Coronary endothelial dysfunction in patients with early coronary artery disease is associated with the increase in intravascular lipid core plaque.

AIMS: Endothelial dysfunction is considered to play a key role in the development of atherosclerosis. However, only a limited number of human imaging studies have been available to demonstrate this hypothesis. The present study used near-infrared spectroscopy (NIRS) to investigate whether coronary endothelial dysfunction is associated with the lipid core plaque (LCP) in patients with early coronary artery disease.

METHODS AND RESULTS: A total of 32 patients with chest pain who had diameter stenosis <30% were enrolled. All patients underwent coronary endothelial function assessment using intracoronary acetylcholine infusion and NIRS of the proximal left anterior descending artery. The lipid core burden index (LCBI), LCBI/L (LCBI divided by the length of scanned artery), maxLCBI4mm (maximum value of LCBI for any of the 4-mm segment) and block chemogram (yellow: probability of LCP presence >0.98, tan: 0.84 ≤ P ≤ 0.98, orange: 0.57 ≤ P ≤ 0.84, red: P < 0.57) were measured. The mean percentage of yellow, tan, and orange colour blocks in patients with epicardial endothelial dysfunction was significantly higher than in those with normal epicardial endothelial function (9.5 ± 11.4 vs. 3.1 ± 6.5%, P = 0.042). There was a significant correlation between LCBI (r = -0.460, P = 0.008), LCBI/L (r = -0.453, P = 0.009), and maxLCBI4mm (r = -0.431, P = 0.014) and the degree of epicardial endothelial function. However, there was no significant correlation between LCBI (r = -0.101, P = 0.58), LCBI/L (r = -0.099, P = 0.59), and maxLCBI4mm (r = -0.063, P = 0.73) and the degree of microvascular endothelial function.

CONCLUSION: Patients with early coronary artery disease and endothelial dysfunction had a higher lipid content in the vascular wall than patients with normal endothelial function. The result of the present study supports the hypothesis that endothelial dysfunction is associated with pathogenesis of early atherosclerosis.