K. Yamamoto et al., THE COAGULATION SYSTEM IS ACTIVATED IN IDIOPATHIC CARDIOMYOPATHY, Journal of the American College of Cardiology, 25(7), 1995, pp. 1634-1640
Objectives. We investigated the plasma levels of molecular markers for
platelet activity and the thrombotic and fibrinolytic status in patie
nts with hypertrophic cardiomyopathy and dilated cardiomyopathy to det
ermine the activating site of coagulation in these disorders. Backgrou
nd. A thromboembolic event is a serious complication in patients with
idiopathic cardiomyopathy. However, the activating site of the coagula
tion system in idiopathic cardiomyopathy has not been fully investigat
ed. Methods. We determined the plasma levels of molecular markers for
platelet activity (platelet factor 4 and beta-thromboglobulin), thromb
otic status (fibrinopeptide A and thrombin-antithrombin III complex) a
nd fibrinolytic status (D-dimer and plasmin-alpha(2)-plasmin inhibitor
complex) in 13 patients with hypertrophic cardiomyopathy, 17 patients
with dilated cardiomyopathy and 20 normal subjects. Results. Plasma l
evels of platelet factor 4, beta-thromboglobulin and plasmin-alpha(2)-
plasmin inhibitor complex did not differ significantly among the three
groups, whereas plasma levels of fibrinopeptide A and thrombin-antith
rombin III complex in both patient groups were significantly higher th
an those in normal subjects. Plasma levels of D-dimer in patients with
dilated cardiomyopathy were significantly higher than those in patien
ts with hypertrophic cardiomyopathy and normal groups. In patients wit
h hypertrophic cardiomyopathy, both fibrinopeptide A and thrombin-anti
thrombin III complex levels were significantly correlated with left at
rial diameter. In patients with dilated cardiomyopathy, fibrinopeptide
A and thrombin-antithrombin III complex levels showed a positive corr
elation with left ventricular end diastolic volume and a negative corr
elation with fractional shortening of the left ventricle. Conclusions.
The activated coagulation system in patients with hypertrophic and di
lated cardiomyopathy mag be triggered by left atrial dilation in hyper
trophic cardiomyopathy and left ventricular enlargement and dysfunctio
n in dilated cardiomyopathy.