Impact of COVID-19 on the Cardiovascular System: A Review of Available Reports

Abstract

The recent emergence of the coronavirus disease 19 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in China is now a global health emergency. The transmission of SARS-CoV-2 is mainly via human-to-human contact. This virus is expected to be of zoonotic origin and has a high genome identity to that of bat derived SARS-like coronavirus. Various stringent measures have been implemented to lower person-to-person transmission of COVID-19. Particular observations and attempts have been made to reduce transmission in vulnerable populations, including older adults, children, and healthcare providers. This novel CoV enters the cells through the angiotensin-converting enzyme 2 (ACE2) receptor. There is a higher risk of COVID-19 infection among those with preexisting cardiovascular diseases (CVD), and it has been connected with various direct and indirect complications, including myocarditis, acute myocardial injury, venous thromboembolism, and arrhythmias. This article summarizes the various cardiovascular complications and mechanisms responsible for the same with COVID-19 infection. For the benefit of the scientific community and public, the effect of COVID-19 on major vital organs such as the kidneys, liver, and intestines has been briefly discussed. In this review, we also discuss drugs in different stages of clinical trials and their associated complications, as well as the details of vaccines in various stages of development.

Impact of COVID-19 infection on the cardiovascular system: An evidence-based analysis of risk factors and outcomes

“…Understanding the risk factors for cardiac involvement in COVID-19 infection is important; previous reports have found an increase in mortality of infections that are associated with cardiac injury ( 15 , 16 ). It has been reported that risk factors for cardiac-specific involvement from established COVID-19 infection include many of the aforementioned risk factors for bad outcomes, including DM, HTN, chronic heart failure, previous CAD, atherosclerotic heart disease, and even cancer ( 11 ).…”

“…Notable laboratory findings have also been associated with increased cardiovascular involvement during infection. D-dimer elevation of patients was linked with increased hospital death, associating hypercoagulation states from SARS-CoV-2 with elevated inflammatory responses to the virus ( 3 , 15 ). In a Chinese cohort, increased levels of NT-proBNP was associated with a need for ICU care, linking heart failure-associated ACE2 upregulation with COVID-19 infection and severity ( 3 ).Elevated levels of troponin I, CRP, ferritin, IL-6, IL-1β, and IFN-γ during cytokine storms can be a predictor of severity of COVID-19.…”

“…In a Chinese cohort, increased levels of NT-proBNP was associated with a need for ICU care, linking heart failure-associated ACE2 upregulation with COVID-19 infection and severity ( 3 ).Elevated levels of troponin I, CRP, ferritin, IL-6, IL-1β, and IFN-γ during cytokine storms can be a predictor of severity of COVID-19. ( 15 , 16 ). Increased states of inflammation impairs the endogenous mechanism of clot dissolution, thereby increasing risk for complications and possibly explaining the increased frequency of myocardial infarction ( 15 ).…”

“…( 15 , 16 ). Increased states of inflammation impairs the endogenous mechanism of clot dissolution, thereby increasing risk for complications and possibly explaining the increased frequency of myocardial infarction ( 15 ).…”

“…COVID-19 can, directly and indirectly, injure the cardiovascular system. Direct inflammation and damage are a result of the COVID-19 virus attaching to angiotensin-converting enzyme 2 (ACE2), found in abundance in cardiomyocytes and alveolar cells, among others ( 61 , 62 ). As COVID-19 attaches to these enzymes, the ability of ACE2 to influence the fluctuation of the renin-angiotensin-aldosterone (i.e., RAAS) system is disturbed, leading to an increased presence of angiotensin II, which is a potent vasoconstrictor.…”