Clinical studies have demonstrated that COVID-19 mortality is predominantly related to thromboembolic disease and coagulation abnormalities, in which the so-called “cytokine storm” and systemic inflammation play an orchestrating role. Inflammation plays an important pathogenic role in atherosclerotic cardiovascular disease in general and in ischemic heart disease in particular. Endothelial dysfunction, hyperinflammation, and coagulopathy contribute to disease severity and death in patients infected with SARS-CoV-2, while also being prevalent features of atherosclerosis. The presence of a cytokine storm in patients with COVID-19 causes ARDS or multiorgan dysfunction, including an increased risk of plaque rupture and direct myocardial injury (i.e., myocarditis), leading to high mortality rates. An optimal regulation of the cytokine storm in the early stages of the disease can contribute to treatment effectiveness and reduce the risk of cardiovascular complications, which are the leading cause of death in these patients.
IL-/TNF- and IFN-Family Cytokines | |
---|---|
Factor | Prognostic Value |
IL-1β | Elevated levels IL-1β have been associated with hypercoagulation, disseminated intravascular coagulation, and severe symptoms [28]. |
IL-2 | Increases in IL-2 or its receptor IL-2R are directly proportional to the severity of the disease [13]. |
IL-4 | IL-4 has negative effects on CD8+ memory T cells; elevated IL-4 levels are associated with cytokine storm and severe respiratory symptoms [29]. |
IL-6 | Higher levels of IL-6 accelerates the inflammatory process, contributing to the cytokine storm and worsening the prognosis [18]. |
IL-12 | NA |
IL-17 | Elevated IL-17 levels have been reported in patients with SARS-CoV-2 as part of the cytokine storm, and they are associated with viral load and disease severity [30]. |
IL-18 | NA |
IL-21 | NA |
IL-33 | Higher IL-33 levels have been associated with lung fibrosis and skeletal muscle wasting [31]. |
TNF-alpha | TNF-alpha was one of the cytokines whose overproduction was related to a poor prognosis in patients with SARS-CoV-2, finding an inverse relationship between TNF-alpha levels and T cell counts [32]. |
TGF-β | NA |
IFN-α | NA |
IFN-γ | IFN-γ levels are associated with greater viral load and lung damage [33]. |
Chemokines | |
CCL2/MCP-1 | CCL2 levels were higher in patients with COVID-19 and even higher among those admitted to the Intensive Care Unit [9]. |
CCL3/MIP-1A | NA |
CCL5 | NA |
CXCL9 | NA |
CXCL10/IP-10 | IP-10 levels were found to be elevated in patients with COVID-19 and even higher in those who required Intensive Care Unit admission, suggesting their relationship with lung damage and disease severity [9]. |
This entry is adapted from the peer-reviewed paper 10.3390/ijms22126607