Objective: Given that recent reports have suggested left atrial disease to be an independent risk factor for ischemic stroke, we sought to examine if advanced interatrial block (aIAB) is an independent stroke risk factor. Methods: We examined the association between aIAB and incident ischemic stroke in 14,716 participants (mean age 54 ± 5.8 years; 55% female; 26% black) from the Atherosclerosis Risk in Communities Study (ARIC). Cases of aIAB were identified from digital ECGs recorded during the baseline ARIC visit (1987–1989) and the first 3 follow-up study visits (1990–1992, 1993–1995, and 1996–1998). Adjudicated ischemic stroke events were ascertained through December 31, 2010. Results: There were 266 (1.8%) participants who had evidence of aIAB. Over a median follow-up of 22 years, 916 (6.2%) ischemic stroke events were detected. The incidence rate (per 1,000 person-years) of ischemic stroke among those with aIAB (incidence rate 8.05, 95% confidence interval [CI] 5.7, 11.4) was more than twice the rate in those without aIAB (incidence rate 3.14, 95% CI 2.94, 3.35). In a multivariable Cox regression analysis adjusted for stroke risk factors and potential confounders, aIAB was associated with an increased risk of ischemic stroke (hazard ratio 1.63, 95% CI 1.13, 2.34). The results were consistent across subgroups of participants stratified by age, sex, and race. Conclusions: In the ARIC, aIAB was associated with incident ischemic stroke, which strengthens the hypothesis that left atrial disease should be considered an independent stroke risk factor.

Background: Onset of postoperative atrial fibrillation ( POAF ) is a common and costly complication of heart surgery despite major improvements in surgical technique and quality of patient care. The etiology of POAF , and the ability of clinicians to identify and therapeutically target high‐risk patients, remains elusive. Methods and Results: Myocardial tissue dissected from right atrial appendage ( RAA ) was obtained from 244 patients undergoing cardiac surgery. Reactive oxygen species ( ROS ) generation from multiple sources was assessed in this tissue, along with total glutathione ( GSH t) and its related enzymes GSH ‐peroxidase ( GP x) and GSH ‐reductase ( GR ). Monoamine oxidase ( MAO ) and NADPH oxidase were observed to generate ROS at rates 10‐fold greater than intact, coupled mitochondria. POAF risk was significantly associated with MAO activity (Quartile 1 [Q1]: adjusted relative risk [ ARR ]=1.0; Q2: ARR =1.8, 95% confidence interval [ CI ]=0.84 to 4.0; Q3: ARR =2.1, 95% CI =0.99 to 4.3; Q4: ARR =3.8, 95% CI =1.9 to 7.5; adjusted P _trend =0.009). In contrast, myocardial GSH t was inversely associated with POAF (Quartile 1 [Q1]: adjusted relative risk [ ARR ]=1.0; Q2: ARR =0.93, 95% confidence interval [ CI ]=0.60 to 1.4; Q3: ARR =0.62, 95% CI =0.36 to 1.1; Q4: ARR =0.56, 95% CI =0.34 to 0.93; adjusted P _trend =0.014). GP x also was significantly associated with POAF ; however, a linear trend for risk was not observed across increasing levels of the enzyme. GR was not associated with POAF risk. Conclusions: Our results show that MAO is an important determinant of redox balance in human atrial myocardium, and that this enzyme, in addition to GSH t and GP x, is associated with an increased risk for POAF . Further investigation is needed to validate MAO as a predictive biomarker for POAF , and to explore this enzyme's potential role in arrhythmogenesis.