Among 980 consecutive selective coronary angiograms performed, nine patients had myocardial bridges of the left anterior descending (LAD) coronary artery. The overall prevalence of myocardial bridges was 0.92%. Among these patients, three patients had coronary artery disease, while six cases were isolated myocardial muscle bridges. With respect to functional abnormality, three had grade III milking effect, three had grade II and three had grade I milking effect. The indications for coronary angiograms were typical chest pain in seven cases and atypical pain in two cases. Myocardial bridges are sections of a coronary artery, almost all the left anterior descending and/or one of its diagonal branches, which run under a strip of left ventricular muscle and dip below the epicardial surface under small areas of the myocardium: During systole, the segment of the artery surrounded by myocardium is narrowed and appears as localized stenosis. This systolic compression is defined as the "milking" effect. The key to recognizing these myocardial bridges is that the apparent localized stenosis returns to normal during diastole.1 In 1976, Noble et al. stated that myocardial bridges with a milking effect on the proximal third of the left anterior descending artery could represent a new type of ischemic heart disease.2 In 1977, Grondin et al. classified the milking effect as grade I when less than 50% of arterial narrowing occurs, grade II when it is between 50% and 75%, and grade III when it is greater than 75%.3 As early as 1951, Geiringer reported the etiology of this anatomical variant to be congenital, explaining that most of the coronary arteries have an intramyocardial course during fetal life.
4As suggested by Binet et al. in 1975, muscle bridges might explain some cases of sudden death occurring during strenuous exercises among athletes in whom no coronary arterial lesions are demonstrated at postmortem examination. 5 In 1993, on an experimental basis, Campbell et al. studied similarities between dynamic elastance responsible for the left ventricular chamber and the papillary muscle of a rabbit heart. They concluded that the dynamic elements responsible for myofiber stiffness were also responsible for left ventricle chamber elastance. Furthermore, it was possible to describe and interpret dynamic chamber elastance and muscle stiffness with a common model based on the muscle-bridge theory. This model did a reasonable job of reproducing all the important features of experimentally observed left ventricular chamber elastance and muscle stiffness. Thus, dynamic homologies between chamber and muscle were established in experimental data and, in fact, this single interpretive model served equally well for both chamber elastance and muscle stiffness. 5,6 The aim of this study is to assess the prevalence of myocardial bridging of the left anterior descending coronary artery in a population of patients referred for diagnostic coronary angiography and to throw some light on the pathophysiology, clinical implications and prognosi...