! Learn more about 👸❤️
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.
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
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
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.
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.
4 examples below. Swipe ↔️ or use arrow keys to veiw more.
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.
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.
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.
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)
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
7 examples below. Swipe ↔️ or use arrow keys to veiw more.
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.
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.
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.)
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.
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.
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.
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
Diffuse STE without reciprocal STD (except in V1 or AVR)
STE in lead II > STE in lead III
🚨 OMI (+) Mimics of Pericarditis:
2 examples below. Swipe ↔️ or use arrow keys to veiw more.
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.
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.
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)
✅ OMI (-) mimics from artifact:
6 examples below. Swipe ↔️ or use arrow keys to veiw more.
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.
Queen's verdict: OMI (Confidence = Mid) This one stumped the Queen but she's still learning! Learn more about 👸❤️
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.
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.
Queen's verdict: OMI (Confidence = Low) This one stumped the Queen but she's still learning! Learn more about 👸❤️
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.
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.
Queen's verdict: OMI (Confidence = High) This one stumped the Queen but she's still learning! Learn more about 👸❤️
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.
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:
10 examples below. Swipe ↔️ or use arrow keys to veiw more.
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.
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
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
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.
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.
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.
6 examples below. Swipe ↔️ or use arrow keys to veiw more.
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 TallR Wave in Lead V1(ie, R=S or R>S in V1) should prompt the following diagnosticconsiderations: 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 rightwardaxis+incompleteRBBB+lowvoltage+ 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 acutedyspnea
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:
Queen's verdict: OMI (Confidence = Low) This one stumped the Queen but she's still learning! Learn more about 👸❤️
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:
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:
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:
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:
7 examples below. Swipe ↔️ or use arrow keys to veiw more.
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).
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.
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.(5859) 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.
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.
Queen's verdict: OMI (Confidence = Low) This one stumped the Queen but she's still learning! Learn more about 👸❤️
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.
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:
1 examples below. Swipe ↔️ or use arrow keys to veiw more.
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
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:
2 examples below. Swipe ↔️ or use arrow keys to veiw more.
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.
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.
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:
7 examples below. Swipe ↔️ or use arrow keys to veiw more.
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
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.
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.
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.
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
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.
Queen's verdict: Not OMI (Confidence = Low) This one stumped the Queen but she's still learning! Learn more about 👸❤️
🚨 OMI (+) Subtle Anterior STE:
7 examples below. Swipe ↔️ or use arrow keys to veiw more.
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.
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.
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.)
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.
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.
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.
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
12 examples below. Swipe ↔️ or use arrow keys to veiw more.
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.
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.
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.
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.
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.
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
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.
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.
5 examples below. Swipe ↔️ or use arrow keys to veiw more.
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.
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
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.
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.
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.
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:
11 examples below. Swipe ↔️ or use arrow keys to veiw more.
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
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.
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.
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
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
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.
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.
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
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:
11 examples below. Swipe ↔️ or use arrow keys to veiw more.
HPI: 67F with chest pain
Cath: 99% mid LAD occlusion
Key ECG: de Winter’s T-waves. They are simply Hyperacute T-waves with depressed ST takeoff.
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)
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
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
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.”
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.
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.
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.
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)
Subjectively, this corresponds to T-waves that are abnormally large by area (both height and width), bulky, and abnormally symmetric, as if being physically inflated, but all relative to QRS size.
Objectively, increased AUC of the T-wave relative to the QRS has been shown by the following 2 quantifiable elements: 1) longer corrected QT interval, 2) greater T-wave to QRS amplitude ratio.
An additional feature of hyperacute T-waves is increased and abnormal T-wave symmetry, which has not yet been well quantified.
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:
7 examples below. Swipe ↔️ or use arrow keys to veiw more.
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
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)
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.
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)
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
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
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
Queen's verdict: Not OMI (Confidence = High) This one stumped the Queen but she's still learning! Learn more about 👸❤️
🚨 OMI (+) Anterior Hyperacute T-waves:
15 examples below. Swipe ↔️ or use arrow keys to veiw more.
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
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).
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
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.
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.
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).
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.
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
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
3 examples below. Swipe ↔️ or use arrow keys to veiw more.
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.)
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.
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
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)
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)
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
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
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).