We aimed to investigate association between mean platelet volume (MVP), platelet distribution width (PDW) and red cell distribution width (RDW) and mortality in patients with COVID-19 and find out in which patients the use of acetylsalicylic acid (ASA) affects the prognosis due to the effect of MPV on thromboxan A2. A total of 5142 patients were divided into those followed in the intensive care unit (ICU) and those followed in the ward. Patient medical records were examined retrospectively. ROC analysis showed that the area under curve (AUC) values were 0.714, 0.750, 0.843 for MPV, RDW and D-Dimer, the cutoff value was 10.45fl, 43.65fl, 500.2 ng/mL respectively. (all P < .001). Survival analysis showed that patients with MPV >10.45 f/l and D-Dimer >500.2 ng/mL, treatment with ASA had lower in-hospital and 180-day mortality than patients without ASA in ICU patients (HR = 0.773; 95% CI = 0.595-0.992; P = .048, HR = 0.763; 95% CI = 0.590-0.987; P = .036). Administration of low-dose ASA in addition to anti-coagulant according to MPV and D-dimer levels reduces mortality.

Purpose Atrial fibrillation (AF) is relatively frequent in the postoperative period, and is associated with an increased frequency of adverse events. The role of right atrial (RA) volume and functions in the development of AF is unknown. In this study, we investigated the effect of RA echocardiographic indices on AF development in the postoperative period. Method We enrolled 142 consecutive patients who underwent coronary artery bypass surgery, and assigned them into two groups depending on the occurrence or not of AF development in the postoperative period. Results A propensity score matching analysis was performed to balance the groups, and 37 pairs were eventually included in the analysis. The median age was 67.5 (63‐75) years and 73.3% of them were males. In the univariate analysis, right atrial volume index (RAVi), right atrial strain during reservoir phase (RASr), left ventricular global longitudinal strain, right ventricular strain, left atrial volume index, left atrial strain during reservoir phase, and systolic pulmonary artery pressure were associated with AF development. In the regression analysis, we found that RAVi (OR: 3.1, 95% CI: 2.2‐6.3, P: .033) and RASr (OR: 0.82, 95% CI: 0.67‐0.93, P: .048) were independent predictors of AF development. Conclusions RA structure and functions are closely associated with AF development in the postoperative period, and screening of RA functions prior to surgery may be useful for preventing AF development.

Recent trials reported that risk of atrial fibrillation (AF) is increased in patients using ivabradine compared with controls. We performed this meta-analysis to investigate the risk of AF association with ivabradine treatment on the basis of data obtained from randomized controlled trials (RCTs). We searched PubMed, EMBASE, Scopus, and the Cochrane Library for RCTs that comprised >100 patients. The incidence of AF was assessed. We obtained data from European Medicines Agency (EMA) scientific reports for the RCTs in which the incidence of AF was not reported. We used trial sequential analysis (TSA) to provide information on when we had reached firm evidence of new AF based on a 15% relative risk increase (RRI) in ivabradine treatment. Three RCTs and 1 EMA overall oral safety set (OOSS) pooled analysis (included 5 RCTs) were included in the meta-analysis (N = 40 437). The incidence of AF was 5.34% in patients using ivabradine and 4.56% in placebo. There was significantly higher incidence of AF (24% RRI) in the ivabradine group when compared with placebo before (RR: 1.24, 95% confidence interval: 1.08-1.42, P = 0.003, I 1980 = 53%) and after excluding OOSS (RR: 1.24, 95% confidence interval: 1.06-1.44, P = 0.008). In the TSA, the cumulative z-curve crossed both the traditional boundary (P = 0.05) and the trial sequential monitoring boundary, indicating firm evidence for ≥15% increase in ivabradine treatment when compared with placebo. Study results indicate that AF is more common in the ivabradine group (24% RRI) than in controls.

(1) To investigate the role of azurocidin, an antimicrobial protein, in patients with ST segment elevation myocardial infarction (STEMI). (2) This single-center prospective observational study included patients with STEMI and healthy age- and sex-matched control subjects. Baseline demographic, clinical and biochemical data were compared between the two groups. Azurocidin levels at baseline were determined using an enzyme-linked immunosorbent assay. Multivariate linear regression analysis with enter method was used to test the association between azurocidin and independent variables, such as the thrombolysis in myocardial infarction (TIMI) score, synergy between percutaneous coronary intervention with TAXUS and cardiac surgery score, global registry of acute coronary events score, Killip class, C-reactive protein (CRP), and creatinine kinase-myocardial band (CK-MB). (3) A total of 76 patients with STEMI and 30 healthy control subjects were enrolled in the study. Mean ± SD azurocidin levels were significantly higher in patients compared with healthy controls (18.07 ± 13.99 versus 10.09 ± 5.29 ng/mL, respectively). In a receiver-operating characteristic curve analysis, an azurocidin cut-off level of >11.46 ng/mL had 74% sensitivity and 58% specificity in predicting myocardial infarction. Azurocidin levels had a positive correlation with TIMI score (r = 0.651). In multivariate linear regression analysis, the TIMI score was an independent predictor of the azurocidin level. (4) Azurocidin is an infection marker that may be important in patients with STEMI.