Background-Experimental studies suggest that low wall shear stress (WSS) promotes plaque development and high WSS is associated with plaque destabilization. We hypothesized that low-WSS segments in patients with coronary artery disease develop plaque progression and high-WSS segments develop necrotic core progression with fibrous tissue regression. Methods and Results-Twenty patients with coronary artery disease underwent baseline and 6-month radiofrequency intravascular ultrasound (virtual histology intravascular ultrasound) and computational fluid dynamics modeling for WSS calculation. For each virtual histology intravascular ultrasound segment (nϭ2249), changes in plaque area, virtual histology intravascular ultrasound-derived plaque composition, and remodeling were compared in low-, Key Words: atherosclerosis Ⅲ coronary artery disease Ⅲ hemodynamics Ⅲ intravascular ultrasonography, interventional Ⅲ wall shear stress A lthough cardiovascular risk factors lead to systemic inflammation, oxidative stress, and endothelial dysfunction, it is recognized that coronary atherosclerotic plaques are focally distributed with highly variable rates of progression. However, prediction of regional plaque progression in an individual coronary segment remains elusive. Editorial see p 763 Clinical Perspective on p 788Alterations in wall shear stress (WSS) have been implicated in the focal distribution and pathophysiology of coronary atherosclerosis. [1][2][3][4][5] Low WSS leads to a proatherogenic endothelial cell phenotype 1-3 and focal development of atherosclerosis and vascular remodeling in experimental models 6 -8 and pilot clinical studies. 9,10 Both low WSS and high WSS have been implicated in the production of matrix metalloproteinases and plasmin by endothelial cells that can destabilize plaque fibrous caps. [11][12][13] In addition, high WSS has been shown to induce apoptosis of smooth muscle cells, 14,15 which might enhance plaque vulnerability.To date, the role of both low WSS and high WSS in the development of plaque progression, change in plaque com- Received January 23, 2011; accepted May 9, 2011 Methods Study PopulationTwenty patients presenting to the cardiac catheterization laboratory at Emory University Hospital between December 2007 and January 2009 with an abnormal noninvasive stress test or stable anginal syndromes and found to have a nonobstructive lesion requiring invasive physiological evaluation were enrolled. Exclusion criteria included myocardial infarction, cardiogenic shock or hemodynamic instability, lesion requiring percutaneous or surgical revascularization, coronary artery bypass surgery, severe valvular heart disease, presence of visual coronary collaterals, inability to provide informed consent, serum creatinine Ͼ1.5 mg/dL, liver disease, or significant hematologic disease. All patients underwent baseline and 6-month follow-up radiofrequency backscatter IVUS (VH-IVUS) and baseline computational fluid dynamics (CFD) modeling for WSS calculation. All patients underwent lipid profile assessm...

Abstract

Patients with myocardial bridges are often asymptomatic but this anomaly may be associated with exertional angina, acute coronary syndromes, cardiac arrhythmias, syncope or even sudden cardiac death. This review presents our understanding of the pathophysiology of myocardial bridging and describes prevailing diagnostic modalities and therapeutic options for this challenging clinical entity.