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Editor,—Williams and colleagues1 recently described two patients in their early 20s presenting with acute myocardial infarction (AMI) in whom subsequent invasive investigation demonstrated no evidence of atheromatous coronary disease. In their review of the pathogenesis of AMI in patients with “normal” coronary arteries, alcohol and cocaine are discussed as potential triggers for coronary spasm or local thrombus, but they do not mention the potential role of myocardial bridging.
Myocardial bridging is usually asymptomatic but has been related to AMI in patients as young as 15 years in the absence of risk factors for coronary artery disease and without evidence of coronary atherosclerosis.2 Although a common postmortem finding,3 myocardial bridging is manifest (as segmental systolic squeezing of a coronary artery) in up to 5% of patients undergoing diagnostic angiography. As coronary arterial blood flow is primarily diastolic, the relevance of bridging in clinical practice has been the subject of extensive debate. However, recent studies suggest that deep muscle bridges can twist the coronary artery and compromise diastolic blood flow3 ,4 and that this disturbance in flow at the site of the bridge might increase the propensity for intimal damage or platelet aggregation.5 Intravascular ultrasound and intracoronary Doppler studies have also indicated that bridging may play an important role in AMI or angina in some patients.4Indeed, de Winter and colleagues6 recently reported a case of recurrent AMI caused by a soft atheromatous plaque within a myocardial bridge. This plaque was invisible during coronary angiography and could only be imaged using intravascular ultrasound. Thus, although myocardial bridging is usually clinically irrelevant, in selected cases it can be the culprit for acute coronary syndromes. In young patients with AMI particularly, documentation of bridging during angiography may be inadequate and complete evaluation using intravascular ultrasound and Doppler is advisable.
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