J Cardiovasc Pharmacol. 2021 Jul 22. doi: 10.1097/FJC.0000000000001116. Online ahead of print.
The novel coronavirus disease (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has rapidly evolved into a global pandemic. The substantial morbidity and mortality associated with the infection has prompted us to understand potential risk factors that can predict patient outcomes. Hypertension has been identified as the most prevalent cardiovascular comorbidity in COVID-19 patients, that demonstrably increases the risk of hospitalization and death. Initial studies implied that renin-angiotensin-aldosterone system (RAAS) inhibitors might increase the risk of viral infection and aggravate disease severity, thereby causing panic given the high global prevalence of hypertension. Nonetheless, subsequent evidence supported the administration of antihypertensive drugs, and noted that they do not increase the severity of COVID-19 infection in patients with hypertension; rather, may have a beneficial effect. To date, the precise mechanism by which hypertension predisposes to unfavorable outcomes in patients with COVID-19 remains unknown. In this mini-review, we elaborate on the pathology of SARS-CoV-2 infection coexisting with hypertension, and summarize potential mechanisms, focusing on the dual roles of angiotensin converting enzyme 2 (ACE2) and the disorders of RAAS in COVID-19 and hypertension. The effects of proinflammatory factors released due to immune response, and gastrointestinal dysfunction in COVID-19 are also discussed.