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COVID-19 and cardiovascular complications: an update from the underlying mechanism to consequences and possible clinical intervention.

ABSTRACT: Introduction: The novel coronavirus has caused significant mortality worldwide and is primarily associated with severe acute respiratory distress syndrome (ARDS). Apart from ARDS, clinical reports have shown noticeable cardiovascular complications among the patients of COVID-19. Infection from virus, stimulation of cytokine storm, altered immune response, and damage to myocardial tissue are some of the proposed mechanisms of cardiovascular complications in COVID-19.Areas covered: Based on the clinical reports of CVDs among COVID-19 patients, we have discussed the molecular mechanisms involved in cardiovascular pathogenesis, its prevalence, and association with COVID-19, and various available therapeutic modality for the treatment.Expert opinion: Seeing the cardiovascular complications in COVID-19 patients and its association with the existing drug, risk-benefit ratio of treatment paradigm, as well as the level of cardiac injury biomarkers must be monitored regularly. Additionally, a well-designed clinical trial should be conducted where head to head comparison can be made with anti-COVID-19 drugs and cardioprotective anti-inflammatory drugs. Nevertheless, vaccines are the best-suited approach, but until then, sanitization, social distancing, and active lifestyle are the best ways to beat this global pandemic situation.

SUBMITTER: Iqubal A

PROVIDER: S-EPMC7938651 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:The novel SARS coronavirus SARS-CoV-2 pandemic may be particularly deleterious to patients with underlying cardiovascular disease (CVD). The mechanism for SARS-CoV-2 infection is the requisite binding of the virus to the membrane-bound form of angiotensin-converting enzyme 2 (ACE2) and internalization of the complex by the host cell. Recognition that ACE2 is the coreceptor for the coronavirus has prompted new therapeutic approaches to block the enzyme or reduce its expression to prevent the cellular entry and SARS-CoV-2 infection in tissues that express ACE2 including lung, heart, kidney, brain, and gut. ACE2, however, is a key enzymatic component of the renin-angiotensin-aldosterone system (RAAS); ACE2 degrades ANG II, a peptide with multiple actions that promote CVD, and generates Ang-(1-7), which antagonizes the effects of ANG II. Moreover, experimental evidence suggests that RAAS blockade by ACE inhibitors, ANG II type 1 receptor antagonists, and mineralocorticoid antagonists, as well as statins, enhance ACE2 which, in part, contributes to the benefit of these regimens. In lieu of the fact that many older patients with hypertension or other CVDs are routinely treated with RAAS blockers and statins, new clinical concerns have developed regarding whether these patients are at greater risk for SARS-CoV-2 infection, whether RAAS and statin therapy should be discontinued, and the potential consequences of RAAS blockade to COVID-19-related pathologies such as acute and chronic respiratory disease. The current perspective critically examines the evidence for ACE2 regulation by RAAS blockade and statins, the cardiovascular benefits of ACE2, and whether ACE2 blockade is a viable approach to attenuate COVID-19.

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Project description: Not available

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