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Background: There is conflicting evidence regarding the association between atrial fibrillation (AF) and the risk of subsequent fractures. Methods: We included participants aged 45 years or older from the Framingham Heart Study Offspring, Third Generation, New Offspring Spouse, Omni 1, and Omni 2 cohorts. We prespecified analyzing index age 65 years as our primary analysis; we repeated analyses for index age 45, 55, and 75 years. The primary outcome was any bone fracture, except finger, toe, foot, skull, and facial fractures. We assessed the association between time-varying AF and subsequent fractures by an illness-death model that accounted for the competing risk of death. We estimated hazard ratios (HR) adjusted for age, sex, body mass index, smoking, diabetes, alcohol intake, and prior fracture. Results: We included 3,403 participants (mean age of 68 years, 53.3% female) in the analysis at index age 65 years and above. In all, 525 (15%) participants developed incident fractures during follow-up. The HR between AF and subsequent fracture was 1.36 95%CI (1.05-1.77). There was no evidence of effect modification by sex (HR 1.63, 95%CI 1.05-2.23 in men; HR 1.22, 95%CI 0.84-1.76; interaction p value 0.27). Results were consistent at other index ages. Conclusion: AF was associated with increased risk of incident fracture in the community-based Framingham Heart Study.

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The last three decades have been characterized by an exponential growth in knowledge and advances in the clinical treatment of atrial fibrillation (AF). It is now known that AF genesis requires a vulnerable atrial substrate and that the formation and composition of this substrate may vary depending on comorbid conditions, genetics, sex, and other factors. Population-based studies have identified numerous factors that modify the atrial substrate and increase AF susceptibility. To date, genetic studies have reported seventeen independent signals for AF at fourteen genomic regions. Studies have established that advanced age, male sex, and European ancestry are prominent AF risk factors. Other modifiable risk factors, including sedentary lifestyle, smoking, obesity, diabetes mellitus, obstructive sleep apnea, and elevated blood pressure predispose to AF and each factor has been shown to induce structural and electrical remodeling of the atria. Both heart failure and myocardial infarction increase risk of AF and vice versa creating a feed forward loop that increases mortality. Other cardiovascular outcomes attributed to AF, including stroke and thromboembolism, are well established and epidemiology studies have championed therapeutics that mitigate these adverse outcomes. However, the role of anticoagulation for preventing dementia attributed to AF is less established. Our review is a comprehensive examination of the epidemiological data associating unmodifiable and modifiable risk factors for AF and of the pathophysiological evidence supporting the mechanistic link between each risk factor and AF genesis. Our review also critically examines the epidemiological data on clinical outcomes attributed to AF and summarizes current evidence linking each outcome with AF.

Multiple features in the presentation of randomized controlled trial (RCT) results are known to influence comprehension and interpretation. We aimed to compare interpretation of cancer RCTs with time-to-event outcomes when the reported treatment effect measure is the hazard ratio (HR), difference in restricted mean survival times (RMSTD), or both (HR+RMSTD). We also assessed the prevalence of misinterpretation of the HR.We carried out a randomized experiment. We selected 15 cancer RCTs with statistically significant treatment effects for the primary outcome. We masked each abstract and created three versions reporting either the HR, RMSTD, or HR+RMSTD. We randomized corresponding authors of RCTs and medical residents and fellows to one of 15 abstracts and one of 3 versions. We asked how beneficial the experimental treatment was (0-10 Likert scale). All participants answered a multiple-choice question about interpretation of the HR. Participants were unaware of the study purpose.We randomly allocated 160 participants to evaluate an abstract reporting the HR, 154 to the RMSTD, and 155 to both HR+RMSTD. The mean Likert score was statistically significantly lower in the RMSTD group when compared with the HR group (mean difference -0.8, 95% confidence interval, -1.3 to -0.4, P 0.01) and when compared with the HR+RMSTD group (difference -0.6, -1.1 to -0.1, P = 0.05). In all, 47.2% (42.7%-51.8%) of participants misinterpreted the HR, with 40% equating it with a reduction in absolute risk.Misinterpretation of the HR is common. Participants judged experimental treatments to be less beneficial when presented with RMSTD when compared with HR. We recommend that authors present RMST-based measures alongside the HR in reports of RCT results.

Background Advancing age is a prominent risk factor for atrial fibrillation ( AF ). Shorter telomere length is a biomarker of biological aging, but the link between shorter telomere length and increased risk of AF remains unclear. We examined the association between shorter leukocyte telomere length ( LTL ) and incident AF . Methods and Results We included AF ‐free participants from the observational Framingham Heart Study Offspring cohort from 1995 to 1998, who had LTL measurements. We examined the association between baseline LTL and incident AF with multivariable Cox models adjusted for age, sex, current smoking, height, weight, systolic and diastolic blood pressure, use of antihypertensive medication, diabetes mellitus, history of myocardial infarction, and history of heart failure. The study sample comprised 1143 AF ‐free participants (52.8% women), with mean age of 60±8 years. The mean LTL at baseline was 6.95±0.57 kb. During 15.1±4.2 years mean follow‐up, 184 participants (64 women) developed AF . Chronological age was associated with increased risk of AF (hazard ratio per 10‐year increase, 2.16; 95% confidence interval, 1.71–2.72). There was no significant association between LTL and incident AF (hazard ratio per 1 SD decrease LTL , 1.01; 95% confidence interval, 0.86–1.19). Our study was observational in nature; hence, we could not exclude residual confounding and we were unable to establish causal pathways. Conclusions In our moderate‐sized community‐based cohort, we did not find evidence for a significant association between LTL and risk of incident AF .

Atrial fibrillation (AF) is the most common arrhythmia worldwide and is associated with significant morbidity and mortality. A number of risk factors have been associated with AF, though few studies have explored the association between gastrointestinal and liver diseases and AF. Additionally, AF and treatment for AF may predispose to gastrointestinal and liver diseases. We review the current literature on the bidirectional associations between gastrointestinal and liver diseases and AF. We highlight the gaps in knowledge and areas requiring future investigation.