药物洗脱支架置入后血栓形成的原因分析

Analysis of the mechanisms of thrombosis after implantation of drug-eluting stents

目的探讨药物洗脱支架置入后血栓形成的发生率以及血栓形成的原因。方法本研究为单中心药物洗脱支架的注册研究,自2001年12月至2005年12月共计3345例冠心病患者接受了药物洗脱支架的治疗,其中使用雷帕霉素洗脱支架(SES)2165例,使用紫杉醇洗脱支架(PES)1180例,完成10个月临床随访为2296例;所有患者均同时口服阿司匹林和氯吡格雷至少9个月。结果 3345例患者中9例发生急性血栓形成(0.27%),其中7例为 SES、2例为 PES 所致(0.32%比0.17%,P=0.637);7例发生亚急性血栓形成(0.21%),其中5例为 SES、2例为 PES 所致(0.23%比0.17%,P=0.526);急性和亚急性血栓发生率为0.485(16/3345);13例有晚期血栓形成,5例为 SES、8例为 PES 所致(0.34%比0.95%,P=0.114);4例晚期血栓形成的主要原因为提前中断抗血小板药物,既往患有心肌梗死病史,心功能差,药物洗脱支架置入后晚期发生血栓致猝死6例。结论支架置入不满意,特别是分叉病变以及支架未能完全覆盖受损伤的病变段是急性和亚急性血栓形成的主要原因;中断抗血小板药物和左心功能不全是晚期血栓形成的主要原因。

Objective Stent thrombosis has been regarded as a severe complication of PCI therapy, therefore, analyzing the causes of thrombosis after implantation of drug-eluting stents （DES） is necessary. Methods This is a single center study with no limitation of entry criteria for using DES in patients with coronary heart disease （CHD）. From Dec. 2001 to Dec. 2005, 3345 consecutive patients underwent implantation with Cypher stents （eluted with sirolimus ：2165 patients, 2362 lesions, 2695 stents） or TAXUS stents （e luted with paclitaxel： 1180 patients, 1453 lesions, 1725 stents） in our hospital. 10-month follow- up was completed in 2296 patients （ 1455 patients with 1632 lesions using 1773 Cypher stents ＆ 841 patients with 1032 lesions used 1182 TAXUS stents）. All patients were treated with aspirin plus clopidogrel at least 9 months after PCI procedure. Results Among 3345 patients, 9 patients had acute stent thrombosis （0. 27% ）： 7 in the sirolimns group, 2 in the paclitaxel group （0. 32% vs 0. 17% , P = 0. 637 ）, 7 patients had subacute stent thrombosis （0. 21% ） ： 5 in the sirolimus group and 2 in the paclitaxel group （0. 23% vs 0. 17%, P = 0. 526） and13 patients had late stent thrombosis （0. 57% ） ： 5 in the sirolimus group and 8 in the paclitaxel group （0. 34% vs 0.95% , P =0. 114） Among the 29 patients with DES thrombosis. 8 patients （26. 7% ） presented as sudden death, 13 nonfatal MI and 8 unstable angina. Stent thrombosis was demonstrated by angingraphy in 21 patients （72.4%）. The causes of acute and subacute DES thrombosis were related to suboptimal stenting in 8 patients including 7 patients with bifurcation lesions or to uncovered injury segment of the diffuse lesions in five patients. The causes for late thrombosis were discontinuation of antiplatelet drugs in four cases and related to poor left ventricular function in 6 cases with history of old myocardial infarction. Conclusions Our study showed that suboptimal stenting, especially for bifurcation lesions and uncovered injury segment of diffuse lesions were the main causes of acute and subacute stent thrombosis. Left ventricular disfunction and premature discontinuation of antiplatelet therapy were the main reasons of late thrombosis.