Hemostatic changes induced by percutaneous mitral valvuloplasty.
A study was conducted of hemostatic changes in 15 patients with mild-to-moderate rheumatic mitral stenosis who underwent percutaneous mitral balloon valvuloplasty (PMV). The patients were divided into two groups according to the degree of valve dilatation as evaluated by Doppler echocardiography before and 2 to 3 months after therapy: one group (n = 7) with suboptimal valvuloplasty (< 0.5 cm2) and one (n = 8) with optimal valvuloplasty (> or = 0.5 cm2). On the day of echocardiographic evaluation, hemostatic testing of the platelet, coagulation, and fibrinolytic systems was performed. Before PMV there were no differences in the hemodynamic and hemostatic variables between the two groups. No favorable hemostatic changes were achieved by PMV in the suboptimal group. In the optimal group, however, platelet-specific protein levels decreased after PMV; the mean levels of platelet factor 4 and beta-thromboglobulin were moderately elevated before and decreased after PMV from 38.5 +/- 22.2 to 8.13 +/- 5.08 ng/ml (p < 0.01) and from 132.5 +/- 78.6 to 38.8 +/- 19.5 ng/ml (p < 0.02), respectively. Coagulation and fibrinolytic systems were unchanged in this study. These data indicate that PMV produces favorable hemostatic effects when sufficient mitral valve dilatation is achieved. Analysis of our data also discloses that platelet activation plays an important role in the initial step of thrombus formation in patients with rheumatic mitral stenosis.
Kataoka
H
H
Second Department of Internal Medicine, Oita Medical University, Japan.
Yano
S
S
Tamura
A
A
Mikuriya
Y
Y
D001780:Blood Coagulation Tests; D002404:Catheterization; D015150:Echocardiography, Doppler; D005260:Female; D006439:Hemodynamics / Q000502:physiology; D006487:Hemostasis / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D008943:Mitral Valve / Q000000981:diagnostic imaging; D008946:Mitral Valve Stenosis / Q000097:blood / Q000503:physiopathology / Q000628:therapy*; D012214:Rheumatic Heart Disease / Q000097:blood / Q000503:physiopathology / Q000628:therapy*; D013923:Thromboembolism / Q000517:prevention & control