Hypercoagulability in patients with mitral stenosis. From the viewpoint of the behavior of plasma antithrombin III and alpha2-plasmin inhibitor.

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Abstract
The concentration of plasma antithrombin [AT] III and the biological activity of plasma alpha-2-plasmin inhibitor (.alpha.2-PI) were measured in cases of mitral stenosis (MS) and rheumatic heart disease (RHD) without MS. Cases of MS showed the findings of the low levels of plasma AT III and normal or a little higher levels of plasma .alpha.2-PI, that was not recognized in RHD without MS. This finding was interpreted to be hypercoagulable because of the acceleration of coagulation and of little or slight retardation of fibrinolysis. The influence of atrial fibrillation and chronic congestive heart failure on hypercoagulability in cases of MS was detected clearly. The influence of them in cases of non-RHD was obscure. The severer the degree of MS, the clearer the hypercoagulable state. The prethrombotic state existed in cases of MS, combined with blood flow disturbance due to atrial fibrillation or chronic congestive heart failure. Endocardial damage resulted from rheumatic fever in an early stage and hypercoagulability. There was no significant difference between cases with and without thrombi in the degree of hypercoagulability in subjects with MS. The consumption of AT III apparently caused the low levels of thrombosis in cases of MS. The low production of AT III in the liver rather than consumption caused the low levels of thrombosis in cases of non-RHD.