Myocardial bridge as a structure of "double-edged sword" for the coronary artery

Abstract

Myocardial bridge (MB) is a chance anatomical structure, comprised of the myocardial tissue, with which the coronary artery running in epicardial adipose tissue is partly covered. It is predominantly present in the left anterior descending artery (LAD) and recognizable through imaging techniques as changes in blood flow within the LAD that arises from MB contraction at cardiac systole. Such changes in blood flow influence the pathophysiology of coronary circulation and atherosclerosis development, thus generating controversy as to whether MB predisposes individual to myocardial infarction (MI). However, recent histomorphometric studies have shown that the individual anatomic properties of MB, such as location, length and thickness, consistently play a critical role in the occurrence of MI. This review article comprehensively addresses the pathophysiological mechanisms of MI occurrence together with the benign suppressive effect of coronary atherosclerosis by MB.

Keywords: atherosclerosis; coronary artery; myocardial bridge; myocardial infarction; pathology.

Fig. 1

Myocardial bridge (MB) in the left anterior descending coronary artery (LAD) after manual removal of epicardial adipose tissue. The LAD is covered with myocardial tissue in its middle course.

Fig. 2

Multi-detector computed tomography imaging of myocardial bridge (MB) in the left anterior descending coronary artery (LAD). MPR: multiplanar reconstruction; VR: volume-rendered.

Fig. 3

Longitude-section of the left anterior descending coronary artery (LAD) in three cases by the patient’s age from left to right direction. LAD thickening is remarkably suppressed at the entrance part of myocardial bridge (MB) (asterisk).

Fig. 4

Changes of endothelial cell shape by the sites within the left anterior descending coronary artery (LAD) with scanning electron microscopy. Flat and polygonal in pavement arrangement of endothelial cell shape becomes spindle and engorged in alignment along the direction of blood flow beneath myocardial bridge (MB). Their shape becomes intermingled with the former two shapes of the site distal to MB. SEM: scanning electron microscopy.

Fig. 5

Cross-section of the left anterior descending coronary artery (LAD) proximal to myocardial bridge (MB) and beneath MB in the normal and infarcted heart. Eccentric intimal thickening of the LAD is abruptly suppressed beneath MB surrounded by myocardial tissue.

Fig. 6

In cholesterol-fed rabbit, changes of endothelial cell shape are basically similar to those of human coronary artery across myocardial covering. Macrophages attached in more numbers at 20 weeks than 2 weeks. Epi-LC: epicardial left coronary artery; Myo-LC: myocardial left coronary artery.

Fig. 7

Changes in immunohistochemical expression of vaso-active agents. They remarkably decrease just at the left anterior descending coronary artery (LAD) segment covered by myocardial bridge (MB). ET-1: endothelin-1; eNOS: e-nitric oxide synthase; ACE: angiotensin converting enzyme.

Fig. 8

Schematic drawing on the difference in the atherosclerotic lesion proximal to myocardial bridge (MB). In the myocardial infarction patient (lower half of the figure), atheosclerotic intimal lesions are extensive 2 cm proximal to MB and plaque fissure preferentially occurs at this site, when compared with those in left anterior descending coronary artery (LAD) of the patient free from myocardial infarction (MI) (upper half of the figure).