BackgroundAtrial fibrillation is associated with higher mortality. Identification of causes of death and contemporary risk factors for all‐cause mortality may guide interventions.Methods and ResultsIn the Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Embolism Trial in Atrial Fibrillation (ROCKET AF) study, patients with nonvalvular atrial fibrillation were randomized to rivaroxaban or dose‐adjusted warfarin. Cox proportional hazards regression with backward elimination identified factors at randomization that were independently associated with all‐cause mortality in the 14 171 participants in the intention‐to‐treat population. The median age was 73 years, and the mean CHADS 2 score was 3.5. Over 1.9 years of median follow‐up, 1214 (8.6%) patients died. Kaplan–Meier mortality rates were 4.2% at 1 year and 8.9% at 2 years. The majority of classified deaths (1081) were cardiovascular (72%), whereas only 6% were nonhemorrhagic stroke or systemic embolism. No significant difference in all‐cause mortality was observed between the rivaroxaban and warfarin arms (P=0.15). Heart failure (hazard ratio 1.51, 95% CI 1.33–1.70, P<0.0001) and age ≥75 years (hazard ratio 1.69, 95% CI 1.51–1.90, P<0.0001) were associated with higher all‐cause mortality. Multiple additional characteristics were independently associated with higher mortality, with decreasing creatinine clearance, chronic obstructive pulmonary disease, male sex, peripheral vascular disease, and diabetes being among the most strongly associated (model C‐index 0.677).ConclusionsIn a large population of patients anticoagulated for nonvalvular atrial fibrillation, ≈7 in 10 deaths were cardiovascular, whereas <1 in 10 deaths were caused by nonhemorrhagic stroke or systemic embolism. Optimal prevention and treatment of heart failure, renal impairment, chronic obstructive pulmonary disease, and diabetes may improve survival.Clinical Trial Registration URL: https://www.clinicaltrials.gov/. Unique identifier: NCT00403767.

Cell-free nuclear (cf-nDNA) and mitochondrial (cf-mDNA) DNA are released from damaged cells in type 2 diabetes mellitus (T2DM) patients, contributing to adverse cardiac remodeling, vascular dysfunction, and inflammation. The purpose of this study was to correlate the presence and type of cf-DNAs with HF in T2DM patients. A total of 612 T2DM patients were prescreened by using a local database, and 240 patients (120 non-HF and 120 HF individuals) were ultimately selected. The collection of medical information, including both echocardiography and Doppler imagery, as well as the assessment of biochemistry parameters and the circulating biomarkers, were performed at baseline. The N-terminal brain natriuretic pro-peptide (NT-proBNP) and cf-nDNA/cf-mtDNA levels were measured via an ELISA kit and real-time quantitative PCR tests, respectively. We found that HF patients possessed significantly higher levels of cf-nDNA (9.9 ± 2.5 μmol/L vs. 5.4 ± 2.7 μmol/L; p = 0.04) and lower cf-mtDNA (15.7 ± 3.3 μmol/L vs. 30.4 ± 4.8 μmol/L; p = 0.001) than those without HF. The multivariate log regression showed that the discriminative potency of cf-nDNA >7.6 μmol/L (OR = 1.07; 95% CI = 1.03–1.12; p = 0.01) was higher that the NT-proBNP (odds ratio [OR] = 1.10; 95% confidence interval [CI] = 1.04–1.19; p = 0.001) for HF. In conclusion, we independently established that elevated levels of cf-nDNA, originating from NT-proBNP, were associated with HF in T2DM patients.

BACKGROUND: Endothelial NO-synthase (eNOS) is constitutive enzyme, which expresses in mature endothelial cells and promotes direct vascular dilatation. Single nucleotide polymorphism (SNP) of T786C in eNOS gene may influence on adverse cardiac remodeling after ST-elevation myocardial infarction (STEMI). Purpose of the study was to investigate possible associations between SNP Т786С in eNOS gene and adverse cardiac remodeling after STEMI. METHODS: 177 acute STEMI patients treated with percutaneous coronary intervention and thrombolysis that were admitted to intensive care unit of GI "L.T.Malaya TNI NAMSU" were enrolled in the study. Anthropometry, cardiovascular risk assay, coronary angiography, echocardiography and biomarkers' measure were performed at baseline. The DNA extraction was performed with a commercial kit using real-time polymerase chain reaction PCR. RESULTS: There were correlations between 786СС polymorphism in eNOs gene and adverse cardiac remodeling (r = 0.48; p =0.001), LDL cholesterol (r = 0.32; p =0.012), type 2 diabetes mellitus (r = 0.30; p =0.042), diastolic BP (r =-0.26; p =0.048), unstable angina prior to STEMI (r = 0.25; p =0.047) and total quantity of complicated STEMI (r = 0.23; p =0.042). Additionally, there were not significant relations between 786СС polymorphism in eNOs gene and multiple coronary vessel injury, STEMI localization, levels of circulating biomarkers of myocardial injury, and amount of damaged coronary arteries. Using univariate and multivariate regressive logistic analysis we found that 786СС genotype of eNOS was independent predictor for late adverse LV remodeling (β-coefficient =1.57342; odds ration = 4.8231; 95% confidence interval = 1.5349-15.1552; p =0.0071). CONCLUSION: The polymorphism 786СС in eNOs gene was found as an independent predictor for late adverse cardiac remodeling after STEMI.

Objectives. To assess the outcomes of cavoatrial tumor thrombus removal using the liver transplantation technique for thrombectomy, a retrospective study was conducted. Materials and Methods. Five patients with atrial tumor thrombi who underwent piggy-back mobilization of the liver, surgical access to the right atrium from the abdominal cavity, and external manual repositioning of the thrombus apex below the diaphragm (milking maneuver) were included into the study. Extracorporeal circulation was used in none of the cases. The average length of the atrial component of the tumor was 20.0 ± 11.7 mm (10 to 35 mm), and the width was 14.8 ± 8.5 mm (10 to 30 mm). In this work, the features of patients and surgical interventions as well as perioperative complications and mortality were analyzed. Results. External manual repositioning of the tumor thrombus apex below the diaphragm was successfully performed in all patients. Tumor thrombi with the length of the atrial part up to 1.5 cm were removed through the extrapericardial approach. For evacuation of the thrombi with the large atrial part (3.0 cm or more), a transpericardial surgical approach was required. Specific complications associated with the access to the right atrium from the abdominal cavity (paresis of the right phrenic nerve, pneumothorax, and mediastinitis) were not detected in any case. The average clamping time of the supradiaphragmatic inferior vena cava (IVC) was 6.3 ± 4.6 min. The volume of intraoperative blood loss varied from 2500 to 5600 ml (an average of 3675 ± 1398.5 ml). Conclusion. Our work represents the initial experience in the liver transplantation technique for thrombectomy in distinct and well-selected patients with atrial tumor thrombi. The effectiveness of this approach needs further study. The video presentation of our research took place in March 2019 at the 34th Annual EAU Congress in Barcelona.

Background: The single nucleotide polymorphism of Val66Metgen of the brain-derived neurotrophic factor (BDNF) gene is a possible candidate that is associated with the development of psychopathology and combines it with cardiovascular events. The purpose of this study was to research the possible associations of single-nucleotide polymorphism of Val66Met BDNF gene with the occurrence of endpoints after 6 months of follow-up after ST-segment elevation myocardial infarction (STEMI). Materials and Methods: 256 acute STEMI patients after successful primary percutaneous coronary intervention (PCI) were enrolled in the study. Thrombolysis in myocardial infarction III blood flow restoring through culprit artery was determined. The study of single-nucleotide polymorphism of Val66Met gene BDNF (rs6265) was performed by real-time polymerase chain reaction. The emotional state of the patients and its relationship with stress were assessed with the questionnaire “Depression, Anxiety, and Stress-21”. Results: The frequency of genotypes Val66Met gene for BDNF in STEMI patients (n = 256) was the following: 66ValVal = 74.2% (n = 190), 66ValMet + 66MetMet - 25.8% (n = 66). The 66ValMet + 66MetMet polymorphism in the BDNF gene, stress, and anxiety on 10–14 days before the event, as well as reduced left ventricular ejection fraction, were independently associated with combined 6 months' clinical endpoint after STEMI. Conclusion: The Val66Met polymorphism in BDNF gene was found as an independent predictor for combined 6-month clinical endpoints after acute STEMI-treated primary PCI.