Background:
Myocardial bridging is an anatomical variant, occurring when an epicardial coronary artery contains an intramyocardial segment that becomes compressed during systole.1 Most commonly, myocardial bridging occurs in the mid-portion of the LAD. The incidence and prevalence vary widely due to variation in diagnostic methods and definitions of myocardial bridging.2,3 Currently, no diagnostic gold standard exists for clinically significant myocardial bridging.
Longstanding debate surrounds the clinical significance of myocardial bridging. Since myocardial perfusion occurs mainly during diastole, it was thought that systolic compression in the setting of a myocardial bridge would not have significant clinical impact. However, angiography and intravascular ultrasound (IVUS) have shown that compression extends into diastole, inducing symptoms from delayed diastolic relaxation and decreased perfusion. Additionally, myocardial bridging may cause persistent reduction in diastolic luminal diameter, retrograde systolic flow, reduced coronary flow reserve, and increased velocity of blood flow.2,4 Often, the tunneled artery segment in symptomatic patients has endothelial dysfunction. The portion of the artery proximal to the bridge may be prone to atherosclerosis due to alterations in flow patterns. The bridged segment has a propensity toward coronary spasm due to endothelial dysfunction.1,3-5 Patient specific features such as the depth and length of myocardial bridge, septal branch involvement, and degree of systolic diameter reduction influence the clinical impact.