Abstract
Myocardial bridging constitutes a congenital, usually benign, coronary abnormality defined as a segment of a major epicardial coronary artery that follows an intramural course through the myocardium. On the basis of clinical and histopathological data, myocardial bridges appear to be spared from atherosclerosis. Although the mechanisms involved are largely unknown, the surrounding myocardium appears to be a key factor by generating a unique atheroprotective hemodynamic microenvironment within bridges. The main components of this environment include low tensile stress and high shear stress. Reduced coronary wall motion due to external support of the surrounding myocardium may also play a role. Better investigation of these mechanisms in appropriate animal models is anticipated to advance our understanding of the pathophysiology of atherosclerosis, providing a framework for the development of new atheroprotective strategies.