Exercise-induced hemostatic activation in patients with dilated cardiomyopathy in sinus rhythm.

Abnormalities of baseline hemostatic variables have been related to a hypercoagulable state in patients with chronic heart failure (CHF). Given that physical exercise leads to an activation of coagulation physiologically, this study addressed the question of whether the exercise-induced hemostatic activation is enhanced in patients with CHF. Ten patients with dilated cardiomyopathy (ejection fraction < 40%) and 10 healthy individuals (matched for sex, age and body mass index) were subjected to a maximal exercise test on a bicycle ergometer. Healthy subjects performed a second exercise test at a submaximal intensity level, in which oxygen consumption (VO2) was adjusted to the peak oxygen consumption (VO2peak) of the corresponding patient. Exercise testing had only marginal effects on markers of thrombin formation in patients and healthy individuals alike. In patients with CHF, exercise-induced changes in fibrinopeptide A, an index of fibrin formation, paralleled those observed in controls after submaximal exercise whereas most pronounced changes occurred in healthy subjects after maximal exercise. Plasmin-antiplasmin complexes increased almost three-fold with maximal exercise in both groups, thus indicating a marked formation of plasmin. Maximal physical exercise does not induce an exaggerated formation of thrombin and fibrin in CHF patients. The fibrinolytic response to exercise in terms of plasmin formation is not compromised in patients with dilated cardiomyopathy.