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.