Laule M, Cascorbi I, Stangl V, Bielecke C, Wernecke K D, Mrozikiewicz P M, Felix S B, Roots I, Baumann G, Stangl K
Medizinische Klinik mit Schwerpunkt Kardiologie, Angiologie und Pneumologie, Humboldt-Universität zu Berlin, Germany.
Lancet. 1999 Feb 27;353(9154):708-12. doi: 10.1016/S0140-6736(98)07257-2.
A five-fold increase in risk of stent thrombosis in carriers of A1/A2 (Leu33Pro) polymorphism of glycoprotein Illa has been described. Whether this increased procedural risk applies to other coronary interventions is unknown. We investigated the role of A1/A2 polymorphism as a putative risk factor.
We genotyped 1000 consecutive patients with angiographically confirmed coronary-artery disease and 1000 controls matched for age and sex. 653 of the 1000 patients received interventions (271 coronary angioplasty, 102 directional coronary atherectomy, and 280 stenting) and were assessed for a 30-day composite endpoint of need for target-vessel revascularisation, myocardial infarction, and death.
The composite endpoint occurred in 41 (6.3%) patients. There was no evidence that the A2 allele was associated with excess procedural risk (relative risk 1.36 [95% CI 0.70-2.70], p=0.37). Nor, in subgroup analyses, did A2 predict events that complicated coronary angioplasty (1.17 [0.40-2.70]), directional coronary atherectomy (1.50 [0.30-8.70]), or stenting (1.45 [0.60-3.50]). Neither heterozygotes (A1/A2) nor homozygotes (A2/A2) were over-represented in any subgroup, including those with acute coronary syndromes, early disease manifestation (age <40 years), and histories of myocardial infarction.
A1/A2 polymorphism is not a major risk factor for 30-day adverse events that complicate coronary angioplasty, directional coronary atherectomy, or stenting. Furthermore, A1/A2 polymorphism has no apparent impact on more chronic processes such as atherogenesis of the coronary arteries.
已有报道称，糖蛋白IIIa的A1/A2（Leu33Pro）多态性携带者发生支架内血栓形成的风险增加了五倍。这种增加的手术风险是否适用于其他冠状动脉介入治疗尚不清楚。我们研究了A1/A2多态性作为一种假定风险因素的作用。
我们对1000例经血管造影证实患有冠状动脉疾病的连续患者以及1000例年龄和性别匹配的对照进行了基因分型。1000例患者中有653例接受了介入治疗（271例冠状动脉成形术、102例定向冠状动脉斑块旋切术和280例支架置入术），并对其进行了为期30天的复合终点评估，该复合终点包括靶血管血运重建需求、心肌梗死和死亡。
41例（6.3%）患者出现了复合终点。没有证据表明A2等位基因与手术风险增加有关（相对风险1.36 [95%置信区间0.70 - 2.70]，p = 0.37）。在亚组分析中，A2也未预测冠状动脉成形术（1.17 [0.40 - 2.70]）、定向冠状动脉斑块旋切术（1.50 [0.30 - 8.70]）或支架置入术（1.45 [0.60 - 3.50]）的并发症。杂合子（A1/A2）和纯合子（A2/A2）在任何亚组中均未占过高比例，包括急性冠状动脉综合征患者、疾病早期表现（年龄<40岁）以及有心肌梗死病史的患者。
A1/A2多态性不是冠状动脉成形术、定向冠状动脉斑块旋切术或支架置入术30天不良事件的主要风险因素。此外，A1/A2多态性对冠状动脉粥样硬化等更慢性的过程没有明显影响。
