Dale J, Myhre E
Am Heart J. 1977 Sep;94(3):359-66. doi: 10.1016/s0002-8703(77)80481-x.
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.
对正常受试者以及植入1200系列和2300系列单枚史塔夫-爱德华兹主动脉球瓣的患者的血小板功能进行了研究。采用海勒姆改良法测定血小板黏附性,发现其变化最为显著。黏附血小板的平均百分比从正常受试者的71.8%降至1200型瓣膜患者的50.9%,以及2300型瓣膜患者的27.2%。血清乳酸脱氢酶水平反映出血小板黏附性与血管内溶血程度呈负相关。2300型瓣膜患者的平均出血时间显著延长,且个体值与黏附性呈负相关。与正常情况相比,血小板计数、胶原蛋白或肾上腺素诱导的不可逆聚集以及血小板存活的平均值均有适度但显著的降低。血小板反应性紊乱背后最重要的机制可能是瓣膜对血小板的机械损伤,而血小板对红细胞释放的二磷酸腺苷的不应性以及血栓形成对黏附血小板的消耗被认为对血小板行为的影响有限。有动脉血栓栓塞并发症病史的患者与无此病史的患者血小板功能改变程度相同。血小板反应性紊乱可能易导致出血,但也可能对动脉血栓栓塞有一定的保护作用。