Myocardial bridging: A 'forgotten' cause of acute coronary syndrome - a case report

Abstract

During a stress test, an asymptomatic 40-year-old man showed an ST depression above 4 mm and a horizontal ST depression above 2 mm in the V3 to V6 precordial leads during the recovery phase, without symptoms related to myocardial ischemia. After several days, he experienced recurrent episodes of oppressive retrosternal pain with radiation to the interscapular region, associated with stress dyspnea. Stress myocardial scintigraphy using technetium sestamibi was performed, which showed a modest push-pull deficit of perfusion in the septal-anterior basal area associated with a small deficit of perfusion in the apical region.

The patient was admitted to hospital with a diagnosis of unstable angina. Repeated episodes of chest pain appeared during this period, which were partially relieved with the administration of sublingual nitrate. There were no significant changes in the electrocardiogram or cardiac enzyme levels. Coronary angiography showed initial parietal hypertrophy with normal segmentary kinesis and global systolic function and, most importantly, the presence of a systolic narrowing (myocardial bridging) of the middle one-third of the left anterior descending artery from the likely intramyocardial route. There was no significant stenosis of the remaining coronary tracts.

Myocardial bridges have traditionally been considered a benign condition, but recent studies have demonstrated that the clinical complications can be dangerous; these complications include acute coronary syndromes, arrhythmias (including supraventricular tachycardia and ventricular tachycardia), exercise-induced atrioventricular conduction blocks, transient ventricular dysfunction and sudden death.