Is this terminal QRS distortion? Is there LVH?

This ECG of a patient was sent to me with the question, "Just LVH, no?"

What do you think?

First, is there Terminal QRS distortion?  We defined terminal QRS distortion as absence of BOTH a J-wave and S-wave in EITHER of V2 or V3, and found that zero of 171 patients with normal variant ST elevation in V2-V4 had this finding.  In other words, it is very specific for LAD occlusion (vs. early repol), though not sensitive.  We found that there was an S-wave in V2 100%, and an S-wave in V3 in 90%.  In the 10% that had no S-wave in V3, all had a J-wave of at least 0.5 mm.

This ECG has no S-wave in V3, but it has a definite J-wave.  Therefore this is NOT TQRSD.

Citation: Lee DH.  Walsh B.  Smith SW.  Terminal QRS distortion is present in anterior myocardial infarction but absent in early repolarization.  The American Journal of Emergency Medicine 34 (11): 2182–85. https://doi.org/10.1016/j.ajem.2016.08.053.

Left ventricular hypertrophy?  There is certainly high voltage.  There are new LVH criteria which say that to add the sum of the deepest S-wave in any lead plus the amplitude of the S-wave in V4.  If the deepest S-wave is in V4, then double that value. If the total is greater than 28 mm for men or 23 for women, then LVH is diagnosed.  I think the S-wave in V2 is 28 mm, so it would qualify for the new criteria.

Citation: Peguero, Julio G., Saberio Lo Presti, Jorge Perez, Omar Issa, Juan C. Brenes, and Alfonso Tolentino. 2017. “Electrocardiographic Criteria for the Diagnosis of Left Ventricular Hypertrophy.” Journal of the American College of Cardiology 69 (13): 1694–1703. https://doi.org/10.1016/j.jacc.2017.01.037.

But LVH can especially be mimicked by young healthy athletic subjects, especially with thin walls. Furthermore, when high voltage is not accompanied by discordant ST depression and T-wave inversion (the typical repolarization abnormalities associated with LVH, formerly called "strain"), the likelihood of clinically significant LVH is much less and the prognosis is much better, especially in patients without hypertension.


This is what I texted back:

"Actually, probably not even LVH. Probably early repolarization in a young person with a thin chest wall. Probably African-American.  But definitely not ischemia."


It turned out he was an otherwise healthy, thin, African American male.  He ruled out for MI.

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Comment by KEN GRAUER, MD (4/27/2019):

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Before I began corresponding with Dr. Stephen Smith — the concept of Terminal QRS Distortion (T-QRS-D) was unknown to me. It’s a beautiful concept that on occasion may provide invaluable assistance for distinguishing between early repolarization vs acute OMI. This case adds insight to what is, and what isn’t TQRSD.

• T-QRS-D — is defined as the absence of both a J-wave and an S-wave in either lead V2 or lead V3. Although simple to define — it’s taken me a bit of practice to become comfortable and confident in its recognition.
• The ECG in this case does not demonstrate T-QRS-D for the reasons stated by Dr. Smith above ( = a well-defined J-wave [notch] is seen in lead V3).

There are an increasing number of other examples of what T-QRS-D is, and what it is not on Dr. Smith’s Blog. For easy reference — Consider these 2 links:

• START WITH THIS ONE = step-by-step discussion by Brooks Walsh & Steve Smith about T-QRS-D.
• MORE PRACTICE = 4 examples (3 positive; 1 not for T-QRS-D).

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The other theme addressed in this post that I’d like to comment on regards ECG criteria for LVH. For “My Take” on a user-friendly method for ECG diagnosis of LVH — CLICK HERE. KEY points to emphasize include the following:

• More than 50 criteria for ECG diagnosis of LVH have been described in the literature. The fact that there have been so many attempts at defining criteria — simply means that none of these criteria are optimally accurate. All criteria suffer from imperfect sensitivity (generally well under 55%).
• Despite suboptimal sensitivity for ECG diagnosis of LVH — specificity can be much higher (ie, >90%) — IF several specific features are present.
• The 2017 Peguero criteria cited above by Dr. Smith now offer an additional ECG option for assessment of LVH — with purported increased sensitivity (up to 62%) compared to previously used criteria. However, their criteria were based on a small (<100 patients) retrospective cohort with limited variability in their patient selection (patients with LVH all had hypertensive crisis) — so in my opinion, their data can be considered, but should not yet replace other criteria.
• Rather than dependence on any one single voltage criterion — I’ve found ( = my experience) that assessment of likelihood of LVH is best based on a series of factors including: i) Patient age (young adults <35 tend to have increased QRS amplitude, not necessarily related to true chamber enlargement); ii) Presence of other cardiovascular disease + demographics (ie, LVH is statistically much more likely before you even look at the ECG if the patient is an adult African-American male with longstanding hypertension); iii) Awareness of different criteria that may assist when certain ECG findings are present (ie, I’ve found voltage criteria of an R≥12mm in lead aVL especially helpful when there is left axis deviation — in which case chest lead voltage criteria may not detect LVH); and, iv) Figure-1 = Presence of LV “Strain” and/or a “Strain Equivalent” pattern (which if either is present in association of clinical features consistent with LVH — likelihood of true chamber enlargement is greatly increased).

Figure-1: The importance of recognizing LV “strain” and/or a “Strain Equivalent” in the ECG diagnosis of LVH (Excerpted from HERE).

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Regarding LVH or Not in this Case:

For clarity — I’ve reproduced the ECG in this case in Figure-2. Assessment is somewhat challenging given the angling distortion, so I’ve counted voltage in several key leads.

Figure-2: The ECG in this case (See text).

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• As per Dr. Smith — the 28mm S wave in lead V2 satisfies Peguero Criteria [deepest S in any lead + SV4 ≥28 (men) or ≥23 (women)].
• Numerous other voltage criteria would be met in Figure-2 (CLICK HERE), given the very deep S wave in lead V2 (28mm) — and, the very tall R waves in V5 (30mm) and V6 (21mm) — IF this patient was ≥35 years of age. Much greater QRS amplitude increase should be seen for true chamber enlargement in younger adults (ie, I’ve used the reverse of 35mm = 53mm for deepest S in V1,2 + tallest R in V5,6 as my voltage criterion in young adults). NOTE — Peguero criteria did not assess QRS amplitudes in their study for adults <35 years of age.
• NOTE — Neither LV “strain” nor a “strain equivalent” are seen in any of the lateral leads in Figure-2. IF this patient was older (say in his 40s or 50s) — then voltage criteria for LVH would be easily met, but without “strain” or a “strain equivalent”. In this situation, I favor the term “Voltage for LVH” — which is an easy way of conveying that despite increased QRS amplitude — specificity for true chamber enlargement is limited (ie, under 50%, and possibly much less depending on other clinical factors).
• As per Dr. Smith, given that the patient in this case turned out to be a young, thin, and otherwise healthy African-American male — the likelihood of true chamber enlargement is minimal.
• BOTTOM LINE: Assessment of age, clinical factors + demographics and the presence or absence of LV “strain” and/or a “strain equivalent” (as discussed in Figure-1) — may be of invaluable assistance for refining your assessment of the likelihood of true LV chamber enlargement.