Friday, October 1, 2021

ECG Blog #254 (26a) — Wellens Syndrome?


The ECG in Figure-1 was obtained from a 30-ish year old man with a history of a bicuspid aortic valve. He presented to the ED (Emergency Department) for a pre-syncopal episode.

 

QUESTION:

  • Is this Wellens' Syndrome?

 

Figure-1: ECG obtained from a 30-ish year old man who presented to the ED for pre-syncope. Is this Wellens' Syndrome?

 

 

  — The Case Continues BELOW today's Audio Pearl ... —

 

 

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NOTE: Some readers may prefer at this point to listen to the 7:40-minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to refer to My Thoughts on this tracing (that appear below ECG MP-26a).

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Today's ECG Media PEARL #26a (7:40 minutes Audio) — Reviews what Wellens' Syndrome is — and what it is not (This is the revised version from 3/30/2021).

 

 

 

MY Approach to this Tracing:

As always — I favor a Systematic Approach for interpretation of every ECG I encounter (This Systematic Approach is 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:

  • Rate & Rhythm: Although we lack a long lead rhythm strip — we can still say that the rhythm is slow (ie, ~60/minute) with slight-but-definite variation in the R-R interval. This is sinus arrhythmia. 
  • Intervals: P waves are small in amplitude — but present and upright in lead II. The PR interval appears to be slightly short (ie, ~0.11-to-0.12 second in duration). The QRS complex is not prolonged — and the QTc is normal. NOTE: The isolated finding of a slightly short PR interval in a young adult is not necessarily a concerning finding. More clinical information is needed to assess this finding. As a result — I usually write "Short PR — Suggest clinical correlation" in my interpretation. It turns out that this slightly short PR interval was not relevant to today's case.
  • Axis: The front plane axis is about +70 degrees, which is normal.


Chamber Enlargement: As noted earlier — P wave amplitude is reduced (ie, there is no sign of atrial enlargement). There is also no sign of RVH. Assessment of the ECG in Figure-1 for LVH (Left Ventricular Hypertrophyis more challenging:

  • QRS amplitude is often increased in younger adults (especially in men less than 35 years of age). As a result — It is difficult to arrive at a definite answer regarding the presence or absence of ECG criteria for LVH in this 30-ish year old man.
  • That said, despite the young adult age of today's patient — QRS amplitude appears to be significantly increased — which I illustrate by coloring in overlapping QRS deflections in the anterior leads (Figure-2). QRS amplitude most probably satisfies voltage criteria for LVH given the very deep S waves in anterior leads V1 and V2 (or 18 mm and 23 mm, respectively) — with what appears to be an extremely deep S wave in lead V3 (which is cut off by the bottom of the paper after an S wave of 16 mm).
  • NOTE: For more on the LVH voltage criteria that I favor — See ECG Blog #245.

 

 

Figure-2: For clarity — I have colored in overlapping QRS deflections in anterior leads V1, V2 and V3 (See text).


 

 

Regarding Q-R-S-T Changes:

  • Slender but fairly deep Q waves are seen in each of the inferior leads (II, III, aVF). Slender Q waves are also seen in lateral chest leads V5, V6.
  • R wave progression — reveals that R wave amplitude is surprising tall (ie, 9 mm) already by lead V1 — with an extremely tall R wave (of more than 20 mm) already by lead V2.

 

Assessment of ST-T waves:

  • The most remarkable finding for the ST-T waves is seen in the anterior leads (ie, leads V1, V2 and V3). Each of these leads manifest ST segment coving with slight elevation — that leads into terminal T wave inversion.
  • Less marked, nonspecific changes are seen in many of the remaining leads, including ST segment flattening and modest T wave inversion in lead III.
  • 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.


Clinical IMPRESSION:

The ECG in today's case shows sinus arrhythmia with borderline bradycardia — a slight short PR interval (of ~0.11-0.12 second) — marked increase in QRS amplitude that probably satisfies voltage criteria for LVH (despite the patient's young adult age) — and a clearly abnormal ST-T wave response in the anterior leads that resembles the ST-T wave appearance of Wellens' T waves.

  • As alluded to earlier — chances are that the short PR interval has no bearing on today's case. Given the tiny P wave amplitude in lead II (that appears slightly smaller than the P wave in lead I) — this could be an ectopic atrial rhythm, which can be a normal variant. Depending on where within the atria the rhythm arises — the PR interval might normally be shorter (ie, if the ectopic atrial rhythm arose from an atrial site close to the AV node).



Why Wellens’ Syndrome is Unlikely in Today's Case:

I review the essentials of Wellens' Syndrome in today's ECG Media PEARL #26a (above) — and in the 2 Figures shown below in the Addendum. In a word, despite the presence of anterior ST-T wave changes that resemble those seen with Wellens' Syndrome — Today's case is unlikely to represent Wellens' Syndrome. This is because:

  • 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. The patient in today's case is a younger adult (ie, therefore in a lower prevalence group for coronary disease) — and there is no mention of a history of preceding chest pain.
  • The QT interval looks to be normal in Figure-2. In contrast — with Wellens' Syndrome, the QTc is often at least borderline prolonged.
  • R wave amplitude in the anterior leads is markedly increased (ie, the R wave in lead V1 is ~9 mm — and the R wave in lead V2 is huge at 24 mm!). Most cases of Wellens' Syndrome are associated with reduced anterior R wave amplitude, often with delayed transition in the chest leads.
  • There is voltage for LVH. The diagnosis of Wellens' Syndrome should be made with caution in the presence of marked increase in QRS amplitude — because of the tendency for this to produce false positive results.
  • Overall — The ECG pattern of increased voltage, early transition and ST-T wave changes similar to those in Figure-2 is commonly seen as a repolarization variant in younger adults. By exclusion — follow-up in today's case suggested this (and not Wellens' Syndrome) to be the explanation for the ECG findings in Figure-1. So YES — Clearly evaluation of this patient was indicated, because the ECG pattern in Figure-1 could potentially be consistent with either LVH or HCM (Hypertrophic CardioMyopathy) — But Echo showed neither LVH nor HCM.

 

 

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ADDENDUM (10/1/2021): 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). 


 

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Acknowledgment: My appreciation to Ghady Rahhal (from Virginia, USA) for the case and this tracing.

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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 — Reviews a case of marked LVH that results in similar ST-T wave changes as may be seen with Wellens' Syndrome.

 

ECG Blog #245 — Reviews my approach to the ECG diagnosis of LVH (outlined in Figures-3 and -4, and the subject of Audio Pearl MP-59 in Blog #245).





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