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 contraction and coronary vasoconstriction, all interacting with diffuse and focal atherosclerotic disease that is beyond anatomic description (3-7). THE CURRENT REPORT Therefore, Uusitalo et al. (8), in this issue of iJACC, deserve congratulations for this first systematic study of quantitative perfusion and CFR by positronemission tomography (PET) in adults with myocardial bridging. The protocol included 100 patients with potential coronary artery disease (CAD) undergoing computed tomographic angiography, PET myocardial perfusion imaging at rest and during vasodilator stress, and invasive coronary angiography; 34 of these patients had 48 coronary artery myocardial bridges classified as superficial in 24 (>1-to 2-mm deep) or deep in 24 (>2-mm deep). CAD was assessed by computed tomography soft or calcified plaque, or by quantitative coronary angiography of atherosclerotic percent diameter stenosis. Myocardial bridging was identified by systolic compression of the coronary artery using visual assessment and quantified by quantified coronary angiography of diastolic and systolic angiographic frames.Absolute stress perfusion during pharmacological vasodilation was comparable in patients with and without either shallow or deep myocardial bridges. Rest perfusion was higher in patients with myocardial bridges compared to patients without bridges, but absolute stress flow was similar and well above low-flow ischemic levels. Frequency and severity of CAD by calcium score or percent stenosis was not different among any of the groups and was located primarily proximally to the bridge. Exercise stress tests in these patients were also benign without ischemia related to the myocardial bridges. The authors conclude that myocardial bridging is common but nearly always anatomically and physiologically mild, and not associated with significant flow impairment, myocardi...