Background and objective: Prevalence of atrial fibrillation is higher in hemodialysis patients as compared to the general population. Atrial electromechanical delay is known as a significant predictor of atrial fibrillation. In this study, we aimed to reveal the relationship between atrial electromechanical delay and attacks of atrial fibrillation. Materials and methods: The study included 77 hemodialysis patients over 18 years of age giving written consent to participate in the study. The patients were divided into two groups based on the results of 24-h Holter Electrocardiogram (Holter ECG) as the ones having attacks of atrial fibrillation and the others without any attack of atrial fibrillation. Standard echocardiographic measurements were taken from all patients. Additionally, atrial conduction times were measured by tissue Doppler technique and atrial electromechanical delays were calculated. Results: Intra- and interatrial electromechanical delay were found as significantly lengthened in the group of patients with attacks of atrial fibrillation (p = 0.03 and p < 0.001 respectively). The optimal cut-off time for interatrial electromechanical delay to predict atrial fibrillation was >21 ms with a specificity of 79.3% and a sensitivity of 73.7% (area under the curve 0.820; 95% confidence interval (CI), 0.716–0.898). In the multivariate logistic regression model, interatrial electromechanical delay (odds ratio = 1.230; 95% CI, 1.104–1.370; p < 0.001) and hypertension (odds ratio = 4.525; 95% CI, 1.042–19.651; p = 0.044) were also associated with atrial fibrillation after adjustment for variables found to be statistically significant in univariate analysis and correlated with interatrial electromechanical delay. Conclusions: Interatrial electromechanical delay is independently related with the attacks of atrial fibrillation detected on Holter ECG records in hemodialysis patients.

Background: Chronic thromboembolic pulmonary hypertension (CTEPH) is a disease characterized by right heart failure following recurrent pulmonary embolism (PE). It is important to know the predictors of the development of CTEPH after PE as it is a treatable cause of pulmonary arterial hypertension. Soluble ST2 is a biomarker closely associated with heart failure and the inflammatory process. The aim of this study was to investigate the relationship between sST2 level and the development of CTEPH in patients with PE. Methodology: Baseline characteristics, electrocardiographic findings, laboratory findings, transthoracic echocardiography (TTE) findings, location, and extent of involvement in CT pulmonary angiography were recorded in 100 patients with acute PE included in our prospective study. Treatment modalities and treatment durations were followed. Ventilation-perfusion scintigraphy was performed in patients with a systolic pulmonary artery pressure (sPAP) of 35 mmHg or more on TTE and residual thrombus on CT pulmonary angiography after at least three months of anticoagulant use. In the case of findings compatible with CTEPH in these examinations, patients were diagnosed with CTEPH by right heart catheterization. The sST2 levels obtained from all patients at admission were evaluated between the groups of patients with and without CTEPH. Results: CTEPH was observed in 11 of the 100 patients who participated in the trial, with a median follow-up of 284 ± 60 days. The mean age of the 11 patients with CTEPH was 67 ± 10 years; five were males and six were females. The mean age of 89 patients without CTEPH was 65 ± 18 years, 36 were males and 53 were females. The sST2 values of the group with CTEPH were found to be statistically significantly higher than those of patients without CTEPH [193.7 (184.3-244.7) vs 58.6 (29.5-122.9) p=0.020]. This receiver operating characteristic (ROC) curve shows that the optimal cutoff point of sST2 levels in the prediction of CTEPH was > 157.4 with specificity of 83.7% and sensitivity of 81.8% (area under the curve = 0.783; 95% CI, 1.005-1.027; p < 0.001). Conclusion: In acute PE patients, sST2 levels may be a useful biomarker to predict the development of CTEPH.

Objectives: Advanced heart failure is the last stage of heart failure in which the life expectancy of patients is significantly reduced. Many mortality markers have been identified in advanced heart failure. Although the nesfatin-1 molecule is known as a satiety hormone, it has also been shown to be associated with many cardiovascular diseases. This study aims to elucidate the association between in-hospital mortality and nesfatin-1 level in advanced heart failure patients. Methods: The research included 74 cases of advanced heart failure. During the coronary intensive care surveillance of these patients, 22 patients had in-hospital mortality. The cases, divided into groups with and without in-hospital mortality, were compared using laboratory data, echocardiography, and demographic properties. Results: The age of the cases with in-hospital mortality was older than the cases without mortality [(74 (66–95) vs. 67 (26–90); p=0.019)]. Serum nesfatin-1 level and tricuspid annular plane systolic excursion (TAPSE) were statistically lower in the in-hospital mortality group (43.8 ± 5.5 vs. 40.5 ± 6.1; p=0.027, 13.5 ± 1.9 vs. 16.2 ± 2.6 p=0.001, respectively). Serum nesfatin-1 level and TAPSE were detected as independent predictors for in-hospital mortality in advanced heart failure via multivariate analysis using parameters that were significant in the univariate analysis. Receiver operator characteristic curve analysis showed that the optimum cut-off level for nesfatin-1 in determining in-hospital mortality was ≤23.57 (pg/mL) with a specificity of 73.1 % and a sensitivity of 77.3 % (AUC=0.763, 95 % CI=0.647–0.879, p<0.001). Conclusions: This research revealed that in advanced heart failure patients, serum nesfatin-1 amounts are associated with mortality and seem to be an independent predictor of mortality.

Background and Objectives: The risk of autonomic dysfunction with COVID-19 vaccines used worldwide in the COVID-19 pandemic remains a topic of debate. Heart rate variability has a number of parameters that can be used to assess autonomic nervous system dynamics. The aim of this study was to investigate the effect of a COVID-19 vaccine (Pfizer-BioNTech) on heart rate variability and autonomic nervous system parameters, and the duration of the effect. Materials and Methods: A total of 75 healthy individuals who visited an outpatient clinic to receive the COVID-19 vaccination were included in this prospective observational study. Heart rate variability parameters were measured before vaccination and on days 2 and 10 after vaccination. SDNN, rMSSD and pNN50 values were evaluated for time series analyses, and LF, HF, and LF/HV values for frequency-dependent analyses. Results: The SDNN and rMSDD values declined significantly on day 2 after vaccination, while the pNN50 and LF/HF values increased significantly on day 10. The values at pre-vaccination and at day 10 were comparable. The pNN50 and LF/HF values declined significantly on day 2 and increased significantly on day 10. The values at pre-vaccination and at day 10 were comparable. Conclusions: This study showed that the decline in HRV observed with COVID-19 vaccination was temporary, and that the Pfizer-BioNTech COVID-19 vaccination did not cause permanent autonomic dysfunction.

Adrenomedullin and non-dipping circadian pattern in newly diagnosed essential hypertension