Myocardial bridging, a congenital coronary anomaly, is a clinical condition with several possible manifestations, and its clinical relevance is debated. This article reviews current knowledge about the anatomy, pathophysiology, clinical relevance, and treatment of myocardial bridging. Myocardial bridging is present when a segment of a major epicardial coronary artery, the 'tunnelled artery', runs intramurally through the myocardium. With each systole, the coronary artery is compressed. Myocardial bridging has been associated with angina, arrhythmia, depressed left ventricular function, myocardial stunning, early death after cardiac transplantation, and sudden death. Evidence indicates that the intima beneath the bridge is protected from atherosclerosis, and the proximal segment is more susceptible to development of atherosclerotic lesions because of haemodynamic disturbances. New techniques (e.g. intravascular ultrasonography and intracoronary Doppler studies) have revealed new characteristics and pathophysiologic processes such as diastolic flow abnormalities. Medical treatment generally includes beta-blockers. Nitrates should be avoided because symptoms may worsen. Intracoronary stents and surgery have been attempted in selected patients. Additional research is needed to define patients in whom myocardial bridging is potentially pathologic, and randomized multicentre long-term follow-up studies are needed to assess the natural history, patient selection, and therapeutic approaches.

In medical intensive care unit patients, admission troponin levels are independently associated with short- and long-term mortality, even after adjustment for severity of disease.