Ratkovec R M, Wray R B, Renlund D G, O'Connell J B, Bristow M R, Gay W A, Karwande S V, Doty D B, Millar R C, Menlove R L
Utah Transplantation Affiliated Hospitals, Cardiac Transplant Program, Salt Lake City.
J Thorac Cardiovasc Surg. 1990 Jul;100(1):6-12.
Although the etiology of allograft coronary artery disease, a major limiting factor in long-term survival after cardiac transplantation, is poorly understood, it is undoubtedly in part immune mediated and not detected by routine endomyocardial biopsy. Therefore it is possible that withdrawal of maintenance corticosteroids, although providing other short- and long-term benefits, could increase the prevalence of allograft coronary artery disease by permitting undetected immune-mediated vascular injury to occur. To assess whether corticosteroid-free maintenance immunosuppression increased the prevalence of allograft coronary artery disease, we reviewed serial angiograms of 102 patients (49% not receiving corticosteroid maintenance therapy) who underwent heart transplantation after March 7, 1985. Multiple variables including serum cholesterol, recipient and donor age, sex, blood pressure, rejection frequency and severity, early rejection prophylaxis protocol (polyclonal versus monoclonal T-cell agents), and corticosteroid use were examined in relation to allograft coronary artery disease by univariate and multivariate analyses. Allograft coronary artery disease was identified in 21 patients (seven severe, four moderate, and 10 mild). The prevalence by Kaplan-Meier life-table analysis was 17% at 1 year and 25% at 2 years. No further allograft coronary artery disease was detected among patients undergoing angiography at three years. Increased allograft coronary artery disease was not noted in patients withdrawn from maintenance corticosteroids when compared with their corticosteroid-requiring counterparts. In fact, with each 1 gm increment in cumulative corticosteroid use, a slightly increased risk (1.04, p less than 0.05) of allograft coronary artery disease was noted (Cox regression model). None of the other variables correlated with the prevalence of allograft coronary artery disease. Thus withdrawal of maintenance corticosteroids is not associated with an increased risk of early allograft coronary artery disease and minimization of corticosteroids may lead to a decreased long-term incidence of coronary artery disease in cardiac transplant recipients.
尽管心脏移植后长期存活的主要限制因素——同种异体移植冠状动脉疾病的病因尚不清楚，但毫无疑问，其部分是由免疫介导的，且常规心内膜心肌活检无法检测到。因此，尽管停用维持性皮质类固醇有其他短期和长期益处，但它可能会因允许未被检测到的免疫介导的血管损伤发生而增加同种异体移植冠状动脉疾病的患病率。为了评估无皮质类固醇维持免疫抑制是否会增加同种异体移植冠状动脉疾病的患病率，我们回顾了1985年3月7日之后接受心脏移植的102例患者（49%未接受皮质类固醇维持治疗）的系列血管造影。通过单因素和多因素分析，研究了包括血清胆固醇、受者和供者年龄、性别、血压、排斥反应频率和严重程度、早期排斥反应预防方案（多克隆与单克隆T细胞制剂）以及皮质类固醇使用等多个变量与同种异体移植冠状动脉疾病的关系。21例患者被诊断为同种异体移植冠状动脉疾病（7例严重，4例中度，10例轻度）。根据Kaplan-Meier生存表分析，1年时患病率为17%，2年时为25%。在三年时接受血管造影的患者中未检测到更多的同种异体移植冠状动脉疾病。与需要皮质类固醇的患者相比，停用维持性皮质类固醇的患者中未发现同种异体移植冠状动脉疾病增加。事实上，随着累积皮质类固醇使用量每增加1克，同种异体移植冠状动脉疾病的风险略有增加（1.04，p<0.05）（Cox回归模型）。其他变量均与同种异体移植冠状动脉疾病的患病率无关。因此，停用维持性皮质类固醇与早期同种异体移植冠状动脉疾病风险增加无关，皮质类固醇的最小化可能会降低心脏移植受者冠状动脉疾病的长期发病率。
