Figure 2).

Mechanisms responsible for the absence of atherosclerosis from myocardial bridges and the development of lesions at the adjacent proximal epicardial segments. The surrounding myocardium creates a unique atheroprotective hemodynamic microenvironment within bridges characterized by low tensile stress (TS) and normal or high shear stress (SS). Reduced wall motion of mural segments may also play a role. Conversely, a highly atherogenic milieu is created at the edge proximal to the bridge with higher TS and low, oscillatory SS. ET-1 Endothelin-1; ICAM-1 Intercellular adhesion molecule-1; IL-1 Interleukin-1; MMP Matrix metalloproteinase; NO Nitric oxide; PDGF Platelet-derived growth factor; TNF-α Tumour necrosis factor-alpha; VCAM-1 Vascular cell adhesion molecule-1