Background The effect of favipiravir on the QTc interval during the treatment of Coronavirus Disease 2019 (COVID-19) patients is unclear. Thus, the current study objective was to evaluate any change in the QTc interval in patients who were hospitalized due to COVID-19 receiving favipiravir treatment. Method Patients hospitalized with COVID-19 were assessed in this single-center retrospective study. 189 patients, whose diagnosis was confirmed using real-time PCR, were included in the study. The patients were divided into three groups: those using hydroxychloroquine (Group 1, n = 66), hydroxychloroquine plus favipiravir (Group 2, n = 66), and favipiravir only (Group 3, n = 57). The QTc interval was measured before treatment (QTc-B) and 48 h after (i.e., the median) starting treatment (QTc-AT). Results The median age was 53 (39–66 IQR) and 97 (51%) of patients were female. The median QTc(Bazett)-change was 7 ms ( p = 0.028) and 12 ms ( p < 0.001) and in Group 1 and 2, respectively. In Group 3, the median QTc(Bazett)-change was observed as −3 ms and was not statistically significant ( p = 0.247). In multivariable analysis, while there was a significant relationship between QTc-AT(Bazett) and hydroxychloroquine (β coefficient = 2687, 95%CI 2599–16,976, p = 0,008), there was no significant relationship with favipiravir (β coefficient = 0,180, 95% CI -6435-7724, p = 0,858). Similarly, there was a significant relationship between the QTc-AT interval calculated using the Fredericia formula and hydroxychloroquine (β coefficient = 2120, 95% CI 0,514–14,398, p = 0,035), but not with favipiravir (β coefficient = 0,111, 95% CI -6450- 7221, p = 0,911). Conclusion In the ECG recordings received in the following days after the treatment was started in COVID-19 patients, there was a significant prolongation in the QTc interval with hydroxychloroquine, but there was no significant change with favipiravir.

Background Recent findings indicate that thrombosis is one of the underlying pathophysiology and complication of COVID‐19 infection. Therefore, the prognosis of the disease may be more favourable in people who were under oral anticoagulant treatment before the COVID‐19 diagnosis. This study aims to evaluate the effects of chronic DOAC use on ICU admission and mortality in hospitalized patients due to COVID‐19 infection. Method Between 1 September and 30 November 2020, 2760 patients hospitalized in our hospital due to COVID‐19 were screened. A total of 1710 patients who met the inclusion criteria were included in the study. The patients were divided into two groups as those who use DOAC due to any cardiovascular disease before the COVID‐19 infection and those who do not. Results Seventy‐nine patients were enrolled in the DOAC group and 1631 patients in the non‐DOAC group. Median age of all study patient was 62 (52‐71 IQR) and 860 (50.5%) of them were female. The need for intensive care, in‐hospital stay, and mechanical ventilation were observed at higher rates in the DOAC group. Mortality was observed in 23 patients (29%) in the DOAC group, and it was statistically higher in the DOAC group ( P = .002). In the multivariable analysis, age (OR: 1.047, CI: 1.02‐1.06, P < .001), male gender (OR: 1.8, CI: 1.3‐2.7, P = .02), lymphocyte count (OR: 0.45, CI: 0.30‐0.69, P < .001), procalcitonin (OR: 1.12, CI: 1.02‐1.23, P = .015), SaO 2 (OR: 0.8, CI: 0.77‐0.82, P < .001) and creatinine (OR: 2.59, CI: 1.3‐5.1, P = .006) were found to be associated with in‐hospital mortality. DOAC treatment was not found to be associated with lower in‐hospital mortality in multivariable analysis (OR:1.17, CI: 0.20‐6.60, P = .850). Conclusion Our study showed that the use of DOAC prior to hospitalization had no protective effect on in‐hospital mortality and intensive care need in hospitalized COVID‐19 patients.

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The non-dipper hypertension (HT) pattern is associated with more end-organ damage and cardiovascular events than is dipper HT. Inflammation is widely established to play a role in the pathophysiology of HT. Recently, a new inflammatory and prognostic marker called the systemic immune-inflammation index (SII) has emerged. Our goal is to determine whether there is a relationship between non-dipper HT and SII. MethodsOur study is a single-center retrospective and ninety-one patients with HT were included. All patients were analyzed with simultaneous 24-hour ambulatory blood pressure monitoring and laboratory parameters. Thirty-five patients had dipper HT while 56 patients had non-dipper HT. SII was calculated according to neutrophil, platelet, and lymphocyte counts. ResultsThe median age was 48 (45-61 interquartile range (IQR)) in the non-dipper HT group, whereas it was 54 (44-64 IQR) in the dipper HT group. Although the neutrophil level, neutrophil-lymphocyte ratio, platelet lymphocyte ratio, SII, sleeping systolic blood pressure (BP), and sleeping diastolic BP were higher (p=0.020, p=0.041, p=0.046, p=0.019, p<0.001, and p=0.001, respectively) in the non-dipper HT group, the lymphocyte level was lower (p=0.040). A multivariate logistic regression model shows that SII (odds ratio (OR)=1.023, 95% confidence interval (CI)=1.002-1.112, p=0.012) may be an independent predictor of non-dipper HT. ConclusionOur study showed that the SII level was higher in the non-dipper HT patient group than in the dipper HT group. Furthermore, SII was an independent predictor of non-dipper HT. The high SII value in hypertension patients can be used as an early warning parameter to identify non-dipper HT patients.