Although increasing levels of regular physical activity are incrementally cardioprotective, 1,2 prolonged strenuous exercise such as marathon running may trigger acute myocardial infarction 3 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. Subjects were attendees at the prerace Scientific Symposia of the American Medical Athletic Association as entrants in the 100th to 105th Boston Athletic Association Marathons from 1966 to 2001 (mean age 47.6 years), who reported no smoking or known coronary heart disease by yearly questionnaire. Blood samples were drawn without stasis from an antecubital vein using
The American Journal of Cardiology – Elsevier
Published: Oct 15, 2001
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