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BackgroundProlongation of the QT interval has been associated with an increased risk of developing atrial fibrillation (AF), but the responsible mechanism remains unknown.ObjectivesThe aims of this study were to subdivide the QT interval into its components and identify the resultant electrocardiographic interval(s) responsible for the association with AF.MethodsPredefined QT-interval components were assessed for association with incident AF in the Atherosclerosis Risk in Communities study using Cox proportional hazards models. Hazard ratios (HRs) were calculated per 1-SD increase in each component. Among QT-interval components exhibiting significant associations, additional analyses evaluating long extremes, defined as greater than the 95th percentile, were performed.ResultsOf the 14,625 individuals, 1505 (10.3%) were diagnosed with incident AF during a mean follow-up period of 17.6 years. After multivariable adjustment, QT-interval components involved in repolarization, but not depolarization, exhibited significant associations with incident AF, including a longer ST segment (HR 1.27; 95% confidence interval [CI] 1.14-1.41; P < .001) and a prolonged T-wave onset to T-wave peak (T-onset to T-peak) (HR 1.13; 95% CI 1.07-1.20; P < .001). Marked prolongation of the ST segment (HR 1.31; 95% CI 1.04-1.64; P = .022) and T-onset to T-peak (HR 1.36; 95% CI 1.09-1.69; P = .006) was also associated with an increased risk of incident AF.ConclusionThe association between a prolonged QT interval and incident AF is primarily explained by components involved in ventricular repolarization: prolongation of the ST segment and T-onset to T-peak. These observations suggest that prolongation of phases 2 and 3 of the cardiac action potential drives the association between the QT interval and AF risk.

Background--It has recently been reported that atrial fibrillation (AF) is associated with an increased risk of myocardial infarction (MI). However, the mechanism underlying this association is currently unknown. Further study of the relationship of AF with the type of MI (ST-segment-elevation MI [STEMI] versus non-ST-segment-elevation MI [NSTEMI]) might shed light on the potential mechanisms. Methods and Results--We examined the association between AF and incident MI in 14 462 participants (mean age, 54 years; 56% women; 26% blacks) from the Atherosclerosis Risk in Communities (ARIC) study who were free of coronary heart disease at baseline (1987-1989) with follow-up through December 31, 2010. AF cases were identified from study visit ECGs and by review of hospital discharge records. Incident MI and its types were ascertained by an independent adjudication committee. Over a median follow-up of 21.6 years, 1374 MI events occurred (829 NSTEMIs, 249 STEMIs, 296 unclassifiable MIs). In a multivariable-adjusted model, AF (n=1545) as a time-varying variable was associated with a 63% increased risk of MI (hazard ratio,1.63; 95% confidence interval, 1.32-2.02). However, AF was associated with NSTEMI (hazard ratio, 1.80; 95% confidence interval, 1.39-2.31) but not STEMI (hazard ratio, 0.49; 95% confidence interval, 0.18-1.34; P for hazard ratio comparison=0.004). Combining the unclassifiable MI group with either STEMI or NSTEMI did not change this conclusion. The association between AF and MI, total and NSTEMI, was stronger in women than in men (P for interaction <0.01 for both).Conclusions--AF is associated with an increased risk of incident MI, especially in women. However, this association is limited to NSTEMI. [ABSTRACT FROM AUTHOR]

Objective: Advanced glycation end products (AGEs) may cause inflammation by binding to their cellular receptors (RAGE). Soluble RAGE (sRAGE) acts as a decoy receptor for AGEs and may prevent inflammation. Chronic low-grade inflammation is a risk factor for cardiovascular disease, including atrial fibrillation (AF). Methods: We studied 1,068 participants in a subsample of the Atherosclerosis Risk in Communities (ARIC) Study who had baseline measurements of sRAGE (mean age 56, 60% female, 21% Black). Inflammation was assessed using measurements of high sensitivity C-reactive protein (hsCRP), fibrinogen, gamma-glutamyl transferase (GGT) and white blood cell (WBC) count. AF events were identified using ECG data, hospitalization discharge codes, and linkage to the National Death Index. Results: Compared to the highest quartile (N1272.4 pg/mL), the lowest quartile of sRAGE (b714 pg/mL) was associated with higher baseline levels of inflammation (hsCRP=3 mg/L: OR = 2.21 [95% CI 1.41-3.49], fibrinogen =400 mg/dL: OR = 4.31 [95% CI 1.50-12.41], GGT =36 U/L in women and =61 U/L in men: OR = 5.22 [95% CI 2.66-10.22],WBC N6.2 × 109/L: OR = 2.38 [95% CI 1.52-3.72]). sRAGE was not prospectively associated with 6-year change in inflammatory markers (hsCRP or GGT). Therewas no significant association of sRAGE and risk of AF (HR 1.49 [95% CI: 0.80-2.78] for the 1st vs. 4th quartile of sRAGE). Conclusions: sRAGE was strongly inversely associated with markers of inflammation at baseline, but not prospectively. sRAGE was not significantly associated with incident AF. This supports a role for sRAGE in attenuating current inflammation, but it remains unclear whether sRAGE plays a role in the development of AF. [ABSTRACT FROM AUTHOR]

Background: Chronic kidney disease (CKD) is associated with sudden cardiac death and some types of cardiac arrhythmias. However, the prevalence of various types of arrhythmias across CKD severity is not well-characterized. We therefore quantified the burden of arrhythmias across CKD severity in community-dwelling older adults in the ARIC study. Methods: In 2202 adults aged 71-94 years who underwent 2 weeks of non-invasive heart rhythm monitoring using the Zio XT Patch, we examined the associations of atrial fibrillation (AF), non-sustained ventricular tachycardia (NSVT), long pause (>3 sec), 2nd (Mobitz II) or 3rd degree atrioventricular block (AVB), ventricular ectopy (VE), and supraventricular tachycardia (SVT) and ectopy (SVE) with CKD severity categorized as no CKD (low risk) and CKD with moderate, high, and very high risk according to kidney function and albuminuria. Results: CKD participants (vs. no-CKD) had a higher prevalence of AF (9% vs. 5%), NSVT (33% vs. 26%), long pause (4% vs. 2%), and major arrhythmias comprising of the 3 types (39% vs. 28%), with significantly higher prevalence across CKD stages [ Table ]. Conversely, they had a similar prevalence of AVB (2% vs. 2%), and a lower prevalence of SVT (82% vs. 89%) and SVE (61% vs. 66%). After adjusting for potential confounders, CKD with higher risk remained significantly associated with major arrhythmias and AF [ Table ]. CKD with higher risk groups also remained associated with a lower prevalence of supraventricular arrhythmias. Conclusions: Based on 2-week monitoring, major arrhythmias are common in older adults with CKD particularly when severe. Of the major arrhythmias, AF is most robustly associated with CKD severity, highlighting the importance of CKD in the pathophysiology of AF. The lower prevalence of SVT in CKD warrants further studies on potential mechanisms and clinical implications. [ABSTRACT FROM AUTHOR]