A BRIDGE INTO TROUBLED MYOCARDIUM

Abstract

SESSION TITLE: Medical Student/Resident Cardiovascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Myocardial bridging refers to the anomalous intra-myocardial course of a segment of a major coronary artery. Though usually benign, it may manifest in peculiar situations. CASE PRESENTATION: A 47-year-old male with a history of moderate persistent asthma presented with a severe acute exacerbation. On arrival to the emergency department, there was a witnessed cardiopulmonary arrest requiring intubation and advanced cardiac life support for an initial rhythm of pulseless electrical activity. Sustained return of spontaneous circulation was achieved after the administration of 1mg of intravenous epinephrine. Subsequent 12 lead electrocardiogram (ECG) demonstrated 3mm ST-segment elevations in leads aVR and V1, with widespread ST-segment depressions (figure 1a). An emergent left heart catheterization revealed hyper-dynamic contractility and a rhythmic occlusion of the proximal left anterior descending with near total occlusion during systole (figure 2b) that became non-obstructed during diastole (figure 2a). On ECG thirty minutes later, at a notably slower heart rate, there was resolution of the ST segment abnormalities (figure 1b). DISCUSSION: The myocardial bridge of an epicardial coronary artery is usually an incidental finding on autopsy. However, scant observational data have revealed potential clinical manifestations including dysrhythmias, acute coronary syndromes and sudden cardiac death.[1] The hemodynamic implications of this phenomenon may depend on certain aspects of the intra-myocardial course such as the depth, length and orientation of fibers. Physiologic stressors have been shown to unmask an otherwise clinically irrelevant bridge by reducing coronary blood flow during both phases of the cardiac cycle; tachycardia results in shortened diastolic filling time, and hyper-contractility augments the dynamic compression of the bridged segment during systole. Ostensibly, exogenous epinephrine may exaggerate these mechanisms resulting in potentially catastrophic consequences, as seen in our case.[2] Therapeutic strategies are primarily aimed at reduction in the hemodynamic disturbance of the bridge. Despite a paucity of randomized clinical trials, beta blockers and calcium channel blockers have proven beneficial. Per contra, pure vasodilators such as nitrates have been shown to worsen the pressure gradient across the bridge leading to poorer clinical outcomes. Stenting, myotomy and bypass grafting may also be considered in refractory cases.[1] CONCLUSIONS: In critically ill patients, especially those in hyper-adrenergic states, fluctuating myocardial ischemia may be a sign of myocardial bridging. Reference #1: Corban MT, Hung OY, Eshtehardi P, Rasoul-Arzrumly E, McDaniel M, Mekonnen G, Timmins LH, Lutz J, Guyton RA, Samady H. Myocardial Bridging. J Am Coll Cardiol. 2014 Jun, 63 (22) 2346-2355. Reference #2: Ge J, Jeremias A, Rupp A, et al. New signs characteristic of myocardial bridging demonstrated by intracoronary ultrasound and Doppler. Eur Heart J. 1995;20:1707–16. Reference #3: Ripa C, Melatini MC, Olivieri F, Antonicelli R. Myocardial bridging: A 'forgotten’ cause of acute coronary syndrome - a case report. Int J Angiol. 2007;16(3):115–118. doi:10.1055/s-0031-1278262. DISCLOSURES: No relevant relationships by William Kogler, source=Web Response No relevant relationships by Michael Omar, source=Web Response No relevant relationships by Pujan Patel, source=Web Response No relevant relationships by Patrisha Shelley, source=Web Response