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.
