In summary, COVID-19 is rapidly spreading around the globe and our understanding of the virus is limited. To date, there is no effective, approved therapy or vaccination to treat the disease or protect against its complications. Although the lungs are considered the main target organ of SARS-CoV-2, the virus can affect many other organs, leading to multiple organ damage. Cardiovascular injury has been noted as a protruding clinical feature in COVID-19 patients. The dysregulation of RAAS can lead to a harmful inflammatory response and worsening of cardiovascular consequences in patients with COVID-19. Therefore, intervention with drugs that counteract Ang II may have a potential role in preventing the deleterious cardiovascular outcomes. Although increased ACE2 levels may raise the concern of increased SARS-CoV-2 infectivity, we propose here that n-3 PUFAs may be beneficial rather than harmful for cardiovascular outcomes in COVID-19 patients by limiting Ang II-induced detrimental signaling and enhancing Ang (1-7) cardioprotective effects.