Saturday, July 16, 2022

ECG Blog #320: Not the Culprit You Think!

The patient whose ECG is shown in Figure-1 — is a 68-year old man with risk factors, who presented with severe chest pain lasting ~1 hour — but which resolved by the time he arrived in the ED (Emergency Department). The patient reports that during the previous week — he experienced 2 similar episodes of severe chest pain, lasting about the same amount of time before spontaneously resolving.
  • The patient was pain-free on arrival in the ED — at which time the ECG in Figure-1 was obtained.

  • In view of the above history — How would YOU interpret the ECG in Figure-1?
  • Physiologically — Can you explain what happened anatomically to produce the ECG picture shown in Figure-1?

  • Should the cath lab be activated?

Figure-1: The initial ECG in today's case — obtained when the patient was pain-free! (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:
The rhythm in ECG #1 is sinus. Regarding intervals — the PR interval and QRS duration are normal; the QTc may be borderline prolonged. There is no chamber enlargement.

Regarding Q-R-S-T Changes:
  • There are Q waves of uncertain significance in high lateral leads I and aVL. 
  • R wave progression shows slightly delayed transition (the R wave becomes taller than the S wave is deep only between leads V4-to-V5).

The most remarkable findings in Figure-1 relate to ST-T wave Changes:
  • The ST segment is coved in high-lateral leads I and aVL. There appears to be significant ST elevation in lead aVL — in view of how tiny QRS amplitude is in this lead (which is why the Q wave in lead aVL may be relevant). Relative to QRS amplitude — there is fairly deep and symmetric T wave inversion in lead aVL. Similar ST-T wave changes are seen in lead I — albeit more modest. 
  • The 3 inferior leads (II,III,aVF) — each show similar reciprocal changes with respect to the ST-T wave appearance in lead aVL. (Note terminal positivity of the T wave in each of the 3 inferior leads — with this terminal positive T wave in lead III being taller than the R wave in this lead!).

  • In the Chest Leads — the most remarkable findings are in lead V2 — which shows straightening of the ST segment — with 1 mm of J-point ST elevation — and a distinct biphasic T wave, with rapid T wave descent into terminal negativity.
  • The ST-T waves in leads V3,V4 look similar to each other — in that they each manifest ST segment straightening (but no elevation) — and, a hint of terminal T wave negativity.
  • Lateral chest leads V5,V6 also look similar to each other — and show ST segment straightening, with slight ST depression.

  • IMPRESSION: The above history, in association with the appearance of the initial ECG in today's case — illustrate the "classic" picture of Wellens' Syndrome

What is Wellens' Syndrome?
The clinical significance of Wellens' Syndrome — is that its recognition tells you that the patient has a high-grade LAD (Left Anterior Descending) coronary artery narrowing with presumably "hot" thrombus having high propensity to propagate and/or totally occlude the LAD at any point in time (including immediately). That said — Wellens' Syndrome remains a misunderstood and often misdiagnosed clinical entity. For clarity — Consider the KEY clinical and ECG features that establish the diagnosis of Wellens' Syndrome:
  • There should be a history of prior chest pain that has resolved at the time the defining ECG is obtained.
  • There should be no more than minimal (if any) troponin elevation
  • There are no new infarction Q waves.
  • There may be slight (but not marked) ST elevation in one or more of the chest leads.
  • There is a characteristic biphasic T wave, with rapid T wave descent into terminal negativity in one or more of the chest leads (most often in lead V2 and/or V3 and/or V4)

What Wellens' Syndrome is NOT:
Greatest misunderstanding relates to what Wellens' Syndrome is not! Avoidance of this misunderstanding is best accomplished by appreciating the pathophysiology of this syndrome. In essence — the characteristic biphasic T wave appearance with terminal negativity reflects a reperfusion T wave! The patient has recently had total LAD occlusion for a brief period of time — but has now spontaneously reperfused.
  • The chest pain required for the definition of Wellens' Syndrome occurred at the time of coronary occlusion. But the reason the definition of Wellens' Syndrome requires the patient to be pain-free at the time the defining ECG is done — is that the "culprit" LAD lesion is now open. IF the "culprit" LAD lesion was still occluded — then rather than a warning of impending infarction (which is the purpose of promptly recognizing Wellens' Syndrome) — there would be ongoing acute infarction.
  • There is no more than minimal (if any) troponin elevation — because the duration of coronary occlusion was so brief that no more than minimal myocardial damage resulted. IF there is greater troponin elevation — this implies that significant myocardial damage has already occurred (which by definition means that you are dealing with a completed infarction — and not with Wellens' Syndrome).
  • For this same reason — there should not be new infarction Q (or QS) waves.
  • There is no more than slight ST elevation — because Wellens' Syndrome is not a STEMI (ie, it is not an "ST Elevation" MI).

  • Instead — the characteristic biphasic T wave with rapid T wave descent into terminal negativity is an indication that there was brief total occlusion of the LAD, which has now reperfused. This ECG finding is a reperfusion T wave. It may look identical to the ST-T wave appearance after a STEMI with marked troponin elevation that has now reperfused (be this reperfusion spontaneous — or by treatment with PCI or thrombolytics).

  • Clinically — the risk posed by Wellens' Syndrome — is that it is proof that there has already been acute thrombotic occlusion of the LAD, albeit brief in duration and followed by spontaneous reopening of the vessel. But what spontaneously occluded and then reopened — is at high-risk of spontaneously occluding again (with no guarantee that there will again be spontaneous reopening the next time the vessel occludes).

  • CAVEAT: The diagnosis of Wellens' Syndrome should be made with caution (if at all) in a patient with marked LVH and ST-T wave changes of LV "strain". This is because the ECG finding of increased QRS amplitude that occurs in association with abrupt precordial transition from predominantly negative to predominantly positive QRS complexes — may result in an ST-T wave appearance identical to the biphasic T wave with terminal negativity characteristic of Wellens' changes (See ECG Blog #209 and Blog #254 and Blog #309for several examples of this "false positive" Wellens' appearance).


CASE Follow-Up:
The above ECG changes of Wellens' Syndrome were not recognized. As a result — cardiac cath was not performed, and the patient was admitted to the hospital with a diagnosis of "unstable angina".
  • About 3 hours after ECG #1 was recorded — the patient had another episode of severe chest pain. A 2nd ECG was done at that time (Bottom tracing in Figure-2).

  • In view of this follow-up history — How would YOU interpret the repeat ECG shown in Figure-2?
  • Physiologically — Can you explain what happened anatomically to produce the ECG picture shown in Figure-2?

  • Should the cath lab be activated at this time?

Figure-2: Comparison of the initial ECG in today's case (when the patient was pain-free) — with the repeat ECG done ~3 hours later during chest pain. (To improve visualization — I've digitized these ECGs using PMcardio).

MY Thoughts on the Repeat ECG:
Compared to the initial ECG done 3 hours earlier — there has been a remarkable increase in the amount of ST segment deviation in selected leads of ECG #2. Specific ECG findings in this repeat tracing shown in Figure-2 include the following:
  • There is now dramatic ST elevation in leads I and aVL. This is associated with small q waves in these high-lateral leads.
  • There is equally dramatic reciprocal ST depression in the inferior leads. Of note — the relative amount of reciprocal ST depression in lead III — is comparable to the mirror-image opposite picture of extreme ST elevation seen in lead aVL. Also of note — is that there is no longer terminal positivity of the T wave in the inferior leads.

  • In addition to leads I and aVL — ST elevation in ECG #2 is also seen in lead V2. Compared to the appearance of the ST-T wave in lead V2 of ECG #1 — there is now more ST elevation — and there is no longer terminal T wave negativity.

  • ST elevation is not seen in any other chest lead. Instead — there is ST segment flattening and slight depression in leads V3-thru-V6 of ECG #2.

PEARL #1: The Distribution of ST Deviation:

The repeat ECG in today’s case brings to mind the color pattern of the South African Flag — in that the leads with the most prominent ST-T wave changes in ECG #2 are leads IIIIaVL and V2 — which correspond to the arrangement of GREEN coloring in the horizontal "Y" of the South African flag (upper most portion of Figure-3).

  • The ECG picture of ST elevation limited to lead V2 in the chest leads (with ST depression in other chest leads) — when seen in association with ST elevation in lead aVL (and sometimes in lead I) — should suggest acute coronary occlusion of either the 1st or 2nd Diagonal Branch of the LAD.
  • PEARL #2: It is sometimes difficult to distinguish early on, between acute OMI (Occlusion-based Myocardial Infarction) of the 1st or 2nd Diagonal — vs an ongoing LAD occlusion, in which ST elevation has not yet evolved to include chest leads other than lead V2. This is clinically relevant to today's case — because it emphasizes the importance of being aware that with acute occlusion of either the 1st or 2nd Diagonal Branch of the LAD — we should expect only this 1 chest lead to show ST elevation.

Figure-3: The pattern of maximal ST-T wave deviation in ECG #2 — corresponds to the the arrangement of GREEN coloring in the horizontal "Y" of the South African Flag (See text).

CASE Follow-Up:
The treating clinicians did recognize the acute STEMI evident on ECG #2. The patient was successfully treated with thrombolytic therapy.

Putting It All Together:
Among the important points emphasized by today's case — is the need for awareness of a "true" Wellens' Syndrome. As noted above — the ST-T wave appearance of lead V2 in ECG #1 fit the criteria perfectly, in this patient with prior episodes of severe chest pain that spontaneously resolved (with the patient pain-free at the time ECG #1 was recorded).
  • The biphasic T wave with terminal negativity in lead V2 of ECG #1 — is evidence of spontaneous reperfusion following brief coronary occlusion.
  • Similarly — T wave inversion in lead aVL (and to a lesser extent, in lead I) of ECG #1 also reflects spontaneous reperfusion.

  • The reason inferior lead T waves in ECG #1 are so tall — is because the reciprocal changes in these leads manifest a mirror-image opposite picture to the reperfusion T wave inversion seen in lead aVL.

  • Take-Home POINT: The episode of chest pain that spontaneously resolved by the time the patient in today's case arrived in the ED — marked the 3rd "warning" episode that this patient had within the space of 1 week. Unfortunately — the "culprit" vessel did not spontaneously reopen with the 4th episode, which resulted in the STEMI evident in ECG #2. This underscores the need to recognize Wellens' Syndrome as prompt indication for cath, with the goal of preventing a large infarction.

PEARL #3: Every instance of Wellens' Syndrome that I am aware of — has involved a high-grade lesion of the LAD coronary artery. An additional reason why today's case proved so insightful — is that it demonstrates Wellens' Syndrome may also be indicative of a high-grade lesion in the 1st or 2nd Diagonal Branch of the LAD, instead of the LAD itself.
  • Recognizing the South African Flag sign can be clinically important! I am aware of a case in which the interventionist only picked up acute occlusion of the 2nd Diagonal — because an ECG similar to that seen in Figure-3 prompted him to look closer at the cath films for the proximal occlusion that was not initially evident.

PEARL #4: I love lead aVL! I summarize in Figure-4 — the clinical utility of this lead for predicting the "culprit" artery in acute OMI.

Figure-4: Optimal use of lead aVL for predicting the "culprit" artery in acute OMI.

Advanced Point (Beyond-the-Core): In recent years — MRI correlations with cardiac anatomy, coronary artery distribution, and ECG findings have revealed that traditional ECG terminology is not as accurate as previously thought (Bayes de Luna et al: Circulation 114:1755, 2006). Thus, the anatomic relationship of the posterior wall of the left ventricle — is in reality not as directly "posterior" as we thought
  • What traditionally has been thought of as “posterior” wall involvement — is more accurately referred to as involvement of part of the lateral LV wall.

A new, more anatomically accurate terminology has been proposed:
  • The new terminology would change reference to the posterior LV wall — to the lateral wall instead.

  • MRI correlations also suggest that classification of lead aVL as a “high-lateral" lead is anatomically inaccurate. Instead, the ECG finding of infarction Q waves in lead aVL and/or lead I — but without a Q wave in lead V6 — indicates a mid-anterior wall MI rather than “high-lateral" involvement. This provides the rationale presented above in Figure-4 as to why lead aVL is so useful in localizing the "culprit" artery!

  • MY BIAS: Realizing the potential tremendous benefit that MRI correlations may provide toward more accurate anatomic localization — traditional ECG terminology appears entrenched at the current time. Rather than confusing the issue with a novel ECG terminology that is not yet in general use — We favor continued use of the term posterior infarction  (with continued distinction between lateral vs posterior walls of the heart— and continued description of lead aVL as a “high-lateral" lead. We fully acknowledge that at some point in the future — more widespread acceptance of MRI-correlated terminology may change the way we localize anatomic areas on ECG.



Acknowledgment: My appreciation to Kianseng Ng and Paul Ling (from Malaysia) for the case and this tracing.




Related ECG Blog Posts to Today’s Case: 

ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation (outlined in Figures-2 and -3, and the subect of Audio Pearl MP-23 in Blog #205).


ECG Blog #209 and ECG Blog #254 and ECG Blog #309 — Review cases of marked LVH that result in similar ST-T wave changes as may be seen with Wellens' Syndrome (but which are not Wellens' Syndrome!).



ADDENDUM (7/16/2021): In the following 2 Figures — I post written summary from my ECG-2014-ePub regarding Wellens’ Syndrome

  • CLICK HERE — for a PDF of this 3-page file on Wellens’ Syndrome that appears in Figure-3 and Figure-4.



Figure-3: Regarding Wellens’ Syndrome (from my ECG-2014-ePub).

Figure-4: Wellens’ Syndrome (Continued). 

Audio PEARL #26a (7:40 minutes) — Reviews what Wellens' Syndrome is — and what it is not (from ECG Blog #254).


  1. Wow! Emeritus Prof KG, I learnt so much today. I have always enjoyed the methodical way you interpret the ECG but this case probably tops the list.