Cardiovascular System during SARS-CoV-2 Infection

Abstract

SARS-CoV-2 virus can not only damage the respiratory system but may also pose a threat to other organs, such as the heart or vessels. This review focuses on cardiovascular complications of COVID-19, including acute cardiac injury, arrhythmias, biomarkers, accompanying comorbidities and outcomes in patients diagnosed with SARS-CoV-2 infection. The research was conducted on the databases: PubMed, Springer, ScienceDirect, UpToDate, Oxford Academic, Wiley Online Library, ClinicalKey. Fifty-six publications from 1 November 2020 till 15 August 2021 were included in this study. The results show that cardiac injury is present in about 1 in 4 patients with COVID-19 disease, and it is an independent risk factor, which multiplies the death rate several times in comparison to infected patients without myocardial injury. New-onset cardiac injury occurs in nearly every 10th patient of the COVID-19-suffering population. Comorbidities (such as hypertension, cardiovascular disease and diabetes) severely deteriorate the outcome. Therefore, patients with SARS-CoV-2 infection should be carefully assessed in terms of cardiac medical history and possible cardiological complications.

SARS‐CoV‐2 infection and multi-organ system damage: a review

“…Identifying the primary processes responsible for the abnormalities in gas exchange and respiratory mechanics, as well as their variations over time, should determine the best configuration of respiratory support. Monitoring inspiratory effort in spontaneously breathing patients (non-invasive or invasive ventilation) is an essential supplementary tool for informing the decision of mechanical support and identifying treatment failure [ 19 ]. Clinical, physiological, and radiological surveillance and early referral to a chest specialist are currently advised for all COVID-19 survivors [ 6 ].…”

Levantamento bibliográfico da relação causal entre afecções Cardiovasculares e Covid-19

“…O organismo em resposta a agressão viral apresenta um estado inflamatório persistente que incluem: alterações plasmáticas (sistema complemento, coagulação/fibrinólise e cininas), gerados pelas células (citocinas, mediadores lipídicos, oxidantes, proteases, óxido nítrico e neuropeptídeos) e indução de síntese proteica, um estágio precoce na produção de citocinas. Esses fatores são considerados responsáveis pela injúria celular e alterações no surfactante, com distúrbio da relação ventilação/perfusão, resultando em hipoxemia (Kozlik, et al, 2022).…”

“…As células cardíacas que expressam receptores ECA2, envolvem o endotélio da microcirculação e estão envolvidas na integridade da parede dos vasos que irrigam o miocárdio. Ao serem danificadas pela infecção viral, estas são preparadas para liberar uma série de fatores de crescimento que tentam restaurar a integridade microvascular, esses fatores contribuem para a inflamação do tecido local, perturbando a eletrofisiologia celular atrial (Kozlik, et al, 2022).…”

3D Lung Tissue Models for Studies on SARS-CoV-2 Pathophysiology and Therapeutics

“…However, these chips are not the only ones used for research on viral diseases. Given that COVID-19, as well as other coronaviruses, can affect several organs, including kidneys, and the gastrointestinal, cardiovascular and nervous systems [ 90 , 91 , 92 , 93 ], 3D models of other organs have been used. Bein et al [ 94 ] recently modeled an immunocompetent human Intestine-on-a-Chip to study enteric NL63 coronavirus infection and treatment, whereas Helms et al [ 95 ], using kidney organoids derived from pluripotent stem cells, showed that SARS-CoV-2 can directly infect and damage kidney tubular epithelial cells.…”