Dataset Information

Negative Affect and Risk of Atrial Fibrillation: MESA.

ABSTRACT: Background Current literature examining the prospective relationship between depression and other measures of negative affect with atrial fibrillation (AF) are limited. We determined the relationships of depression, anger, anxiety, and chronic stress with incident AF in a multiethnic cohort of middle- and older-aged adults. Methods and Results This analysis included 6644 MESA (Multi-Ethnic Study of Atherosclerosis) study participants who were free of AF at baseline. Depressive symptoms were assessed at baseline and defined as either a 20-item Center for Epidemiologic Studies Depression Scale score ?16 or use of antidepressant medications. The Spielberger Trait Anger Scale, Spielberger Trait Anxiety Scale, and Chronic Burden Scale were also administered at baseline to assess anger, anxiety, and chronic stress, respectively. The primary outcome was incident AF , identified by follow-up study visit ECGs, hospital discharge diagnoses, or Medicare claims data. A total of 875 (13%) incident AF cases were detected over a median follow-up of nearly 13 years. A Center for Epidemiologic Studies Depression Scale score ?16 (referent, Center for Epidemiologic Studies Depression Scale score <2) and antidepressant use were associated with a 34% and 36% higher risk of AF , respectively, in separate adjusted Cox proportional hazards analyses (hazard ratio, 1.34; 95% CI 1.04-1.74 for Center for Epidemiologic Studies Depression Scale ?16; hazard ratio, 1.36; 95% CI , 1.04-1.77 for antidepressant use). No significant associations were observed for anger, anxiety, or chronic stress with development of AF . Conclusions Depressive symptoms are associated with an increased risk of incident AF . Further study into whether improving depressive symptoms reduces AF incidence is important.

SUBMITTER: Garg PK

PROVIDER: S-EPMC6405728 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature

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Negative Affect and Risk of Atrial Fibrillation: MESA.

Garg Parveen K PK O'Neal Wesley T WT Diez-Roux Ana V AV Alonso Alvaro A Soliman Elsayed Z EZ Heckbert Susan S

Journal of the American Heart Association 20190101 1

Background Current literature examining the prospective relationship between depression and other measures of negative affect with atrial fibrillation (AF) are limited. We determined the relationships of depression, anger, anxiety, and chronic stress with incident AF in a multiethnic cohort of middle- and older-aged adults. Methods and Results This analysis included 6644 MESA (Multi-Ethnic Study of Atherosclerosis) study participants who were free of AF at baseline. Depressive symptoms were asse ...[more]

PMID: 30563392

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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.

Project description:The mechanisms underlying atrial fibrillation (AF), the most common sustained cardiac rhythm disturbance, remain elusive. Atrial fibrosis plays an important role in the development of AF and rotor dynamics. Both electrical wavelength (WL) and the degree of atrial fibrosis change as AF progresses. However, their combined effect on rotor core location remains unknown. The aim of this study was to analyze the effects of WL change on rotor core location in both fibrotic and non-fibrotic atria. Three patient specific fibrosis distributions (total fibrosis content: 16.6, 22.8, and 19.2%) obtained from clinical imaging data of persistent AF patients were incorporated in a bilayer atrial computational model. Fibrotic effects were modeled as myocyte-fibroblast coupling + conductivity remodeling; structural remodeling; ionic current changes + conductivity remodeling; and combinations of these methods. To change WL, action potential duration (APD) was varied from 120 to 240ms, representing the range of clinically observed AF cycle length, by modifying the inward rectifier potassium current (IK1) conductance between 80 and 140% of the original value. Phase singularities (PSs) were computed to identify rotor core locations. Our results show that IK1 conductance variation resulted in a decrease of APD and WL across the atria. For large WL in the absence of fibrosis, PSs anchored to regions with high APD gradient at the center of the left atrium (LA) anterior wall and near the junctions of the inferior pulmonary veins (PVs) with the LA. Decreasing the WL induced more PSs, whose distribution became less clustered. With fibrosis, PS locations depended on the fibrosis distribution and the fibrosis implementation method. The proportion of PSs in fibrotic areas and along the borders varied with both WL and fibrosis modeling method: for patient one, this was 4.2-14.9% as IK1 varied for the structural remodeling representation, but 12.3-88.4% using the combination of structural remodeling with myocyte-fibroblast coupling. The degree and distribution of fibrosis and the choice of implementation technique had a larger effect on PS locations than the WL variation. Thus, distinguishing the fibrotic mechanisms present in a patient is important for interpreting clinical fibrosis maps to create personalized models.

Project description:BackgroundAfrican Americans are consistently found to have a lower prevalence of clinically detected atrial fibrillation (AF) than whites, despite a higher prevalence of major AF risk factors and higher risk of ischemic stroke. Long-term ambulatory ECG monitors provide the opportunity for unbiased AF detection. We determined differences by race/ethnicity in the prevalence of clinically detected AF and in the proportion with monitor-detected AF.MethodsWe conducted a cross-sectional analysis in the MESA (Multi-Ethnic Study of Atherosclerosis), a community-based cohort study that enrolled 6814 Americans free of clinically recognized cardiovascular disease in 2000 to 2002. At the 2016 to 2018 examination, 1556 individuals participated in an ancillary study involving ambulatory ECG monitoring and had follow-up for clinically detected AF since cohort entry.ResultsAmong 1556 participants, 41% were white, 25% African American, 21% Hispanic, and 14% Chinese; 51% were women; and the mean age was 74 years. The prevalence of clinically detected AF after 14.4 years' follow-up was 11.3% in whites, 6.6% in African Americans, 7.8% in Hispanics, and 9.9% in Chinese and was significantly lower in African Americans than in whites, in both unadjusted and risk factor-adjusted analyses (adjusted rate difference, -6.6% [95% CI, -10.1% to -3.1%]; P<0.001). By contrast, in the same individuals, the proportion with monitor-detected AF using a 14-day ambulatory ECG monitor was similar in the 4 race/ethnic groups: 7.1%, 6.4%, 6.9%, and 5.2%, respectively (compared with whites, all P>0.5).ConclusionsThe prevalence of clinically detected AF was substantially lower in African American than in white participants, without or with adjustment for AF risk factors. However, unbiased AF detection by ambulatory monitoring in the same individuals revealed little difference in the proportion with AF by race/ethnicity. These findings provide support for the hypothesis of differential detection by race/ethnicity in the clinical recognition of AF, which may have important implications for stroke prevention.

Dataset Information

Negative Affect and Risk of Atrial Fibrillation: MESA.

Publications

Negative Affect and Risk of Atrial Fibrillation: MESA.

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