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Background Patients with atrial fibrillation (AF) face an increased risk of death and major adverse cardiovascular events (MACE). We aimed to assess the predictive value of the novel atrial‐specific biomarker BMP10 (bone morphogenetic protein 10) for death and MACE in patients with AF in comparison with NT‐proBNP (N‐terminal prohormone of B‐type natriuretic peptide). Methods and Results BMP10 and NT‐proBNP were measured in patients with AF enrolled in Swiss‐AF (Swiss Atrial Fibrillation Study), a prospective multicenter cohort study. A total of 2219 patients were included (median follow‐up 4.3 years [interquartile range 3.9, 5.1], mean age 73±9 years, 73% male). In multivariable Cox proportional hazard models, the adjusted hazard ratio (aHR) associated with 1 ng/mL increase of BMP10 was 1.60 (95% CI, 1.37–1.87) for all‐cause death, and 1.54 (95% CI, 1.35–1.76) for MACE. For all‐cause death, the concordance index was 0.783 (95% CI, 0.763–0.809) for BMP10, 0.784 (95% CI, 0.765–0.810) for NT‐proBNP, and 0.789 (95% CI, 0.771–0.815) for both biomarkers combined. For MACE, the concordance index was 0.732 (95% CI, 0.715–0.754) for BMP10, 0.747 (95% CI, 0.731–0.768) for NT‐proBNP, and 0.750 (95% CI, 0.734–0.771) for both biomarkers combined. When grouping patients according to NT‐proBNP categories (900 ng/L), higher aHRs were observed in patients with high BMP10 in the categories of low NT‐proBNP (all‐cause death aHR, 2.28 [95% CI, 1.15–4.52], MACE aHR, 1.88 [95% CI, 1.07–3.28]) and high NT‐proBNP (all‐cause death aHR, 1.61 [95% CI, 1.14–2.26], MACE aHR, 1.38 [95% CI, 1.07–1.80]). Conclusions BMP10 strongly predicted all‐cause death and MACE in patients with AF. BMP10 provided additional prognostic information in low‐ and high‐risk patients according to NT‐proBNP stratification. Registration URL: https://www.clinicaltrials.gov ; Unique identifier: NCT02105844.

Background Previous randomized control trials showed mixed results concerning the effect of omega-3 fatty acids (n-3 FAs) on atrial fibrillation (AF). The associations of n-3 FA blood levels with heart rhythm in patients with established AF are unknown. The goal of this study was to assess the associations of total and individual n-3 FA blood levels with AF type (paroxysmal versus nonparoxysmal), heart rate (HR), and HR variability in patients with AF. Methods and Results Total n-3 FAs, eicosapentaenoic acid, docosahexaenoic acid, docosapentaenoic acid, and alpha-linolenic acid blood levels were determined in 1969 patients with known AF from the SWISS-AF (Swiss Atrial Fibrillation cohort). Individual and total n-3 FAs were correlated with type of AF, HR, and HR variability using standard logistic and linear regression, adjusted for potential confounders. Only a mild association with nonparoxysmal AF was found with total n-3 FA (odds ratio [OR], 0.97 [95% CI, 0.89-1.05]) and docosahexaenoic acid (OR, 0.93 [95% CI, 0.82-1.06]), whereas other individual n-3 FAs showed no association with nonparoxysmal AF. Higher total n-3 FAs (estimate 0.99 [95% CI, 0.98-1.00]) and higher docosahexaenoic acid (0.99 [95% CI, 0.97-1.00]) tended to be associated with slower HR in multivariate analysis. Docosapentaenoic acid was associated with a lower HR variability triangular index (0.94 [95% CI, 0.89-0.99]). Conclusions We found no strong evidence for an association of n-3 FA blood levels with AF type, but higher total n-3 FA levels and docosahexaenoic acid might correlate with lower HR, and docosapentaenoic acid with a lower HR variability triangular index.

BACKGROUND The effect of the ventricular repolarization heterogeneity has not been systematically assessed in patients with atrial fibrillation (AF). Aim of this study is to assess ventricular repolarization heterogeneity as predictor of cardiovascular (CV) death and/or other CV events in patients with AF. METHODS From the multicenter prospective Swiss-AF (Swiss Atrial Fibrillation) Cohort Study, we enrolled 1711 patients who were in sinus rhythm (995) or AF (716). Resting ECG recordings of 5-min duration were obtained at baseline. Parameters assessing ventricular repolarization were computed (QTc, Tpeak-Tend, J-Tpeak and V-index). RESULTS During AF, the V-index was found repeatable (no differences when computed over the whole recording, on the first 2.5-min and on the last 2.5-min segments). During a mean follow-up time of 2.6��������1.0���years, 90 patients died for CV reasons. In bivariate Cox regression analysis (adjusted for age only), the V-index was associated with an increased risk of CV death, both in the subgroup of patients in sinus rhythm (SR) as well as those in AF. In multivariate analysis adjusted for clinical risk factors and medications, both prolonged QTc and V-index were independently associated with an increased risk of CV death (QTc: hazard ratio [HR] 2.78, 95% CI 1.79-4.32, p���

BACKGROUND Atrial fibrillation (AF) is associated with cognitive dysfunction. However, neurocognitive function in AF patients undergoing pulmonary vein isolation (PVI) has not been well studied. The aim of this analysis is to compare neurocognitive function in patients who did or did not undergo PVI. MATERIALS AND METHODS We used data from the Swiss Atrial Fibrillation Cohort study (Swiss-AF), a prospective, observational, multicenter study in Switzerland. Patients with documented AF were enrolled and data of 1,576 patients without history of PVI and with complete information on PVI status and neurocognitive function were used. Information on PVI was collected at baseline and during 1 year of follow-up. Neurocognitive testing was performed at baseline and after 1 year of follow-up, using the Montreal Cognitive Assessment (MoCA), trail making test (TMT) A and B, digit symbol substitution test (DSST) and semantic fluency test (SFT). To investigate the association of PVI with neurocognitive function, we use propensity score matching (1:3) and inverse probability of treatment weighting (IPTW). RESULTS The mean age of this population was 74 ± 8 years, 27.1% were women. Overall, 88 (5.5%) patients underwent PVI during 1 year of follow-up. Using ITPW (n = 1576), PVI was weakly associated with the MoCA score after adjusting for time since PVI, baseline MoCA score and other covariates (β (95%CI) 1.19 (0.05; 2.32), p = 0.04). In the propensity matched comparison (n = 352), there was no significant association between PVI and the MoCA score (β (95%CI) 1.04 (-0.19; 2.28), p = 0.1). There were no significant associations between PVI and cognitive function when using the TMT A and B, DSST or SFT independent of the method used. CONCLUSION In this population of AF patients, there was no consistent evidence of an association between PVI and neurocognitive function. CLINICAL TRIAL REGISTRATION [https://clinicaltrials.gov/], identifier [NCT02105844].

Background Diabetes is a major risk factor for atrial fibrillation (AF). However, it remains unclear whether individual AF phenotype and related comorbidities differ between patients who have AF with and without diabetes. This study investigated the association of diabetes with AF phenotype and cardiac and neurological comorbidities in patients with documented AF. Methods and Results Participants in the multicenter Swiss-AF (Swiss Atrial Fibrillation) study with data on diabetes and AF phenotype were eligible. Primary outcomes were parameters of AF phenotype, including AF type, AF symptoms, and quality of life (assessed by the European Quality of Life-5 Dimensions Questionnaire [EQ-5D]). Secondary outcomes were cardiac (ie, history of hypertension, myocardial infarction, and heart failure) and neurological (ie, history of stroke and cognitive impairment) comorbidities. The cross-sectional association of diabetes with these outcomes was assessed using logistic and linear regression, adjusted for age, sex, and cardiovascular risk factors. We included 2411 patients with AF (27.4% women; median age, 73.6��years). Diabetes was not associated with nonparoxysmal AF (odds ratio [OR], 1.01; 95% CI, 0.81-1.27). Patients with diabetes less often perceived AF symptoms (OR, 0.74; 95% CI, 0.59-0.92) but had worse quality of life (��=-4.54; 95% CI, -6.40 to -2.68) than those without diabetes. Patients with diabetes were more likely to have cardiac (hypertension [OR, 3.04; 95% CI, 2.19-4.22], myocardial infarction [OR, 1.55; 95% CI, 1.18-2.03], heart failure [OR, 1.99; 95% CI, 1.57-2.51]) and neurological (stroke [OR, 1.39, 95% CI, 1.03-1.87], cognitive impairment [OR, 1.75, 95% CI, 1.39-2.21]) comorbidities. Conclusions Patients who have AF with diabetes less often perceive AF symptoms but have worse quality of life and more cardiac and neurological comorbidities than those without diabetes. This raises the question of whether patients with diabetes should be systematically screened for silent AF. Registration URL: https://www.clinicaltrials.gov; Unique Identifier: NCT02105844.

AIMS We aimed to investigate the association of clinically overt and silent brain lesions with cognitive function in atrial fibrillation (AF) patients. METHODS AND RESULTS We enrolled 1227 AF patients in a prospective, multicentre cohort study (Swiss-AF). Patients underwent standardized brain magnetic resonance imaging (MRI) at baseline and after 2 years. We quantified new small non-cortical infarcts (SNCIs) and large non-cortical or cortical infarcts (LNCCIs), white matter lesions (WML), and microbleeds (Mb). Clinically, silent infarcts were defined as new SNCI/LNCCI on follow-up MRI in patients without a clinical stroke or transient ischaemic attack (TIA) during follow-up. Cognition was assessed using validated tests. The mean age was 71 years, 26.1% were females, and 89.9% were anticoagulated. Twenty-eight patients (2.3%) experienced a stroke/TIA during 2 years of follow-up. Of the 68 (5.5%) patients with ���1 SNCI/LNCCI, 60 (88.2%) were anticoagulated at baseline and 58 (85.3%) had a silent infarct. Patients with brain infarcts had a larger decline in cognition [median (interquartile range)] changes in Cognitive Construct score [-0.12 (-0.22; -0.07)] than patients without new brain infarcts [0.07 (-0.09; 0.25)]. New WML or Mb were not associated with cognitive decline. CONCLUSION In a contemporary cohort of AF patients, 5.5% had a new brain infarct on MRI after 2 years. The majority of these infarcts was clinically silent and occurred in anticoagulated patients. Clinically, overt and silent brain infarcts had a similar impact on cognitive decline. CLINICAL TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT02105844, https://clinicaltrials.gov/ct2/show/NCT02105844. KEY QUESTION The incidence of clinically overt and silent brain infarcts, white matter lesions, and microbleeds, and their impact on cognition in atrial fibrillation (AF) patients are not known. KEY FINDING Over 2 years of follow-up, 5.5% of AF patients developed new brain infarcts, with the majority of them being clinically silent and occurring in anticoagulated patients. New clinically overt and silent brain infarcts were similarly associated with cognitive decline. TAKE-HOME MESSAGE In a contemporary cohort of AF patients, new brain infarcts are frequent despite a high anticoagulation rate. Our data suggest that anticoagulation alone may not be sufficient to prevent brain damage and cognitive decline in all AF patients.

OBJECTIVE The optimal target heart rate in patients with prevalent atrial fibrillation (AF) is not well defined. The aim of this study was to analyse the associations between heart rate and adverse outcomes in a large contemporary cohort of patients with prevalent AF. METHODS From two prospective cohort studies, we included stable AF outpatients who were in AF on the baseline ECG. The main outcome events assessed during prospective follow-up were heart failure hospitalisation, stroke or systemic embolism and death. The associations between heart rate and adverse outcomes were evaluated using multivariable Cox regression models. RESULTS The study population consisted of 1679 patients who had prevalent AF at baseline. Mean age was 74 years, and 24.6% were women. The mean heart rate on the baseline ECG was 78 (±19) beats per minute (bpm). The median follow-up was 3.9 years (IQR 2.2-5.0). Heart rate was not significantly associated with heart failure hospitalisation (adjusted HR (aHR) per 10 bpm increase, 1.00, 95% CI 0.94 to 1.07, p=0.95), stroke or systemic embolism (aHR 0.95, 95% CI 0.84 to 1.07, p=0.38) or death (aHR 1.02, 95% CI 0.95 to 1.09, p=0.66). There was no evidence of a threshold effect for heart rates 100 bpm. CONCLUSIONS In this large contemporary cohort of outpatients with prevalent AF, we found no association between heart rate and adverse outcome events. These data are in line with recommendations that strict heart rate control is not needed in otherwise stable outpatients with AF.