Coronaviruses and the Cardiovascular System: Acute and Long-term Implications

Tian-Yuan Xiong; Simon Redwood; Bernard Prendergast; Mao Chen


Eur Heart J. 2020;41(19):1798-1800. 

In This Article

Viral Pathology and Links to the Cardiovascular System

Chronic cardiovascular disease may become unstable in the setting of viral infection as a consequence of imbalance between infection-induced increase in metabolic demand and reduced cardiac reserve. Patients with coronary artery disease and heart failure may be at particular risk as a result of coronary plaque rupture secondary to virally induced systemic inflammation, and rigorous use of plaque stabilizing agents (aspirin, statins, beta-blockers, and angiotensin-converting enzyme inhibitors) has been suggested as a possible therapeutic strategy. Pro-coagulant effects of systemic inflammation[13] may increase the likelihood of stent thrombosis and assessment of platelet function and intensified anti-platelet therapy should be considered in those with a history of previous coronary intervention.

The beta-coronavirus virus underlying COVID-19 strains from the same species as SARS and has recently been named SARS-CoV-2. SARS-CoV binds to cells expressing appropriate viral receptors, particularly angiotensin-converting enzyme 2 (ACE2).[14] Angiotensin-converting enzyme 2 is also expressed in the heart, providing a link between coronaviruses and the cardiovascular system. Murine models and human autopsy samples demonstrate that SARS-CoV can down-regulate myocardial and pulmonary ACE2 pathways, thereby mediating myocardial inflammation, lung oedema, and acute respiratory failure.[15] Pro-inflammatory cytokines are up-regulated in the lungs and other organs of SARS patients, and the systemic inflammatory response syndrome provides a possible mechanism for multi-organ failure (usually involving the heart) in severe cases.