DILATED CARDIOMYOPATHY WITH CARDIOGENIC SHOCK SECONDARY TO COVID-19 INFECTION

SESSION TITLE: Extraordinary Cardiovascular Reports SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 01:35 pm - 02:35 pm INTRODUCTION: Acute myocarditis from COVID-19 has been well documented, but there are few cases of COVID -19 patients developing dilated cardiomyopathy (3). We present a case of COVID-19 induced dilated cardiomyopathy leading to cardiogenic shock. CASE PRESENTATION: A 49-year-old African-American female presented to the emergency department (ED) with shortness of breath. She was diagnosed with COVID-19 infection four weeks prior to presentation, and since that time she experienced continuously worsening dyspnea, congestion, and weakness. In the ED, the patient was found to have pulmonary edema and bilateral pleural effusions on chest x-ray, as well as acute kidney injury with a creatinine level of 2.85 mg/dL. An echocardiogram revealed a new diagnosis of dilated cardiomyopathy with reduced ejection fraction of 10-15% with a large left ventricular thrombus. Heparin infusion was initiated and intravenous furosemide was administered for diuresis. Her renal function continued to worsen, which was attributed to cardiorenal syndrome. She became hypotensive and was found to be in cardiogenic shock, which required intensive care unit admission with the initiation of continuous renal replacement therapy (CRRT). The patient improved with CRRT, however her renal function did not recover and she continued to require hemodialysis. She was able to be transferred out of the intensive care unit, and the heparin was bridged to warfarin. Goal-directed medical therapy was initiated for her heart failure. She was eventually discharged home with an external cardioverter-defibrillator vest. A follow-up echocardiogram three months later revealed the left ventricular thrombus had resolved, however, her ejection fraction had improved to only 15-20% despite medication compliance. An implantable cardioverter-defibrillator (ICD) was placed and the patient continues to be followed closely by cardiology. DISCUSSION: Viral infection is a well-documented cause of myocarditis with some patients developing dilated cardiomyopathy (1). Inflammatory dilated cardiomyopathy occurs most commonly in patients infected with Coxsackie B virus, Human Parvovirus B19, Adenovirus, Human Immunodeficiency Virus, Hepatitis C Virus, Cytomegalovirus, Epstein-Barr Virus, and Human Herpes Virus 6 (1). The proposed mechanism of inflammatory cardiomyopathy includes infection of the myocytes, incomplete viral elimination, and persistent retained viral components in the myocytes(2). This may cause direct viral injury or chronic myocardial inflammation leading to remodeling (2). It is documented in the literature that COVID-19 can lead to myocarditis and various types of acute cardiomyopathy (3). However, there have been only a few reported cases of COVID - 19 induced dilated cardiomyopathy (3). CONCLUSIONS: While rarely reported thus far, it should be established that COVID-19 alone can cause dilated cardiomyopathy and lead to heart failure (3). Reference #1: Schultheiss H-P, Baumeier C, Pietsch H, Bock C-T, Poller W, Escher F. Cardiovascular consequences of viral infections: from COVID to other viral diseases. Cardiovascular Research. Published online October 5, 2021. doi:10.1093/cvr/cvab315 Reference #2: Kühl U, Pauschinger M, Seeberg B, et al. Viral Persistence in the Myocardium Is Associated With Progressive Cardiac Dysfunction. Circulation. 2005;(13):1965-1970. doi:10.1161/circulationaha.105.548156 Reference #3: Komiyama M, Hasegawa K, Matsumori A. Dilated Cardiomyopathy Risk in Patients with Coronavirus Disease 2019: How to Identify and Characterise it Early? European Cardiology Review. Published online May 27, 2020. doi:10.15420/ecr.2020.17 DISCLOSURES: No relevant relationships by Amanda Cecchini No relevant relationships by Austin Richardson No relevant relationships by Krupa Solanki

CARDIAC TAMPONADE SECONDARY TO COVID-19 INFECTION

SESSION TITLE: Infections In and Around the Heart Case Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: Due to the novelty of COVID-19 virus, complications of this severe respiratory infection are continually emerging. The inflammatory response to the virus carries a high mortality rate and can lead to a variety of cardiothoracic complications such as acute coronary syndrome, thromboembolism, and heart failure [1]. Here, we present a case of a young female who suffered cardiac tamponade (CT) from a pericardial effusion (PEEF) attributed to COVID-19 infection, which has only been described a handful of times in the literature. CASE PRESENTATION: A 33-year-old female with a history of Down syndrome and morbid obesity presented with worsening dyspnea and fever for one week. Her initial oxygen saturation was 50% on room air, and bilevel noninvasive ventilatory support was initiated. Her viral PCR was positive for COVID-19. A computed tomography angiogram of the chest revealed small bilateral pulmonary emboli, diffuse ground-glass consolidations, and small bilateral pleural effusions. Her respiratory status continued to decompensate and she was placed on mechanical ventilation. She became hypotensive requiring vasopressor support. The following morning, an echocardiogram (TTE) revealed an ejection fraction of 40-45% and a new PEEF with early right ventricular diastolic collapse consistent with CT physiology. She underwent emergent pericardiocentesis, and 220 mL of bloody fluid was drained. PEEF studies revealed a glucose level of 186 mg/dL, LDH of 1380 U/L, and protein of 3.0 g/dL. Total nucleated count was 16,545/uL with 68% neutrophils. Gram stain showed a few white blood cells without organisms, and final bacterial, fungal, and acid-fast cultures were negative. A pericardial drain was left in place, but the procedure was complicated by a pneumothorax and a chest tube was placed. A follow-up TTE the next day revealed improvement of the PEEF without signs of CT. A repeat chest x-ray showed resolution of the pneumothorax. Unfortunately, the patient’s oxygenation and hemodynamic status continued to worsen. She eventually suffered cardiac arrest with pulseless electrical activity and succumbed to her illness. DISCUSSION: New knowledge regarding complications of COVID-19 infection is continually emerging. According to a February 2022 systematic review, only 30 cases of severe PEEFs with CT secondary to COVID-19 have been recorded. The mechanism by which PEEFs form is unclear. It is proposed that the entry of the virus into inflammatory cells causes a release of cytokines such as TNF-alpha, IL-1, IL-6, and IL-8. This resulting cytokine storm allows rapid inflammation and infiltration of fluid into the pericardial sac [1]. CONCLUSIONS: In a decompensated patient with COVID-19, a stat TTE should be obtained to rule out PEEF. Physicians must be cognizant of this uncommon yet highly fatal complication in unstable COVID-19 patients, as cardiac tamponade is a potentially reversible cause of cardiac arrest. Reference #1: Kermani-Alghoraishi, M., Pouramini, A., Kafi, F., & Khosravi, A. (2022). Coronavirus Disease 2019 (COVID-19) and Severe Pericardial Effusion: From Pathogenesis to Management: A Case Report Based Systematic Review. Current problems in cardiology, 47(2), 100933. https://doi.org/10.1016/j.cpcardiol.2021.100933 DISCLOSURES: No relevant relationships by Amanda Cecchini No relevant relationships by Arthur Cecchini No relevant relationships by Kevin Cornwell No relevant relationships by Krupa Solanki

GUILLAIN-BARRÉ SYNDROME FOLLOWING COVID-19 PNEUMONIA: ARE THEY RELATED?

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: Guillain-Barré syndrome (GBS) is an immune-mediated polyneuropathy affecting the peripheral nervous system. Immune system activation in response to a viral or bacterial infection, which cross-reacts with the peripheral nerve components, is GBS's proposed mechanism. Epstein-Barr virus, campylobacter, cytomegalovirus, influenza, and mycoplasma are the most commonly associated infections with GBS development. Since the beginning of the coronavirus 2019 (COVID-19) pandemic, there have been isolated reports of the disease's neurological manifestations and sequelae. In early February 2020 itself, COVID-19 associated GBS has been reported from Italy and China. Here we are reporting the case of a GBS after severe COVID-19 pneumonia. CASE PRESENTATION: A 68-year- old Caucasian male with a history of obstructive sleep apnea, hypertension, and restless leg syndrome came to the hospital with worsening reparatory difficulty. He was diagnosed with COVID-19 pneumonia a week ago and was on remdesivir and dexamethasone therapy at home. At the time of presentation, he was found to be in respiratory failure, which eventually required intubation and mechanical ventilation. After spending 14 days on mechanical ventilation, the patient was extubated. His respiratory status significantly improved, but he was found to have confused mentation on day two after extubation. An MRI scan and EEG showed no significant abnormality. His confusion improved over the next two days, but he gradually developed bilateral upper and lower extremity symmetrical weaknesses with loss of deep tendon reflexes and touch sensation. The patient was also found to have alternating tachycardia and bradycardia around this period. The weakness progressed over the next week. CSF analysis revealed a protein level of 77mg/dL (normal: 8–43 mg/dL) with total nucleated cells of 3 (normal 0-8 ). CSF meningitis/encephalitis PCR panel for the 17 most common pathogens was negative (the panel did not have COVID-19). Nerve conduction studies were not done due to lack of availability. A diagnosis of GBS was made, and the patient was transferred to a higher center for plasmapheresis. DISCUSSION: COVID-19 leading to GBS does not come as a surprise;similar viruses, including Severe acute respiratory syndrome coronavirus and middle east respiratory syndrome coronavirus, had been reported to trigger GBS. If the CSF findings and autonomic nervous system involvement were absent, post-intensive care syndrome and critical care neuropathy might have been close differentials. There are isolated reports of blood transfusions leading to GBS;although unlikely, the patient's reception of convalescent plasma cannot be overlooked. The absence of nerve conduction studies also truncates the confidence of GBS diagnosis here. CONCLUSIONS: GBS may be triggered by COVID-19 infection, although more evidence is needed to establish the causation. REFERENCE #1: Caress JB, Castoro RJ, Simmons Z, Scelsa SN, Lewis RA, Ahlawat A, Narayanaswami P. COVID-19-associated Guillain-Barré syndrome: The early pandemic experience. Muscle Nerve. 2020 Oct;62(4):485-491. doi: 10.1002/mus.27024. Epub 2020 Aug 11. PMID: 32678460;PMCID: PMC7405390. REFERENCE #2: Rajdev K, Victor N, Buckholtz ES, Hariharan P, Saeed MA, Hershberger DM, Bista S. A Case of Guillain-Barré Syndrome Associated With COVID-19. J Investig Med High Impact Case Rep. 2020 Jan-Dec;8:2324709620961198. doi: 10.1177/2324709620961198. PMID: 32981333;PMCID: PMC7545753. REFERENCE #3: Scheidl E, Canseco DD, Hadji-Naumov A, Bereznai B. Guillain-Barré syndrome during SARS-CoV-2 pandemic: A case report and review of recent literature. J Peripher Nerv Syst. 2020 Jun;25(2):204-207. doi: 10.1111/jns.12382. Epub 2020 May 26. PMID: 32388880;PMCID: PMC7273104. DISCLOSURES: No relevant relationships by Arthur Cecchini, source=Web Response No relevant relationships by Bhavesh Gajjar, source=Web Response No relevant relationships by Rasheed Musa, source=Web Response No relevant relati nships by Akesh Thomas, source=Web Response