吸烟与冠状动脉粥样硬化:对右冠状动脉不成比例的影响

Axel Dahlgren MD , David Erlinge MD, PhD , Ryo Torii PhD , Enhui Yong MD , Göran Bergström MD, PhD , Tomas Jernberg MD, PhD , Ole Fröbert MD, PhD , Pernille G. Thrane MD, PhD , Michael Mæng MD, PhD , Gregg W. Stone MD, PhD , Moman A. Mohammad MD, PhD
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引用次数: 0

摘要

研究背景:本研究旨在研究吸烟对冠状动脉粥样硬化发展的长期影响。方法从瑞典冠状动脉造影和血管成形术登记处收集1989-2017年吸烟者、戒烟者和非吸烟者的血管造影数据。西丹麦心脏登记处被用来验证结果。纳入临床指征冠状动脉造影≥2条且无阻塞性冠状动脉疾病的患者。主要结局是15年内斑块进展、经皮冠状动脉介入治疗或冠状动脉旁路移植术。结果共纳入瑞典患者215,364例,冠状动脉993,405条(左前降支[LAD]、左旋支[LCX]、右冠状动脉[RCA])。验证队列包括19613名患者。每1000例患者年,吸烟者斑块进展发生率为11.3 (95% CI, 10.9-11.7),前吸烟者为10.2 (95% CI, 9.9-10.5),非吸烟者为7.7 (95% CI, 7.5-7.9)。吸烟者在RCA中表现出更高的斑块进展的相对风险(风险比,1.87;95% CI, 1.73-2.03),而LAD(风险比,1.21;95% CI, 1.12-1.30)。瑞典和丹麦吸烟者st段抬高型心肌梗死的RCA作为罪魁动脉的比例高于不吸烟者(吸烟者:RCA, 42.4%; LAD, 42.0%; LCX, 15.6%;不吸烟者:RCA, 33.1%; LAD, 51.4%; LCX, 15.5%)。结论:这项观察性队列研究确定了吸烟者和不吸烟者斑块进展模式的明显差异,与不吸烟者的LAD相比,吸烟与RCA斑块进展增加有关。这些发现再次强调了有针对性地预防吸烟的必要性,并为进一步研究斑块进展和心肌梗死的rca特异性机制提供了依据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Smoking and Coronary Atherosclerosis: Disproportionate Impact on the Right Coronary Artery

Background

We aimed to study the long-term effect of smoking on coronary atherosclerosis progression at the segmental level.

Methods

Angiographic data (1989-2017) on current, former, and nonsmokers were collected from the Swedish Coronary Angiography and Angioplasty Registry. The Western Denmark Heart Registry was used to validate the results. Patients with clinically indicated angiography with ≥2 coronary arteries without obstructive coronary artery disease were included. The main outcome was segmental plaque progression, percutaneous coronary intervention, or coronary artery bypass grafting within 15 years.

Results

In total, 215,364 Swedish patients with 993,405 coronary arteries (left anterior descending artery [LAD], left circumflex artery [LCX], and right coronary artery [RCA]) were included. The validation cohort consisted of 19,613 patients. Per 1000 patient-years, plaque progression incidence rate was 11.3 (95% CI, 10.9-11.7) for smokers, 10.2 (95% CI, 9.9-10.5) for former smokers, and 7.7 (95% CI, 7.5-7.9) for nonsmokers. Smokers demonstrated higher relative risk of plaque progression in RCA (hazard ratio, 1.87; 95% CI, 1.73-2.03) vs LAD (hazard ratio, 1.21; 95% CI, 1.12-1.30). Swedish and Danish smokers with ST-segment elevation myocardial infarction had higher proportion of RCA as the culprit artery compared to nonsmokers (smokers: RCA, 42.4%; LAD, 42.0%; LCX, 15.6%; nonsmokers: RCA, 33.1%; LAD, 51.4%; LCX, 15.5%).

Conclusions

This observational cohort study identifies distinct differences in plaque progression patterns between smokers and nonsmokers, with smoking linked to increased plaque progression in the RCA, in contrast to the LAD in nonsmokers. These findings reemphasize the need for targeted smoking prevention and warrant further investigation into RCA-specific mechanisms of plaque progression and MI.
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