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Nitroglycerine Induced Acute Myocardial Infarction in a Patient with Myocardial Bridging

DOI: 10.1155/2014/289879

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Abstract:

Muscle overlying an intramyocardial segment of a coronary artery is termed a myocardial bridge. The intramyocardial segment, the tunneled artery, is compressed during systole. The condition is generally benign but may occasionally cause myocardial ischemia, infarction, arrhythmia, or sudden cardiac death. We present a case regarding a 52-year-old man with exercise-induced angina who was diagnosed with a myocardial bridge overlying the left anterior descending artery. He was initially treated with beta-blockers and later received coronary bypass graft surgery. 1. Introduction The major coronary arteries are normally distributed epicardially, that is, on the surface of the myocardium. Occasionally, these vessels have a segmental intramyocardial course. During systole, this segment is compressed either partially or completely. Muscle overlying the intramyocardial segment is called a myocardial bridge, and the artery coursing within the myocardium is termed a tunneled artery [1–3]. 2. Case Presentation A 52-year-old man with a long-standing history of smoking and a positive family history of coronary artery disease (CAD) had undergone multiple admissions and investigations in several different hospitals during the last 13 years due to exercise-induced chest pain, shortness of breath, and palpitations. The electrocardiogram (ECG) showed sinus rhythm with complete right bundle branch block. The concentration of the myocardial tissue-specific biomarker, troponin T, was within the reference range during each hospitalization. A 7-day Holter-monitor recording and an exercise stress test also showed normal results. A transthoracic echocardiogram showed a slightly increased tricuspid regurgitation jet peak gradient (38?mmHg), and a subsequent computed tomography (CT) of the heart revealed dilatation of the right-sided chambers with a sinus venosus-type atrial septal defect (ASD) with partial anomalous pulmonary venous return (abnormal return of the right upper pulmonary vein into sinus venosus) and poor contrast enhancement of the left anterior descending artery (LAD), but no coronary artery calcification. The anomalous anatomical findings were confirmed by transesophageal echocardiography. To further examine the coronary anatomy, the patient underwent invasive coronary angiography, revealing a myocardial bridge confined to the LAD with mild systolic compression (Figure 1), which worsened during intravenous administration of nitroglycerin (Figure 2). During the angiography, he developed mild chest pain, which continued thereafter in the ward. Despite the

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