Cardiovascular Involvement by COVID-19 (Published: ESC April 21, 2020)

Key points:

• Severe COVID-19 infection is associated with myocardial damage and cardiac arrhythmia;

• Monitoring of cardiac toxicity of antiviral drugs is recommended.

• The pathobiology of coronavirus infection involves SARS-CoV‑2 binding to the host receptor angiotensin-converting enzyme 2 (ACE2) to mediate entry into cells;

• ACE2, which is expressed in the lungs, heart and vessels, is a key member of the renin angiotensin system (RAS) important in the pathophysiology of CVD;

• CVD associated with COVID-19, likely involves dysregulation of the RAS/ACE2 system due to SARS-CoV‑2 infection and due to comorbidities, such as hypertension;

• CVD may be a primary phenomenon in COVID-19, but may be secondary to acute lung injury, which leads to increased cardiac workload, potentially problematic in patients with pre existing HF;

• Cytokine release storm, originating from imbalance of T cell activation with dysregulated release of interleukin (IL)-6, IL-17 and other cytokines, may contribute to CVD in COVID-19. IL-6 targeting is being tested therapeutically;

• Immune system activation along with immunometabolism alterations may result in plaque instability, contributing to development of acute coronary events.