Thursday, May 19, 2022

Chest pain, shortness of breath, T wave inversion, and rising troponin in a young healthy runner.

Written by Pendell Meyers, edits by Smith and Grauer

A man in his late 20s with history of asthma presented to the ED with a transient episode of chest pain and shortness of breath after finishing a 4-mile run. He typically runs 4 to 8 miles per day. This episode was unusual to him because he was still "huffing and puffing" about 30 minutes after finishing his strenuous run in the outdoor heat. No mention of whether the patient had cough.

At the time of evaluation in the ED, his symptoms were resolved. His exam stated that his lungs were clear.

Here is his ECG:

Meyers: This ECG shows sinus rhythm, normal QRS with healthy high voltage, and benign T wave inversion pattern in V3-V5. Dr. Smith and I agree that this is a normal variant ECG, in other words, NORMAL, and no further workup should be based on this ECG, but instead only the patient's symptoms and clinical picture. For in-depth description and examples of BTWI, I'll refer you to my other recent post: Understanding this pathognomonic ECG would have greatly benefitted the patient.

Smith comment: the pattern in this case is indeed benign and normal, but is slightly different than BTWI.  I have seen this particular morphology many times, and it has always been benign and in young males.  There is a prominent U-wave and a much deeper S-wave in V3 and V4 than in the typical BTWI. I doubt it makes a difference in management.

The ECG was read as concerning for Wellens (meaning anterior reperfusion pattern).

Initial high sensitivity troponin I = 27 ng/L (URL for men 20 ng/L for this assay).

CT angio negative for PE or other radiographic pathology.  (No D-dimer was ordered)

A repeat troponin returned at 51 ng/L.

He was given aspirin and heparin and transferred to the local cardiac center for further evaluation.

He was diagnosed with mild AKI which resolved.

Ct coronary angiogram showed normal coronary arteries.  

Smith note: I think CT coronary angiogram is reasonable with the elevated troponins and symptoms.  Exercise test would also have been reasonable.  I would always do a peak flow in a patient like this and if not at predicted value, give albuterol and see if it improves.

Next troponins were 28, then 19, then none further measured.

Several more ECGs were obtained during his admission.

All just normal ECGs with BTWI. 

His symptoms of chest pain and shortness of breath were attributed to an asthma exacerbation during exercise.

He was discharged.

Read about "exercise induced cardiac troponin elevations" here. Here are a couple quotes from the article:

"Exercise intensity and duration, together with exercise‐induced high heart rate, have been the most consistent predictors for the exercise‐induced cardiac troponin elevations."

"Exercise‐induced troponin elevations are common after long‐distance running, but occur rarely (9%) after long‐distance walking, supporting the crucial role of high heart rate in this process."

"The benign troponin release pattern is characterized by relatively low peak concentrations that occur within a few hours after exercise and normalize within 24 hours compared with a more prolonged elevation in myocardial infarction or myocarditis."

Dr. Smith note: I wouldn't necessarily consider this ENTIRELY "benign." It is benign compared to acute MI, but it may be that people with such troponin elevations are at higher risk for long term mortality. It may even be that patients with ECGs with this morphology have a higher long term risk. The important point for our purposes is that they do no represent myocardial infarction. Indeed, they have a higher incidence of structural problems.

Potential Adverse Cardiovascular Effects From Excessive Endurance Exercise

Exercise Is Medicine? The Cardiorespiratory Implications of Ultra-marathon

Bjørkavoll‐Bergseth et al. JAHA 2020.

177 participants of a 91-km recreational mountain bike race had pre-race, 3-hour post race, and 24-hour post race evaluations including cTnI and cTnT measurements. Both cTnI and cTnT increased in all individuals, reaching the highest level at 3 hours after the race. Of all heart rate data recorded during the race, the duration of exercise with HR greater than 150 bpm correlated best with the rise in troponin levels.

Median cTnI at baseline was 1.9 (1.6–3.3) ng/L, increased to 60.0 (36.0–99.3) ng/L at 3 hours (P<0.001) and declined at 24 hours to 10.9 (6.1–22.4) ng/L (P<0.001). A similar profile was found for cTnT: baseline, <3.0 (<3.0–3.8) ng/L; 3 hours, 38.3 (25.6–55.2) ng/L (P<0.001); and 24 hours, 11.0 (7.2–17.4) ng/L (P<0.001).

Paana et al. International Journal of Cardiology 2019.

In this study, 40 presumably healthy male marathon runners had their cardiac troponin and other findings measured before and after running a marathon. 39 pts (97.5%) had baseline cTnT values below the reference limit (less than 14 ng/L). 38 pts (95%) of participants had post-marathon cTnT concentration rise above this reference limit. The median post-marathon cTnT was 41 ng/L, and the 95th percentile concentration was 90 ng/L. None reported "cardiac symptoms" after the race.

See this single post for many examples of BTWI:

Understanding this pathognomonic ECG would have greatly benefitted the patient.

Comment by KEN GRAUER, MD (5/17/2022):
Concise but important presentation by Dr. Meyers that emphasizes the following points:
  • The History is KEY.
  • BTWI (Benign T-Wave Inversion) Syndromes are often mistaken for more serious pathology.
  • Exercise-Induced Troponin Elevation — is a real entity. As per Dr. Meyers — today’s case was typical of this entity because: i) Troponin elevation occurred in an otherwise healthy adult after an episode of long-distance running; ii) Peak troponin was no more than minimally elevated; andiii) Troponin levels rapidly returned to normal (whereas the troponin elevation of acute MI is generally higher and lasts much longer).

Regarding the History: 
It sounds from the History as if this patient has at least a significant component of EIA (Exercise-Induced Asthma). It also sounds from events described that he was unaware of this possibility. Many variations of asthma exist — including non-exercise-induced — primarily exercise-induced — and/or — some combination of these 2 entities. Clearly, overexertion from excessive hot temperature during this patient's run may have predisposed to precipitating bronchospasm on the day of admission.
  • Attention to the history could help elicit how likely it is that this patient’s symptoms were (or were not) the result of EIA.
  • definitive diagnosis could be made by a combination of history (regarding the circumstances of symptom occurrence, treatments tried, and the course over time of this patient’s asthma) — and — by lung auscultation and/or peak flow measurement (that can be easily taught to the patient) before and after exercise.
  • Effective management of EIA can usually be achieved by patient awareness of this entity — and — with appropriate prophylactic and/or post-exercise bronchodilator use.
  • Referral to the patient’s primary care clinician (added as an essential part of this patient’s hospital discharge instructions) — can facilitate optimal longterm management (and hopefully avoid recurrent ED visits in the future for the same problem).
  • A nice Review of EIA by Molis and Molis can be found in Sports Health 2:311-317, 2010.

Regarding the ECGs in Today’s Case:
While I immediately suspected that the initial ECG in today's case was benign — I thought it somewhat atypical, because T wave inversion is minimal in leads V1,V2 — and much more impressive in leads V3,V4 (See ECG #1 in Figure-1).
  • NOTE #1: There clearly is misplacement of the lead V1 and V2 electrodes (which are placed too high on the chest) — because: i) There is a terminal r’ complex in lead V1 — with an overall QRS morphology that closely resembles the PQRST complex in lead aVR — and, with an all negative P wave in this lead V1; andii) I would not expect the inverted T wave amplitude to decrease from lead V1-to-V2 — and then to increase again from lead V2-to-V3.
  • Please see My Comment at the bottom of the page in the April 17, 2022 post of Dr. Smith's Blog — for concise review on how to quickly recognize too-high placement of the lead V1 and V2 electrodes.
  • Given that the reason for admitting today's patient to the hospital was mainly because his initial ECG was perceived as “abnormal” and possible Wellens' Syndrome — I would have immediately repeated the initial ECG as soon as I recognized the obvious misplacement of the V1,V2 electrodes. Doing so would have immediately produced a repeat tracing similar to ECG #2 — which I feel is even more typical for a BTWI variant with ST elevation (because of a much more logical progression of QRS complexes and ST-T wave appearance as one moves from leads V1-thru-V4).

  • NOTE #2: In support that the lead V1,V2 electrodes in ECG #1 were in fact placed too high — is the appearance of these leads in ECG #2, in which: i) There is no longer any r' component in lead V1; ii) The P wave in lead V1 now has an initial positive component; iii) The rS complex in lead V1 of ECG #2 no longer resembles the Qr complex in lead aVR; andiv) There is now a much more natural R wave progression as one moves from lead V1-to V2- to V3, compared to the less logical R wave progression that there was in ECG #1.

  • NOTE #3: For review of the "many faces" of benign ST-T wave variants — numerous examples are shown and discussed in the March 22, 2022 post by Dr. Meyers — and earlier, in the January 7, 2015 post in Dr. Smith's Blog.

Final Points:
  • We know that the patient in today's case is athletic (he runs 4-8 miles daily!) — but we were not told his race. This is relevant — because many of the benign ST-T wave variants are far more common in young adult, athletic, African-American males. Awareness of this racial predominance may be helpful in estimating the likelihood of a normal variant ECG pattern.

  • Did YOU notice the rhythm in ECG #1? This is not a simple sinus rhythm. In addition to marked variation in the R-R interval throughout the long lead II rhythm strip — there appears to be a change in P wave morphology (ie, the P wave being of much smaller amplitude at the slower rates, before beats #1, 2 and 12 in the long lead II rhythm strip — compared to the larger and notched P wave in front of beats #3-thru-11). This gradual change in P wave morphology as the heart rate varies could be consistent with a wandering atrial pacemaker.
  • To Emphasize: WAP (Wandering Atrial Pacemaker) is typically a benign variant rhythm that is not important clinically to today's case. That said — My point is to illustrate how EASY it is to overlook non-sinus rhythms if you are not systematic in your approach to ECG interpretation (and if you do not routinely spend an "educated" 3-to-5 seconds looking at regularity and consistency in P wave morphology in the long lead rhythm strip of every ECG you encounter)!

  • Technically — We cannot diagnose WAP with certainty from the 12-beat rhythm strip shown in ECG #1 — because shift between at least 3 different atrial pacemaker sites is needed to satisfy criteria for WAP — and we only see 2 different P wave shapes in the long lead II of ECG #1.
  • In contrast — the difference in P wave morphology is more subtle in ECG #2 (and more difficult to distinguish from the slight variation in sinus P wave morphology that is sometimes normally seen). 
  • NOTE: Please see the Addendum below if interested in more detail regarding the ECG diagnosis of WAP.

Figure-1: I've reproduced the first 2 ECGs in today's case (See text).


I review KEY features of a Wandering Atrial Pacemaker (as opposed to MAT) in the 3:30 minute Audio Pearl below:


Figure-2: Written review of wandering atrial pacemaker (from ECG Blog #200 — which illustrates a case).

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