Myocardial bridge (MB), which covers a part of the left anterior descending coronary artery (LAD), is a normal anatomical variant structure (45% in frequency by autopsy) in LAD. MB contraction plays the role of a “double-edged sword” on the coronary events, suppressing coronary atherosclerosis under the MB, yet generating abnormal blood flow associated with coronary heart diseases (CHDs). High shear stress driven by MB compression causes the suppression of vascular permeability and vasoactive protein expression such as e-NOS and endothelin-1, which leads to the suppression of atherosclerosis in the LAD segment under the MB. However, despite the prevalent view of MB as benignancy by conventional coronary angiography (5-6% in frequency), with advance of imaging technique such as multislice spiral computed tomography [(MSCT); 16% in frequency], cardiologists are now frequently aware of symptomatic MB occurring not only in hospitalized patients, but also in young athletes free from atherosclerosis. Moreover, the large mass volume of MB muscle induces atherosclerosis evolution at the settled site in LAD proximal to MB and contributes to the occurrence of myocardial infarction.
These events upon the coronary events result from the different pathophysiological mechanisms induced by contractile force of MB, which is solely determined just by the integration of anatomical properties of MB, such as the location, length and thickness of MB in an individual LAD. A recent MSCT provides the objective quantification of the anatomical variables that correlate with the histopathological results in relation to the occurrence of CHD. In this review, we therefore discuss the necessity to explore MB as a inherent chance anatomical risk factor for CHD.