Monday, January 18, 2021

ECG Blog #185 (Audio Pearl-3) — Ps, Qs & 3R Approach to Arrhythmias


The KEY to interpreting cardiac arrhythmias — is to use a Systematic Approach, as emphasized in today's Audio Pearl. It doesn't matter if you use my system — or some other system you were taught, as long as each time you interpret an arrhythmia, you use the same system you have adapted.

  • The Audio Pearl below concisely reviews my approach (in < 4 minutes).

  • My ECG Video #10 reviews the basics of the Ps, Qs & 3R Approach in more detail (28 minutes). As with all my ECG Videos — if you click on SHOW MORE (under the video, on the YouTube page) — you'll see a detailed linked Contents that allows rapid access to any specific part of the video that interests you.
  • Section 2.0 (62 pages) from my ECG-2014 Pocket Brain book reviews the basics of ECG Arrhythmia Interpretation (This is a free download).

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ECG Audio PEARL #3 (3:40 minutes): — reviews my systematic approach to arrhythmia interpretation, as summarized by the saying — "Watch your Ps, Qs & 3Rs".


NOTE: Outlined below are the 5 elements in the Ps, Qs & 3R Approach:

Friday, January 15, 2021

ECG Blog #184 (Audio Pearl-2) — Magical Lead 3- Lead aVL Relationship

Interpreting ECGs is a visual skill — but important ECG concepts are sometimes more effectively conveyed by a brief audio message. This is the purpose of this new feature I’ve added to supplement content on my ECG Blog posts. 

  • I illustrate today’s Audio Pearl with several tracings excerpted from other blog posts.

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ECG Audio PEARL #2 (2:45 minutes): — relates to the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL.


Figure-1: ECG obtained from a 54-year old man. No history was available. How would you interpret this tracing? (Excerpted from ECG Blog #171).

Figure-2: Focusing on the 6 limb leads from Figure-1 — Note how the mirror-image of the ST-T wave in lead aVL (within the light BLUE insert) — looks identical to the shape of the elevated ST-T wave in lead III (within the WHITE rectangle). Similarly, the mirror-image of the elevated ST-T wave in lead III (within the light BLUE insert) — looks identical to the shape of the inverted ST-T wave in lead aVL (within the WHITE rectangle). This all but confirms ongoing acute inferior MI (Full details of this case discussed in ECG Blog #171).


Figure-3: ECG obtained from a man in his 50s with chest pain. Although the amount of ST elevation in leads I, aVL and V6 is not a lot — the reason we KNOW that this is an important real finding — is that the SHAPE of the ST elevation in lead aVL is the precise mirror-image opposite of the shape of the ST segment depression in lead III. (Excerpted from My Comment, which is found at the bottom of the page in the October 6, 2018 post in Dr. Smith’s ECG Blog. The mirror-image picture of the ST-T wave of lead aVL is within the GREEN rectangle; and the mirror-image of lead III is within the BLUE rectangle).

Sunday, January 10, 2021

ECG Blog #183 (Repolarization Variant – Hyperacute - deWinter)

NOTE: SEE BELOW for today’s ECG Audio Pearl — which relates to the phenomenon of deWinter-like T waves.

The patient whose ECG is shown in Figure-1 is a middle-aged man who presented to the ED with new-onset chest pain.

Which 2 of the following 5 choices are most correct?

  • Extra Credit: WHY are the remaining 3 choices either less correct or wrong?


CHOICES to Consider:

  • Choice A: The T waves in anterior leads may reflect a repolarization variant.
  • Choice B: The anterior T waves and inferior ST-T waves suggest possible ischemia.
  • Choice C: The cath lab should be immediately activated with an “OMI alert”.
  • Choice D: The “classical” deWinter T wave pattern is present in the anterior leads. 
  • Choice E: Although a “classical” deWinter T wave pattern is not seen in ECG #1 — clinical implications are essential the same as if one was present.

Figure-1: ECG obtained from a middle-aged man with new chest pain (See text).


As always — it BEST to begin by systematic assessment of the ECG in question before moving on to clinical implications.

  • NOTE: It could be easy to overlook that the rhythm in ECG #1 is not regular if one didn’t start by reviewing the long lead II rhythm strip at the bottom of the tracing. The mechanism of the rhythm is sinus — and all QRS complexes are preceded by similar-looking P waves with a constant PR interval. Variation in the R-R interval during the first half of the tracing is consistent with sinus arrhythmia — which then regularizes to normal sinus rhythm at ~80-85/minute toward the end of the rhythm strip.
  • All intervals (PR, QRS, QTc) and the axis are normal. There is no chamber enlargement.


Regarding Q-R-S-T Changes:

  • There are no Q waves.
  • The R wave in anterior leads V1, V2, V3 is a bit slow to develop until transition occurs between V3-to-V4 (but there are no anterior Q waves or QS complexes).
  • The most remarkable finding is the presence of hyperacute T waves that are seen in leads V2V3 and V4. This is most marked in lead V3 (especially given relatively small S wave amplitude in this lead) — albeit there is no ST elevation in this lead. T waves in these 3 chest leads are clearly taller-than-they-should-be and overly “voluminous” (ie, fatter-at-their-peak and wider-at-their-base than would be expected given QRS amplitude in each respective lead).
  • There is slight ST elevation in leads V1 and V2. 
  • Of note — there is subtle-but-definite J-point ST depression in leads V4, V5 and V6.
  • There is some ST segment scooping, with slight depression in the inferior leads (including terminal T wave positivity after the ST-T depression).


Clinical IMPRESSION of ECG #1: This is not a repolarization variant (Choice A). Much more than “possible ischemia” (Choice B) — there are definite ECG abnormalities on this tracing in this patient with new-onsetchest pain. Given this history — ECG #1 should be interpreted as acute proximal LAD OMI (Occlusion-based MI) until proven otherwise — and the cath lab should be immediately activated (Choice C).

  • PEARL #1: There are a number of findings in ECG #1 that suggest LAD occlusion is at a proximal location in this vessel. These include: i) ST elevation begins as early as in lead V1 — with hyperacute T waves also beginning early (in lead V2); andii) Reciprocal ST-T wave changes are seen in the inferior leads. Proximal LAD occlusion is usually also associated with at least slight ST elevation in lead aVL — but that is not present here.
  • PEARL #2: Did YOU notice the lack of R wave progression until lead V4? The presence of a tiny-but-real initial r wave in leads V1 and V2 suggests that the septum remains intact — but lack of any increase in R wave amplitude until lead V4 may be indication of ongoing anterior infarction (ie, loss of anterior forces).


De Winter T Waves:

In 2008 — Robert J. de Winter and colleagues (Drs. Verouden, Wellens, and Wilde) submitted a Letter to the Editor to the New England Journal of Medicine (N Engl J Med 359:2071-2073, 2008) — in which they described a “new ECG pattern” without ST elevation that signifies acute occlusion of the proximal LAD (Left Anterior Descending) coronary artery.

  • The authors recognized this pattern in 30 of 1532 (~2%) patients with acute anterior MI. Cardiac cath confirmed LAD occlusion in all cases — with ~50% of patients having a “wraparound” LAD. Left mainstem occlusion was not present.
  • This was the authors’ original description of the new ECG pattern: “Instead of the signature ST-segment elevation — the ST segment showed 1-3 mm of upsloping ST depression at the J point in leads V1-to-V6— that continued into tall, positive symmetrical T waves”.
  • The QRS complex was usually not widened (or no more than minimally widened).
  • Most patients also manifested 1-2 mm of ST elevation in lead aVR.
  • NOTE: I’ve adapted Figure-2 from the original de Winter manuscript, published in this 2008 NEJM citation.


Figure-2: The de Winter T Wave Pattern, as first described by Robbert J. de Winter et al in N Engl J Med 359:2071-2073, 2008. ECGs for the 8 patients shown here were obtained between 26 and 141 minutes after the onset of symptoms. (See text).

In their original 2008 manuscript — de Winter et al went on to describe the following additional features:

  • “Although tall, symmetrical T waves have been recognized as a transient early feature that changes into overt ST elevation in the precordial leads — in this group of patients, this new pattern was static, persisting from time of the 1st ECG until the pre-cath ECG.”
  • Hyperkalemia was not a contributing factor to this ECG pattern (ie, Serum K+ levels on admission were normal for these patients).  


NOTE: Technically speaking — the de Winter T wave pattern as described in 2008 by de Winter et al differs from the finding of simple “hyperacute” anterior T waves — because ECG findings with a strict de Winter T wave pattern persist for an hour or more until the “culprit” LAD vessel has been reperfused. 

  • As I note above (and as illustrated in the example ECGs taken from the de Winter manuscript that are shown in Figure-2) — there should be involvement in all 6 chest leads with the strict de Winter pattern, with most leads showing several mm of upsloping J-point ST depression and giant T waves.

MY Observations regarding De Winter T Waves: Over the past decade — I have observed literally hundreds of cases in numerous international ECG-internet Forums of deWinter-like T waves in patients with new cardiac symptoms.

  • Many (most) of these cases do not fit strict definition of “de Winter T waves” — in that fewer than all 6 chest leads may be involved — J-point ST depression is often minimal (if present at all) in many of the chest leads — and, giant T waves are limited.
  • ECG changes in many of these cases are not “static” until reperfusion, as was initially reported in 2008 by de Winter et al. Nevertheless, cath follow-up routinely confirms LAD occlusion.
  • MY “Take” on this Phenomenon: I believe there is a spectrum of ECG findings, that in the setting of new-onset cardiac symptoms is predictive of acute LAD occlusion as the cause. What will be seen on the ECG depends greatly on when during the process the ECG was obtained. While many of these patients do not manifest “true de Winter T waves” (because their ECG pattern does not remain static until reperfusion by coronary angioplasty) — for the practical purpose of promptly recognizing acute OMI — I don’t feel ( = my opinion) that it matters whether a “true” de Winter T wave pattern vs simple “hyperacute” T waves (that are deWinter-like) is present.


NOTE: SEE BELOW for today’s ECG Audio Pearl — which relates to the phenomenon of deWinter-like T waves.



Regarding Today’s Case: Comparing the chest lead ST-T wave appearance in ECG #1 with the 8 example tracings from the original de Winter et al manuscript shown in Figure-2 — ECG #1 is lacking in several features:

  • Hyperacute T waves are not nearly as prominent in ECG #1 as in the 8 examples shown in Figure-2.
  • The chest lead in ECG #1 that shows the most prominent T wave ( = lead V3) does not show any J-point ST depression.
  • Only a single lead in ECG #1 shows both J-point ST depression and a hyperacute T wave ( = lead V4).
  • BOTTOM LINE: ECG #1 does not satisfy criteria for a “STEMI” — because there is not enough ST elevation. It does not quite meet the original 2008 description for de Winter T waves. That said — it should still be obvious in this patient with new-onset chest pain that acute proximal LAD occlusion must be assumed until proven otherwise!


 The 2nd ECG in Today’s Case:

follow-up ECG was obtained about 3 hours after ECG #1. For purposes of comparison — I have put this ECG #2 under the initial tracing in Figure-3.

  • How would YOU describe the ECG changes that have occurred since the initial tracing?


Figure-3: Comparison of the initial ECG in today’s case — with the follow-up ECG done about 3 hours later (See text).

MY THOUGHTS on the Follow-Up Tracing:

ECG #2 shows that there has been extensive evolution during the 3 hours since the initial tracing was done:

  • A significant Q wave is now seen in lead aVL of ECG #2, with suggestion of a tiny q wave in lead I. This is associated with loss of R wave amplitude (compared to ECG #1) in both of these high lateral leads.
  • The poor R wave progression in leads V1, V2, and V3 persists — with loss of this initial r wave in lead V4 — leading to prominent Q waves in leads V4 and V5.
  • There is now frank ST elevation in multiple leads, including leads I, aVL and V2-thru-V6.
  • Inferior lead reciprocal changes of ST depression have deepened since ECG #1.
  • Cardiac Cath was performed after ECG #2. It confirmed acute proximal LAD occlusion. Underlying multi-vessel disease (with ~50-60% stenoses) was present.


In CONCLUSION: Based on my experience over the past decade in commenting on hundreds of ECGs posted on various ECG internet forums — there are many “variants” of the original de Winter T wave pattern. 

  • Often, there won’t be J-point ST depression in anterior leads that also manifest overly large positive T waves — and“deWinter-like T wave patterns such as the one in today’s case may not necessarily persist until coronary reperfusion is accomplished. 
  • That said — despite not quite satisfying strict criteria for the de Winter T wave pattern described in the original 2008 NEJM manuscript — clinical implications of the findings in ECG #1are essentially the same as if those strict criteria were present = acute proximal LAD occlusion until proven otherwise (Choice E).



  • Acknowledgment: My appreciation to 유영준 (from Seoul, Korea) for the case and this tracing.



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ODAY’s ECG Audio PEARL (3:30 minutes): — relates to the phenomenon of deWinter-like T waves.

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.