期刊
CORONARY ARTERY DISEASE
卷 24, 期 2, 页码 154-159出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MCA.0b013e32835c46bd
关键词
acute coronary syndromes; atherosclerosis; coronary angiography; myocardial infarction; pathophysiology
Aims Nonobstructive coronary atherosclerotic lesions can lead to ST-elevation myocardial infarction (STEMI). Thrombus aspiration during a primary percutaneous coronary intervention provides a setting to evaluate the degree of stenosis of culprit lesions leading to STEMI. The aim of this study was to assess the degree of culprit lesion residual stenosis after thrombus aspiration and to compare the demographic, clinical, and angiographic characteristics between patients with obstructive versus nonobstructive residual stenosis. Methods and results From a single-center registry of 483 consecutive patients with STEMI undergoing a primary percutaneous coronary intervention, 172 patients underwent thrombus aspiration and were eligible for our study. We defined two groups according to the residual stenosis after thrombus aspiration: group A (n = 119, 69%) with residual stenosis greater than or equal to 50%, and group B (n= 53, 31%) with residual stenosis less than 50%. In terms of the baseline angiographic characteristics, patients with residual stenosis less than 50% had significantly lower prevalence of multivessel disease (15.1 vs. 46.2%, P< 0.001). On multivariable analysis of the preprocedural variables, absence of vascular disease (odds ratio 4.99, 95% confidence interval 1.08-23.12, P = 0.040) and age less than 59 years (odds ratio 2.67, 95% confidence interval 1.25-5.73, P = 0.011) were independent predictors of culprit residual stenosis less than 50%. Conclusion In this population, a significant proportion of patients with STEMI had nonobstructive residual stenosis after thrombus aspiration. These patients were younger, had a lower prevalence of vascular disease in other vascular territories, and less multivessel disease, suggesting an earlier stage of atherosclerosis. Coron Artery Dis 24: 154-159 (C) 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins.
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