Abstract

SESSION TITLE: Cardiovascular Disease 2 SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Chest pain of cardiac origin is commonly ischemic in etiology. However, the phenomenon of myocardial bridging as a cause of chest pain has come to attention recently. Herein, an epicardial coronary artery develops a transient myocardial course. During systole, a portion of the vessel is mechanically compressed and results in ischemia. This has been attributed to as a rare cause of angina. Here we present our experience with a patient who was diagnosed with the same. CASE PRESENTATION: A 51 year old man with no past medical history, presented to the emergency room with pressure like chest pain of two days duration. He had multiple episodes of pain and each lasted for around 20 minutes. It was associated with palpitations, and exacerbated by physical exertion. He was a former smoker and reportedly quit smoking 20 years back. His blood pressure was 153/95 mmHg; temperature 98.1F; heart rate 73/min regular; respiratory rate 18/min. ECG showed Type 1 Wellen's biphasic pattern in V2, V3. Three sets of cardiac troponins were normal. Wellens pattern on ECG is highly specific (89%) for critical left anterior descending artery (LAD) stenosis. [1] [2]. Therefore, the patient was sent for emergent cardiac catheterization. Coronary angiography revealed normal left main, left circumflex and right coronary artery. However, LAD artery showed moderate myocardial bridging. DISCUSSION: In myocardial bridging, a coronary artery that normally runs on the epicardium, develops a transient intra-myocardial course. This section of the artery gets compressed during ventricular systole. Generally asymptomatic, bridging sometimes results in angina, arrhythmias myocardial ischemia. Most myocardial bridging has been found to occur in the middle portion of the LAD artery. However, on autopsy right coronary and left circumflex arteries have shown bridging at comparable rates. [3]. Proximal portion of the bridged segment is prone to accelerated atherosclerosis.Hypertrophic obstructive cardiomyopathy (HOCM) has shown increased association with myocardial bridging. Treatment is with beta blockers and non-dihydropyridine calcium channel blockers. Therapeutic benefit results from decreased chronotropy and inotropy. In cases refractory to medical management, surgical myotomy, coronary artery stenting or coronary artery bypass grafting (CABG) can be pursued. Our patient was started on aspirin, amlodipine, metoprolol, and rosuvastatin. His hospital course was uneventful and he was discharged on pharmacological therapy. CONCLUSIONS: Myocardial Bridging is being recognized increasingly as a cause of refractory angina. However, it is still not widely included as a differential diagnosis. Since the treatment is fairly specific, we wish to underscore the importance of recognizing myocardial bridging as an atypical cause of chest pain. Reference #1: C. de Zwaan, F.W. Bar, H.J. Wellens. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J, 103 (1982), pp. 730-736. Reference #2: C. de Zwaan, F.W. Bar, J.H. Janssen, et al. Angiographic and clinical characteristics of patients with unstable angina showing an ECG pattern indicating critical narrowing of the proximal LAD coronary artery. . Am Heart J, 117 (1989), pp. 657-665. Reference #3: Polacek P, Kralove H. Relation of myocardial bridges and loops on the coronary arteries to coronary occlusions. Am Heart J. 1961;61:44-52 DISCLOSURES: No relevant relationships by Paurush Ambesh, source=Web Response No relevant relationships by Stephan Kamholz, source=Web Response No relevant relationships by Dikshya Sharma, source=Web Response No relevant relationships by Ankur Sinha, source=Web Response

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