Thursday, June 20, 2019

Do you recognize these ECGs? STEMI? LVH? What?

What do you think of these ECGs?

I came across the first one reading it blind for a study.  I was certain I knew the diagnosis, and went to the chart to confirm.

The first 3 were recorded on one day.

ECG 1:

ECG 2:

ECG 3:

ECG 4, recorded 12 days later:

These ECGs are classic for a benign variant in Black males.  I was certain it would be a relatively young black male without cardiac pathology.

Result from chart:

It was a black male in his 40s.

The first ECG, and then the next two (1-3), were recorded for chest and abdominal pain.  The patient was ultimately diagnosed with biliary colic.

The patient ruled out for MI by serial trops.

The second presentation (ECG 4) was for epigastric pain due to GERD.

After ruling out for MI both times, the formal ECG diagnosis was LVH. But we know that this pattern is nearly always a normal pattern for black men (although one cannot be 100% certain and an echo is important especially to rule out hypertrophic cardiomyopathy).

An echocardiogram was completely normal.  No LVH.

See this article published this month by Brooks Walsh, Smith, and others in Journal of Electrocardiology: 

Volume 56, September–October 2019, 

Pages 15-23

Comment by KEN GRAUER, MD (6/20/2019):
This case illustrates an important ECG pattern to recognize! For clarity and simplicity — I’ve chosen to comment on the first 2 ECGs done in this case — which I reproduce in Figure-1.
Figure-1: The initial ECG done in the ED ( = ECG #1) — and, the 2nd ECG done in this case later that day = ECG #2 (See text).

Reasons WHY without any history — I immediately thought that ECG #1 was unlikely to represent acute ischemiaiThere is NO loss of anterior forces. On the contrary — there is early transition with already a huge R wave (of ~18mmby lead V2; iiThere is a dramatic increase in wave amplitude in the chest leads, beginning with lead V2 (R wave amplitude in leads V4, V5 and V6 is ≥25 mm! — going off the page in lead V4)iiiConsidering this early transition and dramatic R wave amplitude increase in so many leads — ST-T wave depression in the inferior and lateral precordial leads is at most quite modest (NOTE: Significant ST depression should not be seen with benign repolarization variants)ivIn view of the slow heart rate — the QTc looks to be relatively shortandvThe SHAPE of the ST-T wave in leads V2 and V3 can be seen in non-ischemic repolarization patterns — especially when accompanied by preserved anterior forces and marked increase in R wave amplitude. PEARL: Memorize this shape for the ST-T waves that we see in leads V2 and V3 of ECG #1.

That said — My Thoughts on seeing ECG #1 ( my opinion— was that while I doubted the presence of acute ischemia — the diagnosis of a “benign variant” is one of exclusion. Before “going there” — I felt we needed to know.
  • What was the age and ethnicity of this patient?
  • What was the History?
NOTE: The SHAPE of the ST-T wave elevation that we see in ECG #1 in leads V2 and V3 (ie, ST coving with J-point elevation in V— andJ-point notching that blends into an upward concavity rising ST segment, that terminates in T wave inversion in V3— is most common as a repolarization variant in younger adult black males (even if they are not necessarily athletically inclined).

Reasons WHY without any history — I also contemplated the possibility of LVH and/or HCM (Hypertrophic CardioMyopathyfrom ECG #1 were iDespite my awareness that younger adults often manifest increased QRS amplitude without true LVH — the increase in R wave amplitude in ECG #1 is extreme! — andiiThe ECG is notorious for poor sensitivity and specificity in detection of HCM. There simply is NO specific ECG finding that reliably predicts HCM. That said — marked increase in QRS amplitude and early transition with huge R wave by lead V2 (signaling increased anterior and/or septal forcesare 2 potential ECG findings that have been associated with HCM. BOTTOM LINE: In my opinion, Echo would be needed to rule out these 2 considerations (ie, LVH & HCM) — IF doing an Echo was clinically relevant to the case at hand.

I then looked at ECG #2, which was done some time later that same day. There are some differences between ECG #1 and ECG #2:
  • From a technical standpoint — comparison of ECG #1 and ECG 2 is valid — because there is no significant change either in frontal plane axis or in R wave progression/chest lead QRS morphology.
  • There is less ST elevation in leads V2 and V3 in ECG #2 — and perhaps slightly deeper T wave inversion in most of the chest leads than was seen in ECG #1.
BOTTOM LINE: still thought both ECG #1 and ECG #2 were unlikely to represent acute ischemia for the reasons I initially stated above. BUT
  • There is ST-T inversion/depression (primarily T wave inversion) in no less than 8-to-9 leads in ECGs #1 and #2 — and that is more diffuse involvement than is usually seen in most repolarization variants (T wave inversion is most often limited to to leads V1-thru-V4 with simple repolarization variants). And despite my awareness that there may be variations in ST-T wave morphology in serial tracings of patients with benign repolarization — there has been a change in ST-T wave morphology between ECG #1 and #2.
  • Before proceeding — We needed to find out the ageethnicity and clinical history of this case! IF the patient presented with a history of potentially worrisome chest discomfort (especially if the patient was an older adult) — then additional evaluation would be indicated to ensure no acute ischemia.
  • IF the patient had a history of significant hypertension — then these ECGs would suggest significant LVH until proven otherwise (ie, by Echo). Remember that some young black males are especially prone to developing even malignant hypertension.
  • IF this patient had a personal history of syncope/presyncope — and/or a positive family history — and/or a suggestive heart murmur on exam — then HCM would become a consideration. The early transition with huge R wave by lead V2 + markedly increased chest lead R wave amplitude are findings that should suggest the possibility of HCM whenever they are seen on the ECG of a young adult. Whether formal Echo (with complete measurements) is indicated as an evaluative study in a patient presenting to the ED would depend on specifics of the case at hand.
  • Additional REFERENCE: IF the patient in question is an athlete — this international consensus paper from 2017 has excellent information on normal vs abnormal ECG findings in athletes — with suggestions for follow-up (See especially Figure 1 and Tables 1 & 2 on pages 2,3,4 of this article CLICK HERE to download a bookmarked copy of this Reference).

    _ _ _ _ _ _ _ _ _ _ _ _ _
    NOTE: As it turned out — this patient was a black male, and he did not have acute ischemic heart disease. His Echo was normal. But the point of my comment was to think through the possibilities based on the 2 ECGs shown in Figure-1 above.


  1. Anterior TWI were preceded by J-point elevation and convex (domed) ST segment elevation. But, are these TWI in the lower territory normal?

  2. Very interesting thank you. I'm guessing these patterns are seen in males of African racial background. Are they found in other dark skinned ethnic groups?

    1. Good question, to which I do not know the answer!

    2. Interesting question. Brief search of the internet reveals a VERY interesting set of slides by Dr. Sanjay Sharma, who specializes in the area of assessing for sudden death risk in athletes. He studied a group of Afro- and Caribbean-origin blacks — GO TO — — I found it worthwhile going through this series of slides! Unfortunately, I don't see breakdown between blacks of Afro- vs Caribbean origin — but I suppose there is similar prevalence of ECG (and underlying cardiac) changes .... And perhaps Brooks Walsh (primary author in the above article that Dr. Smith references) might know more on this (I am writing to ask Dr. Walsh for comment about your interesting question). My hunch is those with initial African origin (which should include both Afro & most Caribbean blacks) would manifest such changes — but simply "darker-skinned" individuals without initial origin out of Africa might not .... — but I have no data on this ...

    3. There is enormous cultural/geographic/generic diversity among the people living in the African continent. The likelihood of manifesting such ECG patterns likely has far more to do with geographic/genetic origins than simply dark skin.
      See recent data by Riding et al:


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