Exercise-Induced Cardiac Troponin I Increase and Incident Mortality and Cardiovascular Events

Abstract

Background: Blood concentrations of cardiac troponin above the 99 th percentile are a key criterion for the diagnosis of acute myocardial injury and infarction. Troponin concentrations, even below the 99 th percentile, predict adverse outcomes in patients and the general population. Elevated troponin concentrations are commonly observed after endurance exercise, but the clinical significance of this increase is unknown. We examined the association between postexercise troponin I concentrations and clinical outcomes in long-distance walkers. Methods: We measured cardiac troponin I concentrations in 725 participants (61 [54–69] yrs) before and immediately after 30 to 55 km of walking. We tested for an association between postexercise troponin I concentrations above the 99 th percentile (>0.040 µg/L) and a composite end point of all-cause mortality and major adverse cardiovascular events (myocardial infarction, stroke, heart failure, revascularization, or sudden cardiac arrest). Continuous variables were reported as mean ± standard deviation when normally distributed or median [interquartile range] when not normally distributed. Results: Participants walked 8.3 [7.3–9.3] hours at 68±10% of their maximum heart rate. Baseline troponin I concentrations were >0.040 µg/L in 9 participants (1%). Troponin I concentrations increased after walking ( P <.001), with 63 participants (9%) demonstrating a postexercise troponin concentration >0.040 µg/L. During 43 [23–77] months of follow-up, 62 participants (9%) experienced an end point; 29 died and 33 had major adverse cardiovascular events. Compared with 7% with postexercise troponin I ≤0.040 µg/L (log-rank P <.001), 27% of participants with postexercise troponin I concentrations >0.040 µg/L experienced an end point. The hazard ratio was 2.48 (95% CI, 1.29–4.78) after adjusting for age, sex, cardiovascular risk factors (hypertension, hypercholesterolemia or diabetes mellitus), cardiovascular diseases (myocardial infarction, stroke, or heart failure), and baseline troponin I concentrations. Conclusions: Exercise-induced troponin I elevations above the 99 th percentile after 30 to 55 km of walking independently predicted higher mortality and cardiovascular events in a cohort of older long-distance walkers. Exercise-induced increases in troponin may not be a benign physiological response to exercise, but an early marker of future mortality and cardiovascular events.

Highly increased Troponin I levels following high-intensity endurance cycling may detect subclinical coronary artery disease in presumably healthy leisure sport cyclists: The North Sea Race Endurance Exercise Study (NEEDED) 2013

“…A very recent study by Aengevaeren et al also assessed long-term outcomes of exercise-induced cTnI increase (83). In this study, a highly significant association was identified between all-cause mortality and major adverse cardiovascular events, and cTnI increase above the upper reference limit following a prolonged walking exercise in 725 participants (83).…”

“…Cardiac troponins are markers of myocardial injury, and increased levels have been associated with increased risk of cardiovascular mortality and morbidity, recently also following exercise (83). This biomarker is therefore of major interest in detecting potentially pathological responses to exercise.…”

“…There was a highly significant (P<.001) increase in CRP following exercise in all four measures of physical fitness, with the highest CRP levels in the least fit study participants (Figure 1). Max heart rate (bpm) 180 (174)(175)(176)(177)(178)(179)(180)(181)(182)(183)(184)(185)(186)(187)(188) Max heart rate of expected max heart rate (%) 96.7 (95)(96)(97)(98)(99)(100) Mean heart rate (bpm) 158 Mean heart rate of expected max (%) 86 (82)(83)(84)(85)(86)(87)(88) Study participants with the fastest race times (Q1) were taller and consisted only of men; they also reported higher self-assessed fitness level (Table 3). There were no differences in age and BMI between riders in the different race time quartiles (Table 3).…”

The impact of exercise modality and menstrual cycle phase on circulating cardiac troponin T

“…Nevertheless, this feature allows assessment of a homogeneous cohort, free of potential confounding issues associated with training status or health status. 25 In addition, a new stricter luteal phase verification limit of >16 nmol l −1 for progesterone has just been proposed. 23 It is, therefore, recommended that future research follow this criterion to reduce the risk of inclusion of anovulatory or luteal phase deficient cycles in a large and heterogeneous cohort.…”

Determination of high sensitive cardiac troponin I 99th percentile upper reference limits in a healthy Pakistani population

“…Cardiac troponin I (cTnI) and T (cTnT) are regulatory proteins in cardiac tissue that regulate actin and myosin calcium-mediated interactions. 4 It is a protein that aids in the contraction of cardiomyocytes. Troponin is a heterotrimeric protein consisting of a tropomyosin-binding subunit troponin T (TnT), a Ca 2+ -binding subunit, troponin C (TnC), and a troponin I (TnI) inhibitory subunit.…”