COVID-19-Associated Cardiovascular Complications

Abstract

Coronavirus disease 2019 (COVID-19) has been reported to cause cardiovascular complications such as myocardial injury, thromboembolic events, arrhythmia, and heart failure. Multiple mechanisms-some overlapping, notably the role of inflammation and IL-6-potentially underlie these complications. The reported cardiac injury may be a result of direct viral invasion of cardiomyocytes with consequent unopposed effects of angiotensin II, increased metabolic demand, immune activation, or microvascular dysfunction. Thromboembolic events have been widely reported in both the venous and arterial systems that have attracted intense interest in the underlying mechanisms. These could potentially be due to endothelial dysfunction secondary to direct viral invasion or inflammation. Additionally, thromboembolic events may also be a consequence of an attempt by the immune system to contain the infection through immunothrombosis and neutrophil extracellular traps. Cardiac arrhythmias have also been reported with a wide range of implicated contributory factors, ranging from direct viral myocardial injury, as well as other factors, including at-risk individuals with underlying inherited arrhythmia syndromes. Heart failure may also occur as a progression from cardiac injury, precipitation secondary to the initiation or withdrawal of certain drugs, or the accumulation of des-Arg⁹-bradykinin (DABK) with excessive induction of pro-inflammatory G protein coupled receptor B₁ (BK1). The presenting cardiovascular symptoms include chest pain, dyspnoea, and palpitations. There is currently intense interest in vaccine-induced thrombosis and in the treatment of Long COVID since many patients who have survived COVID-19 describe persisting health problems. This review will summarise the proposed physiological mechanisms of COVID-19-associated cardiovascular complications.

Keywords: COVID-19; Long COVID; SARS-CoV-2; cardiovascular system.

Figure 1

Summary of the cardiovascular complications associated with COVID-19.

Figure 2

Summary of the possible pathophysiological mechanisms underlying COVID-19-associated cardiovascular complications. p38 Mitogen-Activated Protein Kinase (p38 MAPK); Angiotensin II (Ang II); T-Helper-1 (Th1); Nicotinamide Adenine Dinucleotide Phosphate Oxidase 2 (Nox2); Neutrophil Extracellular Traps (NETs); von Willebrand (vWF) factor; Toll-Like Receptor (TLR); Tissue-Factor (TF); Damage-Associated Molecular Patterns (DAMPs); Factor VIII (VIII); Human Ether-a-go-go-Related Gene (hERG); Interleukin (IL); Tumour Necrosis Factor (TNF); Des-Arg⁹-Bradykinin (DABK); G-protein coupled receptor B1 (BK₁).