Abstract
This article reviews current knowledge about morphology, pathophysiology, clinical relevance and treatment of myocardial bridges. Myocardial bridging (MB) is a congenital coronary abnormality defined as a segment of a major epicardial coronary artery running intramurally through the myocardium, usually affecting the left anterior descending artery (LAD). Because of incomplete understanding of the pathophysiology of MB, their clinical significance has been the subject of debate for the last 20 years. Although MB is generally considered as benign condition, there are many reports suggesting that this anomaly is associated with angina, acute coronary syndrome, myocardial infarction, arrhythmias and even sudden death. MB may cause ischemic heart disease by two distinct mechanisms. One is systolic compression of the intramural segment of LAD, resulting in delayed early diastolic artery relaxation, reduced blood flow reserve and decreased myocardial perfusion. The other is the development of atherosclerotic lesions of the LAD proximal to the MB, occurring because of hemodynamic disturbances influenced by retrograde blood flow up toward the LAD ostium at systole. New investigational tools in the cardiac catheterization laboratory (quantitative coronary angiography, intravascular ultrasound, intracoronary Doppler, fractional flow reserve) have revealed morphological and hemodynamical alterations during diastole. Medical therapy (beta-blockers, calcium channel-blockers) has a major role in the treatment of symptomatic patient with MB. Nitrates are contraindicated because they have been shown to increase the systolic compression of the affected portion of the vessel.
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