key: cord-264327-uzlavmhx
authors: Singh, Rajat; Domenico, Christopher; Rao, Sriram; Urgo, Kimberly; Prenner, Stuart; Wald, Joyce; Atluri, Pavan; Birati, Edo Y.
title: Novel Coronavirus Disease 2019 in a Patient on Durable Left Ventricular Assist Device Support
date: 2020-04-17
journal: J Card Fail
DOI: 10.1016/j.cardfail.2020.04.007
sha: 
doc_id: 264327
cord_uid: uzlavmhx

nan

In December 2019, an outbreak of a severe respiratory viral illness was first identified in the Hubei province of China. The illness was later discovered to be caused by infection with a novel coronavirus known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).

To the best of our knowledge, we present here the first confirmed case of COVID-19 in a patient on left ventricular assist device (LVAD) support. Our case patient is a 66-year-old man with a history of end-stage ischemic cardiomyopathy, on HeartMate II (Abbott Laboratories, Abbott Park, IL) LVAD as destination therapy, hypertension, atrial flutter and ischemic stroke who presented with a four-day history of fever, cough and shortness of breath following recent two-month travel to Egypt. Initial physical examination revealed a body temperature of 100.9 degrees Fahrenheit (38.3 degrees Celsius), normal mean arterial pressure by Doppler, and oxygen saturation of 70% on room air. Arterial blood gas revealed a PaO 2 of 46 mmHg despite delivery of 100% FiO 2 via non-rebreather ventilation. LVAD parameters were stable on presentation. A chest radiograph showed bilateral pulmonary infiltrates suggestive of multifocal pneumonia (Figure 1a ). The patient appeared to be in moderate respiratory distress, with tachypnea and accessory muscle use. Due to concern for developing respiratory muscle fatigue and impending respiratory failure, the decision was made to pursue intubation and mechanical ventilation.

Testing for novel coronavirus returned positive for SARS-CoV-2 by PCR. Salient features of the patient's initial clinical laboratory trend include lymphocytopenia, transaminitis, hyperbilirubinemia and elevated creatinine, lactate dehydrogenase, Ddimer and ferritin levels. In the following days, the patient developed progressive hypotension requiring initiation of vasopressor agents, acute oliguric renal failure requiring continuous renal replacement therapy, and refractory hypoxemia consistent with acute respiratory distress syndrome (ARDS).

Right ventricular failure was considered as a potential etiology of hypotension in the setting of LVAD and inflammatory surge. The patient was unable to be transferred to the catheterization laboratory for invasive hemodynamic assessment due to COVID-19.

Pulmonary artery catheterization was attempted at the bedside but placement was unsuccessful. A central line was utilized to measure central venous pressure (17 mmHg) and oxygen saturation (ScvO 2 75%). Transthoracic echocardiogram revealed baseline moderate right ventricular dysfunction. LVAD parameters otherwise remained stable.

Management of ARDS was further complicated by refractory hypoxemia despite mechanical ventilation. Implementation of prone positioning was considered to assist with oxygenation, however the presence of LVAD was determined to be a relative contraindication. While it has previously been shown that prone positioning unloads the right ventricle in ARDS due to improved pulmonary pressures, (1) the use of this maneuver in the setting of LVAD has not been well described and may be adversely associated with increase in RV pressures and subsequent RV failure.

The patient's clinical course was later complicated by septic shock in setting of Escherichia coli and Lactobacillus species bacteremia, hyperbilirubinemia secondary to acalculous cholecystitis with requirement for percutaneous cholecystostomy, and acute blood loss anemia secondary to gastrointestinal bleed requiring blood transfusion. Due to prolonged ventilator dependent respiratory failure, the patient underwent placement of tracheostomy.

The patient was treated with hydroxychloroquine 600 mg twice daily following initial diagnosis. Oseltamivir 75 mg twice daily was added and once liquid lopinavirritonavir was available at our institution, the patient was switched to lopinavir-ritonavir 400-100 mg twice daily on treatment day 5, but was discontinued in the setting of hyperbilirubinemia on treatment day 9. He was transitioned back to hydroxychloroquine 200 mg twice daily to complete a total fourteen-day course. The patient was deemed not a candidate for the compassionate use of remdesivir due to poor creatinine clearance.

This report describes the first known presentation of illness secondary to SARS-CoV-2 in a patient with long-term LVAD support. At the time of writing, the patient remains critically ill, however with clinical improvement. Recent evidence suggests that patients with cardiovascular comorbidities appear to be at increased risk of morbidity and mortality with COVID-19. (2) Notably, prior studies have shown that cellular immunity is compromised among long-term LVAD recipients. (3, 4) This "functionally immunocompromised state" may in part explain the patient's rapid clinical deterioration and prolonged critical illness following infection with SARS-CoV-2. Increased susceptibility to viral infections, particularly COVID-19, in the setting of LVAD has not been reported previously in the literature. Furthermore, this case highlights an important consideration for management of ARDS as the safety and efficacy of prone positioning in the presence of LVAD is currently unknown. Finally, we propose the establishment of a COVID-LVAD registry to further understand the impact of COVID-19 on this advanced heart failure population.

Protecting the Right Ventricle in ARDS: The Role of Prone Ventilation

Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study

Activation-induced T-cell death and immune dysfunction after implantation of left-ventricular assist device

Cellular immunity impaired among patients on left ventricular assist device for 6 months