Abstract
Hypertension is one of the most common risk factors for COVID-19 clinical progression. The identification of plasma biomarkers for anticipating worse clinical outcomes and to better understand the shared mechanisms between hypertension and COVID-19 are needed. A hypothesis-generating study was designed to compare plasma proteomics and metabolomics between 22 hypertensives (HT) and 41 non-hypertensives (nHT) patients with the most unfavorable COVID-19 progression. A total of 43 molecules were significantly differed between HT (n = 22) and nHT (n = 41). Random Forest (RF) analysis identified myo-inositol, gelsolin and phosphatidylcholine (PC) 32:1 as the top molecules for distinguishing between HT and nHT. Plasma myo-inositol and gelsolin were higher (P = 0.03 and P = 0.02, respectively) and plasma PC 32:1 was lower (P = 0.03) in HT compared to nHT. Biological processes like stress response and blood coagulation, along with KEGG pathways including ascorbate and aldarate metabolism (P = 0.021) and linoleic acid metabolism (P = 0.028), were altered in hypertensive patients with the most unfavorable COVID-19 progression. There is a clear link between hypertension and severe COVID-19. Key biological pathways to consider for improving the prognosis and quality of life of hypertensive patients who become infected with SARS-CoV-2 include oxidative stress, ascorbate and aldarate metabolism, lipid metabolism, immune system and inflammation.