Article Text

Download PDFPDF
Cardiac involvement in COVID-19: cause or consequence of severe manifestations?
  1. Bruno Ramos Nascimento1,2,
  2. Craig Sable3
  1. 1 Serviço de Cardiologia e Cirurgia Cardiovascular e Centro de Telessaúde, Hospital das Clínicas da Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil
  2. 2 Departamento de Clínica Médica, Faculdade de Medicina da Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil
  3. 3 Department of Pediatric Cardiology, Children's National Health System, Washington, District of Columbia, USA
  1. Correspondence to Dr Bruno Ramos Nascimento, Departamento de Clínica Médica, Faculdade de Medicina da Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, 30130-100, Brazil; ramosnas{at}gmail.com

Statistics from Altmetric.com

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Since the inception of the COVID-19 pandemic, the identification of factors associated with unfavourable outcomes has been a topic of intense investigation. With limited disease-specific therapies, early stratification of those at highest risk of complications can guide who needs intensive clinical monitoring and supportive management. The large body of evidence in the early phases of the pandemic strongly suggested that cardiac involvement could potentially be one of these prognostic factors, and several hypotheses have been raised for the cardiovascular abnormalities observed, especially in severely ill patients. Markers of acute myocardial injury have been reported in up to one-fifth of patients with COVID-19,1 and several mechanisms have been implicated: (a) direct myocardial injury due to viral invasion of cardiomyocytes; (b) systemic inflammatory response and cytokine storm; (c) increased cardiometabolic demand associated with acute hypoxic respiratory failure; (d) increased vascular shear stress precipitating plaque rupture in the setting of a prothrombotic state; (e) deleterious cardiovascular effects of empirical drug regimens; (f) critical electrolyte disturbances. These disease-related mechanisms may be exacerbated by underlying cardiac disease and increase risk of adverse outcomes.1

The present study by Singh et al 2 brings a significant contribution to this growing body of evidence. Fifty-two patients recovered from COVID-19 (one-third with intensive care admission and one-fifth requiring mechanical ventilation) underwent a comprehensive imaging protocol with gadolinium and manganese-enhanced MRI, with 23 additionally undergoing CT coronary angiography for evaluation of underlying coronary artery disease. They were compared with 10 healthy controls and 26 volunteers propensity matched for cardiovascular morbidity. COVID-19-recovered patients demonstrated impaired left (LV) and right (RV) ventricular systolic function, elevated myocardial T1 values and extracellular volume fraction, and reduced myocardial manganese uptake compared with healthy controls. In contrast, when comparing with comorbidity-matched volunteers, patients with COVID-19 had preserved LV function but reduced RV systolic function …

View Full Text

Footnotes

  • Twitter @ramosnas

  • Contributors Conception and design of the research: Nascimento, BR; Acquisition of data: Nascimento, BR, Sable, C; Analysis and interpretation of data: Nascimento, BR, Sable, C; Obtaining financing: Nascimento, BR, Sable, C; Writing of the manuscript: Nascimento, BR; Critical revision of the manuscript for intellectual content: Sable, C, Nascimento, BR; Authors responsible for the overall content as guarantors: Nascimento, BR, Sable, C.

  • Funding BN is supported in part by Conselho Nacional de Desenvolvimento Científico e Tecnológico (Bolsa de produtividade em pesquisa, 312382/2019-7), by the Edwards Lifesciences Foundation (Improving the Prevention and Detection of Heart Valve Disease Across the Lifespan, 2021) and by Fundação de Amparo à Pesquisa do Estado de Minas Gerais (grant APQ-000627-20).

  • Competing interests None declared.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

  • Provenance and peer review Commissioned; internally peer reviewed.

Linked Articles

  • Heart failure and cardiomyopathies
    Trisha Singh Thomas A Kite Shruti S Joshi Nick B Spath Lucy Kershaw Andrew Baker Helen Jordan Gaurav Singh Gulsin Michelle Claire Williams Edwin J R van Beek Jayanth Ranjit Arnold Scott I K Semple Alastair James Moss David E Newby Marc Dweck Gerry P McCann