Exercise-Induced Increases in Cardiac Troponins and Prothrombotic Markers

Abstract

Cardiac troponin I and T are potent tools for risk stratification and clinical decision-making for patients in the appropriate clinical setting of an acute coronary syndrome. Although these findings are relevant to patients with a typical clinical presentation, caution should be exercised in generalizing the results to troponin-positive athletes with a low clinical suspicion of coronary artery disease. This review addresses the clinical relevance of increased troponin levels induced by strenuous exercise. The imprecision and lack of standardization of currently available troponin assays merit caution with the application of these findings. In addition, it may well be that if reparative processes are present and/or the release is not due to irreversible injury that increases in troponins after vigorous exercise are normal and should not be expected to be of pathophysiological significance. Due to this potential for misclassification, the crux of appropriate interpretation of troponin testing is careful consideration of the corresponding clinical scenario. Troponin-positive patients often have complex coronary lesion morphology with intracoronary thrombus and understandably derive particular benefit from platelet glycoprotein GpIIb/IIa inhibitors as well as low molecular weight heparins. Studies on exercise-induced activation of blood coagulation have produced conflicting results. At present, there is no clear evidence that a hemostatic imbalance may trigger acute cardiac events after strenuous exercise. In contrast to troponin-positive patients, it may thus be premature and even dangerous to recommend pharmacologic intervention (low molecular weight heparins) to (troponin-positive) endurance athletes even when exercising during high-altitude exposure.

Reference Population and Marathon Runner Sera Assessed by Highly Sensitive Cardiac Troponin T and Commercial Cardiac Troponin T and I Assays

“…The concentration difference was minor, however, and the increases occurred in the absence of any clinical symptoms. Two opposing theories attempt to explain the link between exercise-induced cTn release and (acute) cardiac events (34 ). First, the reversibility concept proposes that exercise increases the number of radicals and thereby membrane permeability, causing cTn leakage from the cytosolic cellular pool (35,36 ).…”

Cardiac drift during prolonged exercise with echocardiographic evidence of reduced diastolic function of the heart

“…Prolonged exercise may also provoke an increase in serum levels of the myofibrillar protein cardiac troponin T (cTnT; Mair et al 1992;Koller 2001;Neumayr et al 2001Neumayr et al , 2002Shave et al 2002bShave et al , 2004aShave et al , 2004b, but whether that indicates myocardial damage remains unknown (Koller 2003) and the association between serum cTnT and EICF is not clear.…”

Cardiac Marker Troponin in Dubai Marathon Runners

“…Some have suggested that exercise-induced cardiac troponin release precedes physiologic cardiac hypertrophy [6,8,26,27]. Release of acidic and basic fibroblast growth factor (> FGF and AFGF, respectively) from the cytosol of cardiac myocytes has been demonstrated, occurring in response to membrane damage caused by an increase in the rate and force of cardiac contraction.…”

“…Recent studies [6][7][8][9][10][11] have demonstrated the risks of exercise-associated cardiac damage and/or dysfunction, as evidenced by a rise in cardiac biomarkers. Of particular interest is the transient rise in activities of creatine kinase MB [12] following marathon run.…”