Abstract
Patients with underlying cardiovascular conditions are particularly vulnerable to severe COVID-19. In this project, we aimed to characterize similarities in dysregulated immune pathways between COVID-19 patients and patients with cardiomyopathy, venous thromboembolism (VTE), or coronary artery disease (CAD). We hypothesized that these similarly dysregulated pathways may be critical to how cardiovascular diseases (CVDs) exacerbate COVID-19. To evaluate immune dysregulation in different diseases, we used four separate datasets, including RNA-sequencing data from human left ventricular cardiac muscle samples of patients with dilated or ischemic cardiomyopathy and healthy controls; RNA-sequencing data of whole blood samples from patients with single or recurrent event VTE and healthy controls; RNA-sequencing data of human peripheral blood mononuclear cells (PBMCs) from patients with and without obstructive CAD; and RNA-sequencing data of platelets from COVID-19 subjects and healthy controls. We found similar immune dysregulation profiles between patients with CVDs and COVID-19 patients. Interestingly, cardiomyopathy patients display the most similar immune landscape to COVID-19 patients. Additionally, COVID-19 patients experience greater upregulation of cytokine- and inflammasome-related genes than patients with CVDs. In all, patients with CVDs have a significant overlap of cytokine- and inflammasome-related gene expression profiles with that of COVID-19 patients, possibly explaining their greater vulnerability to severe COVID-19.
Highlights
Introduction iationsIn December 2019, widespread infection by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was reported in Wuhan, China [1]
We found a significant overlap between COVID-19 patients and ischemic cardiomyopathy (ICM) and nonischemic dilated cardiomyopathy (NIDCM)
We observe that CASP4 functions in recurrent VTE and COVID-19. These results show that VTE and COVID-19 patients share similar upregulation of inflammation-associated genes, which could explain why rates of venous thromboembolism events are higher in COVID-19 patients, as well as why venous thromboembolism events are associated with higher risk of death in COVID-19 patients [68,69]
Summary
Introduction iationsIn December 2019, widespread infection by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was reported in Wuhan, China [1]. SARS-CoV-2, which causes COVID-19, has spread rapidly, and COVID-19 was declared a pandemic by the World Health Organization (WHO) on 11 March 2020 [2] Current research suggests that patients with existing comorbidities, including hypertension, cardiovascular disease, diabetes, and obesity are more likely to develop severe COVID-19 [3,4,5]. COVID-19 has been known to induce myocardial injury, arrhythmia, acute coronary syndrome, and venous thromboembolism (VTE) [6,7,8]. Such cardiovascular damage has been attributed to cytokine storms triggered by the SARS-CoV-2 infection that can cause multi-organ damage [9,10].
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