Parveen K Garg1, Traci M Bartz2, Faye L Norby3, Neal W Jorgensen2, Robyn L McClelland2, Christie M Ballantyne4, Lin Y Chen5, John S Gottdiener6, Philip Greenland7, Ron Hoogeveen4, Nancy S Jenny8, Jorge R Kizer9, Robert S Rosenson10, Elsayed Z Soliman11, Mary Cushman12, Alvaro Alonso13, Susan R Heckbert14. 1. Division of Cardiology, Keck School of Medicine, University of Southern California, Los Angeles, CA. Electronic address: parveeng@med.usc.edu. 2. Department of Biostatistics, University of Washington, Seattle, WA. 3. Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN. 4. Section of Atherosclerosis and Vascular Medicine, Baylor College of Medicine, Houston, TX; The Center for Cardiovascular Disease Prevention, Methodist DeBakey Heart Center, Houston, TX. 5. Cardiovascular Division, University of Minnesota Medical School, Minneapolis, MN. 6. Division of Cardiology, University of Maryland School of Medicine, Baltimore, MD. 7. Departments of Preventive Medicine and Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL. 8. Department of Pathology, Larner College of Medicine at the University of Vermont, Burlington, VT. 9. Department of Medicine, Albert Einstein College of Medicine, Bronx, NY; Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY. 10. Mount Sinai Heart, Icahn School of Medicine at Mount Sinai, New York, NY. 11. Epidemiological Cardiology Research Center (EPICARE), Department of Epidemiology and Prevention, Wake Forest School of Medicine, Winston-Salem, NC; Department of Medicine, Section on Cardiology, Wake Forest School of Medicine, Winston-Salem, NC. 12. Department of Pathology, Larner College of Medicine at the University of Vermont, Burlington, VT; Department of Medicine, Cardiovascular Research Institute, Larner College of Medicine at the University of Vermont College of Medicine, Burlington, VT. 13. Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA. 14. Department of Epidemiology, University of Washington, Seattle, WA.
Abstract
BACKGROUND: Multiple prospective studies have established an association between inflammation and higher risk of atrial fibrillation (AF), but the association between lipoprotein-associated phospholipase A2 (Lp-PLA2) mass and activity and incident AF has not been extensively evaluated. METHODS: Using data from 10,794 Atherosclerosis Risk In Communities (ARIC) study participants aged 53-75 years, 5,181 Cardiovascular Health Study (CHS) participants aged 65 to 100 years, and 5,425 Multi-Ethnic Study of Atherosclerosis (MESA) participants aged 45-84 years, we investigated the association between baseline Lp-PLA2 levels and the risk of developing AF. Incident AF was identified in each cohort by follow-up visit electrocardiograms, hospital discharge coding of AF, or Medicare claims data. RESULTS: Over a mean of 13.1, 11.5, and 10.0 years of follow-up, 1,439 (13%), 2,084 (40%), and 615 (11%) incident AF events occurred in ARIC, CHS, and MESA, respectively. In adjusted analyses, each SD increment in Lp-PLA2 activity was associated with incident AF in both ARIC (hazard ratio [HR] 1.13, 95% CI 1.06-1.20) and MESA (HR 1.24, 95% CI 1.05-1.46). Each SD increment in Lp-PLA2 mass was also associated with incident AF in MESA (HR 1.25, 95% CI 1.11-1.41). No significant associations were observed among CHS participants. CONCLUSIONS: Although higher Lp-PLA2 mass and activity were associated with development of AF in ARIC and MESA, this relationship was not observed in CHS, a cohort of older individuals.
BACKGROUND: Multiple prospective studies have established an association between inflammation and higher risk of atrial fibrillation (AF), but the association between lipoprotein-associated phospholipase A2 (Lp-PLA2) mass and activity and incident AF has not been extensively evaluated. METHODS: Using data from 10,794 Atherosclerosis Risk In Communities (ARIC) study participants aged 53-75 years, 5,181 Cardiovascular Health Study (CHS) participants aged 65 to 100 years, and 5,425 Multi-Ethnic Study of Atherosclerosis (MESA) participants aged 45-84 years, we investigated the association between baseline Lp-PLA2 levels and the risk of developing AF. Incident AF was identified in each cohort by follow-up visit electrocardiograms, hospital discharge coding of AF, or Medicare claims data. RESULTS: Over a mean of 13.1, 11.5, and 10.0 years of follow-up, 1,439 (13%), 2,084 (40%), and 615 (11%) incident AF events occurred in ARIC, CHS, and MESA, respectively. In adjusted analyses, each SD increment in Lp-PLA2 activity was associated with incident AF in both ARIC (hazard ratio [HR] 1.13, 95% CI 1.06-1.20) and MESA (HR 1.24, 95% CI 1.05-1.46). Each SD increment in Lp-PLA2 mass was also associated with incident AF in MESA (HR 1.25, 95% CI 1.11-1.41). No significant associations were observed among CHS participants. CONCLUSIONS: Although higher Lp-PLA2 mass and activity were associated with development of AF in ARIC and MESA, this relationship was not observed in CHS, a cohort of older individuals.
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