Reverse takotsubo cardiomyopathy in fulminant COVID-19 associated with cytokine release syndrome and resolution following therapeutic plasma exchange: a case-report.

Abstract

BACKGROUND:

Fulminant (life-threatening) COVID-19 can be associated with acute respiratory failure (ARF), multi-system organ failure and cytokine release syndrome (CRS). We present a rare case of fulminant COVID-19 associated with reverse-takotsubo-cardiomyopathy (RTCC) that improved with therapeutic plasma exchange (TPE).

CASE PRESENTATION:

A 40 year old previous healthy male presented in the emergency room with 4 days of dry cough, chest pain, myalgias and fatigue. He progressed to ARF requiring high-flow-nasal-cannula (flow: 60 L/minute, fraction of inspired oxygen: 40%). Real-Time-Polymerase-Chain-Reaction (RT-PCR) assay confirmed COVID-19 and chest X-ray showed interstitial infiltrates. Biochemistry suggested CRS: increased C-reactive protein, lactate dehydrogenase, ferritin and interleukin-6. Renal function was normal but lactate levels were elevated. Electrocardiogram demonstrated non-specific changes and troponin-I levels were slightly elevated. Echocardiography revealed left ventricular (LV) basal and midventricular akinesia with apex sparing (LV ejection fraction: 30%) and depressed cardiac output (2.8 L/min) consistent with a rare variant of stress-related cardiomyopathy: RTCC. His ratio of partial arterial pressure of oxygen to fractional inspired concentration of oxygen was < 120. He was admitted to the intensive care unit (ICU) for mechanical ventilation and vasopressors, plus antivirals (lopinavir/ritonavir), and prophylactic anticoagulation. Infusion of milrinone failed to improve his cardiogenic shock (day-1). Thus, rescue TPE was performed using the Spectra Optia™ Apheresis System equipped with the Depuro D2000 Adsorption Cartridge (Terumo BCT Inc., USA) without protective antibodies. Over 5 days he received daily TPE (each lasting 4 hours). His lactate levels, oxygenation, and LV function normalized and he was weaned off vasopressors. His inflammation markers improved, and he was extubated on day-7. RT-PCR was negative on day-17. He was discharged to home isolation in good condition.

CONCLUSION:

Stress-cardiomyopathy may complicate the course of fulminant COVID-19 with associated CRS. If inotropic therapy fails, TPE without protective antibodies may help rescue the critically ill patient.

• Authors: Fahad Faqihi, Abdulrahman Alharthy, Rayan Alshaya, John Papanikolaou, Demetrios J Kutsogiannis, Peter G Brindley, Dimitrios Karakitsos
• Journal: BMC cardiovascular disorders (BMC Cardiovasc Disord) Vol. 20 Issue 1 Pg. 389 (08 26 2020) ISSN: 1471-2261 [Electronic] England
• PMID: 32842957 (Publication Type: Case Reports, Journal Article, Research Support, Non-U.S. Gov't, Video-Audio Media)

Chemical References

• Antiviral Agents
• Cardiotonic Agents
• Drug Combinations
• lopinavir-ritonavir drug combination
• Lopinavir
• Ritonavir

Topics

• Adult
• Antiviral Agents (therapeutic use)
• Betacoronavirus
• COVID-19
• Cardiotonic Agents (therapeutic use)
• Coronavirus Infections (complications, diagnosis, drug therapy, therapy)
• Cytokine Release Syndrome (complications, diagnosis, therapy)
• Drug Combinations
• Echocardiography
• Humans
• Lopinavir (therapeutic use)
• Male
• Pandemics
• Plasma Exchange
• Pneumonia, Viral (complications, diagnosis, therapy)
• Respiration, Artificial
• Respiratory Distress Syndrome (etiology, therapy)
• Ritonavir (therapeutic use)
• SARS-CoV-2
• Shock, Cardiogenic (etiology, therapy)
• Takotsubo Cardiomyopathy (diagnostic imaging, etiology, therapy)
• COVID-19 Drug Treatment