Mechanisms of COVID-19-induced heart failure: a short review

Abstract

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes coronavirus disease 2019 (COVID-19) has infected more than 42.5 million people globally resulting in the death of over 1.15 million subjects. It has inflicted severe public health and economic hardships across the world. In addition to acute respiratory distress syndrome, respiratory failure, sepsis, and acute kidney injury, COVID-19 also causes heart failure (HF). COVID-19-induced HF is manifested via different mechanisms, including, but not limited to, (1) virus-induced infiltration of inflammatory cells, which could impair the function of the heart; (2) pro-inflammatory cytokines (monocyte chemoattractant protein-1, interleukin-1β; interleukin-6; tumor necrosis factor-α) that could cause necrosis and death of the myocardium; (3) endothelial injury coupled with micro-thrombosis which could damage the endocardium; and (4) acute respiratory distress syndrome and respiratory failure that could lead to heart failure due to severe hypoxia. It is concluded that the etiology of COVID-19-induced HF is multifactorial and mitigation of the development of HF in patients with COVID-19 will require different approaches such as social distancing, drug therapy, and the urgent development of a vaccine to eradicate the disease.

Long covid—mechanisms, risk factors, and management

“…Studies have shown that sarcomere disruption and fragmentation, enucleation, transcriptional changes, and an intense local immune response occurs in cardiomyocytes infected by SARS-CoV-2 9192. Pathological responses to acute cardiac injury and viral myocarditis, such as endothelial damage and microthrombosis, can lead to the development of coagulopathy,93 while chronic hypoxia and an increase in pulmonary arterial pressure and ventricular strain may further precipitate the incidence of cardiac injury in people who have had covid-19 94. Furthermore, sustained immune activation can lead to fibrotic changes95 and displacement of desmosomal proteins,96 which could be arrhythmogenic.…”

A possible role for ST2 as prognostic biomarker for COVID-19

“…The association between COVID-19 infection and HF has been increasingly demonstrated in the last few months, [ 40 ]. It is currently known that myocarditis, endothelial damage, coagulopathies and respiratory failure can be considered as possible risk factors for the onset of HF in severe COVID-19 patients [ [40] , [41] , [42] ].…”

The SARS-CoV-2/Receptor Axis in Heart and Blood Vessels: A Crisp Update on COVID-19 Disease with Cardiovascular Complications

“…The tropism exhibited by the SARS-CoV-2 virus towards cardiac tissues due to several aforementioned SARS-CoV-2 receptors on the cardiac system, especially on cardiomyocytes and pericytes, could culminate in cardiac injuries, where the virus directly invades into the myocardial cells by binding to the ACE2 receptor to cause myocardial injuries. In addition to this, the bystander effect plays a significant role in mediating cardiac injuries, which include (a) systemic hyper responsiveness due to cytokine storm; (b) cardiac tissue hypoxia due to respiratory failure; (c) coronary plaque destabilization, (d) induction of coronary thrombosis, which are elicited by high SARS-CoV-2 load, are also responsible for cardiac muscle dysfunction and injuries, causing acute or fulminant myocarditis [ 28 , 29 ]. Though direct cardiac injury mediated by SARS-CoV-2 virus is not completely understood, it was evident that this virus does replicate inside cardiomyocytes and are localized at the perinuclear region of the cytoplasm, causing viral-mediated cytopathic effects, including apoptosis which was reflected by the cleaved caspase-3 expression and cessation of beating in 72 h post-infection, as demonstrated by beat rate contractility analysis [ 30 ].…”