The coagulation system is activated in idiopathic cardiomyopathy

Objectives. We investigated the plasm levels of molecular markers for platelet activity and the thrombotic and fibrinolytic status in patients with hypertrophic cardiomyopathy and dilated cardiomyopathy to determine the activating site of coagulation in these disorders. Background. thromboembolic event is serious complication in patients with idiopathic cardiomyopathy. However, the activating site of the coagulation system in idiopathic cardiomyopathy has not been fully investigated. Methods. We determined the plasm levels of molecular markers for platelet activity (platelet factor 4 and beta-thromboglobulin), thrombotic status (fibrinopeptide and thrombin-antithrombin III complex) and fibrinolytic status (D-dimer and plasmin-alpha2-plasmin inhibitor complex) in 13 patients with hypertrophic cardiomyopathy, 17 patients with dilated cardiomyopathy and 20 normal subjects. Results. Plasm levels of platelet factor 4, beta-thromboglobulin and plasmin-alpha2-plasmin inhibitor complex did not differ significantly among the three groups, whereas plasm levels of fibrinopeptide and thrombin-antithrombin III complex in both patient groups were significantly higher than those in normal subjects. Plasm levels of D-dimer in patients with dilated cardiomyopathy were significantly higher than those in patients with hypertrophic cardiomyopathy and normal groups. In patients with hypertrophic cardiomyopathy, both fibrinopeptide and thrombin-antithrombin III complex levels were significantly correlated with left atrial diameter. In patients with dilated cardiomyopathy, fibrinopeptide and thrombin-antithrombin III complex levels showed positive correlation with left ventricular end-diastolic volume and negative correlation with fractional shortening of the left ventricle. Conclusions. The activated coagulation system in patients with hypertrophic and dilated cardiomyopathy may be triggered by left atrial dilation in hypertrophic cardiomyopathy and left ventricular enlargement and dysfunction in dilated cardiomyopathy.