Tuesday, May 31, 2022

ECG Blog #309 — Syncope and Wellens?

The ECG in Figure-1 was obtained from a middle-aged man — who presented to the ED (Emergency Department) with syncope. No other clinical information available.

  • How would YOU interpret this ECG?
  • In view of this history — what are your diagnostic considerations?

Figure-1: ECG obtained from a middle-aged man with syncope.

MY Thoughts on the ECG in Figure-1:
The rhythm is sinus at ~65/minute. 

  • Regarding Intervals: The PR interval is normal. The QRS complex is not wide. However,  the QTc appears to be at least slightly prolonged (taking into account the relatively slow rate — and some uncertainty where to define the end point of the T wave given its biphasic appearance with terminal positivity in a number of leads).
  • Axis: Normal (about +40 degrees).
  • Chamber Enlargement: Obvious LVH (Left Ventricular Hypertrophy) — but no sign of other chamber enlargement. 

NOTE: The increase in R wave amplitude in some of the leads in Figure-1 is about as marked as you will ever encounter (ie, R wave amplitude attains ~50 mm in leads V4, V5). For clarity — I’ve used different colors to shade in QRS complexes in those leads in which voltage overlap is greatest (Figure-2).

  • Sugggestion: The amount of voltage overlap seen in Figure-1 complicates interpretation because of how difficult this makes it to determine where one QRS complex ends — and the next begins. Immediately repeating the ECG at HALF-standardization resolves the issue.

Regarding Q-R-S-T Wave Changes:

  • Q Waves: A small and narrow q wave is seen in lead III.
  • R Wave Progression: The R wave becomes predominant already in lead V2 (YELLOW outline of the QRS in this lead) — thus transition occurs early (ie, between leads V1-to-V2).

  • ST-T Waves Changes: There is diffuse and exceedingly deep, symmetric T wave inversion. ST segments in most leads are coved in shape — with several millimeters of J-point ST depression in those leads with very tall R waves. Isolated leads show modest ST elevation (ie, leads III, aVR, V1, V2) — but the predominant finding is clearly the ST coving with J-point depression and the very deep, symmetric T wave inversion.

PEARL #1: In a similar way that modified-Smith-Sgarbossa criteria incorporate the concept of “proportionality” into decisions about whether with LBBB, the amount of J-point elevation or depression is excessive (ECG Blog #282)this same concept is applied to Figure-2. That is, when assessing the size of the giant inverted T wave in lead V4 (that attains 20 mm in depth!) — We need to consider this in the context of the huge R wave in this same lead V4 that exceeds 50 mm in amplitude!

Figure-2: I've colored in selected QRS complexes in those leads in which voltage overlap is greatest (See text).

Putting It All Together:
The patient in today’s case is a middle-aged man who presented with syncope. No other information available. The principal findings in his initial tracing include sinus rhythm — marked LVH — diffuse ST segment coving with J-point depression and diffuse, symmetric T wave invertion, including a number of exceedingly deep T waves measuring 15-20 mm in depth. Even considering the marked increased in QRS amplitude — these are Giant" T-waves.

  • I’ve previously reviewed a number of cases in which there are Giant T Waves (See ECG Blog #276Blog #277and Blog #59). For clarity — I’ve reproduced in Figure-3 a summary defining “Giant” T waves, and listing the common causes that should be considered whenever you encounter this finding.

Giant T-Wave Syndrome
The designation of "Giant" T waves is reserved for a limited number of clinical entities that are likely to produce truly deep (>5-10 mm amplitude) T wave inversion.
  • The definition of "Giant" T waves is easily satisfied for the tracing in Figure-2 by the 15-20 mm depth of multiple T waves. 
  • Truly "giant" T waves are not overly common. The advantage of identifying this entity — is that doing should immediately suggest the diagnostic considerations listed in Figure-3.

  • While impossible to determine which of the entities listed in Figure-3 is (are) most likely in today's case — the relatively modest amount of QTc prolongation would seem to make a severe CNS disorder and Takotsubo Cardiomyopathy less likely. Ischemia is clearly a possibility given symmetric T wave inversion with J-point ST depression — but no mention of chest pain in the history makes this less likely.

  • My Suspicion: The overwhelming finding on today's tracing is the huge R wave amplitude in multiple leads. This strongly suggests that some form of hypertrophic cardiomyopathy is contributing (of which Apical Cardiomyopathy is the most common hypertrophic cardiomyopathy associated with Giant T waves).

Figure-3: Summary of the ECG criteria for "Giant" T Waves — with a list of the most common diagnostic entities to consider (See text).

For clarity — I've reproduced the initial ECG in today's case in Figure-4.
  • Doesn't the steep descent of the T wave in lead V2 look like the picture of Wellens' Syndrome?

Figure-4: I've reproduced Figure-1, which shows the initial tracing in today's case. Doesn't steep descent of the T wave in lead V2 resemble the ECG picture of Wellens' Syndrome?

It is tempting in Figure-4 — to interpret the slightly elevated ST segment with steep descent of the T wave in lead V2 as suggestive of Wellens' Syndrome. That said — Wellens’ Syndrome is unlikely to be present in today's case
  • While acute coronary disease is a definite possibility when there are Giant T waves (ie, acute ischemia is included among the entities listed in Figure-3) — it is well to remember that there are other causes of the ST-T wave picture seen in lead V2 of Figure-4. These include (among others) — LVH, cardiomyopathy, coronary reperfusion. 

  • In Figure-4 — I suspect the reason for the slight ST elevation, followed by steep descent of the T wave in lead V2 — is simply a reflection of the overall increased QRS and ST-T wave amplitude that we see, with lead V2 representing a “transition lead” placed between the ST elevation with upright T wave that we see in lead V1and — the J-point ST depression with very deep negative T wave that we see in lead V3.

  • PEARL #2: Remember the following KEY points about the ECG diagnosis of Wellens' Syndromei) A history of recent chest pain that has now resolved is an essential part of the diagnosis; ii) R wave amplitude in the anterior leads is markedly increased (ie, the R wave in lead V2 is ~15 mm). Most cases of Wellens' Syndrome are associated with reduced anterior R wave amplitude, often with delayed (not early) transition in the chest leads; iii) T wave inversion is not nearly so widespread in Wellens' Syndrome, as it is here; and, iv) There is marked LVH! The diagnosis of Wellens' Syndrome is far less reliable when there is LVH with LV "strain".

  • NOTE: For more on what Wellens' Syndrome is and is notSee ECG Blog #254

CASE Follow-Up:
The patient in today's case was found to have AHC (Apical Hypertrophic Cardiomyopathy — also known as Yamaguchi Cardiomyopathy). No other explanation for his syncope was detected. He was discharged from the hospital on ß-blocker therapy.
  • AHC is an uncommon variant of HCM (Hypertrophic CardioMyopathy). It was first described in Asian patients — and is still more prevalent in this population.
  • While AHC is most often a hereditary condition — not all patients have a positive family history.
  • The clinical course of AHC is highly variable. Patients may be asymptomatic (with AHC discovered incidentally when an ECG showing similar findings as in today's case is done for some other reason). Alternatively — patients may present with palpitations, dyspnea, cardiac-sounding chest pain — or — with otherwise unexplained syncope.
  • Although many patients with AHC do well — there is potential for adverse cardiac outcome (including cardiac arrest from malignant arrhythmias). As a result — Risk Stratification of patients detected with AHC is recommended to determine potential need for an ICD (Implantable Cardioverter Defibrillator).

  • For Review of AHC — See Kasirye et al (Clin Med & Research 10: 26-31, 2012) — and — Yusuf et al (World J Cardiology 3: 256-259, 2011).

Acknowledgment: My appreciation to Mubarak Al-Hatemi (from Qatar) 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.
  • ECG Blog #245 — Reviews the ECG diagnosis on LVH (with a 9-minute Audio Pearl in this post on this topic).
  • ECG Blog #254 — Reviews what Wellens' Syndrome is — and what it is not (with a 7:40 minute Audio Pearl in this post on this topic).
  • ECG Blog #46 — Reviews ECG findings with Takotsubo Cardiomyopathy.
  • ECG Blog #276 — Works through the differential diagnosis of Giant T Waves.
  • The June 22, 2020 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) reviews the case of Giant T-Waves with prolonged QTc that is shown in the TOP panel of Figure-5 above.


  1. Another great great post. Your comments on Wellens is enlightening. Thanks Professor KG