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Background: Several reports have demonstrated that prolongation of the QT interval is associated with sudden cardiac death (SCD). However, it is unknown whether any of the components within the QT interval are responsible for its association with SCD.Methods and Results: We examined the association of the individual QT-interval components (R-wave onset to R-peak, R-peak to R-wave end, ST-segment, T-wave onset to T-peak, and T-peak to T-wave end) with SCD in 12 241 participants (54±5.7 years; 26% black; 55% women) from the ARIC study (Atherosclerosis Risk in Communities). The QT interval and its components were measured at baseline (1987-1989) from 12-lead ECGs. SCD cases were adjudicated by a group of physicians through December 31, 2012. During a median follow-up of 23.6 years, a total of 346 cases of SCD were identified. Although prolongation of the QT interval was associated with a 49% increased risk of SCD (hazard ratio, 1.49; 95% confidence interval, 1.01-2.18), only the T-wave onset to T-peak component (per 1-SD increase: hazard ratio, 1.19; 95% confidence interval, 1.06-1.34) was associated with SCD and not any of the other components in separate models. When all of the QT-interval components were included in the same model, T-wave onset to T-peak remained the strongest predictor of SCD (per 1-SD increase: hazard ratio, 1.21; 95% confidence interval, 1.06-1.37).Conclusions: The risk of SCD with the QT interval is driven by prolongation of the T-wave onset to T-peak component. This suggests that shifting the focus from the overall QT interval to its individual components will refine SCD prediction in the community. [ABSTRACT FROM AUTHOR]

Background--Coronary artery calcium (CAC) measured at a single time point has been associated with an increased risk for atrial fibrillation (AF). It is unknown whether CAC progression over time carries a similar risk. Methods and Results--This analysis included 5612 participants (mean age: 62±10; 52% women; 39% whites; 27% blacks; 20% Hispanics; 12% Chinese Americans) from the Multi-Ethnic Study of Atherosclerosis. Phantom-adjusted Agatston scores for baseline and follow-up measurements were used to compute change in CAC per year (≤0, 1-100, 101-300, and >300 U/year). AF was ascertained by review of hospital discharge records and from Medicare claims data through December 31, 2010. Cox regression was used to compute hazard ratios (HR) and 95% confidence intervals (CI) for the association between CAC progression and AF. Over a median follow-up of 5.6 years (25th, 75th percentiles=5.1, 6.8), a total of 203 (3.6%) incident AF cases were detected. Any CAC progression (>0/year) was associated with an increased risk for AF (HR=1.55, 95% CI=1.10, 2.19), and the risk increased with higher levels of CAC progression (≤0/year: HR=1.0 [reference]; 1-100/year: HR=1.47, 95% CI=1.03, 2.09; 101-300/year: HR=1.92, 95%CI=1.15, 3.20; >300/year: HR=3.23, 95%CI=1.48, 7.05). An interaction was observed by age with the association of CAC progression with AF being stronger for younger (<61 years: HR=3.53, 95% CI=1.29, 9.69) compared with older (≥61 years: HR=1.42, 95% CI=0.99, 2.04) participants (P interaction=0.037). Conclusions--CAC progression during an average of 5 to 6 years of follow-up is associated with an increased risk for AF. [ABSTRACT FROM AUTHOR]

Objective: This study examines the association between environmental tobacco smoke (ETS) exposure and atrial fibrillation (AF). Methods: We examined the cross-sectional association between ETS exposure and AF in 12,021 participants (mean age: 65 ± 9.9 years; 60% women; 40% blacks) from the REasons for Geographic And Racial Differences in Stroke study who self-identified as never smokers between 2003 and 2007. Results: A total of 2503 (21%) participants reported ETS exposure. In a multivariate logistic regression model adjusted for sociodemographics and potential confounders, ETS exposure was significantly associated with AF (odds ratio = 1.27, 95% confidence interval = 1.08, 1.50). Conclusions: Our findings suggest that the harmful effects of ETS exposure extend to sustained arrhythmias such as AF. [ABSTRACT FROM AUTHOR]

Background: Limited information exists on the lifetime risk of atrial fibrillation (AF) in African Americans and by socioeconomic status.Methods: We studied 15 343 participants without AF at baseline from the ARIC (Atherosclerosis Risk in Communities) cohort recruited in 1987 to 1989 from 4 communities in the United States when they were 45 to 64 years of age. Participants have been followed through 2014. Incidence rates of AF were calculated dividing the number of new cases by person-years of follow-up. Lifetime risk of AF was estimated by a modified Kaplan-Meier method considering death as a competing risk. Participants' family income and education were obtained at baseline.Results: We identified 2760 AF cases during a mean follow-up of 21 years. Lifetime risk of AF was 36% (95% confidence interval, 32%-38%) in white men, 30% (95% confidence interval, 26%-32%) in white women, 21% (95% confidence interval, 13%-24%) in African American men, and 22% (95% confidence interval, 16%-25%) in African American women. Regardless of race and sex, incidence rates of AF decreased from the lowest to the highest categories of income and education. In contrast, lifetime risk of AF increased in individuals with higher income and education in most sex-race groups. Cumulative incidence of AF was lower in those with higher income and education compared with their low socioeconomic status counterparts through earlier life but was reversed after age 80.Conclusions: Lifetime risk of AF in the ARIC cohort was ≈1 in 3 among whites and 1 in 5 among African Americans. Socioeconomic status was inversely associated with cumulative incidence of AF before the last decades of life. [ABSTRACT FROM AUTHOR]

Introduction: Lower neighborhood socioeconomic status (SES) has been associated with several cardiovascular diseases, but its relationship with atrial fibrillation (AF) is unclear. Hypothesis: In a national cohort of black and white adults, lower neighborhood SES will be associated with increased risk of incident AF. Methods: This analysis consisted of 12481 participants (42% black, 58% white), aged 45 and older, enrolled in the REasons for Geographic and Racial Differences in Stroke (REGARDS) Study between 2003 and 2007. Included participants had geocoded addresses, were free of AF at baseline and completed a 10-year follow-up assessment. Incident AF was defined by electrocardiogram or self-report of physician diagnosis. A neighborhood SES score was constructed using 6 neighborhood-level variables from linked 2000 census data (median household income, median value of owner-occupied units, % of households receiving interest or rental income, % of adults with HS diploma, % of adults with college degree, % of adults employed in professional occupations), and then divided into quartiles. Logistic regression was used to estimate the association of neighborhood SES quartile with incident AF, adjusting for demographics, individual SES measures, AF risk factors, and access to care factors. Results: During follow-up, 1474 incident AF cases were identified (11.7%). In multivariable adjusted models, neighborhood SES was not associated with increased risk of incident AF: (Odds ratio (OR) (95% confidence interval (CI)): Q1: 1.04 (0.87, 1.25); Q2: 0.96 (0.81, 1.13); Q3: 0.87 (0.74, 1.02)) for the lowest three quartiles of neighborhood SES score compared to the highest quartile (Q4). However, individual SES measures, including low household income (<$20K vs. $75K+ OR (95% CI): 1.27 (1.01, 1.61)) and housing instability (lived in 3 or more places during follow-up vs. same residence OR (95% CI): 1.19 (1.04, 1.36)) were each independently associated with increased risk of incident AF. Conclusions: In this analysis from a large geographically diverse biracial cohort of adults, there was no association between neighborhood SES and incident AF, although there was an association between different individual SES variables and risk of AF. [ABSTRACT FROM AUTHOR]

Background: Circulating N-terminal pro-B-type natriuretic peptide (NT-proBNP) concentrations and body mass index (BMI), both strong risk markers for AF, are inversely correlated. Their potential interaction in relation to incident atrial fibrillation (AF), however, has not been explored. Hypothesis: Atherosclerosis Risk in Communities Study (ARIC) participants with high NT-proBNP and obese BMI will be at the highest risk of developing AF, and that increases in both risk factors between visits 2 and 4 will be associated with increased AF risk. Methods: We studied 9692 individuals without prevalent AF in 1996-1998 and with available NT-proBNP measurements and BMI obtained in 1990-1992 and 1996-1998 participating in the ARIC Study. Participants were followed through the end of 2015. AF was ascertained from electrocardiograms, hospital discharge codes, and death certificates. BMI values were dichotomized to obese (BMI ≥ 30 kg/m2) and non-obese (BMI < 30 kg/m2). NT-proBNP levels were dichotomized as low vs. high using the cohort's median as the cut-point. Multivariable Cox regression was used to calculate the hazard ratios (HR) and 95% confidence intervals (CI) of NT-proBNP and BMI with incident AF. We also assessed the impact of NT-proBNP and BMI change on incidence AF. Results: Over a median follow up of 17.4 years, there were 1,451 incident cases of AF. The median NT-proBNP at visit 4 was 68.2 pg/ml. Considering non-obese individuals with low NT-proBNP at visit 4 as the reference group, obese participants with high NT-proBNP had the highest hazards of incident AF (HR 3.79, 95% CI, 3.27, 4.39). The corresponding HRs for non-obese participants with high NT-proBNP and obese participants with low NT-proBNP were 2.45 (95%CI, 2.14, 2.81) and 1.72 (95%CI, 1.46, 2.02), respectively. However, the effect of obesity on AF risk was not modified by NT-proBNP levels (interaction P=0.62). When assessing associations of AF with a change in BMI and NT-proBNP between visits 2 and 4, increases in NT-proBNP between both visits were associated with higher risk of AF, while no association was found between increased BMI and AF risk. The association of change in BMI with AF risk was not modified by NT-proBNP change (Interaction P=0.17). Conclusion: Individuals with high NT-proBNP or obese BMI are at a greater risk of AF than those with low NT-proBNP and non-obese BMI. However, the association of BMI with AF risk is not modified by NT-proBNP and vice versa. [ABSTRACT FROM AUTHOR]

Background: Women are less likely to develop atrial fibrillation (AF) compared with men. It is unclear if this is related to difference in risk factors leading to AF or due to a differential impact of the same risk factors between sexes. Methods: This analysis included 11,806 participants (55.2 % women) free of AF at baseline from the REGARDS study. Incident AF was ascertained by study-scheduled electrocardiograms and self-reported history at a follow-up examination. Logistic regression was used to examine baseline associations with incident AF. Backwards elimination logistic regression was used to identify AF risk factors in men and women, separately. Results: Over a median follow-up of 9.0 years, 588 (11.1%) men and 428 (6.6%) women (p-value <0.001) developed AF. Men had a higher risk of AF than women in a logistic regression model adjusted for age and race [OR (95%CI): 1.61(1.26, 1.75)]. Age, white race, height, weight, use of blood pressure lowering medications and history of cardiovascular disease were identified by backward elimination as AF risk factors shared by both sexes. On the other hand, diabetes was an AF risk factor in women but not in men (Table). Among the shared risk factors between men and women, only age showed a stronger association in women than in men [Interaction p-value=0.003]. Adjustment for the shared risk factors eliminated the sex difference in AF risk [OR (95%CI): 0.90 (0.74, 1.09)], which was more noticeable in those younger than the median age (62 years) compared to those who were older [interaction p-value 0.003]. Conclusions: Women and men share several AF risk factors, and these shared risk factors explain the sex differences. However, age association with AF differs by sex, and age modifies the associations between sex and other AF risk factors. [ABSTRACT FROM AUTHOR]

Background: Acute stress may trigger atrial fibrillation, but the mechanisms are not clear. We hypothesized that acute mental stress results in abnormal atrial remodeling via electrophysiologic effects. Methods: We examined our hypothesis in 168 patients (mean age=63±8.7 years; 74% men; 65% Caucasian) with stable coronary heart disease who underwent mental (speech task) stress testing. PTFV1 duration (ms) times the value of the depth (μV) of the downward deflection (terminal portion) of the median P-wave in lead V1, and was automatically measured on digital electrocardiograms (ECG) at rest, stress, recovery. Electrocardiographic left atrial abnormality was defined as P-wave terminal force in lead V1 (PTFV1) ≤ -4000 μV*ms. The mean values of PTFV1 during stress and recovery were compared with rest. Additionally, the percentage of participants who had left atrial abnormality during stress and recovery was compared with those at rest. Results: The mean PTFV1 at rest was -2857±2459 μV*ms. There were 51 (30%) participants who had baseline left atrial abnormality. Compared with rest, PTFV1 became more negative with stress [mean change=-474, 95%CI=(-103, -845); p=0.013] and during recovery [mean change=-420, 95%CI=(-79, -761); p=0.016]. A larger percentage of participants showed left atrial abnormality during stress (n=63, 38%) and recovery (n=67, 40%) compared with rest. Similar changes in PTFV1 with stress [mean change=-833, 95%CI=(-372, -1295); p<0.001] and recovery [mean change=-796, 95%CI=(-389, -1204); p<0.001] were observed when we excluded those with baseline left atrial abnormality. No differences were noted in the PTFV1 response based on age, gender, race, or hemodynamic response to stress. Conclusion: Acute mental stress alters left atrial electrophysiology, as measured by PTFV1, suggesting that stressful situations promote adverse atrial remodeling. This possibly explains the poor cardiovascular outcomes associated with acute mental stress that are triggered by left atrial abnormalities such as atrial arrhythmias and stroke. [ABSTRACT FROM AUTHOR]

Background: In people with atrial fibrillation (AF), periods of sinus rhythm present an opportunity to detect prothrombotic atrial remodeling through measurement of P-wave indices (PWIs)-prolonged P-wave duration, abnormal P-wave axis, advanced interatrial block, and abnormal P-wave terminal force in lead V1. We hypothesized that the addition of PWIs to the CHA 2 DS 2 -VASc score would improve its ability to predict AF-related ischemic stroke., Methods: We included 2229 participants from the ARIC study (Atherosclerosis Risk in Communities) and 700 participants from MESA (Multi-Ethnic Study of Atherosclerosis) with incident AF who were not on anticoagulants within 1 year of AF diagnosis. PWIs were obtained from study visit ECGs before development of AF. AF was ascertained using study visit ECGs and hospital records. Ischemic stroke cases were based on physician adjudication of hospital records. We used Cox proportional hazards models to estimate hazard ratios and 95% CIs of PWIs for ischemic stroke. Improvement in 1-year stroke prediction was assessed by C-statistic, categorical net reclassification improvement, and relative integrated discrimination improvement., Results: Abnormal P-wave axis was the only PWI associated with increased ischemic stroke risk (hazard ratio, 1.84; 95% CI, 1.33-2.55) independent of CHA 2 DS 2 -VASc variables, and that resulted in meaningful improvement in stroke prediction. The β estimate was approximately twice that of the CHA 2 DS 2 -VASc variables, and thus abnormal P-wave axis was assigned 2 points to create the P 2 -CHA 2 DS 2 -VASc score. This improved the C-statistic (95% CI) from 0.60 (0.51-0.69) to 0.67 (0.60-0.75) in ARIC and 0.68 (0.52-0.84) to 0.75 (0.60-0.91) in MESA (validation cohort). In ARIC and MESA, the categorical net reclassification improvements (95% CI) were 0.25 (0.13-0.39) and 0.51 (0.18-0.86), respectively, and the relative integrated discrimination improvement (95% CI) were 1.19 (0.96-1.44) and 0.82 (0.36-1.39), respectively., Conclusions: Abnormal P-wave axis-an ECG correlate of left atrial abnormality- improves ischemic stroke prediction in AF. Compared with CHA 2 DS 2 -VASc, the P 2 -CHA 2 DS 2 -VASc is a better prediction tool for AF-related ischemic stroke.

Objective: This study examines the association between environmental tobacco smoke (ETS) exposure and atrial fibrillation (AF)., Methods: We examined the cross-sectional association between ETS exposure and AF in 12,021 participants (mean age: 65 ± 9.9 years; 60% women; 40% blacks) from the REasons for Geographic And Racial Differences in Stroke study who self-identified as never smokers between 2003 and 2007., Results: A total of 2503 (21%) participants reported ETS exposure. In a multivariate logistic regression model adjusted for sociodemographics and potential confounders, ETS exposure was significantly associated with AF (odds ratio = 1.27, 95% confidence interval = 1.08, 1.50)., Conclusions: Our findings suggest that the harmful effects of ETS exposure extend to sustained arrhythmias such as AF.

Objective: It is unknown whether endothelial dysfunction precedes atrial fibrillation (AF) development. The objective of this study was to examine the association of brachial flow-mediated dilation (FMD) with incident AF., Approach and Results: A total of 2936 participants (mean age, 61±9.9 years; 50% women; 66% nonwhites) from the Multi-Ethnic Study of Atherosclerosis with available ultrasound brachial FMD measurements who were free of baseline AF were included in this analysis. Baseline (2000-2002) FMD was computed from the percentage difference (%FMD) in brachial artery diameter and maximum diameter during measured vasodilator response. AF was ascertained from hospitalization data including Medicare claims during a median follow-up of 8.5 years. Probability-weighted Cox proportional-hazards regression was used to compute hazard ratios and 95% confidence intervals for the association between FMD as a continuous variable (%FMD values per 1-SD increase) and incident AF. Incident AF was detected in 137 (4.7%) participants. Those with %FMD values below the sex-specific median value (median %FMD; men, 3.6%; women, 4.2%; incidence rate per 1000 person-years, 7.3; 95% confidence interval, 5.9-9.0) were more likely to develop AF than people whose %FMD values were above the median value (incidence rate per 1000 person-years, 4.5; 95% confidence interval, 3.4-5.8; log-rank P=0.0043). In a multivariable Cox regression analysis, each 1-SD increase in %FMD values (SD, 2.8%) was associated with less incident AF (hazard ratio, 0.84; 95% confidence interval, 0.70-0.99). These results were consistent across subgroups stratified by age, sex, and race/ethnicity., Conclusions: Smaller brachial FMD values are associated with higher rates of AF, suggesting a role for endothelial dysfunction in AF pathogenesis., (© 2014 American Heart Association, Inc.)