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脂蛋白(a)浓度如何影响经皮冠状动脉介入治疗后接受不同双联抗血小板治疗的稳定性冠心病患者的临床结局?

How Do Lipoprotein(a) Concentrations Affect Clinical Outcomes for Patients With Stable Coronary Artery Disease Who Underwent Different Dual Antiplatelet Therapy After Percutaneous Coronary Intervention?

机构信息

Cardiometabolic Medicine Center Department of Cardiology Fuwai HospitalNational Center for Cardiovascular DiseasesState Key Laboratory of Cardiovascular DiseaseChinese Academy of Medical Sciences and Peking Union Medical College Beijing China.

出版信息

J Am Heart Assoc. 2022 May 3;11(9):e023578. doi: 10.1161/JAHA.121.023578. Epub 2022 Apr 27.

DOI:10.1161/JAHA.121.023578
PMID:35475627
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9238589/
Abstract

Background Lp(a) (lipoprotein[a]) plays an important role in predicting cardiovascular events in patients with coronary artery disease through its proatherogenic and prothrombotic effects. We hypothesized that prolonged dual antiplatelet therapy (DAPT) might be beneficial for patients undergoing percutaneous coronary intervention who had elevated Lp(a) levels. This study aimed to evaluate the effect of Lp(a) on the efficacy and safety of prolonged DAPT versus shortened DAPT in stable patients with coronary artery disease who were treated with a drug-eluting stent. Methods and Results We selected 3201 stable patients with CAD from the prospective Fuwai Percutaneous Coronary Intervention Registry, of which 2124 patients had Lp(a) ≤30 mg/dL, and 1077 patients had Lp(a) >30 mg/dL. Patients were divided into 4 groups according to Lp(a) levels and the duration of DAPT therapy (≤1 year versus >1 year). The primary end point was major adverse cardiovascular and cerebrovascular event, defined as a composite of all-cause death, myocardial infarction, or stroke. The median follow-up time was 2.5 years. Among patients with elevated Lp(a) levels, DAPT >1 year presented lower risk of major adverse cardiovascular and cerebrovascular event and definite/probable stent thrombosis compared with DAPT ≤1 year. In contrast, in patients with normal Lp(a) levels, the risks of major adverse cardiovascular and cerebrovascular event and definite/probable stent thrombosis were not significantly different between the DAPT >1 year and DAPT ≤1 year groups. Prolonged DAPT had 2.4-times higher risk of clinically relevant bleeding than shortened DAPT in patients with normal Lp(a) levels, although without statistical difference. Conclusions In stable patients with coronary artery disease, who underwent percutaneous coronary intervention with a drug-eluting stent, prolonged DAPT was associated with reduced risk of cardiovascular events among those with elevated Lp(a) levels, whereas it did not show statistically significant evidence of benefit for reducing ischemic events and tended to increase clinically relevant bleeding among those with normal Lp(a) levels.

摘要

背景脂蛋白(a)(Lp(a))通过其促动脉粥样硬化和促血栓形成作用,在预测冠心病患者的心血管事件方面发挥着重要作用。我们假设,对于接受经皮冠状动脉介入治疗且 Lp(a)水平升高的患者,延长双联抗血小板治疗(DAPT)可能是有益的。本研究旨在评估 Lp(a)对接受药物洗脱支架治疗的冠心病稳定患者延长 DAPT 与缩短 DAPT 疗效和安全性的影响。

方法和结果我们从前瞻性阜外经皮冠状动脉介入治疗注册中心中选择了 3201 例稳定型 CAD 患者,其中 2124 例患者的 Lp(a)≤30mg/dL,1077 例患者的 Lp(a)>30mg/dL。根据 Lp(a)水平和 DAPT 治疗持续时间(≤1 年与>1 年),将患者分为 4 组。主要终点是主要不良心血管和脑血管事件,定义为全因死亡、心肌梗死或卒中的复合终点。中位随访时间为 2.5 年。在 Lp(a)水平升高的患者中,与 DAPT≤1 年相比,DAPT>1 年的主要不良心血管和脑血管事件和明确/可能的支架血栓形成风险较低。相比之下,在 Lp(a)水平正常的患者中,DAPT>1 年与 DAPT≤1 年之间主要不良心血管和脑血管事件和明确/可能的支架血栓形成风险无显著差异。在 Lp(a)水平正常的患者中,与缩短 DAPT 相比,延长 DAPT 使临床相关出血的风险增加了 2.4 倍,但无统计学差异。

结论在接受药物洗脱支架经皮冠状动脉介入治疗的冠心病稳定患者中,与 Lp(a)水平正常的患者相比,延长 DAPT 与 Lp(a)水平升高的患者心血管事件风险降低相关,而在统计学上没有证据表明其可降低缺血性事件风险,且在 Lp(a)水平正常的患者中倾向于增加临床相关出血。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b05/9238589/401b655c514b/JAH3-11-e023578-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b05/9238589/ae6433d78139/JAH3-11-e023578-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b05/9238589/f7c18c9bb370/JAH3-11-e023578-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b05/9238589/edc88b14c20d/JAH3-11-e023578-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b05/9238589/c3099f039fcc/JAH3-11-e023578-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b05/9238589/401b655c514b/JAH3-11-e023578-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b05/9238589/ae6433d78139/JAH3-11-e023578-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b05/9238589/f7c18c9bb370/JAH3-11-e023578-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b05/9238589/edc88b14c20d/JAH3-11-e023578-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b05/9238589/c3099f039fcc/JAH3-11-e023578-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b05/9238589/401b655c514b/JAH3-11-e023578-g005.jpg

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