Coronary Myocardial Bridge Updates: Anatomy, Pathophysiology, Clinical Manifestations, Diagnosis, and Treatment Options.

Abstract

Myocardial bridging is a frequent anomaly of the heart in humans and other animals. A myocardial bridge is typically characterized by the systolic narrowing seen with traditional catheter angiography, but this abnormality is not by itself a sign of ischemia or the need for intervention. In particular, transient spontaneous angina must be corroborated by reproducible narrowing during acetylcholine testing; this narrowing occurs during resting conditions and is responsive to nitroglycerin administration. Ischemia in myocardial bridging can result from acquired arterial wall disease (coronary artery atherosclerotic disease) or from instances of coronary spasm. Clinical evaluation should seek to identify baseline features such as myocardial bridge thickness (by using computerized axial tomography or intravascular ultrasonography) and the severity of systolic compression or reproducible spasticity (by administering acetylcholine). Nuclear myocardial scintigraphy is usually negative in patients with isolated myocardial bridging. Spastic coronary hyperactivity must be treated initially with antispasmodic medications, such as calcium channel blockers and nitrates, rather than by percutaneous stent placement or bypass surgery. Only exceptionally prolonged and critically severe spasm can induce intraluminal clotting and acute myocardial infarction. Recognizing the exceptionality and variability of ischemic presentations related to myocardial bridging is essential, as is establishing appropriate investigational methods for each of these facets of the condition.