Hooman Kamel1, Kathleen Alwell2, Brett M Kissela2, Heidi J Sucharew3,4, Daniel Woo2, Matthew Flaherty2, Simona Ferioli2, Stacie L Demel2, Charles J Moomaw2, Kyle Walsh5, Jason Mackey6, De Los Rios La Rosa Felipe7, Adam Jasne8, Sabreena Slavin9, Sharyl Martini10, Opeolu Adeoye5, Tehniyat Baig11, Monica L Chen11, Emily B Levitan12, Elsayed Z Soliman13, Dawn O Kleindorfer2. 1. Clinical and Translational Neuroscience Unit, Feil Family Brain and Mind Research Institute and Department of Neurology, Weill Cornell Medicine, New York, NY; hok9010@med.cornell.edu. 2. Department of Neurology and Rehabilitation Medicine, University of Cincinnati, Cincinnati, OH. 3. Division of Biostatistics and Epidemiology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH. 4. Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH. 5. Department of Emergency Medicine, University of Cincinnati, Cincinnati, OH. 6. Department of Neurology, Indiana University School of Medicine, Indianapolis, IN. 7. Baptist Health Neuroscience Center, Miami, FL. 8. Department of Neurology, Yale University, New Haven, CT. 9. Department of Neurology, University of Kansas Medical Center, Kansas City, KS. 10. Michael E. DeBakey VA Medical Center, Houston, TX. 11. Clinical and Translational Neuroscience Unit, Feil Family Brain and Mind Research Institute and Department of Neurology, Weill Cornell Medicine, New York, NY. 12. Department of Epidemiology, University of Alabama at Birmingham, Birmingham, AL. 13. Division of Cardiology and Epidemiological Cardiology Research Center, Department of Epidemiology and Prevention, and Department of Internal Medicine-Cardiology, Wake Forest School of Medicine, Winston-Salem, NC.
Abstract
OBJECTIVE: To test the hypothesis that thrombogenic atrial cardiopathy may be relevant to stroke-related racial disparities, we compared atrial cardiopathy phenotypes between Black versus White ischemic stroke patients. METHODS: We assessed markers of atrial cardiopathy in the Greater Cincinnati/Northern Kentucky Stroke Study, a study of stroke incidence in a population of 1.3 million. We obtained ECGs and reports of echocardiograms performed during evaluation of stroke during the 2010/2015 study periods. Patients with atrial fibrillation (AF) or flutter (AFL) were excluded. Investigators blinded to patients' characteristics measured P-wave terminal force in ECG lead V1 (PTFV1), a marker of left atrial fibrosis and impaired inter-atrial conduction, and abstracted left atrial diameter from echocardiogram reports. Linear regression was used to examine the association between race and atrial cardiopathy markers after adjustment for demographics, body mass index, and vascular comorbidities. RESULTS: Among 3,426 ischemic stroke cases in Black or White patients without AF/AFL, 2,391 had a left atrial diameter measurement (mean, 3.65 ±0.70 cm). Black race was associated with smaller left atrial diameter in unadjusted (β coefficient, -0.11; 95% CI, -0.17 to -0.05) and adjusted (β, -0.15; 95% CI, -0.21 to -0.09) models. PTFV1 measurements were available in 3,209 patients (mean, 3,434 ±2,525 μV*ms). Black race was associated with greater PTFV1 in unadjusted (β, 1.59; 95% CI, 1.21 to 1.97) and adjusted (β, 1.45; 95% CI, 1.00 to 1.80) models. CONCLUSIONS: We found systematic Black-White racial differences in left atrial structure and pathophysiology in a population-based sample of ischemic stroke patients. CLASSIFICATION OF EVIDENCE: This study provides class II evidence that the rate of atrial cardiopathy is greater among Black people with acute stroke compared to White people.
OBJECTIVE: To test the hypothesis that thrombogenic atrial cardiopathy may be relevant to stroke-related racial disparities, we compared atrial cardiopathy phenotypes between Black versus White ischemic stroke patients. METHODS: We assessed markers of atrial cardiopathy in the Greater Cincinnati/Northern Kentucky Stroke Study, a study of stroke incidence in a population of 1.3 million. We obtained ECGs and reports of echocardiograms performed during evaluation of stroke during the 2010/2015 study periods. Patients with atrial fibrillation (AF) or flutter (AFL) were excluded. Investigators blinded to patients' characteristics measured P-wave terminal force in ECG lead V1 (PTFV1), a marker of left atrial fibrosis and impaired inter-atrial conduction, and abstracted left atrial diameter from echocardiogram reports. Linear regression was used to examine the association between race and atrial cardiopathy markers after adjustment for demographics, body mass index, and vascular comorbidities. RESULTS: Among 3,426 ischemic stroke cases in Black or White patients without AF/AFL, 2,391 had a left atrial diameter measurement (mean, 3.65 ±0.70 cm). Black race was associated with smaller left atrial diameter in unadjusted (β coefficient, -0.11; 95% CI, -0.17 to -0.05) and adjusted (β, -0.15; 95% CI, -0.21 to -0.09) models. PTFV1 measurements were available in 3,209 patients (mean, 3,434 ±2,525 μV*ms). Black race was associated with greater PTFV1 in unadjusted (β, 1.59; 95% CI, 1.21 to 1.97) and adjusted (β, 1.45; 95% CI, 1.00 to 1.80) models. CONCLUSIONS: We found systematic Black-White racial differences in left atrial structure and pathophysiology in a population-based sample of ischemic stroke patients. CLASSIFICATION OF EVIDENCE: This study provides class II evidence that the rate of atrial cardiopathy is greater among Black people with acute stroke compared to White people.
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