Abstract des Autors

We examined the hypothesis that physical exercise might give rise to an exaggerated activation of coagulation in patients with coronary artery disease (CAD). Molecular markers of in vivo thrombin (prothrombin fragment l+2; PTF1+2) and fibrin formation (fibrinopeptide A; FPA) were determined in 12 patients with angiographically documented CAD (55+/-9 years) and 12 healthy control subjects (52+/-7 years) before and after a group-exercise session for cardiac rehabilitation lasting 1 hour. All patients were treated with beta-blockers and aspirin. PTF1+2 at baseline was significantly lower in patients than in controls (0.7+/-0.2 vs. 1.0+/-0.2 nmol/l; P<0.001). Following exercise PTF1+2 remained unchanged in patients and increased to 1.3+/-0.5 nmol/l (P<0.01) in controls. Exercise gave rise to significant increases of FPA in both groups with more pronounced changes, however, in controls (from 1.3+/-0.4 to 2.0+/-0.5 ng/ml, P<0.05 vs. from 1.3+/-0.4 to 1.6+/-0.4 ng/ml, P<0.05 in patients). Examinations in controls after administration of aspirin indicate that aspirin did not significantly affect exercise-induced hemostatic activation. We conclude that exercise training in patients with CAD has no detrimental effects on thrombin and fibrin formation. Verf.-Referat