Exercise-induced increases in cardiac troponins and prothrombotic markers.

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.