Debra L. Beck and Eugene Braunwald, MD
Published: April 13, 2020
There is some evidence that COVID-19, the disease caused by the novel coronavirus SARS-CoV-2, preferentially afflicts the elderly and those with chronic comorbidities. However, the clinical profile of COVID-19 in refractory heart failure (HF) patients is unknown. Hong et al describe 4 hospitalized severe HF patients infected with COVID-19 between January 7th and March 15th at one hospital in China.
All patients were transferred to isolation wards when COVID-19 diagnosis was confirmed or suspected. In 3, hospital-transmission was suspected because they were previously in the same ward. Interestingly, 1 patient was negative on two consecutive nucleic acid tests but tested positive for serum antibodies.
All 4 patients were male. Age ranged from 38 to 67 in 3 patients. One patient (a survivor) was 11 years old and had been hospitalized for myocarditis 10 years after a tetralogy of Fallot operation.
None of the patients had fever during their illness. Symptoms were restricted to mild cough and fatigue at time of diagnosis.
Two patients had typical ground-glass changes on lung computed tomography. An enlarged left ventricle and reduced left ventricular ejection fraction was seen in all 4 patients (between 22-30%) and all were in NYHA class IV HF.
Three of 4 patients had elevated troponin I (TNI) later in the course of their disease. Two of four had exacerbations and were transferred to the ICU where they both died 10 days after testing positive for COVID-19. Neither received mechanical ventilation. Both showed increases in troponin I before their deaths. They also had higher levels of C-reactive protein and brain natriuretic peptide compared to the 2 patients who survived.
Of note, patient 2, who survived, tested positive after two negative tests for nucleic acid.
Summary
Dong et al report on 4 patents with end-stage heart failure who were infected with COVID-19. Two presentations were relatively mild and two severe and fatal. “The most novel finding was that the TNI level of the two critically ill patients increased significantly by more than 20-fold, indicating myocardial injury,” wrote the authors. This provides stronger evidence of myocardial injury by COVID-19 than previous reports, although the exact mechanism of this injury remains unknown.
Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine features a unique update program by Dr. Braunwald, creating a “living textbook” by featuring twice monthly updates including “Hot off the Press” and Late-Breaking Clinical Trials (links to authors’ presentation slides are also included).
Learn more about Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine, 11th Edition. Download a free chapter here.
The SARS-CoV-2 virus induces an autoimmune response similar to other viral induced autoimmune diseases. We have submitted a paper, pending review, that demonstrates the disconnect between the cardiology community and the basic science community concerning the pathophysiology and potential treatments. T cell depleting therapies, never even cited in current reviews, but used by our group for over 20 years, have support from the basic science literature. Eleven other Clinical papers have reported similar positive results.
The addition of anti-CD20 monoclonal antibodies seems to eliminate self reactive plasmablasts to stop the production of autoantibodies. It’s all in the basic science literature.