Tuesday, March 30, 2021

ECG Blog #209 (ECG MP-26) — Is this Wellens’ Syndrome?

The ECG shown in Figure-1 was obtained from a 53-year-old African American man. No additional information about this patient was available. The computer interpretation of this tracing read as follows — “Sinus bradycardia; LVH with repolarization abnormality; abnormal ECG.”  

  • Do you agree with the computer interpretation?
  • In the absence of any history — WHAT are your diagnostic considerations?
  • Is this ECG diagnostic of Wellens’ Syndrome?


Figure-1: Is this ECG diagnostic of Wellens’ Syndrome? (See text).



NOTE #1: Some readers may prefer at this point to listen to the 6:00 minute ECG Audio PEARL beforereading My Thoughts regarding the ECG in Figure-1. Feel free at any time to review to My Thoughts on this tracing (that appear below ECG MP-26).



Today’s ECG Media PEARL #26a (7:40 minutes Audio) — What Wellens’ Syndrome is — and what it is not ... (P.S. — I updated this Audio Pearl on 9/28/2021).



NOTE #2: I have excerpted a brief written summary regarding Wellens’ Syndrome from my ECG-2014-ePub. This appears below in the Addendum (in Figure-3 and Figure-4).

  • CLICK HERE — to download a PDF of this 3-page file on Wellens’ Syndrome.



MY Approach to this Tracing:

As always — I favor a Systematic Approach for interpretation of every ECG I encounter (This Systematic Approach reviewed in ECG Blog 205). The 1st Step in interpretation is Descriptive Analysis — which I find especially helpful for organizing your thoughts with complex tracings, such as the ECG shown in Figure-1. My Descriptive Analysis for this ECG is as follows:

  • The rhythm is fairly (albeit not completely) regular at ~45-50/minute. Upright P waves with a constant PR interval are seen in lead II — so the rhythm is sinus bradycardia. 
  • The PR interval is normal at 0.20 second. 
  • NOTE: Given the uncertain clinical significance of 1st-degree AV block as an isolated conduction defect finding — the term “borderline” 1st-degree is essentially meaningless. As a result, my bias is not to call the PR interval “prolonged” (ie, abnormal) — unless the PR interval clearly exceeds 1 large box ( = 0.20 second) in duration, which it does not in Figure-1.
  • Assessing QRS duration from the lead(s) in which the QRS appears to be longest — I measure QRS duration in leads III, V2 and V3 at 0.11 second, which is slightly prolonged (ie, the QRS is prolonged if it clearly measures more than half a large box [ = >0.10 second] in duration).
  • I measure a QT interval of ~0.52 second — which is long. That said, assessment of the clinical significance of QTc prolongation is much more difficult when there is marked bradycardia — as the bradycardia itself may be associated with some QT lengthening. Serial QT readings may be insightful (ie, if on serial recordings there is clear increase or decrease from the baseline QT value) — but as an isolated finding, I find it difficult to know what to do with a QT value ~0.52 second when the heart rate is under 50/minute.
  • The frontal plane axis (which is about +45 degrees) is normal.
  • QRS amplitude is markedly increased — easily satisfying voltage criteria for LVH (See ECG Blog #73 for review of the LVH voltage criteria I favor). Criteria for atrial abnormality and RVH are not satisfied.


Regarding Q-R-S-T Changes:

  • There are no Q waves in Figure-1 (NOTE: Given how common and normal it is to see a QS complex in lead aVR — I generally don’t even mention this finding).
  • R wave progression is remarkable in Figure-1 for a taller-than-expected R wave in lead V1 (that measures 9mm!). That said — transition (where the R wave becomes taller than the S wave is deep) is normal (occurring between leads V2-to-V3 in this tracing).


Assessment of ST-T waves:

  • The most remarkable finding for the ECG shown in Figure-1 is the deep, diffuse and symmetric T wave inversion seen in no less than 9 of the 12 leads of this tracing. The depth of T wave inversion reaches a maximum of 14 mm in lead V3!
  • The J-point is depressed in virtually all of the leads that manifest deep T wave inversion (except in leads aVF and V2). The amount of J-point depression attains 2 mm in lead V3.
  • The shape of ST segments in several leads that manifest J-point ST depression is coved (ie, with a “frowny”-configuration). This abnormal ST segment shape is best appreciated in leads I, aVL; V3 and V4.
  • There is ~2 mm of J-point ST elevation in leads V1 and V2. The T wave in lead V2 is biphasic with terminal negativity.


Unfortunately — Our interpretation of the ECG shown in Figure-1 needs to proceed without the benefit of any history. The only information available is that the patient is a 53-year-old African American man. With this in mind — my Clinical Impression was as follows:

  • The rhythm is sinus bradycardia at 45-50/minute.
  • There is marked LVH with diffusely abnormal ST-T waves consistent with LV “strain” and/or ischemia, that could be recent or acute. Clinical Correlation is essential!

COMMENT: There is a lot to discuss about the ECG findings on this tracing. 

  • Given the age and race of the patient in today’s case (ie, a 53-year-old African American man) — there should be little doubt about the presence of severe LVH. The increase in QRS amplitude is extreme (ie, a 22 mm R wave in lead II; S waves exceeding 20 mm in leads V1 and V2; 20-25 mm R waves in leads V3 and V4). Likely diagnoses include: i) Severe, longstanding hypertension; ii) Hypertrophic or apical cardiomyopathy; iii) Congestive (dilated) cardiomyopathy; and/or, iv) Other forms of severe underlying heart disease.
  • The overly slow heart rate is of potential concern. Whether this is the result of rate-slowing medication (ie, such as a beta-blocker) — an early sign of SSS (Sick Sinus Syndrome) — or part of this patient’s underlying (acute or chronic) cardiac disorder needs clinical explanation.
  • Although severe LVH with longstanding hypertensive heart disease may produce fairly deep and symmetric T wave inversion in multiple leads — there are a number of additional findings on this tracing that prompt concern for potential recent or acute ischemia. These findings include: i) Marked J-point depression in multiple leads (which is usually not seen to this extent in so many leads with simple LVH); ii) ST segment coving in leads I, aVL, V3, V4 (ST coving is generally not seen with simple LVH); iii) Excessively deep T wave inversion (over 10 mm deep in lead V3); iv) Potential reciprocal (mirror-image opposite) changes for the ST-T waves in leads III and aVL; andv) The marked sinus bradycardia.


Returning to 2 ECG findings I noted earlier:

  • The QRS complex is slightly prolonged (ie, at ~0.11 second). That said — QRS morphology does notresemble that of any conduction defect (ie, neither RBBB, LBBB nor a hemiblock). Although some clinicians might call this a nonspecific IVCD — I believe the “theme” of this tracing is marked LVH. A thicker left ventricle takes more time to depolarize — so I thought the slight QRS widening that we see here is most likely the result of the LVH.
  • The QT interval appears to be prolonged (ie, ~0.52 second). That said — it is difficult clinically to “correct the QT for rate” with a bradycardia in the 40s. Clinically, once we learn the history — common potential causes of QT prolongation should be inquired about (ie, medication effect; serum electrolyte disorders; CNS catastrophes — which I review in ECG Blog #89 and Blog #152) — but if no other obvious cause of QT prolongation is elicited, the increased QT interval seen here may be the result of the marked ST-T wave abnormalities.

BOTTOM Line regarding the ECG in Figure-1: 

The computer interpretation picked up sinus bradycardia and LVH with “strain”. It said nothing about the possibility of ischemia that could be acute (For more on the Pros & Cons of the Computer ECG Report — See ECG Blog #207).

  • Finding a prior ECG on this patient would be invaluable for determining whether the above-noted ST-T wave changes are new or old. 
  • Clinical Correlation is the essential next step!

Is the ECG in Figure-1 Diagnostic of Wellens’ Syndrome?

I review the essentials of Wellens' Syndrome in today's ECG Media PEARL #26 (above) — and in the 2 Figures shown below in the Addendum. In a word — this ECG is not diagnostic of Wellens' Syndrome.

  • As emphasized in my review of Wellens’ Syndrome — a history of recent chest pain that has now resolved is an essential part of the diagnosis of Wellens’ Syndrome. The history is unknown in today’s case.
  • The picture of modest ST elevation in lead V2 with very sharp (steep) descent of the T wave in this lead, that goes on to terminal negativity is identical to the shape of a Wellens’-like T wave. That said — there are 2 reasons why we can not make the diagnosis of Wellens’ Syndrome from this tracing: i) There is marked LVH — which is notorious for producing false positive T wave findings that simulate the T wave appearance in Wellens’ Syndrome; andii) I suspect the reason for the Wellens’-like T wave in lead V2 — is that V2 is a transitional lead between the all-positive T wave (with slight ST elevation) that we see in lead V1 — and— the ST segment coving with very deep and symmetric T wave inversion in lead V3 (See Figure-2).
  • BOTTOM Line: As discussed in my Clinical Impression and Comment above — there are a number of ECG findings in Figure-1 that should prompt concern for possible ischemia that may be acute. But the diagnosis of Wellens’ Syndrome can not be made from this tracing alone.


Figure-2: Magnified view of leads V1, V2 and V3. I suspect that the ST-T wave changes seen in lead V2 are most likely the result of this being a “transition” lead. IF you were to “average out” R wave amplitude, S wave amplitude, and the ST-T wave appearance in lead V1 with that of lead V3 — Wouldn’t you expect to see a QRST complex similar to what we see here in lead V2?



ADDENDUM (3/30/2021): 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).




Relevant 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 subject of Audio Pearl MP-23-LINK in Blog #205).
  • ECG Blog #73 — Reviews “My Take” on the ECG Diagnosis of LVH.
  • ECG Blog #207 — The ECG Computer Report: Friend or Foe?
  • ECG Blog #152 — Tachycardia with a long QTc.
  • ECG Blog #89 — ECG Basics: Assessment of Intervals (PR, QRS, QTc).


  1. Dr Ken, thanks for educating us with a wonderful teaching ECG
    (Tuesday- March 30th 2021 ). Your explanation about the Wellen like ST-T morphology in V2 is indeed ingenious and quite convincing. Regarding, the QT interval in bradycardia (HR=46/mt), I noted your point that it is difficult to clinically obtain a reliable QTc. Sir, I think Fredricia's formula is suitable for bradycardic patients and going by that I got a QTc of 500 ms , which puts this patient in the dangerous threshold for TdP. Again, going by Chan's QT-HR
    Nomogram,for a HR of 46/mt and a raw QT of 540 ms,this patient
    clearly falls in the danger zone. With regards, Dr.R.Balasubramanian - PONDICHERRY - INDIA

    1. @ Dr. R. Balaubramanian — THANKS so much for your kind words and comment! I fully acknowledge that my approach to QTc assessment at either extreme (ie, at relatively fast or significantly slow rates) will differ from that cited by many experts ( = my opinion). I feel what is MUCH MORE important than selecting one’s preferred QTc assessment tool are the CLINICAL CIRCUMSTANCES of why you are following the QTc in THAT particular patient. Knowing the “increment” or “decrement” in the QTc in THAT patient compared to prior and serial tracings (correlated to ongoing clinical circumstances) I believe is KEY to determining IF the QTc measurement is “good”, “bad”, “improving” or “getting more concerning”.

      Dr. Stephen Smith did a “deep dive” on the QTc in his November 24, 2017 post in his ECG Blog (http://hqmeded-ecg.blogspot.com/2017/11/qt-correction-formulas-compared-to-rule.html ). I’ve excerpted 3 paragraphs related to assessing the QTc when the heart rate is slow — but given your interest in this subject, you may wish to review this entire post (SPOILER ALERT — Tremendous credit to Dr. Smith for his thorough investigation! — but this is NOT easy reading … )

      From Dr. Smith’s Nov. 24, 2017 Post:
      “Several formulas have been developed.  In all of them, the QT interval is corrected to a SHORTER duration than the measured value at low heart rates (less than 60) — and to a LONGER duration than the measured value at high heart rates (greater than 60).

      To make things more confusing, bradycardia is a major contributor to TdP, especially in acquired long QT (due to drugs or electrolytes), and TdP in these situations is thus frequently called "pause-dependent."  The long RR interval of bradycardia lengthens the QT interval, providing a greater time interval for an R-on-T PVC to initiate TdP.   Accordingly, bradycardia alone is a significant predictor of TdP — and yet bradycardia reduces the corrected QTc.  As far as we can tell, it is unknown whether, for any given raw QT interval, bradycardia has more of a good prognostic effect in reducing the QTc, or an adverse effect in promoting TdP.  I (Smith) suspect the latter.

      Consequently, even more important than the calculation of the corrected QT at slow heart rates is the calculation of a long QTc at normal or high heart rates, such that if the patient becomes bradycardic, then that patient is then at particularly high risk.   In addition, the QT can be volatile especially in ill hospitalized patients and some recommend continuous monitoring of the QTc for those at high risk.

      BOTTOM LINE regarding the ECG in my ECG Blog #210 (about which you commented) — I still feel the same as I wrote (above) under the Section, “Returning to 2 ECG findings I noted earlier” = The QT interval appears to be prolonged (ie, ~0.52 second). That said — it is difficult clinically to “correct the QT for rate” with a bradycardia in the 40s. Clinically, once we learn the history — common potential causes of QT prolongation should be inquired about (ie, medication effect; serum electrolyte disorders; CNS catastrophes) — but if no other obvious cause of QT prolongation is elicited, the increased QT interval seen here may be the result of the marked ST-T wave abnormalities.

      Dr. B — I appreciate that your opinion may differ from mine — and that’s fine! THANKS AGAIN (as always!) for you comment! — :)