COVID-19 and cardiovascular consequences: Is the endothelial dysfunction the hardest challenge?

Area of Science:

• Cardiology
• Infectious Diseases
• Pathology

Background:

• Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV-2) causes Coronavirus Disease-19 (COVID-19), a pandemic with a wide clinical spectrum.
• Severe COVID-19 can lead to life-threatening cardiovascular collapse, and pre-existing cardiovascular comorbidities increase mortality risk.

Purpose of the Study:

• To review the pathogenetic mechanisms of cardiovascular complications in severe COVID-19.
• To clarify the role of endothelial dysfunction, inflammation, and coagulation in COVID-19-related cardiac injury.
• To discuss the impact of SARS-CoV-2 on the renin-angiotensin system and implications for treatment.

Main Methods:

• Literature review of studies on severe COVID-19.
• Analysis of pathogenetic mechanisms linking viral infection to cardiovascular events.
• Discussion of the interplay between inflammation, coagulation, and endothelial function.

Main Results:

• Endothelial dysfunction, driven by inflammation and coagulation, is a key mechanism for cardiovascular complications in severe COVID-19.
• SARS-CoV-2 infection can compromise endothelial homeostasis, leading to systemic inflammatory complications.
• The virus's effect on the ACE2 receptor warrants consideration regarding ACE inhibitors and ARBs in COVID-19 patients.

Conclusions:

• Severe COVID-19 poses significant cardiovascular risks primarily through sustained endothelial dysfunction.
• The "cytokine storm" and "coagulative storm" in COVID-19 severely impact endothelial function.
• Understanding these mechanisms is crucial for managing COVID-19 patients with cardiovascular comorbidities.