Key result
SARS-CoV-2 infection induces cardiovascular damage through mechanisms including direct myocardial infection, ACE2 downregulation, cytokine storm, coagulation abnormalities, and hypoxia.
Why the study?
The large volume of rapidly accumulating literature made it difficult to keep up with the mechanisms behind SARS-CoV-2-induced cardiovascular damage.
This review provides a comprehensive overview of the molecular mechanisms by which SARS-CoV-2 infection leads to cardiovascular complications, highlighting direct viral injury, immune overactivation, and coagulopathy.
Severe COVID-19 may involve myocardial injury warranting monitoring; leaves open impact on outcomes and interventions.
Since its emergence in late December 2019, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) - the causative agent of coronavirus disease 2019 (COVID-19) - has spread rapidly world-wide, becoming a global pandemic in March 2020 that is still active. In addition to the severe pulmonary damage, clinical studies have reported that COVID-19 is associated with the development of cardiovascular alterations such as myocardial injury, particularly in its most severe manifestations. At the same time, pre-existing cardiovascular conditions in COVID-19 cases have been related to an increased risk of adverse outcomes. To date, several mechanisms have been described to participate in the development of cardiovascular damage related to COVID-19, including direct SARS-CoV-2 infection of the cardiovascular system, Angiotensin-Converting Enzyme 2 (ACE2) downregulation, cytokine storm, coagulation abnormalities, hypoxia and drug-induced cardiotoxicity. However, the large amount of information gathered so far makes it difficult to keep up with this new pandemic. In the present review, we provide a clear insight of the extensive literature available and summarize the current understanding of COVID-19-related mechanisms behind SARS-CoV-2-induced damage to the cardiovascular system.
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Pinsach‐Abuin et al. (2021) conducted a review in COVID-19. SARS-CoV-2 was evaluated. SARS-CoV-2 infection induces cardiovascular damage through mechanisms including direct myocardial infection, ACE2 downregulation, cytokine storm, coagulation abnormalities, and hypoxia.
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