Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19)

Abstract

IMPORTANCE Virus infection has been widely described as one of the most common causes of myocarditis. However, less is known about the cardiac involvement as a complication of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. OBJECTIVE To describe the presentation of acute myocardial inflammation in a patient with coronavirus disease 2019 (COVID-19) who recovered from the influenzalike syndrome and developed fatigue and signs and symptoms of heart failure a week after upper respiratory tract symptoms. DESIGN, SETTING, AND PARTICIPANT This case report describes an otherwise healthy 53-year-old woman who tested positive for COVID-19 and was admitted to the cardiac care unit in March 2020 for acute myopericarditis with systolic dysfunction, confirmed on cardiac magnetic resonance imaging, the week after onset of fever and dry cough due to COVID-19. The patient did not show any respiratory involvement during the clinical course.EXPOSURE Cardiac involvement with COVID-19.MAIN OUTCOMES AND MEASURES Detection of cardiac involvement with an increase in levels of N-terminal pro-brain natriuretic peptide (NT-proBNP) and high-sensitivity troponin T, echocardiography changes, and diffuse biventricular myocardial edema and late gadolinium enhancement on cardiac magnetic resonance imaging. RESULTSAn otherwise healthy 53-year-old white woman presented to the emergency department with severe fatigue. She described fever and dry cough the week before. She was afebrile but hypotensive; electrocardiography showed diffuse ST elevation, and elevated high-sensitivity troponin T and NT-proBNP levels were detected. Findings on chest radiography were normal. There was no evidence of obstructive coronary disease on coronary angiography. Based on the COVID-19 outbreak, a nasopharyngeal swab was performed, with a positive result for SARS-CoV-2 on real-time reverse transcriptasepolymerase chain reaction assay. Cardiac magnetic resonance imaging showed increased wall thickness with diffuse biventricular hypokinesis, especially in the apical segments, and severe left ventricular dysfunction (left ventricular ejection fraction of 35%). Short tau inversion recovery and T2-mapping sequences showed marked biventricular myocardial interstitial edema, and there was also diffuse late gadolinium enhancement involving the entire biventricular wall. There was a circumferential pericardial effusion that was most notable around the right cardiac chambers. These findings were all consistent with acute myopericarditis. She was treated with dobutamine, antiviral drugs (lopinavir/ritonavir), steroids, chloroquine, and medical treatment for heart failure, with progressive clinical and instrumental stabilization.CONCLUSIONS AND RELEVANCE This case highlights cardiac involvement as a complication associated with COVID-19, even without symptoms and signs of interstitial pneumonia.

COVID-19 for the Cardiologist

“…Heart failure and myocardial dysfunction have been described in COVID-19 (53,55,58,60,63 The general pattern of fatalities across the age groups appears to be consistent throughout the world. In general, greater age is associated with greater risk of severe disease as well as death.…”

“…Based on serial assessment of troponin, researchers in China reported that the median time to the development of acute cardiac injury was 15 days (IQR 10 -17) after illness onset, occurring after the development of ARDS (53). Of note, early cardiac injury has been reported, even in the absence of respiratory symptoms (60). In a case series by Shi et al, the mortality rate for those hospitalized with subsequent evidence of cardiac injury was significantly higher than those without cardiac injury (51.2% vs 4.5%, p<0.001) and, along with ARDS, was an independent predictor of death (56).…”

“…The presence of ACE2 receptors on the myocardium and vascular endothelial cells provides a theoretical mechanism for direct viral infection of the heart with resultant myocarditis. Reports have documented clear cases of myocarditis syndromes (60,63). However, to date there no reports of biopsy proven SARS-CoV2 viral myocarditis with viral inclusions or viral DNA detected in myocardial tissue.…”

COVID-19 Clinical Trials

“…COVID-19 can also directly result in a number of cardiovascular complications, including fulminant myocarditis, myocardial injury, heart failure, and arrhythmia (1,3,4). There have been a number of published case reports of clinically suspected myocarditis with markedly elevated troponin levels, ST-segment elevations on electrocardiogram without obstructive coronary disease in the presence of severely decreased left ventricular systolic function and shock (5), with cardiac magnetic resonance imaging evidence of diffuse myocardial edema and gadolinium enhancement (6). However, in another isolated autopsy report from a patient who suffered from SARS-CoV-2related pneumonia and cardiac arrest, no obvious histological changes in the myocardium were observed with the exception of few interstitial mononuclear inflammatory infiltrates (7).…”

Préconisations cardiologiques lors de l’utilisation d’un traitement pouvant entraîner des troubles conductifs ou un allongement de l’intervalle QT dans le COVID-19

“…. Des altérations cardiaques structurelles ou inflammatoires ont également été rapportées [2,3] avec jusqu'à 23 % d'insuffisance cardiaque dans certaines séries hospitalières [4]. De nombreuses thérapeutiques sont en cours d'évaluation clinique (au 8 avril 2020), certaines pouvant éventuellement favoriser l'allongement de l'intervalle QT (chloroquine, hydroxychloroquine, azithromycine, lopinavir/ritonavir et d'autres).…”