Cardiovascular aspects of COVID-19

• Published in: Swiss medical weekly 2020-12, Vol.150 (5153), p.w20417-w20417
• Main Authors: Kurz, David J., Eberli, Franz Robert
• Format: Article
• Language: English
• Subjects: Age Factors; Angiotensin-Converting Enzyme 2 - metabolism; Angiotensin-Converting Enzyme Inhibitors; Biomarkers; cardiogenic shock; Cardiovascular Diseases - epidemiology; Cardiovascular Diseases - physiopathology; cardiovascular risk factors; Comorbidity; COVID-19; COVID-19 - drug therapy; COVID-19 - epidemiology; COVID-19 - physiopathology; Humans; Inflammation - physiopathology; Inflammation Mediators - metabolism; multisystem inflammatory syndrome in children; Myocardial Infarction - physiopathology; myocardial injury; myocarditis; Myocardium - pathology; Renin-Angiotensin System - physiology; Sex Factors; Systemic Inflammatory Response Syndrome - physiopathology
• ISSN: 1424-3997; 1424-3997
• DOI: 10.4414/smw.2020.20417

Coronavirus disease 2019 (COVID-19) is primarily a pulmonary disease, but also affects the cardiovascular system in multiple ways. In this review, we will summarise and put into perspective findings and debates relating to the diverse aspects of cardiovascular involvement of COVID-19. We will review evidence for the role of the renin-angiotensin-aldosterone system (RAAS), the risk of pre-existing cardiovascular disease in COVID-19 susceptibility and course, and the mechanism of acute and long-term myocardial injury. The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) uses membrane-bound angiotensin converting-enzyme-2 (ACE2) as a receptor for cell entry. ACE2 is part of an important counter-regulatory circuit antagonising the harmful effects of angiotensin II on lung and heart. Modulation of ACE2 may therefore affect disease susceptibility and disease course. However, observational clinical studies and one randomised trial have so far not yielded evidence for harmful or beneficial effects of blockers of the RAAS during COVID-19. Age, gender, and multi-morbidity all increase susceptibility to SARS-CoV-2. In contrast, pre-existing cardiovascular diseases do so only minimally, but they may aggravate the disease course. Direct SARS-CoV-2 infection of the heart tissue and myocytes is rare. Nevertheless, COVID-19 may lead to myocarditis-like acute cardiac injury, characterised by myocardial oedema, but lacking extensive myocyte loss and lymphocytic infiltration. Independent of this, increases in cardiac biomarkers (troponin, N-terminal pro-brain natriuretic peptide, D-dimer) are frequent, especially in the phase of severe systemic inflammation and acute respiratory distress syndrome, and quantitatively associated with poor outcome. The pulmonary infection may result initially in right ventricular dysfunction, but in cases with severe systemic infection hypoxia, hyperinflammation and cytokine storm heart failure may eventually ensue. Unlike other infections and inflammatory states, COVID-19 does not appear to trigger acute coronary syndromes. In children, even mild COVID-19 can induce a multisystem inflammatory syndrome with Kawasaki-like symptoms frequently accompanied by cardiogenic shock.