Occult obstructive coronary artery disease is associated with prolonged cardiac troponin elevation following strenuous exercise.

BACKGROUND: Sudden cardiac death among middle-aged recreational athletes is predominantly due to myocardial ischaemia. This study examined whether measuring cardiac troponin I and T (cTnI and cTnT) after strenuous exercise could identify occult obstructive coronary artery disease. DESIGN: Prospective observational study. METHODS: Subjects were recruited from 1002 asymptomatic recreational cyclists completing a 91-km mountain bike race (North Sea Race Endurance Exercise Study). No subject had known cardiovascular disease or took cardiovascular medication. Blood samples were collected within 24 h before and 3 h and 24 h after the race. Coronary computed tomography angiography was performed in 80 participants with the highest post-exercise cTnI and in 40 reference subjects with moderately elevated cTnI values. RESULTS: Study subjects (N = 120) were 45 (36-52) years old and 74% were male. There were similar demographics in the High-cTnI group and the Reference group. The cTn concentrations were highest at 3 h post-race: cTnI, 224 (125-304) ng/L; cTnT, 89 (55-124) ng/L. Nine subjects had obstructive coronary artery disease on coronary computed tomography angiography, eight of whom were High-cTnI responders. Two subjects had myocardial bridging, both High-cTnI responders. Troponin concentrations at 24 h post-race were higher in subjects with obstructive coronary artery disease than in the rest of the cohort (n = 109): cTnI, 151 (72-233) ng/L vs. 24 (19-82) ng/L, p = 0.005; cTnT, 39 (25-55) ng/L vs. 20 (14-31) ng/L, p = 0.002. The areas under the receiver operating characteristic curves for predicting obstructive coronary artery disease were 0.79, p = 0.005 (cTnI) and 0.82, p = 0.002 (cTnT). CONCLUSION: In subjects with occult obstructive coronary artery disease there was a prolonged elevation of cTn following strenuous exercise.

Race duration and blood pressure are major predictors of exercise-induced cardiac troponin elevation.

BACKGROUND: The underlying mechanisms of the exercise-induced increase in cardiac troponins (cTn) are poorly understood. The aim of this study was to identify independent determinants of exercise-induced cTn increase in a large cohort of healthy recreational athletes. METHODS: A total of 1002 recreational cyclists without known cardiovascular disease or medication, participating in a 91-km mountain bike race were included. Median age was 47 years and 78% were males. Blood samples were obtained 24 h prior to, and 3 and 24 h after the race. RESULTS: Cardiac TnI concentrations increased markedly from baseline [1.9 (1.6-3.0) ng/L] to 3 h after the race [52.1 (32.4-91.8) ng/L], declining at 24 h after the race [9.9 (6.0-20.0) ng/L]. Similarly, cTnT increased from baseline [3.0 (3.0-4.2) ng/L] to 3 h after the race [35.6 (24.4-54.4) ng/L], followed by a decline at 24 h after the race [10.0 (6.9-15.6) ng/L]. The 99th percentile was exceeded at 3 h after the race in 84% (n = 842) of subjects using the cTnI assay and in 92% (n = 925) of study subjects using the cTnT assay. Shorter race duration and higher systolic blood pressure (SBP) at baseline were highly significant (p < 0.001) independent predictors of exercise-induced cTn increase both in bivariate and multivariable analysis. The age, gender, body mass index, training experience and cardiovascular risk of participants were found to be less consistent predictors. CONCLUSION: Systolic blood pressure and race duration were consistent predictors of the exercise-induced cTn increase. These variables likely reflect important mechanisms involved in the exercise-induced cTn elevation. TRIAL REGISTRATION NUMBER: NCT02166216 https://clinicaltrials.gov/ct2/show/NCT02166216.

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.

Background Circulating cardiac troponin levels increase following prolonged intense physical exercise. The aim of this study was to identify participants with highly elevated cardiac troponins after prolonged, high intensity exercise, and to evaluate these for subclinical coronary artery disease. Methods and results Ninety-seven recreational cyclists without known cardiovascular disease or diabetes, participating in a 91 km mountain bike race were included, 74 (76%) were males, age: 43 ± 10 years, race duration: 4.2 (3.6-4.7) h. Blood samples, rest electrocardiogram and physical examination were obtained 24 h prior to, and at 0, 3 and 24 h following the race. Median cardiac troponin I level at baseline: 3.4 (2.1-4.9) ng/l (upper limit of normal: 30.0 ng/l). There was a highly significant ( p < 0.0001) increase in circulating cardiac troponin I in all participants: immediately following the race; 50.5 (28.5-71.9) ng/l, peaking at 3 h 69.3 (42.3-97.7) ng/l and declining at 24 h: 14.2 (8.5-27.9) ng/l. No cyclist had symptoms or rest electrocardiogram changes compatible with coronary artery disease during or following the race. Coronary artery disease was detected by coronary angiography in the three cyclists with the three of the four highest cardiac troponin values (>370 ng/l) at 3 and 24 h following the race. Computed tomographic coronary angiography was performed in an additional 10 riders with the subsequently highest cardiac troponin I values, without identifying underlying coronary artery disease. Conclusions This study suggests that there is a pathologic cardiac troponin I response following exercise in individuals with subclinical coronary artery disease. This response may be associated with an excessive cardiac troponin I increase at 3 and 24 h following prolonged high-intensity exercise.