Cardiovascular risk and complications associated with COVID-19

Abstract

In December 2019, an unprecedented outbreak of pneumonia cases associated with acute respiratory distress syndrome (ARDS) first occurred in Wuhan, Hubei Province, China. The disease, later named Coronavirus disease 2019 (COVID-19) by the World Health Organization (WHO), was caused by the Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), and on January 30, 2020, the WHO declared the outbreak of COVID-19 to be a public health emergency. COVID-19 is now a global pandemic impacting more than 43,438,043 patients with 1,158,596 deaths globally as of August 26th, 2020. COVID-19 is highly contagious and has caused more deaths than SARS in 2002-2003 or the Middle East Respiratory Syndrome (MERS) in 2012-2013 combined and represents an unprecedented human affliction not seen since the influenza pandemic of 1918. COVID-19 has been associated with several cardiac complications, including hypercoagulability, acute myocardial injury and myocarditis, arrhythmias, and acute coronary syndromes. Patients with pre-existing cardiovascular disease (CVD) are at the highest risk for myocardial injury and mortality among infected patients. The mechanism by which COVID-infected patients develop cardiac complications remains unclear, though it may be mediated by increased ACE-2 gene expression. Despite initial concerns, there is no evidence that angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) therapy increases risk for myocardial injury among those infected with COVID-19. In the current report, we summarize the peer-reviewed and preprint literature on cardiovascular risks and complications associated with COVID-19, as well as provide insights into its pathogenesis and management.

Keywords: COVID-19; SARS-CoV-2; cardiovascular complications; cardiovascular risks; corona; coronavirus.

Figure 1

The potential pathogenesis of SARS-CoV-2 infection-related cardiovascular diseases. A spike protein of SARS-CoV-2 has high susceptibility in individuals who have increased ACE2 gene expression (e.g., pre-existing CVD), leading a downregulation of ACE2. ACE2 downregulation could result in the upregulation of inflammatory cytokines (e.g., IL-6), a reduction in the degradation of angiotensin II, and decreased angiotensin 1-7. Decreased angiotensin 1-7 could lead to subsequent decreased activation of Mas receptors on platelets which in combination of inflammatory cytokine upregulation (e.g. IL-6, IFN-, MCP-1) may result in acquired platelet dysfunction and intravascular thrombosis. Additionally, increased angiotensin II mediated AT1 receptor activation may have multiple physiologic effects including myocardial hypertrophy and dysfunction, interstitial fibrosis, endothelial dysfunction, enhanced inflammation, increased endothelin-1 expression and decreased NO release which can manifest as cardiac injury, arrhythmias and hypertension.

Figure 2

COVID-19 and Cardiac phenotypes. Patients with acute ST-elevation myocardial infarction (STEMI) requiring intubation should be intubated prior to arrival to the catheterization laboratory. If no dedicated catheterization laboratory is available, thrombolysis should be considered. Patients with severe cardiac phenotypes should be admitted to the coronary care unit (CCU) for close monitoring, and should be considered for ECMO support as well as referred to the cath lab for an invasive strategy or surgery. High risk patients with non-severe cardiac phenotypes should be hospitalized at the very least. Low risk patients with non-severe cardiac phenotypes should be discharged for self-isolation and followed up closely with telehealth platforms.

Figure 3

Proposed STEMI management in the COVID-19 era. Patients with acute ST-elevation myocardial infarction (STEMI) should be tested for COVID-19. If the rapid test is negative, and the patient is not a person under investigation (PUI), then primary percutaneous coronary intervention (PCI) should be considered. Primary PCI should be considered in a PUI with hemodynamic instability, myocarditis or a ventricular arrhythmia. Fibrinolytic strategy should be considered in a PUI who is hemodynamically stable. Primary PCI should be considered once COVID-19 has been ruled out. In patients with confirmed COVID-19 cath lab or rescue PCI may be needed if fibrinolytic strategy has failed.