Monday, January 4, 2021

ECG Blog #182 (Reciprocal Changes — Covid — Myocarditis — Acute OMI)

Today’s case emphasizes the importance of the History in our clinical interpretation. So — Imagine you are given the ECG shown in Figure-1 — and told only that the patient is a man in his 30s.

  • How would YOU interpret this ECG?
  • Are the findings you see likely to reflect a normal variant?

Figure-1: ECG obtained from a man in his 30s. How would you interpret this ECG? (See text).


The rhythm in ECG #1 is sinus. All intervals (PR, QRS, QTc) are normal. The frontal plane axis is normal at +40 degrees. There is no chamber enlargement. Regarding Q-R-S-T Changes:

  • There are tiny (and normalseptal Q waves in lateral leads I, aVL, V5 and V6.
  • R wave progression shows a somewhat abrupt transition (ie, where the R wave becomes taller than the S wave is deep), which occurs between leads V2-to-V3. The abruptness of this change in R wave amplitude may reflect slight error in electrode lead placement — but it is probably not an important finding.

The ECG findings that are of concern in Figure-1 relate to the abnormal ST-T wave morphology that is seen in multiple leads. These ECG findings are subtle-but-real, and include the following:

  • ST segment coving in both high lateral leads (within the RED rectangles in leads I and aVL of Figure-2). There may be slight ST elevation in lead aVL.
  • Reciprocal ST depression in 2 of the 3 inferior leads ( = leads III and aVF, within the BLUE rectangles in Figure-2). The ST-T wave in lead II is not depressed — but it is flatter-than-it-should-be.

PEARL #1: In support that the shape of these ST-T wave segments is not normal is the suggestion of ever-so-slight terminal T wave negativity in leads I and aVL — and — the equally ever-so-slight terminal positivity of the T wave in leads III and aVF. This is not normal.

PEARL #2: When T waves in each of the chest leads are upright (as they are in ECG #1) — the T wave in lead V1 is usually not taller than the T wave in lead V6.

  • NOTE: This is not to say that tall, upright T waves in lead V1 might not sometimes be the result of a repolarization variant or a mirror-image reflection of LV “stain” that can sometimes be seen in anterior leads. Instead — it is simply to say that on occasion — I have found recognition of a tall, upright T wave in lead V1 that is clearly much taller than the T wave in lead V6 to be a tip-off to an acute coronary syndrome that I might not otherwise have recognized.
  • Look within the PURPLE rectangles in leads V1 and V6 of Figure-2. Given that there is no LVH in ECG #1 — the finding of an obviously taller (and more voluminous) T wave in lead V1 compared to the barely positive T wave in lead V6 is simply not a normal finding!
  • In the context of this clearly taller-than-it-should-be T wave in lead V1 — I wondered if the T waves in leads V2 and V3 might not also be taller-than-they-should-be ...

Figure-2: Abnormal ECG findings in ECG #1 are highlighted within the colored rectangles (See text).


The above ECG findings make up my Descriptive Analysis of ECG #1. The KEY clinical question — is HOW to interpret ECG #1 in light of the patient’s history? To illustrate the importance of the History in clinical decision-making — Consider EACH of the following 3 Clinical ScenariosWhat IF:

  • Scenario #1: This patient presented with severe, new-onset chest pain?
  • Scenario #2: The patient denies symptoms. He insists he has had no chest pain.
  • Scenario #3: The patient denies chest pain — but he does indicate recent shortness of breath on exertion for activities he previously completed without difficulty. He adds that his wife recently tested positive for Covid-19.

What would YOUR Clinical Impression of ECG #1 be for each of these 3 clinical scenarios?

MY THOUGHTS on Clinical Scenario #1:

IF told that ECG #1 was obtained from a patient with severe new-onset chest pain — I would be suspicious of acute OMI ( = Occlusion-based MI) until proven otherwise.

  • As described earlier — proof that ST segment coving in both high lateral leads ( = leads I and aVL) is not a simple “normal variant” finding is forthcoming from: i) The mirror-image opposite picture of ST depression with terminal T wave positivity in inferior leads III and aVF; andii) The finding of a taller and more voluminous T wave in lead V1 compared to the T wave in lead V6.
  • NOTE: It is sometimes quite difficult to distinguish between the prominent anterior T waves of a normal repolarization variant from the hyperacute T waves of early OMI. That said — in a patient with new chest pain in which the tall T wave in lead V1 is highly suspicious (as it would be in ECG #1) — I would wonder IF the T waves in leads V2 and V3 might not also be larger-than-they-should-be, and therefore “hyperacute”. After all — ST elevation with acute antero-septal OMI is often associated with ST elevation in the high lateral leads.

MY THOUGHTS on Clinical Scenario #2:

IF instead, I was told that ECG #1 was obtained from a patient with absolutely no symptoms — I’d strongly suspect the ECG findings described above were not acute.

  • PEARL #3: I’ll emphasize that many patients (more commonly in males) downplay, and even deny symptoms. In my experience, if one carefully (in a completely nonjudgmental manner) goes back over the history — you will often detect description of events that indeed may have been cardiac-related, but were not initially reported by the patient. For example, you might ask the patient who initially denied symptoms: “Think back over the past few days-to-weeks. Was there ever any period of time (even brief) — in which you either experienced some discomfort (even mild) in your chest or - found it more difficult than usual to do some of your daily activities?”. Please note my strategic avoidance of the word “pain” when inquiring in this manner about possible symptoms.
  • NOTE: Even if the patient has absolutely no history of possible cardiac-related symptoms — It should be recognized that ECG #1 is still not a “normal” tracing. Additional evaluation might not necessarily need to be pursued — but it is essential to recognize that ECG #1 is not a normal tracing.

MY THOUGHTS on Clinical Scenario #3:

It turns out that the actual history for the patient in today’s case was the one presented in Clinical Scenario #3 — namely, that this man in his 30s presented to a primary care clinic and reported decreased exercise tolerance, but without any chest pain. His wife was recently found to be Covid-positive.

  • Given this history (especially in the absence of chest pain) — there was concern that the patient was probably Covid-positive with few overt symptoms other than effort-related dyspnea — which given his clearly abnormal ECG, was likely to reflect acute myocarditis as the diagnosis (with this as a complication of Covid).

Regarding the Entity of Covid Myocarditis:

My reading of current literature regarding cardiac involvement as a Covid-related complication — is that this is a rapidly changing field, in which even the “experts” do not have all of the answers! As a result — clinical decision-making must often be based on common sense recommendations, realizing that definitive answers are often not yet available.

  • What is known — is that cardiac injury (including acute infarction) has been increasingly observed among patients hospitalized with Covid (especially but not exclusively among patients in older age groups with underlying co-morbidities). The finding of elevated troponin in such patients is clearly correlated with increased mortality and severity of disease — although reasons for increased troponin in these hospitalized patients may be multiple (ie, including acute ischemia/infarction, acute myocarditis, intravascular thrombosis, damage from inflammatory mediators, and/or other factors not yet elucidated) — Kavsak et al; Clinical Chemistry, Nov., 2020.
  • Less is known about the natural history of mild-severity (or even asymptomatic) Covid-19 infection in athletic individuals. The obvious concern is the risk that might be imposed on asymptomatic (or minimally symptomatic) athletic individuals found to be Covid-positive who have “silent” (therefore undetected) myocarditis. Unrestricted participation in endurance or competitive sports could be potentially lethal for such individuals. Available literature suggests that subclinical myocarditis does occur — albeit the frequency of this form of cardiac involvement in athletes without overt symptoms is unknown. It is unfortunate that the optimal approach for assessment and risk stratification of Covid-positive athletic individuals remains uncertain at this time (Kim et al — JAMA Cardiology, Oct., 2020 — and Rajpal et al — JAMA Cardiology, Sept., 2020).
  • Among strategies suggested for determining athletes that may be at higher risk include cardiac troponin testing. Unfortunately, unlike the case for the generally older population hospitalized for Covid-related illness — clinical implications among minimally symptomatic athletes for slight high-sensitivity troponin elevations are uncertain (Kim et al — JAMA Cards, 2020).
  • Other potential cardiac assessment tools include CMR (Cardiac Magnetic Resonance imaging) — an ECG — Echo — an ETT (Exercise Tolerance/Stress Test) — and a 24-Hour Holter monitor. Protocols for when and how many of these assessment tools to perform for athletic individuals with presumed cardiac involvement before allowing resumption of training/competition are complex and extend beyond the scope of this ECG Blog post (For an idea of some general Guidelines — See Kim et al — JAMA Cardiology, Oct., 2020).

Follow-Up to Today’s Case:

The patient in today’s case was seen outside of the hospital. Although details and follow-up were limited — the patient was rechecked 4 days after his initial visit, at which time ECG #2 was obtained (See Figure-3). Of note — the patient was no longer experiencing effort-related dyspnea at the time ECG #2 was obtained!

  • HOW would you interpret ECG #2 in relation to the above clinical history?

Figure-3: Comparison of this patient’s initial tracing ( = ECG #1) — with a follow-up ECG done 4 days later (See text).

FINAL Thoughts:

Realizing that information in this clinical case is limited — I would make a presumptive diagnosis of Covid-related Myocarditis because:

  • This patient had high-risk exposure to Covid-19 (his wife was Covid-positive).
  • Even though he did not report any of the usual symptoms of Covid (ie, NO fever, headache, myalgias, “cold” symptoms, loss of taste or smell) — he did report exertion-related dyspnea at the time of his initial visit — and his initial ECG ( = ECG #1) was clearly abnormal and consistent with myocarditis.
  • The complete absence of chest pain makes it much less likely that the ECG abnormalities seen on this patient’s initial tracing were the result of acute infarction. This leaves acute myocarditis as the condition most likely to account for the abnormalities we noted above for ECG #1.
  • The patient was no longer experiencing effort-related dyspnea at the time ECG #2 was obtained!
  • Assessment of ECG #2 (in Figure-3) — suggests definite improvement compared to the ECG abnormalities that were seen in ECG #1. Specifically — i) ST segment coving in high lateral leads (and the slight ST elevation in lead aVL) is no longer present in ECG #2; ii) Reciprocal ST-T wave depression in leads III and aVF — and the ST-T wave flattening in lead II — are greatly reduced in ECG #2; andiii) The imbalance in T wave size between leads V1 and V6 is clearly less marked in ECG #2 than it was in ECG #1.
  • Putting It All Together — The fact that there clearly has been serial improvement in ECG abnormalities at the time of this patient’s follow-up visit 4 days later, in association with resolution of his effort-induced dyspnea provides further support that: i) the ECG abnormalities seen on ECG #1 were real; ii) that the presumptive diagnosis of acute myocarditis is most likely accurate; andiii) that the patient’s clinical condition has significantly improved.

In Retrospect:

  • A more definitive diagnosis of acute myocarditis might have been made on this patient’s initial visit by additional testing (ie, troponin, serial ECGs, Echo — and Covid antigen & antibody studies).
  • Long-term “risk” to this patient from his presumed Covid-related myocarditis is uncertain. In addition to the above suggested testing — CMR and stress testing may help to guide return to full, unsupervised activity. In the interim — excessive activity is best avoided.


Additional READING:

  • For another example of the phenomenon in which the T wave in lead V1 should not be taller than the T wave in lead V6 — CHECK OUT the October 23, 2020 post on Dr. Smith’s ECG Blog. Please SCROLL DOWN the page to reach My Comment at this link.
  • IF the concept of “OMI” ( = Occlusion-based MI) as the preferred term instead of “STEMI” is new to you — Please CHECK OUT the July 31, 2020 and the September 13, 2020 posts on Dr. Smith’s ECG Blog. Please SCROLL DOWN the page to reach My Comment for these links to Dr. Smith’s Blog.
  • IF the concept of mirror-image reciprocal changes for the appearance of the ST-T wave in lead III compared to lead aVL is new to you — Please CHECK OUT my ECG Blog #171 and the August 9, 2018 and October 6, 2018 posts on Dr. Smith’s ECG Blog. Please SCROLL DOWN the page to reach My Comment for the links to Dr. Smith’s Blog.
  • As noted in my above discussion — general notions regarding assessment and management of potential cardiac involvement in athletes, with guidance for when resumption of training/competition might safely be allowed are suggested in Kim et al — JAMA Cardiology, Oct., 2020.




  • Acknowledgment: My appreciation to Kristijan Todoroski (from Macedonia) for today's case and tracings.


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