title: Electrocardiographic left atrial abnormality and stroke subtype in the atherosclerosis risk in communities study.
abstract: OBJECTIVE
  The aim of this study was to assess the relationship between abnormally increased P-wave terminal force in lead V1 , an electrocardiographic (ECG) marker of left atrial abnormality, and incident ischemic stroke subtypes. We hypothesized that associations would be stronger with nonlacunar stroke, given that we expected left atrial abnormality to reflect the risk of thromboembolism rather than in situ cerebral small-vessel occlusion.
  
  
  METHODS
  Our cohort comprised 14,542 participants 45 to 64 years of age prospectively enrolled in the Atherosclerosis Risk in Communities study and free of clinically apparent atrial fibrillation (AF) at baseline. Left atrial abnormality was defined as PTFV1 >4,000μV*ms. Outcomes were adjudicated ischemic stroke, nonlacunar (including cardioembolic) ischemic stroke, and lacunar stroke.
  
  
  RESULTS
  During a median follow-up period of 22 years (interquartile range, 19-23 years), 904 participants (6.2%) experienced a definite or probable ischemic stroke. A higher incidence of stroke occurred in those with baseline left atrial abnormality (incidence rate per 1,000 person-years, 6.3; 95% confidence interval [CI]: 5.4-7.4) than in those without (incidence rate per 1,000 person-years, 2.9; 95% CI: 2.7-3.1; p < 0.001). In Cox regression models adjusted for potential confounders and incident AF, left atrial abnormality was associated with incident ischemic stroke (hazard ratio [HR]: 1.33; 95% CI: 1.11-1.59). This association was limited to nonlacunar stroke (HR, 1.49; 95% CI: 1.07-2.07) as opposed to lacunar stroke (HR, 0.89; 95% CI: 0.57-1.40).
  
  
  CONCLUSIONS
  We found an association between ECG-defined left atrial abnormality and subsequent nonlacunar ischemic stroke. Our findings suggest that an underlying atrial cardiopathy may cause left atrial thromboembolism in the absence of recognized AF.
authors.affiliation: Department of Neurology and Feil Family Brain and Mind Research Institute, Weill Cornell Medical College, New York, NY.
authors.forename: Hooman
authors.initials: H
authors.lastname: Kamel
authors.affiliation: Department of Medicine, Wake Forest School of Medicine, Winston-Salem, NC.
authors.forename: Wesley T
authors.initials: WT
authors.lastname: O'Neal
authors.affiliation: Division of Cardiology, Weill Cornell Medical College, New York, NY.
authors.forename: Peter M
authors.initials: PM
authors.lastname: Okin
authors.affiliation: Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC.
authors.forename: Laura R
authors.initials: LR
authors.lastname: Loehr
authors.affiliation: Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, MN.
authors.forename: Alvaro
authors.initials: A
authors.lastname: Alonso
authors.affiliation: Epidemiological Cardiology Research Center, Department of Epidemiology and Prevention, Wake Forest School of Medicine, Winston-Salem, NC.
authors.forename: Elsayed Z
authors.initials: EZ
authors.lastname: Soliman
mesh_terms: D050197:Atherosclerosis / Q000175:diagnosis* / Q000503:physiopathology; D016279:Atrial Function, Left; D002545:Brain Ischemia / Q000473:pathology; D059345:Cerebral Small Vessel Diseases / Q000473:pathology; D015331:Cohort Studies; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D015994:Incidence; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D018570:Risk Assessment; D012307:Risk Factors; D020521:Stroke / Q000145:classification / Q000175:diagnosis* / Q000503:physiopathology; D059409:Stroke, Lacunar / Q000473:pathology; D013923:Thromboembolism / Q000473:pathology