A 62-year-old male smoker presented with having 2 hours of chest pain. Electrocardiography showed ST-segment elevation (STE) in leads V1-V4, equivocal STE in leads I, aVL and V5-V6 and ST-segment depression in leads III and aVF ( Figure A). Vital signs were stable. Physical examination revealed no jugular vein engorgement, a regular heart beat without heart murmur and clear breath sounds. Coronary angiography revealed anomalous origination of the left coronary artery (LCA) from the right sinus of Valsalva with relative hypoplasia of the left anterior descending artery and left circumflex artery. The infarct was in the proximal right coronary artery (RCA) (Figure B). Balloon angioplasty and a bare metal stent deployment were performed successfully. Follow-up electrocardiography showed nearly complete resolution of STE with inverted T-wave in leads V1-V6, I and aVL, and normalized leads III and aVF (Figure C). Echocardiography revealed hypokinesis of the apex of left ventricle (LV) with preserved LV and right ventricle systolic function. The patient׳s peak creatine kinase was 1,279 U/L and myocardial creatine kinase was 132 U/L. Multidetector computed tomography performed several months later revealed anomalous origination of the LCA from the right sinus of Valsalva with anterior and prepulmonary artery course and normal position of the RCA without in-stent restenosis. The dominant RCA gave rise to the distal left anterior descending artery and obtuse marginal branches through the posterior descending artery and posterolateral artery to supply the anteroapical and lateral walls of the LV (Figure D), which were located in the downstream area and more susceptible to ischemia than the inferior wall when proximal RCA occlusion occurred. This explains why the STE occurred in the precordial but not in the inferior leads.
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The authors have no conflicts of interest to disclose.
© 2016 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.