Platelet functions in patients with aortic ball valves.
Platelet functions were studied in normal subjects and patients with single Staff-Edwards aortic ball valves of series 1200 and 2300. The most pronounced changes were found in platelet adhesiveness, measured with Hellem's modified method. The mean percentage of adhesive platelets was reduced from 71.8 in normal subjects to 50.9 in patients with valve type 1200 and to 27.2 in those with type 2300. An inverse correlation was found between platelet adhesiveness and the degree of intravascular hemolysis, as reflected by serum LDH levels. The mean bleeding time was significantly prolonged in patients with valve 2300, and the individual values correlated inversely to the adhesiveness. The mean values of platelet counts, or irreversible aggregation induced by collagen or epinephrine, and of platelet survival were all moderately-but significantly-reduced as compared to normal. The most important mechanism behind the disturbed platelet reactivity is probably mechanical damage of the platelets by the valve, whereas refractoriness of platelets toward ADP liberated from red cells as well as consumption of adhesive platelets by thrombus formation is thought to have limited influence on platelet behavior. Platelet function was altered to the same extent in patients with a history of arterial thromboembolic complications as in those without. The disturbed platelet reactivity may predispose to bleeding, but may also offer some protection against arterial thromboembolism.
D001021:Aortic Valve; D001772:Blood Cell Count; D001780:Blood Coagulation Tests; D001792:Blood Platelets / Q000502:physiology*; D006350:Heart Valve Prosthesis / Q000009:adverse effects; D006461:Hemolysis; D006801:Humans; D007770:L-Lactate Dehydrogenase / Q000097:blood; D010973:Platelet Adhesiveness; D010974:Platelet Aggregation; D013923:Thromboembolism / Q000097:blood / Q000209:etiology
D007770:L-Lactate Dehydrogenase