Sustained endothelial dysfunction in the infarct-related coronary artery is associated with left ventricular adverse remodeling in survivors of ST-segment elevation myocardial infarction.

Background: Ischemia-reperfusion causes endothelial injury and dysfunction in the infarct-related coronary artery (IRA). Using serial assessment of coronary endothelial vasomotor function and left ventriculography (LVG), this study prospectively investigated the clinical impact of endothelial vasomotor dysfunction in the patent IRA on left ventricular (LV) remodeling in survivors of ST-elevation myocardial infarction (STEMI).

Methods: This study included 78 patients with STEMI due to occlusion of the left anterior descending coronary artery (LAD) and successful reperfusion therapy with percutaneous coronary intervention. All of them had LV ejection fraction (LVEF) <55%. LVG and the vasomotor responses to acetylcholine (ACh) in the LAD were examined within 2 weeks (1st test) and 6 months (2nd test) after MI. Cut-off values for coronary vasomotor dysfunction in response to ACh were based on the lower 10% of the distribution of coronary vasomotor responses to ACh in 20 control subjects.

Results: LV adverse remodeling, defined as a >10% increase in either LV end-diastolic volume index (LVEDVI) and/or end-systolic volume index (LVESVI) from the 1st to the 2nd test, occurred in 21 (70%) of 30 patients with sustained impairment of the coronary flow response to ACh at both the 1st and 2nd tests and 14 (29%) of 48 in the other coronary flow response group (p < 0.01). In multivariate logistic regression analysis, a >10% increase in LVEDVI and LVESVI was respectively associated with sustained impairment of the coronary diameter and flow responses to ACh (OR 4.9 and 3.5, 95% CI 1.7-14.1 and 1.1-10.9, p < 0.01 and p = 0.03, respectively), that was independent of hypertension, peak creatine phosphokinase, and the baseline coronary flow response to ACh at the 1st test.

Conclusions: Sustained endothelial vasomotor dysfunction in the IRA was associated with LV adverse remodeling in STEMI survivors with successful reperfusion therapy.