Taha T H, Durrant S, Crick J, Bowcock S, Bradshaw A, Oakley C M
Department of Medicine (Clinical Cardiology and Haematology Units), Royal Postgraduate Medical School, Hammersmith Hospital, London, UK.
Heart Vessels. 1991;6(2):102-6. doi: 10.1007/BF02058756.
Local and generalized changes in coagulation may be important in the genesis of vegetations and embolism in infective endocarditis. To characterize such alterations, serial hematological investigations were performed on nine consecutive patients who satisfied the inclusion criteria. Platelet survival was measured by Indium111 labeling. Acute and convalescent samples were analyzed for fibrinogen, factor VIIIc, antithrombin III (AT III), fibrin/fibrinogen degradation products (FDPs), and platelet aggregation. The results suggest that in the active stage of the disease: (1) hypercoagulability may be caused by a rise in acute phase reactants, (2) an acceleration of coagulation and fibrinolysis may supervene, and (3) in some cases there is a reduction in platelet aggregation, possibly as a result of continued circulation of previously activated "exhausted" platelets.
凝血的局部和全身性变化在感染性心内膜炎中赘生物和栓塞的发生过程中可能起重要作用。为了描述这些改变的特征，对9例符合纳入标准的连续患者进行了系列血液学检查。通过铟111标记测量血小板生存期。对急性期和恢复期样本分析纤维蛋白原、因子VIIIc、抗凝血酶III（AT III）、纤维蛋白/纤维蛋白原降解产物（FDPs）和血小板聚集情况。结果表明，在疾病的活动期：（1）高凝状态可能由急性期反应物升高引起；（2）可能随后出现凝血和纤维蛋白溶解加速；（3）在某些情况下，血小板聚集减少，这可能是先前激活的“耗竭”血小板持续循环的结果。
