New Study Shows Elevated Levels of Troponin After Exercise Associated with Increased Rate of Cardiovascular Events

Fahad Alkhalfan, M.D.
By Fahad Alkhalfan, M.D. on

A study led by Dr. Vincent Aengevaeren, published in Circulation, showed that an elevated exercise-induced troponin I was associated with an increased risk of mortality and cardiovascular events in older long-distance workers. This may suggest that exercise-induced troponin elevations could be a marker of a future cardiovascular event and not a physiological response to exercise.

Cardiac troponin is a protein that is typically used to help diagnose myocardial infarction. However, higher troponin levels that are still below the upper reference limit have been associated with an increased risk of mortality and cardiovascular disease morbidity in the general population. Additionally, while exercise and physical activity are associated with better cardiovascular outcomes, studies have also demonstrated that troponin can rise during moderate or high-intensity exercise. The exercise-induced elevation in troponin is typically considered benign as it occurs in otherwise healthy individuals. However, the mechanism underlying this increase in troponin is not understood. The investigators aimed to determine whether post-exercise troponin concentrations were associated with cardiovascular outcomes in older long-distance walkers.

“Elevated troponin concentrations are frequently observed after exercise of varying duration and intensity. This exercise-associated elevation has commonly been considered to represent a benign phenomenon. We examined the potential clinical relevance of exercise-induced troponin elevations and found that postexercise troponin I concentrations above the URL after recreational walking exercise were associated with a lower event-free survival.” – Dr. Vincent Aengevaeren, M.D.

The investigators identified volunteers who participated in long-distance walking events. Participants were asked to complete a medical questionnaire and blood was drawn at baseline and ten minutes after long-distance walking. The primary study endpoint was a composite of all-cause mortality, major adverse cardiovascular events (MACE, defined as myocardial infarction, stroke, heart failure, revascularization, or sudden cardiac arrest). Participants walked a median of 8.3 hours and were followed up for a median of 43 months. Baseline troponin levels were detectable in 233 participants (33%) with 9 participants (1%) having a troponin level above the upper limit of normal (>0.04 ug/l). Troponin levels increased after exercise (p <0.001) and 418 participants (58%) had detectable troponin concentrations, with 63 participants (9%) having a troponin level above the upper limit of normal. During follow up, 62 participants had the primary endpoint (29 died and 33 had a MACE event). Compared with patients who had a post-exercise level below the upper limit of normal, those who had a higher troponin level were more likely to have the primary outcome (7% vs 27%, p <0.001). Even after adjusting for other known risk factors such as age, sex, and cardiovascular risk factors, the association remained significant (Hazard ratio of 2.48, 95% CI 1.29-4.78).

Elevated troponin levels are frequently observed after exercise. While this phenomenon was previously believed to be benign, the findings of this study suggest that patients with a higher troponin level after exercise may be at increased risk of future cardiovascular events. The results of this study suggest that exercise-induced troponin changes may be a prognostic indicator. The authors suggest that higher troponin levels could suggest myocardial injury as a result of an underlying subclinical pathology that has yet to manifest. When discussing the clinical relevance of the study, Dr. Aengevaeren wrote, “It is currently unclear how these findings impact troponin testing before and after clinical stress testing. A recent meta-analysis found no difference in post-stress (either bicycle exercise or pharmacological test) troponin concentrations in individuals with inducible or noninducible myocardial ischemia. However, only a nonsignificant 0 to 2 ng/L change in troponin concentrations was found, suggesting that the exercise intensity may not have been sufficiently high to maximally stress the heart and identify individuals at risk.” The investigators also highlight some of the limitations of this study which include the relatively short follow up period and small sample size.

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