A REMARKABLE RESPONSE TO ANGIOTENSIN II THERAPY IN SEVERE SARS-COV-2 INFECTION

ABSTRACT

SESSION TITLE Medical Student/Resident Critical Care Posters SESSION TYPE Med Student/Res Case Rep Postr PRESENTED ON October 18-21, 2020 INTRODUCTION: During the COVID19 pandemic, a subset of patients presented with hypoxemia and shock as a complication of SARS-CoV-2 infection. CASE PRESENTATION A 68-year-old Black male presented with ARDS due to SARS-CoV-2. He had dyspnea and cough for the preceding 6 days. At the time of admission, he developed respiratory failure, was placed on mechanical ventilation, and transferred to our facility for further care. His co-morbidities include diabetes, hypertension treated with an ACE inhibitor, CKD stage III, and obstructive sleep apnea. On arrival, he was afebrile, blood pressure was 117/56 mmHg (mean arterial pressure 75 mmHg) without vasopressor support, oxygen saturation was 85% on 100% FiO2. Exam was significant for diminished breath sounds and trace lower extremity edema. The patient's hemodynamics, renal function, and oxygenation worsened within hours of arrival, prompting use of multiple vasopressors, deep sedation, and paralytic agents. An angiotensin II (AngII) infusion was started due to refractory shock. Within 30 minutes of starting AngII, other vasoactive medications were successfully weaned. Interestingly, oxygenation subsequently improved by 30% (P/F 128 to 168) during this same time period in the absence of other interventions (Figure). The AngII infusion was tapered and the patient did not develop further shock. The patient continues to convalesce. DISCUSSION: The renin-angiotensin-aldosterone system (RAAS) has been implicated in the pathogenesis of COVID-19. The SARS-CoV-2 virus enters tissues through the ACE2 receptor. ACE2 converts AngII into Angiotensin-(1-7) and may offset the effects against vasoconstrictive, inflammatory, and pro-fibrotic responses associated with AngII. Loss of this protective mechanism could be responsible for some of the ventilation/perfusion mismatch observed in ARDS related to COVID-19. CONCLUSION(S) Our patient's brisk hemodynamic and oxygenation response to AngII suggests that alterations to RAAS are relevant in COVID-19, and that this pathway can be therapeutically targeted. These observations merit further investigation. Reference #1 Zhou, P., Yang, X., Wang, X. et al. A pneumonia outbreak associated with a new coronavirus of probable bat origin. Nature 579, 270-273 (2020) Reference #2 Santos RAS, Sampaio WO, Alzamora AC, et al. The ACE2/Angiotensin-(1-7)/MAS Axis of the Renin-Angiotensin System Focus on Angiotensin-(1-7). Physiol Rev. 2018;98(1)505-553. DISCLOSURES Stock holder relationship with Amgen Pharmaceuticals Please note $5001 - $20000 Added 06/01/2020 by Joe Chiles, source=Web Response, value=25 shares of stock No relevant relationships by Ryan Goetz, source=Web Response No relevant relationships by Rutwij Joshi, source=Web Response Speaker/Speaker's Bureau relationship with Boehringer Ingelheim Please note $1001 - $5000 by Tracy Luckhardt, source=Web Response, value=Honoraria No relevant relationships by Daniel Scullin, source=Web Response No relevant relationships by Raymond Wade, source=Web Response Advisory Committee Member relationship with GSK, AZ, Mereo BioPharma Please note $1001 - $5000 Added 04/24/2020 by James Wells, source=Web Response, value=Consulting fee Contracts to Conduct Clinical Trials relationship with Mereo BioPharma, Bayer Please note >$100000 Added 04/24/2020 by James Wells, source=Web Response, value=Contracts via my institutionCopyright © 2020 American College of Chest Physicians