Abstract

Although increasing levels of regular physical activity are incrementally cardioprotective,1,2 prolonged strenuous exercise such as marathon running may trigger acute myocardial infarction3 and sudden cardiac death.4,5 The mechanism of such events is not well understood but may be due to hemodynamic, vasoconstrictive, and prothrombotic effects with disruption of unstable coronary plaques leading to acute coronary thrombosis.6,7 Although several studies have demonstrated exercise-induced activation of fibrinolysis and coagulation,8 the effect of marathon running on hemostatic balance has not been well studied. We therefore measured changes in C-reactive protein (CRP), von Willebrand factor (vWF), D-dimer, fibrinogen, fibrinolytic activity, white blood cell (WBC) counts, and platelet activation in middle-aged runners before and after the Boston Marathon. An imbalance in prothrombotic and fibrinolytic factors after strenuous physical exertion may transiently increase the risk for intravascular—including coronary—thrombosis and trigger acute ischemic events.

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