Abstract

SESSION TITLE: Medical Student/Resident Obstructive Lung Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Takotsubo cardiomyopathy (TCM) is a form of sudden transient LV dysfunction often associated with severe emotional and physical stressors; that mimics ACS. Currently, there are limited studies showing the relationship between COPD and TCM. We present a case of Takotsubo cardiomyopathy in a post-menopausal female secondary to AECOPD. CASE PRESENTATION: A 70-year-old female with a history of COPD, HTN, and smoking presented with severe midsternal chest pain and SOB associated with increased cough and sputum production. On arrival, she was tachycardic, tachypneic, and hypoxic. She had decreased air entry in bilateral lung fields with expiratory wheeze, respiratory acidosis, and hyperinflated lungs on CXR. She received multiple Ipratropium-Albuterol nebulizations for AECOPD resulting in symptomatic improvement. Further workup revealed EKG findings of new hyperacute T waves in V3-V6, TWI in V1 and V2; and up-trending Troponin I which peaked at 7.13. She was managed as Type I NSTEMI with Aspirin, Clopidogrel & IV Heparin. Emergent LHC showed 60% occlusion of RCA. TTE revealed a hyperkinetic base with hypokinetic apical and mid anterior wall, new-onset reduced LVEF of 40 to 45%, consistent with TCM. Her noncritical coronary artery disease was not considered to be contributing to her symptom burden and did not correspond to her EKG and echocardiographic findings. Follow up TTE in 6 months revealed improvement in LVEF to 55 to 60% with a resolution of apical hypokinesis. Given the history of no further psychosocial stressors most likely etiology for her TCM was stress related to acute COPD. DISCUSSION: AECOPD related respiratory failure leading to hypoxemia and hypercapnia has been identified as a potential physical trigger of TCM. Catecholamine excess plays a central role in stress-related apical myocardial stunning and coronary vasospasm; reducing the viability of myocytes via cAMP-mediated calcium overload resulting in contraction band necrosis. Hypoxia with coexisting acidosis causes cardiomyocyte damage through activation of BCL-2 family of proapoptotic proteins leading to changes in mitochondrial permeability and DNA fragmentation. Potential mechanisms include sympathetic overstimulation due to the administration of beta-agonist in the setting of endogenous catecholamine excess from the stress of respiratory failure and concurrent administration of ipratropium resulting in inhibition of parasympathetic system, tachycardia, and rarely paradoxical bronchospasm. It is unclear whether respiratory failure from COPD leading to hypoxia and hypercapnia or repeated use of Albuterol-Ipratropium caused TCM in our patient. CONCLUSIONS: In our case, we highlight that by early recognition of COPD induced TCM; complications could be minimized by limiting the use of beta-agonists and treating ongoing cardiac dysfunction. Further studies are required to establish the exact mechanism of COPD induced TCM. Reference #1: Sharkey S, Windenburg D, et al. "Natural History and Expansive Clinical Profile of Stress (Tako-Tsubo) Cardiomyopathy.” J Am Coll Cardiol., 2010 Jan 26; 55(4):333-341. DOI: https://doi.org/10.1016/j.jacc.2009.08.057 Reference #2: Wittstein I, Thiemann D, et al. "Neurohumoral features of myocardial stunning due to sudden emotional stress.” N Engl J Med. 2005 Feb 10; 352:539-548 https://doi.org/10.1056/NEJMoa043046 Reference #3: Kubasiak, Lori A. and Hernandez, Olga M. and Bishopric, Nanette H. and Webster, Keith A., "Hypoxia and acidosis activate cardiac myocyte death through the Bcl-2 family protein BNIP3.” Proceedings of the National Academy of Science, 2002 Oct; 99(20): 12825-12830. DOI = 10.1073/pnas.202474099 DISCLOSURES: No relevant relationships by Tahreem Ahmad, source=Web Response No relevant relationships by Khubaib Ahmad, source=Web Response No relevant relationships by Waqas Ali, source=Web Response No relevant relationships by Pranali Santhoshini Pachika, source=Web Response

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