Warkentin Theodore E, Greinacher Andreas, Koster Andreas
Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada.
Ann Thorac Surg. 2009 May;87(5):1633-40. doi: 10.1016/j.athoracsur.2008.10.060.
Heparin-induced thrombocytopenia (HIT) is caused by platelet-activating antiplatelet factor 4/heparin antibodies. However, clinical HIT (thrombocytopenia or thrombosis, or both) develops in only a minority of patients who form antibodies. It is difficult to distinguish HIT from non-HIT thrombocytopenia in patients after ventricular assist device (VAD) implantation. Further, the risks of heparin-induced immunization and clinical HIT approach 65% and 10%, respectively, in this patient population, with a particularly high risk of cerebrovascular ischemia/infarction. Given the apparent high risk of HIT and its complications, and the diagnostic challenges, we suggest that the VAD patient population be evaluated using alternative, nonheparin agents for routine postimplantation anticoagulation.
肝素诱导的血小板减少症（HIT）由血小板活化的抗血小板因子4/肝素抗体引起。然而，只有少数产生抗体的患者会出现临床HIT（血小板减少或血栓形成，或两者兼有）。心室辅助装置（VAD）植入术后的患者中，很难区分HIT和非HIT血小板减少症。此外，在该患者群体中，肝素诱导免疫和临床HIT的风险分别接近65%和10%，脑血管缺血/梗死风险尤其高。鉴于HIT及其并发症的明显高风险以及诊断挑战，我们建议对VAD患者群体使用替代的非肝素药物进行常规植入后抗凝评估。
