Introduction: Atrial fibrillation (AF) is the most common cardiac arrhythmia, affecting millions of individuals. Left atrial (LA) strain, a measure of LA function and remodeling, holds potential as a prognostic indicator for AF development. We aimed to examine whether LA strain is associated with new onset AF. Methods: We performed a nested case-control study within an electronic health record-based longitudinal cohort of primary care patients from a multi-institutional healthcare system spanning 2001 to 2018. Cases included patients who developed new-onset AF during a follow-up period of 7.3 years and had undergone transthoracic echocardiography (TTE) within three years of the follow-up start. Several LA strain parameters were compared between the case and control groups, including Peak Atrial Longitudinal Strain (PALS), Left Atrial Conduit Strain (LACS), and Peak Atrial Contraction Strain (PACS). Results: The study included 216 patients who developed AF during follow-up each matched with a corresponding age- and sex-matched control without AF. The AF group had significantly lower PALS (25.9 ± 8.9 vs. 34.3 ± 10.4, p<0.001) and LACS (13.6 ± 5.2 vs. 19.9 ± 7.6, p<0.001) compared to the non-AF group. Subgroup analyses of AF patients, stratified by the time to AF development, revealed more substantial differences between the AF and non-AF groups when the initial TTE was conducted closer to the onset of AF. Specifically, when the TTE was performed within 2 years prior to AF onset, the disparities in LA strain parameters were more pronounced compared to TTEs conducted between 2-5 years prior or beyond 5 years prior to AF onset. Conclusions: Impaired left atrial strain is strongly associated with new-onset AF, particularly when measured 2 years prior to AF onset, indicating a higher risk of developing AF in the near future. Incorporating LA strain assessment into clinical decision-making can enhance the evaluation of individuals at risk for AF.

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Background There is conflicting evidence regarding the association between atrial fibrillation 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 ages 45, 55, and 75 years. The primary outcome was any incident bone fracture, except finger, toe, foot, skull, and facial fractures. We assessed the association between time-varying atrial fibrillation 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 3403 participants (mean age of 68 years, 53.3% female) in the analysis at index age 65 years and above. In all, 525 (15%) participants suffered incident fractures during follow-up (median 12.5 years). The HR between atrial fibrillation and subsequent fracture was 1.37; 95% confidence interval (CI), 1.06-1.79. There was no evidence of effect modification by sex (HR 1.55; 95% CI, 1.06-2.26 in men; HR 1.22; 95% CI, 0.84-1.77 in women; interaction P value .27). Results were consistent at other index ages. Conclusion Atrial fibrillation was associated with increased risk of incident fracture in the community-based Framingham Heart Study.

Background Frailty is associated bidirectionally with cardiovascular disease. However, the relations between frailty and atrial fibrillation (AF) have not been fully elucidated. Methods and Results Using the FHS (Framingham Heart Study) Offspring cohort, we sought to examine both the association between frailty (2005–2008) and incident AF through 2016 and the association between prevalent AF and frailty status (2011–2014). Frailty was defined using the Fried phenotype. Models adjusted for age, sex, and smoking. Cox proportional hazards models, adjusted for competing risk of death, assessed the association between prevalent frailty and incident AF. Logistic regression models assessed the association between prevalent AF and new‐onset frailty. For the incident AF analysis, we included 2053 participants (56% women; mean age, 69.7±6.9 years). By Fried criteria, 1018 (50%) were robust, 903 (44%) were prefrail, and 132 (6%) were frail. In total, 306 incident cases of AF occurred during an average 9.2 (SD, 3.1) follow‐up years. After adjustment, there was no statistically significant association between prevalent frailty status and incident AF (prefrail versus robust: hazard ratio [HR], 1.22 [95% CI, 0.95–1.55]; frail versus robust: HR, 0.92 [95% CI, 0.57–1.47]). At follow‐up, there were 111 new cases of frailty. After adjustment, there was no statistically significant association between prevalent AF and new‐onset frailty (odds ratio, 0.48 [95% CI, 0.17–1.36]). Conclusions Although a bidirectional association between frailty and cardiovascular disease has been suggested, we did not find evidence of an association between frailty and AF. Our findings may be limited by sample size and should be further explored in other populations.

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.

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.

The past 3 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 17 independent signals for AF at 14 genomic regions. Studies have established that advanced age, male sex, and European ancestry are prominent AF risk factors. Other modifiable risk factors include 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 electric 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.

The past 3 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 17 independent signals for AF at 14 genomic regions. Studies have established that advanced age, male sex, and European ancestry are prominent AF risk factors. Other modifiable risk factors include 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 electric 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.

BackgroundAdvancing 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 ResultsWe 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. ConclusionsIn our moderate‐sized community‐based cohort, we did not find evidence for a significant association between LTL and risk of incident AF.