Hourigan Lisa A, Walters Darren L, Keck Sally A, Dec G William
Heart Failure and Transplantation Unit, Massachusetts General Hospital, Bigelow 645, Boston, MA 02114, USA.
J Heart Lung Transplant. 2002 Dec;21(12):1283-9. doi: 10.1016/s1053-2498(02)00458-8.
Heparin-induced thrombocytopenia (HIT) is an idiosyncratic complication of heparin therapy triggered by the development of immunoglobulin G (IgG) antibodies to platelet factor 4 heparin. It typically results in a 50% decrease in platelet count. Paradoxically, although bleeding is rare, there is a high risk of venous or arterial thrombotic events. Given that many patients awaiting transplantation are exposed to heparin for prolonged periods, we sought to determine the frequency of HIT and its consequences among patients before and after cardiac transplantation.
We reviewed retrospectively the clinical, pathologic, and laboratory databases for all patients who underwent heart transplantation at our institution between January 1, 1998, and December 31, 2000. An enzyme-linked immunoabsorption assay (ELISA) that detected IgG, IgA, and IgM antibodies directed against platelet factor 4 heparin complex confirmed the diagnosis of HIT. We analyzed bleeding and thrombotic complications and determined the influence of HIT on post-transplant outcomes.
An assay for HIT antibody was performed before or after transplantation in 26 of 46 patients (46% of the entire cohort). In all cases, the clinical indication for testing was thrombocytopenia. Among patients screened, HIT antibody was detected in 11 patients (39%); HIT developed in 10 of 11 patients before transplantation. The mean platelet count at diagnosis was 88,000 +/- 22,000/mm(3). Heparin-induced thrombocytopenia with thrombosis syndrome developed in 5 of 11 patients (45%). Manifestations included splenic and renal infarctions, renal artery occlusion, coronary artery embolism with myocardial infarction, pulmonary embolism, and femoral and jugular venous occlusions. Alternative pre-operative anti-coagulation included lepirudin (n = 7), argatroban (n = 1), dalteparin (n = 1), and abciximab (n = 1). Two deaths occurred in the HIT-positive group; neither bleeding nor thrombosis caused either death. Actuarial 36-month survival did not differ between HIT-positive and HIT-negative cohorts (78% and 79%, respectively).
Heparin-induced thrombocytopenia is a frequent complication among patients hospitalized for heart failure who are awaiting heart transplantation. Timely HIT-antibody screening and the use of alternative forms of systemic anti-coagulation may permit successful transplantation with intermediate survival rates comparable to those of HIT-negative recipients.
肝素诱导的血小板减少症（HIT）是肝素治疗的一种特异质性并发症，由针对血小板因子4 - 肝素的免疫球蛋白G（IgG）抗体产生所引发。它通常导致血小板计数下降50%。矛盾的是，尽管出血罕见，但静脉或动脉血栓形成事件的风险却很高。鉴于许多等待移植的患者长期暴露于肝素，我们试图确定心脏移植前后患者中HIT的发生率及其后果。
我们回顾性分析了1998年1月1日至2000年12月31日在本机构接受心脏移植的所有患者的临床、病理和实验室数据库。通过酶联免疫吸附测定（ELISA）检测针对血小板因子4 - 肝素复合物的IgG、IgA和IgM抗体来确诊HIT。我们分析了出血和血栓形成并发症，并确定了HIT对移植后结局的影响。
46例患者中的26例（占整个队列的46%）在移植前或移植后进行了HIT抗体检测。在所有病例中，检测的临床指征均为血小板减少症。在接受筛查的患者中，11例（39%）检测到HIT抗体；11例患者中有10例在移植前发生了HIT。诊断时的平均血小板计数为88,000±22,000/mm³。11例患者中有5例（占45%）发生了肝素诱导的血小板减少伴血栓形成综合征。表现包括脾梗死和肾梗死、肾动脉闭塞、冠状动脉栓塞伴心肌梗死、肺栓塞以及股静脉和颈静脉闭塞。术前的替代抗凝药物包括重组水蛭素（n = 7）、阿加曲班（n = 1）、达肝素（n = 1）和阿昔单抗（n = 1）。HIT阳性组发生了2例死亡；出血和血栓形成均未导致死亡。HIT阳性和HIT阴性队列的36个月精算生存率无差异（分别为78%和79%）。
肝素诱导的血小板减少症是因心力衰竭住院并等待心脏移植患者中的常见并发症。及时进行HIT抗体筛查并使用替代形式的全身抗凝治疗，可能使移植成功，且中期生存率与HIT阴性受者相当。
