Myocardial Bridges: Lessons in Clinical Coronary Pathophysiology.

M yocardial perfusion occurs primarily in diastole since systolic contraction transiently impedes coronary blood flow especially to the subendocardium. Thus, myocardial bridges replicate the normal microvascular physiology of high diastolic and low systolic flow, albeit at the level of the epicardial coronary artery. Because marked myocardial bridges are not common during invasive angiography, and hence “abnormal,” they have the potential to trigger a similar “oculostenotic” reflex typical for atherosclerotic stenosis. As a relative coronary flow reserve (rel CFR) derived from pressure measurements, fractional flow reserve (FFR) to guide percutaneous coronary intervention has redefined coronary stenosis “severity” from anatomy to physiology, although the journey took 20 years (1,2). Similarly, the severity and effects of myocardial bridges are even more appropriately defined by physiology than anatomy. The physiologic dynamics of myocardial bridges reflect time-varying interactions among aortic pressure, arterial and myocardial compression, diastolic flow, transmural perfusion gradients, heart rate or diastolic perfusion time, and sympathetically driven myocardial