SESSION TITLE: Monday Abstract Posters SESSION TYPE: Original Investigation Posters PRESENTED ON: 10/21/2019 02:30 PM - 03:15 PM INTRODUCTION: Takotsubo cardiomyopathy (TCM) is a form of nonischemic cardiomyopathy that is characterized by transient regional systolic dysfunction of the left ventricle. It often mimics acute myocardial infarction but has a minimal release of cardiac enzymes. The hallmark is an absence of angiographic evidence of obstructive coronary artery disease or acute plaque rupture. In most cases of TCM, the regional wall motion abnormality extends beyond the territory perfused by a single epicardial coronary artery. Classically, TCM is associated with a ballooned left ventricular apex and basal segmental hyperkinesis. While there have been reports of atypical TCM with midventricular hypokinesia and apical sparing, here we present a novel variant in which there is left ventricular hypokinesis of the anterior, septal, and lateral segments, with preservation of motion only in the inferior wall. CASE PRESENTATION: A 56 year old female presented with recent increased stress, poor sleep, and epigastric abdominal pain with radiation to the right shoulder for 4 days. EKG showed ST elevations in V1-V4 and reciprocal ST depressions in II, III, and aVF. Troponin-T peaked to 1.250. Left heart ventricular angiogram showed a left ventricular ejection fraction (LV EF) of 10-15%, with no obstructive coronary artery disease visualized on the angiogram. Transthoracic echocardiography showed LV wall hypokinesis of the anterior, septal, and lateral segments, with preserved motion only in the inferior wall. (Fig. A - F). Follow up TTE showed improvement of LV EF to 35%. DISCUSSION: TCM is a non-ischemic cardiomyopathy with transient contractility changes, presenting in middle-aged women with acute stress. This patient’s presentation - with EKG concerning for acute ST elevation myocardial infarction, no evidence of coronary artery disease, and extensive LV cardiomyopathy - implies a diagnosis of TCM. The pathogenesis of Takotsubo cardiomyopathy is not well understood. Postulated mechanisms include catecholamine excess, coronary artery spasm, and microvascular dysfunction. It is thought that catecholamines play a role in TCM because of the correlation of the disorder with physical or emotional stress. A catecholamine surge may cause diffuse microvascular spasm or dysfunction, resulting in myocardial stunning. Catecholamines can also have a direct myocardial toxicity effect, further contributing to the cardiomyopathy. On resolution of the catecholamine surge, the myocardium recovers and LV EF improves. CONCLUSIONS: This case demonstrates a novel, as of yet unseen, variant of TCM with hypokinesis of all but the inferior wall. Such specific sparing supports etiologies of TCM not related to epicardial coronary artery distribution, and lends credence to etiologies involving stress-induced catecholamine excess causing neurogenic stunned myocardium. Reference #1: Murthy, A., Arora, J., Singh, A., Gedela, M., Karnati, P., & Nappi, A. (2014). Takotsubo Cardiomyopathy: Typical and Atypical Variants, A Two-Year Retrospective Cohort Study. Cardiology research, 5(5), 139-144. Reference #2: Velankar, P., & Buergler, J. (2012). A mid-ventricular variant of Takotsubo cardiomyopathy. Methodist DeBakey cardiovascular journal, 8(3), 37-9. DISCLOSURES: no disclosure on file for Mandeep Kainth; No relevant relationships by Sharmila Sarkar, source=Web Response No relevant relationships by Alexander Volodarskiy, source=Web Response