Epicardial plaque burden and endothelial function are recognized predictors of coronary events. We aimed to investigate mechanistic relationships between atheroma volume and endothelial function in patients with non–ST-segment–elevation myocardial infarction (NSTEMI) using intravascular ultrasound.Methods and Results—
In coronary vessels of patients with near-normal or minimal angiographic disease (n=23) and NSTEMI (n=24), intravascular ultrasound-derived measures (percent atheroma volume), arterial remodeling index, and segmental lumen volumes were performed in contiguous 5-mm epicardial segments. Repeat intravascular ultrasound imaging was performed after consecutive 5-minute intracoronary infusions (vehicle solution, 0.30 μg/min and 0.60 μg/min intracoronary salbutamol) to measure changes in segmental lumen volume (endothelium-dependent function). Male sex, diabetes mellitus, smoking, higher triglycerides, and lower high-density lipoprotein cholesterol were more prevalent in the NSTEMI group. Patients with NSTEMI demonstrated greater segmental percent atheroma volume (40.4±12 versus 27.5±14%, P<0.001), remodeling index (1.2 [1.0–1.5] versus 1.0 [0.9–1.0], P<0.001), and displayed less endothelium-dependent vasomotion (% change segmental lumen volume: 2.1±0.89 versus 5.1±0.89%, P=0.02) compared to patients with minimal angiographic disease. No significant difference in endothelial function between both groups was observed when controlling for plaque burden. Multivariate analysis for change in segmental lumen volume identified percent atheroma volume (β=−0.18, P=0.0004), high-sensitivity C-reactive protein >2 mg/L (β=−3.1, P=0.03), diabetes mellitus (β=−6.9, P<0.0001), low-density lipoprotein cholesterol levels (β=−0.04, P=0.01), and smoking (β=–3.2, P=0.01) as independent associates.Conclusions—
Although coronary endothelial vasoreactivity is blunted in the setting of NSTEMI, this is a reflection of the greater volume of atherosclerosis and cardiovascular risk factors. Thus, the relationship between coronary endothelium-dependent vasomotor reactivity and atheroma volume remains constant irrespective of the nature of the clinical presentation.