Cardiovascular disturbances in COVID-19: an updated review of the pathophysiology and clinical evidence of cardiovascular damage induced by SARS-CoV-2

Abstract

Severe acute respiratory coronavirus-2 (SARS-Co-2) is the causative agent of coronavirus disease-2019 (COVID-19). COVID-19 is a disease with highly variable phenotypes, being asymptomatic in most patients. In symptomatic patients, disease manifestation is variable, ranging from mild disease to severe and critical illness requiring treatment in the intensive care unit. The presence of underlying cardiovascular morbidities was identified early in the evolution of the disease to be a critical determinant of the severe disease phenotype. SARS-CoV-2, though a primarily respiratory virus, also causes severe damage to the cardiovascular system, contributing significantly to morbidity and mortality seen in COVID-19. Evidence on the impact of cardiovascular disorders in disease manifestation and outcome of treatment is rapidly emerging. The cardiovascular system expresses the angiotensin-converting enzyme-2, the receptor used by SARS-CoV-2 for binding, making it vulnerable to infection by the virus. Systemic perturbations including the so-called cytokine storm also impact on the normal functioning of the cardiovascular system. Imaging plays a prominent role not only in the detection of cardiovascular damage induced by SARS-CoV-2 infection but in the follow-up of patients’ clinical progress while on treatment and in identifying long-term sequelae of the disease.

Contribution of genetics and lifestyle to the risk of major cardiovascular and thromboembolic complications following COVID-19

“…However, the magnitude of gene association was reduced for all arterial-related events (CAD, AF, and ISS), suggesting that distinctive pathogenic mechanisms may be involved when arterial disorders develop during COVID-19 infection 2,20 , such as the virus directly mediating heart injury by entering cardiomyocytes. 21,22 Importantly, the polygenic risk for conventional VTE was remarkably retained for COVID-19-related VTE, which echo the finding in our previous study showing that the monogenic such as factor V Leiden mutation also consistently predisposed post-COVID-19 VTE complications. 6…”

Contribution of genetics and lifestyle to the risk of major cardiovascular and thromboembolic complications following COVID-19

“…However, the magnitude of gene association was reduced for all arterial-related events (CAD, AF, and ISS), suggesting that distinctive pathogenic mechanisms may be involved when arterial disorders develop during COVID-19 infection 2,20 , such as the virus directly mediating heart injury by entering cardiomyocytes. 21,22 Importantly, the polygenic risk for conventional VTE was remarkably retained for COVID-19-related VTE, which echo the nding in our previous study showing that the monogenic such as factor V Leiden mutation also consistently predisposed post-COVID-The role of genetics in variable COVID-19 representations is not yet well-understood. Although a large genome-wide association study (GWAS) was performed for COVID-19, it focused on SARS-COV-2-induced critical respiratory complications.…”

Cardiac manifestations in critically ill patients with COVID-19: do we really know what hit us?

“…An excellent article by Helms et al on COVID-19 and the heart, highlights some of the pathophysiology and relates it to clinical manifestations seen in ICU al [ 10 ]. Lawal et al highlight the point that the cardiovascular system expresses the angiotensin-converting enzyme-2, which as we know is the receptor used by COVID-19 for binding, making it vulnerable to infection by the virus [ 11 ]. The severe inflammation or cytokine storm previously experienced by COVID-19 patients, many of which are now prevented or managed by dexamethasone and other anti-inflammatory drugs can also impact on the normal functioning of the cardiovascular system [ 11 ].…”