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The persistent COVID-19 epidemic has exerted significant pressure on worldwide healthcare systems, particularly due to its severe cardiovascular and respiratory complications. Understanding the molecular foundation of SARS-CoV-2 infection and its effects on the heart and lungs is essential, particularly for patients with pre-existing heart failure who face a markedly elevated risk of negative consequences. Due to the swift proliferation of the virus and its emerging forms, there is an immediate necessity for focused therapeutic approaches and comprehensive molecular understanding to guide clinical management. This review focuses on how key mechanisms—ACE2- mediated RAAS imbalance, cytokine-driven inflammation, and troponin-indexed myocardial injury—converge to worsen heart failure in COVID-19. This research is pertinent and timely as the global health burden of heart failure escalates with COVID-19, aiming to enhance patient outcomes and inform effective treatment strategies.
Tomar et al. (Sun,) studied this question.
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