Current understanding of the link between COVID-19 and cardiovascular disease

The rapid outbreak of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) resulted in an ongoing pandemic of Coronavirus Disease 2019 (COVID-19). To date, the pandemic has claimed the lives of more than 5 million people worldwide. Scientists have shown that older people with comorbidities such as cardiovascular disease (CVD) and diabetes are more susceptible to severe COVID-19 infections.

study: Increased COVID-19 complications in people with cardiovascular disease: the role of renin-angiotensin-aldosteron system (RAAS) dysregulation.. Image Credit: Irina Shatilova / Shutterstock

Therefore, understanding the mechanisms linking CVD to SARS-CoV-2 susceptibility and why this group is more susceptible to SARS-CoV-2 infection is important to protect them from disease. ..Review published in Chemobiological interaction It focuses on the prevalence of COVID-19 in CVD patients associated with the ACE2 mechanism.

COVID-19 and cardiovascular disease

SARS-CoV-2 is an RNA virus belonging to the genus Betacoronavirus in the family Coronaviridae. It mainly infects the lungs and symptoms range from mild flu-like to severe pneumonia. Acute COVID-19 infections have many complications such as lymphopenia, disseminated intravascular coagulation (DIC), coagulopathy, myositis, nephropathy or liver damage.

Previous studies of the clinical manifestations of SARS-CoV in the cardiovascular system have shown infiltration of monocyte plasma cells (B cells) and other lymphocytes into the vessel wall and fibrinoid necrosis. These events lead to vasculitis of various organs such as the heart, lungs, liver and kidneys, and the formation of blood clots in small veins. Similarly, previous studies have shown that patients with underlying CVD such as pericarditis, cardiac arrhythmias, and acute myocarditis suffer from severe MERS-CoV infection compared to individuals in the healthy group. It became clear.

Previous studies Cytokine storm Interleukin (IL) -2, IL-6, IL-7, interferon gamma-inducing protein 10 (IP10), granulocyte colony stimulator (GSCF), macrophage inflammatory protein 1 A (MIP1A), and SARS-CoV-2 Tumor necrosis factor α (TNFα) after infection. Scientists have shown that cytokine storms lead to a sharp increase in left ventricular (LV) dysfunction in CVD patients.

A large cohort study of 5000 SARS-CoV-2 patients found that patients with existing diseases (CVD, cancer, diabetes, etc.) were at greatest risk of increased mortality.Scientists say that the main mechanism behind the increased susceptibility of CVD patients to COVID-19 infection is the angiotensin converting enzyme 2 (ACE2) receptor in this group of patients, especially those who were under ACE inhibitors. Said increased expression of (ACEI) or Angiotensin receptor blocker (ARB) Treatment.

However, another group of researchers strongly denied this theory, stating that patients receiving ACEI / ARB therapy were less susceptible to severe COVID-19 and hospitalization. Therefore, more research is needed to better understand the actual mechanisms behind the association between CVD and severe COVID-19 infection. Recent studies have shown that the use of two common treatments, hydroxychloroquine (an antimalarial drug) and azithromycin (an antibiotic), has serious side effects in CVD patients.

ACE2 and COVID-19 Meinfection NSPatients with cardiovascular disease

ACE2 is a metalloprotease that is abundantly expressed in endothelial cells, cardiomyocytes, and cardiac fibroblasts. These cells make up most of the heart tissue. Elevated ACE2 levels have been found in patients after myocardial infarction (MI).Scientists believe this may be a mechanism that prevents activation Renin-angiotensin-aldosteron system (RAAS). Therefore, the ACE2 system acts as a prophylactic mechanism against MI, hypertension, lung disease, and diabetic complications.

ACE2 is also the major host receptor for SARS-CoV-2 infection. The SARS-CoV-2 spike protein binds to the host’s ACE2 receptor and then penetrates the host cell. Angiotensin 1-9 and angiotensin 1-7 have important cardiac protection functions such as lowering blood pressure. Infection with SARS-CoV-2 impairs the conversion of angiotensin I to angiotensin 1-9 and the conversion of angiotensin II to angiotensin 1-7, thus reversing this protective effect.

Previous studies have shown that coronavirus affects a variety of endocrine and metabolic pathways through the RAAS system. Animal models have shown that increased ACE2 expression is effective in ameliorating acute lung injury, and treatment with RAAS inhibitors reduces lung injury. Recent studies have reported that RAAS inhibitors used to treat hypertension and CVD performed better in COVID-19 patients than other antihypertensive drugs (such as calcium channel blockers).

A mouse model of SARS-CoV infection revealed that reduced expression of ACE2 led to increased levels of angiotensin II, which increased vascular permeability and respiratory complications. These complications were reversed by treatment with recombinant ACE2 or ARB (losartan). In addition, analysis of mouse models and human autopsy samples showed that SARS-CoV infection downregulated ACE2 expression in both cardiomyocytes and type 2 alveolar epithelial cells. This led to an inflammatory response and dyspnea in COVID-19 patients.

Conclusion

The authors recommended that future research focus on development In vitro When In vivo Models similar to various cardiovascular complications. This allows scientists to understand better pathogenic mechanisms associated with increased susceptibility to SARS-CoV-2 infection and complications in CVD patients. More research is needed to test the hypothesis that one of the plausible reasons for the increased complications of SARS-CoV-2 in CVD patients is the excessive accumulation of angiotensin II.