Abstract 15888: Low Endothelial Shear Stress Promotes Diffuse Coronary Endothelial Dysfunction in Patients With Early Coronary Atherosclerosis
Introduction: Local hemodynamic factors are important determinants of atherosclerotic plaque development and progression.
Hypothesis: Low endothelial shear stress (ESS) is associated with epicardial endothelial dysfunction in patients with early atherosclerosis.
Methods: Fifty one subjects (age 53±10 y) with mild coronary atherosclerosis (diameter stenosis <40% throughout entire coronary arteries) were included. Epicardial coronary endothelial function was assessed using intracoronary acetylcholine (Ach) infusion and endothelial dysfunction was defined as change in coronary diameter <-20% after ACh. Vascular profiling, using 2-plane coronary angiography and intravascular ultrasound, was used to reconstruct the 3-D anatomy of left anterior descending artery (LAD). Each reconstructed artery was divided into sequential 3mm segments and analyzed for the assessment of local ESS with computational fluid dynamics. Each segment was characterized by local predominant ESS values, including the average ESS and the lowest ESS in a 90° arc around circumference of the artery. Plaque characteristics (plaque area, maximum plaque thickness) were also assessed.
Results: Twelve patients had diffuse epicardial endothelial dysfunction and thirty-nine patients had normal epicardial endothelial function. Plaque area and max plaque thickness were similar between the two groups (p=0.87 and 0.10 respectively). Importantly, coronary segments in arteries with abnormal endothelial function (n=185 segments) exhibited significantly lower ESS compared to segments in arteries with normal endothelial function (n=563 segments) (average ESS: 1.39±0.91 vs. 1.86±1.34 Pa, p<0.001; lowest ESS 90°arc: 1.16±0.74 vs. 1.48±1.15 Pa, p<0.001) (Figure).
Conclusions: These novel data support a significant contribution of the local hemodynamic environment initiating endothelial dysfunction at the early stage of coronary atherosclerosis.
Author Disclosures: G. Siasos: None. J. Sara: None. M. Zaromitidou: None. K.H. Park: None. S. Yang: None. A. Coskun: None. L.O. Lerman: None. D. Fotiadis: None. L. Michalis: None. M. Papafaklis: None. K. Stefanou: None. C. Feldman: None. A. Lerman: None. P.H. Stone: None.
- © 2016 by American Heart Association, Inc.