Background: Biomarkers were correlated with mortality in critically ill COVID-19 patients. No prediction tools exist for noncritically ill COVID-19 patients. We aimed to compare the independent prognostic value of inflammation and cardiac biomarkers for post-acute COVID-19 patients and the 30-day mortality rate in noncritically ill COVID-19 patients, as well as the relation with the virus variant involved. Methods: This observational cohort study was conducted at an emergency clinical hospital between 1 October 2020 and 31 December 2021. We included consecutive patients with biomarkers determined within 24 h of presentation, followed up at least 30 days postdischarge. Results: Post-acute COVID-19 was diagnosed in 20.3% of the cases and the all-cause 30-day mortality rate was 35.1% among 978 patients infected with variants of concern. Neutrophil-to-lymphocyte ratio (1.06 [95%CI, 1.01–1.11], p = 0.015) and NT-pro BNP were correlated with 30-daymortality, while the monocyte-to-lymphocyte ratio (2.77 [95%CI, 1.10–6.94], p = 0.03) and NT-pro BNP (1.68 [95%CI, 1.00–2.84], p = 0.05) were correlated with post-acute COVID-19. High-sensitivity to troponin was associated with 30-day mortality (1.55 [95%CI, 1.00–2.42], p = 0.05). A Cox proportional-hazards model confirmed that NT-pro BNP was independently associated with mortality. NT-pro BNP remained independently associated with 30-day mortality during follow-up (1.29 [95%CI, 1.07–1.56], p = 0.007) after adjustment for confounders. Conclusion: Inflammation and cardiac biomarkers, determined upon admission and predischarge, in a cohort of hospitalized noncritically ill COVID-19 patients throughout successive pandemic waves, showed a predictive value for post-acute COVID-19 and 30-day mortality.
Magnesium is the fourth most common mineral in the human body and the second richest intracellular cation. This element is necessary for many physiological reactions, especially in the cardiovascular and respiratory systems. COVID-19 is an infectious disease caused by SARS-CoV-2. The majority of people who become ill as a result of COVID-19 have mild-to-moderate symptoms and recover without specific treatment. Moreover, there are people who develop severe forms of COVID-19, which require highly specialized medical assistance. Magnesium deficiency may play a role in the pathophysiology of infection with SARS-CoV-2. The primary manifestation of COVID-19 remains respiratory, but the virus can spread to other organs and tissues, complicating the clinical picture and culminating in multiorgan failure. The key mechanisms involved in the disease include direct viral cytotoxicity, endothelial dysfunction, and exaggerated release of inflammatory cytokines. The aim of this review was to summarize the available data regarding the role of magnesium in COVID-19 patients and its particularities in different clinical settings.
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