SESSION TITLE: Cardiovascular Disease SESSION TYPE: Med Student/Res Case Report PRESENTED ON: 10/09/2018 07:30 AM - 08:30 AM INTRODUCTION: Aneurysmal disease of the coronary artery tree (CAA) is a rare condition with an incidence of 0.3-4.9% of patients undergoing coronary angiography. The majority of cases occur in the proximal segments of the epicardial arteries and typically involve only one artery [1]. Involvement of three coronary vessels or the left main coronary artery is particularly rare, found in only 3.5% of CAA patients [2]. Multi-vessel CAA can present as an ischemic coronary syndrome, and can be challenging to manage. CASE PRESENTATION: A 48 year old African American non-smoking female with history of Parry Romberg syndrome, hypertension, obesity, and chronic kidney disease presented with progressive, intermittent, non-exertional chest pain. EKG showed voltage criteria for left ventricular hypertrophy (LVH). Bedside echocardiogram showed moderate LVH and akinesis of the basal inferior myocardial segment. Initial troponin I was 0.7ng/mL, and rose to peak of 6.16ng/mL. She was given aspirin, clopidogrel, and intravenous heparin drip. Coronary angiography showed aneurysmal disease of the left main, left anterior descending, left circumflex, and right coronary arteries, without evidence of thrombus angiographically. There were diffuse mild luminal irregularities, and a discrete 90% stenosis of the proximal right posterior descending artery. Percutaneous intervention was not performed. The patient denied history of Kawasaki’s disease. Subsequent vascular evaluation included an MR angiogram of the head, chest, abdomen and pelvis which were negative. Antinuclear antibodies, rheumatoid factor, and antineutrophil cytoplasmic antibodies were all negative. C-reactive protein and erythrocyte sedimentation rate were mildly elevated (1.01mg/dL and 32mm/Hr respectively). Her lipid profile demonstrated LDL 114mg/dL. She was discharged with dual antiplatelet therapy and high intensity statin. At 3 month follow up, she reported occasional palpitations with no chest pain, and at one year follow up she reported no symptoms. DISCUSSION: CAA is typically atherosclerotic in origin, as in our patient, although other causes exist. Previously it was believed that atherosclerosis caused CAA by increased pressure and shear stress due to luminal narrowing; however, it is now postulated that it may be due to generalized endovascular inflammation [2]. There is no known association between Parry Romberg syndrome and atherosclerosis or CAA. Medical management of CAA is limited to anticoagulant, antiplatelet, and anti-atherosclerotic therapy. Consensus Indications for percutaneous or surgical interventions are limited given the rarity of the disease; however, they are typically reserved for symptomatic flow limiting disease or if there is high risk of rupture. CONCLUSIONS: CAA is a rare condition that may mimic myocardial ischemia on presentation. Treatment options for multi-vessel CAA are limited given the paucity of data on the disease. Reference #1: 1. Abou Sherif, S. et al. “Coronary Artery Aneurysms: A Review of the Epidemiology, Pathophysiology, Diagnosis, and Treatment.” Frontiers in Cardiovascular Medicine 4 (2017): 24. PMC. 17 Feb. 2018. Reference #2: 2. Mata, Karina M. et al. “Coronary Artery Aneurysms: An Update.” Novel Strategies in Ischemic Heart Disease, 2017. Dr.Umashankar Lakshmanadoss (Ed.) DISCLOSURES: No relevant relationships by Michael Berlowitz, source=Web Response No relevant relationships by Andrew Mehlman, source=Web Response