Association between red blood cell distribution width and mortality and severity among patients with COVID-19: A systematic review and meta-analysis.

Emerging evidence has underscored the potential usefulness of red blood cell distribution width (RDW) measurement in predicting the mortality and disease severity of COVID-19. This study aimed to assess the association of the plasma RDW levels with adverse prognosis in COVID-19 patients. A comprehensive literature search from inception to September 2020 was performed to harvest original studies reporting RDW on admission and clinical outcomes among patients hospitalized with COVID-19. RDW levels were compared between cases (patients who died or developed more severe symptoms) and controls (patients who survived or developed less severe symptoms). A total of 14,866 subjects from 10 studies were included in the meta-analysis. Higher levels of RDW were associated with adverse outcomes in COVID-19 patients (mean differences = 0.72; 95% CI = 0.47-0.97; I2 = 89.51%). Deceased patients had higher levels of RDW compared to patients who survived (mean differences = 0.93; 95% CI = 0.63-1.23; I2 = 85.58%). Severely ill COVID-19 patients showed higher levels of RDW, as opposed to patients classified to have milder symptoms (mean differences = 0.61; 95% CI = 0.28-0.94; I2 = 82.18%). Elevated RDW levels were associated with adverse outcomes in COVID-19 patients. This finding warrants further research on whether RDW could be utilized as a simple and reliable biomarker for predicting COVID-19 severity and whether RDW is mechanistically linked with COVID-19 pathophysiology.

COVID-19: A double threat to takotsubo cardiomyopathy and spontaneous coronary artery dissection?

Coronavirus disease 2019 (COVID-19) is an ongoing pandemic that has affected millions of individuals worldwide. Prior studies suggest that COVID-19 may be associated with an increased risk for various cardiovascular disorders, such as myocardial injury, arrhythmia, acute coronary syndrome, and venous thromboembolism. Early reports of non-COVID-19 patients have described the concurrence of takotsubo cardiomyopathy (TTC) and spontaneous coronary artery dissection (SCAD). However, the interplay between COVID-19, TTC and SCAD has not been well established. We herein propose two sets of two-hit hypotheses for the development of SCAD and TTC in the context of COVID-19. The first two-hit hypothesis explains the development of SCAD, in which TTC-associated formation of vulnerable coronary substrate serves as the first hit (predisposing factor), and COVID-19-associated inflammation and vascular disruption serves as the second hit (precipitating factor). The second two-hit hypothesis is proposed to explain the development of TTC, in which SCAD-associated formation of vulnerable myocardial substrate serves as the first hit, and COVID-19-associated sympathetic overactivity serves as the second hit. Under this conceptual framework, COVID-19 poses a double threat for the development of SCAD (among patients with underlying TTC) as well as TTC (among patients with underlying SCAD), thereby forming a reciprocal causation. This hypothesis provides a rationale for the joint assessment of TTC and SCAD in COVID-19 patients with pertinent cardiovascular manifestations.