Association between Age of Onset of Hypertension and Incident Atrial Fibrillation.
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SUBMITTER: Lee Y
PROVIDER: S-EPMC9317856 | biostudies-literature | 2022 Jul
REPOSITORIES: biostudies-literature
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Association between Age of Onset of Hypertension and Incident Atrial Fibrillation.
Lee Yonggu Y Shin Jeong-Hun JH Kim Byung Sik BS Kook Hyungdon H Kim Woohyeun W Heo Ran R Lim Young-Hyo YH Shin Jinho J Kim Chun Ki CK Park Jin-Kyu JK
Journal of personalized medicine 20220721 7
We investigated whether age at hypertension (HTN) onset was associated with the risk of atrial fibrillation (AF) in the general population. This prospective longitudinal community-based cohort study included 9892 participants without AF at baseline, who underwent biennial electrocardiography for a median duration of 11.5 years. The participants were divided into five groups, consisting of a normotensive group (Group-N) and four HTN groups based on HTN onset age: <45 years (Group-H1); 45−54 years ...[more]
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Project description:Background Limited evidence is available on sex differences about the association between hypertension and incident atrial fibrillation (AF). Methods and Results We used a nationwide health checkup and claims database to analyze 3 383 738 adults (median age, 43 (36-51) years, 57.4% men). We investigated the relationship between hypertension and incident AF in men and women using a Cox regression model. We used restricted cubic spline functions to identify the association of blood pressure (BP) as a continuous parameter with incident AF. We categorized the men and women into 4 groups according to the 2017 American College of Cardiology/American Heart Association BP guidelines. During a mean follow-up of 1199±950 days, 13 263 AF diagnoses were recorded. The incidence (95% CI) of AF was 15.8 (15.5-16.1) per 10 000 person-years in men and 6.1 (5.9-6.3) per 10 000 person-years in women. Compared with normal BP, elevated BP, stage 1 hypertension, and stage 2 hypertension were associated with an increased risk AF in both men and women. However, the hazard ratios were greater in women than in men, and the P value for interactions in the multivariable model was 0.0076. The models using restricted cubic spline showed that the risk of AF associated with elevated systolic BP increased steeply above an approximate threshold of systolic BP of 130 mm Hg in men and 100 mm Hg in women. Although our primary findings were consistent across subgroup analyses, this association was most significant in younger individuals. Conclusions Although the incidence of AF was higher in men, the association between hypertension and incident AF was more pronounced in women than in men, suggesting a potential sex difference in the relationship between hypertension and incident AF.
| S-EPMC10111461 | biostudies-literature
Project description:CONTEXT:Although the heritability of atrial fibrillation (AF) is established, the contribution of familial AF to predicting new-onset AF remains unknown. OBJECTIVE:To determine whether familial occurrence of AF is associated with new-onset AF beyond established risk factors. DESIGN, SETTING, AND PARTICIPANTS:The Framingham Heart Study, a prospective community-based cohort study started in 1948. Original and Offspring Cohort participants were aged at least 30 years, were free of AF at the baseline examination, and had at least 1 parent or sibling enrolled in the study. The 4421 participants in this analysis (mean age, 54 [SD, 13] years; 54% women) were followed up through December 31, 2007. MAIN OUTCOME MEASURES:Incremental predictive value of incorporating different features of familial AF (any familial AF, premature familial AF [onset ?65 years old], number of affected relatives, and youngest age of onset in a relative) into a risk model for new-onset AF. RESULTS:Across 11,971 examinations during the period 1968-2007, 440 participants developed AF. Familial AF occurred among 1185 participants (26.8%) and premature familial AF occurred among 351 participants (7.9%). Atrial fibrillation occurred more frequently among participants with familial AF than without familial AF (unadjusted absolute event rates of 5.8% and 3.1%, respectively). The association was not attenuated by adjustment for AF risk factors (multivariable-adjusted hazard ratio, 1.40; 95% confidence interval [CI], 1.13-1.74) or reported AF-related genetic variants. Among the different features of familial AF examined, premature familial AF was associated with improved discrimination beyond traditional risk factors to the greatest extent (traditional risk factors, C statistic, 0.842 [95% CI, 0.826-0.858]; premature familial AF, C statistic, 0.846 [95% CI, 0.831-0.862]; P = .004). Modest changes in integrated discrimination improvement were observed with premature familial AF (2.1%). Net reclassification improvement (assessed using 8-year risk thresholds of <5%, 5%-10%, and >10%) did not change significantly with premature familial AF (index statistic, 0.011; 95% CI, -0.021 to 0.042; P = .51), although categoryless net reclassification was improved (index statistic, 0.127; 95% CI, 0.064-0.189; P = .009). CONCLUSIONS:In this cohort, familial AF was associated with an increased risk of AF that was not attenuated by adjustment for AF risk factors including genetic variants. Assessment of premature familial AF was associated with a very slight increase in predictive accuracy compared with traditional risk factors.
| S-EPMC3073054 | biostudies-literature
Project description:BackgroundThe most prominent risk factor for atrial fibrillation (AF) is chronological age; however, underlying mechanisms are unexplained. Algorithms using epigenetic modifications to the human genome effectively predict chronological age. Chronological and epigenetic predicted ages may diverge in a phenomenon referred to as epigenetic age acceleration (EAA), which may reflect accelerated biological aging. We sought to evaluate for associations between epigenetic age measures and incident AF.MethodsMeasures for 4 epigenetic clocks (Horvath, Hannum, DNA methylation [DNAm] PhenoAge, and DNAm GrimAge) and an epigenetic predictor of PAI-1 (plasminogen activator inhibitor-1) levels (ie, DNAm PAI-1) were determined for study participants from 3 population-based cohort studies. Cox models evaluated for associations with incident AF and results were combined via random-effects meta-analyses. Two-sample summary-level Mendelian randomization analyses evaluated for associations between genetic instruments of the EAA measures and AF.ResultsAmong 5600 participants (mean age, 65.5 years; female, 60.1%; Black, 50.7%), there were 905 incident AF cases during a mean follow-up of 12.9 years. Unadjusted analyses revealed all 4 epigenetic clocks and the DNAm PAI-1 predictor were associated with statistically significant higher hazards of incident AF, though the magnitudes of their point estimates were smaller relative to the associations observed for chronological age. The pooled EAA estimates for each epigenetic measure, with the exception of Horvath EAA, were associated with incident AF in models adjusted for chronological age, race, sex, and smoking variables. After multivariable adjustment for additional known AF risk factors that could also potentially function as mediators, pooled EAA measures for 2 clocks remained statistically significant. Five-year increases in EAA measures for DNAm GrimAge and DNAm PhenoAge were associated with 19% (adjusted hazard ratio [HR], 1.19 [95% CI, 1.09-1.31]; P<0.01) and 15% (adjusted HR, 1.15 [95% CI, 1.05-1.25]; P<0.01) higher hazards of incident AF, respectively. Mendelian randomization analyses for the 5 EAA measures did not reveal statistically significant associations with AF.ConclusionsOur study identified adjusted associations between EAA measures and incident AF, suggesting that biological aging plays an important role independent of chronological age, though a potential underlying causal relationship remains unclear. These aging processes may be modifiable and not constrained by the immutable factor of time.
| S-EPMC8671333 | biostudies-literature
Project description:ObjectiveLimited data exist on the association between menopause and atrial fibrillation (AF). We sought to examine the relationship between menopausal age, postmenopausal hormone therapy (PHT) use and incident AF.MethodsThe Women's Health Study (WHS) enrolled 39 876 female health professionals between 1992 and 1995. We prospectively examined 30 034 women in WHS using Cox proportional-hazard models. Participants were free of cardiovascular disease and AF at baseline and had not undergone hysterectomy without bilateral oophorectomy prior to menopause. Incident AF was confirmed by medical record review.ResultsAt baseline, median age was 53 years (IQR 49-60), median menopausal age was 50 years (IQR 46-52) and 14 415 (48.0%) had prior PHT use. Over a median follow-up of 20.5 years, 1350 AF events occurred. In multivariable analysis, relative hazards for AF were lower among women with younger age at menopause but did not differ significantly from women with the oldest menopausal age (<45: HR 0.82, 95% CI 0.67 to 1.02; 45-49: HR 0.90, 95% CI 0.74 to 1.08; 50-54: HR 0.89, 95% CI 0.75 to 1.06; >54 years: referent). Use of oestrogen-alone PHT, but not oestrogen and progesterone, was independently associated with AF risk (HR 1.22; 95% CI 1.02 to 1.45 vs HR 1.04; 95% CI 0.86 to 1.26). This relationship was not attenuated by intermediary cardiovascular events.ConclusionsIn this large prospective study, menopausal age was not significantly related to incident AF, while use of oestrogen monotherapy was associated with increased AF risk. Our findings suggest a pathophysiological link between unopposed oestrogen exposure and AF in women.Clinical trial registrationNCT000000479; Post-results.
| S-EPMC5831356 | biostudies-literature
Project description:Chronic inflammation is a continuous low-grade activation of the systemic immune response. Whereas downstream inflammatory markers are associated with atrial fibrillation (AF), upstream inflammatory effectors including eicosanoids are less studied. To examine the association between eicosanoids and incident AF. We used a liquid chromatography-mass spectrometry for the non-targeted measurement of 161 eicosanoids and eicosanoid-related metabolites in the Framingham Heart Study. The association of each eicosanoid and incident AF was assessed using Cox proportional hazards models and adjusted for AF risk factors, including age, sex, height, weight, systolic/diastolic blood pressure, current smoking, antihypertensive medication, diabetes, history of myocardial infarction and heart failure. False discovery rate (FDR) was used to adjust for multiple testing. Eicosanoids with FDR < 0.05 were considered significant. In total, 2676 AF-free individuals (mean age 66 ± 9 years, 56% females) were followed for mean 10.8 ± 3.4 years; 351 participants developed incident AF. Six eicosanoids were associated with incident AF after adjusting for multiple testing (FDR < 0.05). A joint score was built from the top eicosanoids weighted by their effect sizes, which was associated with incident AF (HR = 2.72, CI = 1.71-4.31, P = 2.1 × 10-5). In conclusion, six eicosanoids were associated with incident AF after adjusting for clinical risk factors for AF.
| S-EPMC9684401 | biostudies-literature
Project description:BackgroundAtrial fibrillation (AF) is a leading cause of cardiovascular morbidity and mortality. While neighborhood-level factors, such as poverty, have been related to prevalence of AF risk factors, the association between neighborhood poverty and incident AF has been limited.ObjectiveUsing a large cohort from a health system serving the greater Chicago area, we sought to determine the association between neighborhood-level poverty and incident AF.DesignRetrospective cohort study.ParticipantsAdults, aged 30 to 80 years, without baseline cardiovascular disease from January 1, 2005, to December 31, 2018.Main measuresWe geocoded and matched residential addresses of all eligible patients to census-level poverty estimates from the American Community Survey. Neighborhood-level poverty (low, intermediate, and high) was defined as the proportion of residents in the census tract living below the federal poverty threshold. We used generalized linear mixed effects models with a logit link function to examine the association between neighborhood poverty and incident AF, adjusting for patient demographic and clinical AF risk factors.Key resultsAmong 28,858 in the cohort, patients in the high poverty group were more often non-Hispanic Black or Hispanic and had higher rates of AF risk factors. Over 5 years of follow-up, 971 (3.4%) patients developed incident AF. Of these, 502 (51.7%) were in the low poverty, 327 (33.7%) in the intermediate poverty, and 142 (14.6%) in the high poverty group. The adjusted odds ratio (aOR) of AF was higher for the intermediate poverty compared with that for the low poverty group (aOR 1.23 [95% CI 1.01-1.48]). The point estimate for the aOR of AF incidence was similar, but not statistically significant, for the high poverty compared with the low poverty group (aOR 1.25 [95% CI 0.98-1.59]).ConclusionIn adults without baseline cardiovascular disease managed in a large, integrated health system, intermediate neighborhood poverty was significantly associated with incident AF. Understanding neighborhood-level drivers of AF disparities will help achieve equitable care.
| S-EPMC9086074 | biostudies-literature
Project description:ImportanceAtrial fibrillation (AF) is the most common arrhythmia affecting 1% of the population. Young individuals with AF have a strong genetic association with the disease, but the mechanisms remain incompletely understood.ObjectiveTo perform large-scale whole-genome sequencing to identify genetic variants related to AF.Design, setting, and participantsThe National Heart, Lung, and Blood Institute's Trans-Omics for Precision Medicine Program includes longitudinal and cohort studies that underwent high-depth whole-genome sequencing between 2014 and 2017 in 18 526 individuals from the United States, Mexico, Puerto Rico, Costa Rica, Barbados, and Samoa. This case-control study included 2781 patients with early-onset AF from 9 studies and identified 4959 controls of European ancestry from the remaining participants. Results were replicated in the UK Biobank (346 546 participants) and the MyCode Study (42 782 participants).ExposuresLoss-of-function (LOF) variants in genes at AF loci and common genetic variation across the whole genome.Main outcomes and measuresEarly-onset AF (defined as AF onset in persons <66 years of age). Due to multiple testing, the significance threshold for the rare variant analysis was P = 4.55 × 10-3.ResultsAmong 2781 participants with early-onset AF (the case group), 72.1% were men, and the mean (SD) age of AF onset was 48.7 (10.2) years. Participants underwent whole-genome sequencing at a mean depth of 37.8 fold and mean genome coverage of 99.1%. At least 1 LOF variant in TTN, the gene encoding the sarcomeric protein titin, was present in 2.1% of case participants compared with 1.1% in control participants (odds ratio [OR], 1.76 [95% CI, 1.04-2.97]). The proportion of individuals with early-onset AF who carried a LOF variant in TTN increased with an earlier age of AF onset (P value for trend, 4.92 × 10-4), and 6.5% of individuals with AF onset prior to age 30 carried a TTN LOF variant (OR, 5.94 [95% CI, 2.64-13.35]; P = 1.65 × 10-5). The association between TTN LOF variants and AF was replicated in an independent study of 1582 patients with early-onset AF (cases) and 41 200 control participants (OR, 2.16 [95% CI, 1.19-3.92]; P = .01).Conclusions and relevanceIn a case-control study, there was a statistically significant association between an LOF variant in the TTN gene and early-onset AF, with the variant present in a small percentage of participants with early-onset AF (the case group). Further research is necessary to understand whether this is a causal relationship.
| S-EPMC6436530 | biostudies-literature
Project description:BackgroundQRS duration (QRSd), a measure of ventricular conduction, has been associated with adverse cardiovascular outcomes, but its relationship with incident atrial fibrillation (AF) is poorly understood.Methods and resultsThis study included 15,314 participants from the Atherosclerosis Risk in Communities (ARIC) study who were free of AF at baseline. QRSd was automatically measured from resting 12-lead electrocardiograms (ECGs) at baseline. Incident AF cases were systematically ascertained using ECGs, hospital discharge diagnoses and death certificates. Multivariable adjusted Cox regression analyses were performed to investigate the relationship between QRSd and incident AF. Mean age of our population was 54 ± 6 years (55% females). During a median follow-up of 21.2 years, 2041 confirmed incident AF cases occurred. In multivariable adjusted Cox models, a 1-SD increase in QRSd was associated with a hazard ratio (HR) (95% CI) for AF of 1.05 (1.01; 1.10), p = 0.01. This relationship was significant among women (HR per 1-SD increase in QRSd (95% CI) 1.13 (1.06; 1.20), p < 0.001), but not among men (1.00 (0.95; 1.06), p = 0.97) (p for interaction 0.005). Compared to individuals with a QRSd <100 ms, the HRs for incident AF in individuals with a QRSd of 100-119 and ≥120 ms were 1.13 (1.02; 1.26) and 1.35 (1.08; 1.68), respectively (p for trend 0.002). Again, this relationship was significant among women (p for trend <0.001) but not among men (p for trend 0.23).ConclusionIn this large population-based study, QRSd was an independent predictor of incident AF among women, but not in men. Further studies are needed to better understand the underlying mechanisms.
| S-EPMC6027639 | biostudies-literature
Project description:BackgroundLow-density lipoprotein (LDL) cholesterol is a strong risk factor for atherosclerosis but has an inverse association with atrial fibrillation (AF). We aimed to provide insight into the paradoxical association of LDL cholesterol with AF by evaluating the relationship of various lipoprotein measures and incident AF.Methods and resultsWe prospectively evaluated lipoprotein measures among 23 738 healthy middle-aged and older women (median follow-up 16.4 years; N=795 incident AF events). Baseline LDL cholesterol was directly measured, lipoprotein particle concentrations and size were measured by nuclear magnetic resonance spectroscopy, and apolipoproteins were measured by immunoassay. Cox regression models were adjusted for age, AF risk factors, inflammatory, and dysglycemic biomarkers. After multivariable adjustment, inverse associations with AF were observed (hazard ratio, 95% confidence interval for top versus bottom quintile, P value) for LDL cholesterol (0.72, 0.56-0.92, P=0.009), the total number of LDL particles (0.77, 0.60-0.99, P=0.045), and very-low-density lipoprotein particles (0.78, 0.61-0.99, P=0.04), which was driven by the number of cholesterol-poor small LDL (0.78, 0.61-1.00, P=0.05) and small very-low-density lipoprotein particles (0.78, 0.62-0.99, P=0.04). By contrast, the larger cholesterol-rich LDL particles and all high-density lipoprotein measures were not associated with AF in multivariable models. Adjustment for inflammatory and dysglycemic biomarkers had minimal impact on these associations.ConclusionsIn this prospective study, the inverse association between LDL cholesterol and AF extended to several other atherogenic lipoproteins, and these associations are unlikely to be mediated by direct cholesterol effects.Clinical trial registrationClinicalTrials.gov; Unique Identifier: NCT00000479.
| S-EPMC4591535 | biostudies-literature
Project description:BackgroundThe association between nonalcoholic fatty liver disease (NAFLD) and atrial fibrillation (AF) has been inconsistent, and the impact of hepatic fibrosis on this relationship remains uncertain. We investigated the association between NAFLD and the risk of new-onset AF across different age groups.MethodsA total of 3,179,582 participants from the 2009 Korean National Health Screening Program were divided into five groups based on NAFLD status: no NAFLD (fatty liver index [FLI] < 30); grade 1 NAFLD without advanced fibrosis (FLI 30-59 & BARD < 2); grade 1 NAFLD with advanced fibrosis (FLI 30-59 & BARD ≥ 2); grade 2 NAFLD without advanced fibrosis (FLI ≥ 60 & BARD < 2); and grade 2 NAFLD with advanced fibrosis (FLI ≥ 60 & BARD ≥ 2). The primary outcome was incident AF.ResultsDuring the median follow-up of 9.3 years, 62,542 patients were diagnosed with new-onset AF. In the age- and sex-adjusted model, the risk of new-onset AF increased across NAFLD grades and fibrosis categories: grade 1 NAFLD without advanced fibrosis (hazard ratio [HR] 1.120, 95% confidence interval [CI]: 1.081-1.161); grade 1 NAFLD with advanced fibrosis (HR 1.275, 95% CI 1.251-1.300); grade 2 NAFLD without advanced fibrosis (HR 1.305, 95% CI: 1.252-1.360); and grade 2 NAFLD with advanced fibrosis (HR 1.627, 95% CI: 1.586-1.670). In the multivariate model, the excess risk of AF in patients with NAFLD and advanced fibrosis remained significant, even in participants aged 20-39 years.ConclusionPatients with NAFLD had a higher risk of new-onset AF, which increased progressively with NAFLD severity, particularly in those aged 20-29 years.
| S-EPMC11395983 | biostudies-literature