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.

ObjectivePostpericardiotomy syndrome (PPS), which is thought to be related to autoimmune phenomena, represents a common postoperative complication in cardiac surgery. Late pericardial effusions after cardiac surgery are usually related to PPS and can progress to cardiac tamponade. Preventive measures can reduce postoperative morbidity and mortality related to PPS. In a previous study, diclofenac was suggested to ameliorate autoimmune diseases. The aim of this study was to determine whether postoperative use of diclofenac is effective in preventing early PPS after cardiac surgery.MethodsA total of 100 patients who were administered oral diclofenac for postoperative analgesia after cardiac surgery and until hospital discharge were included in this retrospective study. As well, 100 patients undergoing cardiac surgery who were not administered nonsteroidal anti-inflammatory drugs were included as the control group. The existence and severity of pericardial effusion were determined by echocardiography. The existence and severity of pleural effusion were determined by chest X-ray.ResultsPPS incidence was significantly lower in patients who received diclofenac (20% vs 43%) (P<0.001). Patients given diclofenac had a significantly lower incidence of pericardial effusion (15% vs 30%) (P=0.01). Although not statistically significant, pericardial and pleural effusion was more severe in the control group than in the diclofenac group. The mean duration of diclofenac treatment was 5.11±0.47 days in patients with PPS and 5.27±0.61 days in patients who did not have PPS (P=0.07). Logistic regression analysis demonstrated that diclofenac administration (odds ratio [OR] 0.34, 95% confidence interval [CI] 0.18–0.65, P=0.001) was independently associated with PPS occurrence.ConclusionPostoperative administration of diclofenac may have a protective role against the development of PPS after cardiac surgery.

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AimThe pathophysiology of slow coronary flow (SCF) involves atherosclerosis, small vessel dysfunction, platelet function disorders, and inflammation. It has been known that eosinophils also play a significant role in inflammation, vasoconstriction, thrombosis, and endothelial dysfunction. We propose to evaluate the relationship between eosinophilia and SCF.MethodsAll patients who underwent coronary angiography between January 2011 and December 2013 were screened retrospectively. Of 6,832 patients, 102 patients with SCF (66 males, mean age 52.2±11.7 years) and 77 control subjects with normal coronary angiography (50 males, mean age 50.7±8.1 years) were detected. Baseline characteristics, hematological test results, and biochemical test results were obtained from the hospital database.ResultsBaseline characteristics of the study groups were comparable between groups. There was no significant difference between groups regarding leukocyte count, paletelet count, and mean platelet volume. However, patients with SCF had a higher eosinophil count than the controls (0.24±0.17×103/μL vs 0.16±0.15×103/μL, P=0.002). In addition, eosinophil count was found to be correlated with thrombolysis in myocardial infarction (TIMI) frame count in the SCF group (r=0.3, P<0.01). There was no significant correlation between eosinophil count and the number of coronary arteries showing slow flow.ConclusionPatients with SCF have higher blood eosinophil count, and this may play an important role in the pathogenesis of SCF. Elevated baseline eosinophil count may indicate the presence of SCF.

Nadir hematocrit levels on CPB less than 20% and allogenic blood transfusions were independently associated with postoperative hyperglycemia in nondiabetic patients. Patients with a nadir hematocrit levels less than 20 % during CPB should be closely monitored for hyperglycemia in the perioperative period.