SESSION TITLE: Medical Student/Resident Cardiovascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Left ventricular noncompaction (LVNC) is a cardiomyopathy characterized by prominent trabeculae and deep intertrabecular recesses in communication with the ventricular cavity. LVNC affects up to 1.3% of the population and is responsible for 3-4% of all heart failure syndromes. CASE PRESENTATION: A 76-year-old male presented to the emergency department due to increasing dyspnea. He endorsed lower extremity swelling and orthopnea. He was tachypneic and hypoxemic. Lung auscultation revealed bibasilar crackles. Bilateral pitting pedal edema was noted. BNP was elevated at 861 pg/mL and troponins were elevated at 0.6 ng/L. Electrocardiogram demonstrated normal sinus rhythm with T-wave inversions in the inferolateral leads. Chest radiograph showed cardiomegaly, vascular congestion and bilateral pleural effusions suggestive of congestive heart failure syndrome. Transthoracic echocardiogram revealed left ventricular ejection fraction of 25-30%. Prominent trabeculae and deep interventricular recesses were noted, concerning for LVNC. Coronary angiography showed moderate nonobstructive coronary artery disease without need for percutaneous coronary intervention. His clinical condition improved with diuretic therapy, blood pressure control, and initiation of guideline-directed medical therapy. During his hospitalization, telemetry captured 6 beats of non-sustained ventricular tachycardia. Lifevest was placed to evaluate need for ICD implantation after optimization of medical therapy. He was scheduled for follow up echocardiogram in 3 months and counseled on the need for family screening. DISCUSSION: LVNC is thought to be a congenital cardiomyopathy caused by failure of cardiac sinusoids to compact during embryogenesis. However, studies demonstrate development of LV trabeculations on serial echocardiograms suggesting LVNC may be an acquired cardiomyopathy. Predisposition to trabeculation development may be genetically determined, LVNC has a 30% rate of familial recurrence. Excessive preload and afterload are thought to contribute as the development of trabeculations is noted in chronic renal failure and valvular heart disease. Criteria for diagnosis of LVNC vary and are not universally agreed upon. Thus, a multi-modality imaging approach involving echocardiography and cardiac MRI is recommended. LVNC is associated with significant complications, 56% of patients will develop heart failure syndrome and up to 40% will require heart transplantation. Additionally, 11% of patients undergo ICD implantation for ventricular arrhythmias and 7.6% of patients die of sudden cardiac death. Risk of thromboembolism ranges from 21-38%, likely due to turbulent flow through intertrabecular recesses. Three-year mortality rate is estimated at 14%. CONCLUSIONS: LVNC is a relatively common cardiomyopathy with significant morbidity and mortality. We urge clinician awareness to facilitate prompt diagnosis and management. Reference #1: Bhatia, Nisha L., et al. “Isolated Noncompaction of the Left Ventricular Myocardium in Adults: A Systematic Overview.” Journal of Cardiac Failure, vol. 17, no. 9, 2011, pp. 771–778., doi:10.1016/j.cardfail.2011.05.002. Reference #2: Tian, Julia, et al. “Left Ventricular Noncompaction: A Rare Case of Nonischemic Cardiomyopathy.” Case Reports in Cardiology, vol. 2019, 2019, pp. 1–3., doi:10.1155/2019/5637638. Reference #3: Gati, Sabiha, et al. “Adult Left Ventricular Noncompaction.” JACC: Cardiovascular Imaging, vol. 7, no. 12, 2014, pp. 1266–1275., doi:10.1016/j.jcmg.2014.09.005. DISCLOSURES: No relevant relationships by Gopika Dasari, source=Web Response No relevant relationships by Anneka Hutton, source=Web Response No relevant relationships by Eli Levine, source=Web Response No relevant relationships by Shaheen Mizyed, source=Web Response