Coronary Artery Ectasia in the Pathophysiology of Myocardial Infarction With Nonobstructive Coronary Arteries

医学 心脏病学 内科学 冠状动脉扩张 心肌梗塞 冠状动脉疾病 冠状动脉 扩张 优势比 置信区间 动脉 冠状动脉造影
作者
Mehmet Eyuboglu,Cagrı Eyuboglu
出处
期刊:American Journal of Cardiology [Elsevier BV]
卷期号:171: 28-31 被引量:2
标识
DOI:10.1016/j.amjcard.2022.01.043
摘要

Coronary artery ectasia (CAE) is associated with an increased risk for acute myocardial infarction (AMI). A significant proportion of patients with AMI have no obstructive coronary artery disease (CAD), however, the underlying mechanism of myocardial infarction with nonobstructive coronary arteries (MINOCA) is poorly understood. Therefore, the present study aimed to investigate whether CAE has a role in the pathogenesis of MINOCA. A total of 1,284 patients who were admitted with a diagnosis of non-ST-segment elevation myocardial infarction were included in the study. Patients were divided into 2 groups according to the presence or absence of obstructive CAD (≥50% stenosis). Patients without obstructive CAD (MINOCA group) and patients with obstructive CAD (no-MINOCA group) were compared regarding the frequency of CAE. Additionally, the association between CAE and MINOCA was investigated. In the study participants, 101 patients (7.9%) were diagnosed with MINOCA, whereas 1,183 (92.1%) had AMI with obstructive CAD. Importantly, the frequency of patients with CAE was significantly higher in patients with MINOCA compared with those with obstructive CAD (22.8% vs 3.5%, p <0.001). Moreover, CAE was observed in 64 patients (4.9%). The frequency of MINOCA was found to be significantly higher in patients with CAE compared with patients without CAE (35.9% vs 6.4%, p <0.001). Furthermore, multivariate analysis demonstrated that the presence of CAE was an independent predictor of MINOCA in patients presented with a diagnosis of non-ST-segment elevation myocardial infarction (odds ratio 1.812, 95% confidence interval 1.376 to 2.581, p <0.001). In conclusion, CAE may be considered as a risk factor for MINOCA and may have a role in the pathophysiology of MINOCA.

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