Publication Date

10-1-2017

Journal

The Texas Heart Journal

DOI

10.14503/THIJ-16-5905

PMID

29259501

Publication Date(s)

October 2017

Language

English

PMCID

PMC5731584

PubMedCentral® Posted Date

10-1-2017

PubMedCentral® Full Text Version

Post-Print

Published Open-Access

yes

Keywords

Acute coronary syndrome/complications/diagnostic imaging, analysis of variance, coronary stenosis/complications/diagnostic imaging/physiopathology, coronary vessels/pathology, diagnostic errors/prevention & control, models, cardiovascular, plaque, atherosclerotic/pathology, retrospective studies, rupture, spontaneous, stress, mechanical

Abstract

The prevalence of the left circumflex coronary artery (LCx) as the culprit vessel in ST-segment-elevation myocardial infarction (STEMI) is reportedly lowest among that of the 3 main epicardial arteries, and has not been described for non-STEMI (NSTEMI) and stable angina pectoris. We sought to define the distribution of culprit arteries in these clinical presentations and suggest mechanisms for the differences.

We reviewed 189 coronary angiograms of patients with STEMI, 203 with NSTEMI, and 548 with stable angina (n=940), and compared distributions of stenotic and culprit coronary arteries (lesions prompting intervention).

Obstructive coronary lesions (≥50% narrowing) were more prevalent in the left anterior descending coronary artery (LAD) (36%–38%) and similar in the LCx and right coronary artery (RCA) (27%–29%), regardless of clinical presentation (P <0.01). In NSTEMI and stable angina, culprit vessels and total obstructive disease had the same distribution. In STEMI, however, a culprit LCx was significantly less prevalent (17%) than was total obstructive disease (27%; P <0.01), or a culprit LAD (47%) or RCA (34%) (both P <0.001). In our computed tomographic angiographic model of coronary longitudinal strain (percentage of shortening), LCx strain was only 1.5% ± 2.4%, versus 9.5% ± 2.9% for LAD strain and 10.1% ± 3.9% for RCA strain.

In STEMI, LCx plaques seem less prone to rupturing. Culprit and total disease distributions are similar in NSTEMI and angina, suggesting a different ischemic pathophysiology in these presentations. Lower LCx longitudinal strain might contribute to reduced plaque rupture in STEMI.

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