Myocardial bridging is a congenital anomaly in which a segment of a coronary artery takes a "tunneled" intramuscular course under a "bridge" of overlying myocardium. This causes vessel compression in systole, resulting in hemodynamic changes that may be associated with angina, myocardial ischemia, acute coronary syndrome, left ventricular dysfunction, arrhythmias, and even sudden cardiac death. While described on autopsy for centuries, technological advances such as coronary computed tomography angiography and intravascular ultrasound have contributed greatly to our understanding of the anatomic, hemodynamic, and pathophysiological consequences of systolic compression. Atherosclerosis preferentially develops immediately proximal to the bridged segment, likely due to alterations in shear stress, while the compressed segment itself is often spared. First-line therapy of symptomatic bridging remains medical treatment with beta-blockers and non-dihydropyridine calcium-channel blockers, and nitrates are contraindicated. Surgical myotomy, intracoronary stenting, and coronary artery bypass graft surgery have been used for refractory symptoms, but long-term outcomes remain uncertain. Further research is required to better define the patient population that would derive the greatest benefit from surgical and percutaneous intervention.