Background: Little is known about the clinical features and outcome of patients with left circumflex artery (LCX) infarct-related acute myocardial infarction (AMI). This study was conducted to investigate the clinical features and outcome of patients who underwent direct percutaneous coronary intervention (d-PCI) for AMI caused by LCX occlusion, and to discover prognostic determinants in this clinical setting.
Methods and results: Between May 1993 and October 2000, a total of 819 patients with AMI underwent d-PCI in our hospital. Sixty-seven patients (8.2%) who had LCX infarct-related AMI constituted the population of this study. Ten of 67 patients (14.9%) were in cardiogenic shock. Angiographic findings demonstrated that the incidences of triple-vessel disease, reference lumen diameter (RLD) of the LCX ≥ 4.0 mm, and LCX as the dominant artery in these patients were 26.9%, 22.4%, and 34.3%, respectively. Sixteen patients (23.9%) had unsuccessful reperfusion (defined as Thrombolysis in Myocardial Infarction flow ≤ 2). Univariate analysis showed that dominant LCX, RLD of the LCX ≥ 4.0 mm, cardiogenic shock, precordial ST-segment depression, and complete atrioventricular block were significantly related to unsuccessful reperfusion. Multiple stepwise logistic regression analysis demonstrated that dominant LCX and cardiogenic shock were significant independent predictors of unsuccessful reperfusion. The 30-day mortality rate in the 67 patients was 14.9%. Univariate analysis demonstrated that triple-vessel disease, dominant LCX, cardiogenic shock, poor left ventricular ejection fraction, and unsuccessful reperfusion were significantly associated with 30-day mortality. By multiple stepwise logistic regression analysis, dominant LCX, cardiogenic shock, and triple-vessel disease were significant independent predictors of increased 30-day mortality.
Conclusions: LCX infarct-related AMI has its unique clinical features. The presence of dominant LCX and cardiogenic shock were independent determinants of unsuccessful reperfusion, and the presence of dominant LCX, cardiogenic shock, and triple-vessel disease were independent determinants of increased 30-day mortality in this clinical setting.