No-reflow can be predicted by systemic inflammation markers including WBC count, NLR and CAR measured from the blood sample obtained on admission. CAR has a higher clinical value than CRP, albumin level, WBC count and NLR in NR prediction.

SYNTAX score II (SS-II) has a powerful prognostic accuracy in patients with stable complex coronary artery disease who have undergone revascularization; however, there is limited data regarding the prognosis of patients with ST segment elevation myocardial infarction (STEMI). The aim of this study is to examine both the predictive performance of SS-II in determining in-hospital and long term mortality of STEMI patients and to compare SYNTAX score (SS) and TIMI risk score (TRS). Consecutive 1912 STEMI patients treated with primary percutaneous coronary intervention (p-PCI) retrospectively reviewed, and the remaining 1708 patients constituted the study population after exclusion. The patients were divided into three groups according to increased SS-II value: low (n:562; SS-II ≤ 24.6); intermediate (n:563; 24.6 < SS-II < 34.4); and high tertile (n:583; SS-II ≥ 34.4). In-hospital and long term mortality rate from all causes (0 vs. 0.5 vs. 10.6% and 1.8 vs. 3.2 vs. 18.1% respectively, p ≤ 0.001) were significantly increased with SS-II tertiles and SS-II was found to be independent predictor of in-hospital and long term mortality (HR: 1.076 95% CI 1.060-1.092, p < 0.001) and (HR: 1.070 95% CI 1.050-1.090, p < 0.0001). The predictive power of SS-II, SS, and TRS were compared by ROC curve and decision curve analysis. SS-II surpassed SS and TRS in long-term and in-hospital mortality prediction. SS-II is a powerful tool to predict in-hospital and long-term mortality from all causes in STEMI patients treated with p-PCI.

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.

Left ventricular diastolic dysfunction (LVDD) is commonly seen in hypertensive patients, and it is associated with increased morbidity and mortality. Hence, the detection of LVDD with a simple, inexpensive, and easy‐to‐obtain method can contribute to improving patient prognosis. Therefore, we aimed to evaluate whether there was any association between the electrocardiographic P wave peak time (PWPT) and invasively measured left ventricular end‐diastolic pressure (LVEDP) in hypertensive patients who had undergone coronary angiography following preliminary diagnosis of coronary artery disease. A total of 78 patients were included in this cross‐sectional study. The PWPT was defined as the time from the beginning of the P wave to its peak, and it was calculated from the leads DII and VI. In all patients, LVEDP was measured in steady state. The PWPT in lead DII was significantly longer in patients with high LVEDP; however, there was no significant difference between groups in terms of PWPT in the lead VI. In multivariable analysis, PWPT in lead DII was found to be independent predictor of increased LVEDP (OR: 1.257, 95% CI: 1.094‐1.445; P = 0.001). In receiver operating characteristic curve analysis, the optimal cut‐off value of PWPT in the lead DII for prediction of elevated LVEDP was 64.8 ms, with a sensitivity of 68.7% and a specificity of 91.3% (area under curve: 0.882, 95% CI: 0.789‐0.944, P < 0.001). In conclusion, this study result suggested that prolonged PWPT in the lead DII may be an independent predictor of increased LVEDP among hypertensive patients.

Introduction and objectives The aim of this study was to investigate the association of serum albumin (SA) level with long‐term prognosis in patients with acute pulmonary embolism (PE). Materials and methods We retrospectively enrolled 269 patients with acute PE. The SA level was obtained within 12‐24 hours following admission. The primary endpoints were the incidence of short‐ and long‐term mortality in acute PE patients. The mean duration of the study follow‐up was 21 ± 19 months. Results During the follow‐up period, short‐ and long‐term mortality rates were higher in patients who had low SA level compared to those who did not have. In multivariate Cox regression analysis, the SA level was found to be independently associated with long‐term mortality (HR: 0.47, 95%CI: 0.28‐0.78, P = 0.004). In receiver operating characteristics analysis, the SA level of ≤3.17 predicted long‐term mortality with a sensitivity of 77.5% and a specificity of 79.5% (area under the curve 0.82, 95%CI: 0.76‐0.87, P < 0.001). In addition, when the SA plus simplified pulmonary embolism severity index (sPESI) risk score compared to the sPESI risk score alone, it produced a net reclassification improvement of 0.22 with P < 0.001, that is a 22% improved classification. Conclusion To the best of our knowledge, this is the first study to demonstrate that the low SA level is a strong and independent predictor for long‐term mortality in patients with acute PE.