{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T14:45:31Z","timestamp":1792421131564,"version":"4.5.0"},"reference-count":40,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2014,5,22]]},"abstract":"\n Background<\/jats:title>\n \n Once atrial fibrillation (\n AF<\/jats:styled-content>\n ) progresses to sustained forms, adverse outcomes increase and treatment success rates decrease. Therefore, identification of risk factors predisposing to persistence of\n AF<\/jats:styled-content>\n may have a significant impact on\n AF<\/jats:styled-content>\n morbidity.\n <\/jats:p>\n <\/jats:sec>\n \n Methods and Results<\/jats:title>\n \n We prospectively examined the differential associations between traditional, lifestyle, and biomarker\n AF<\/jats:styled-content>\n risk factors and development of paroxysmal versus nonparoxysmal\n AF<\/jats:styled-content>\n (persistent\/permanent) among 34\u00a0720 women enrolled in the Women's Health Study who were free of cardiovascular disease and\n AF<\/jats:styled-content>\n at baseline.\n AF<\/jats:styled-content>\n patterns were defined based on current guidelines and classified according to the most sustained form of\n AF<\/jats:styled-content>\n within 2\u00a0years of diagnosis. During a median follow\u2010up of 16.4\u00a0years, 690 women developed paroxysmal\n AF<\/jats:styled-content>\n and 349 women developed nonparoxysmal\n AF<\/jats:styled-content>\n . In multivariable time\u2010varying competing risk models, increasing age (hazard ratio [\n HR<\/jats:styled-content>\n ] 1.11, 95% CI 1.10 to 1.13, versus\n HR<\/jats:styled-content>\n 1.08, 1.07 to 1.09, per year), body mass index (\n HR<\/jats:styled-content>\n 1.07, 1.05 to 1.09, versus\n HR<\/jats:styled-content>\n 1.03, 1.02 to 1.05, per kg\/m\n 2<\/jats:sup>\n ), and weight (\n HR<\/jats:styled-content>\n 1.30, 1.22 to 1.39, versus\n HR<\/jats:styled-content>\n 1.14, 1.08 to 1.20, per 10\u00a0kg) were more strongly associated with the development of nonparoxysmal\n AF<\/jats:styled-content>\n compared with paroxysmal\n AF<\/jats:styled-content>\n . Hemoglobin A1c levels at baseline were directly related to the development of nonparoxysmal\n AF<\/jats:styled-content>\n but inversely associated with paroxysmal\n AF<\/jats:styled-content>\n in multivariable competing risk models (\n P<\/jats:italic>\n for nonequal association=0.01).\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n In women without\n AF<\/jats:styled-content>\n or\n CVD<\/jats:styled-content>\n at baseline, increasing age, adiposity, and higher hemoglobin A1c levels were preferentially associated with the early development of nonparoxysmal\n AF<\/jats:styled-content>\n . These data raise the hypothesis that efforts aimed at weight reduction or glycemic control may affect the proportion of the population with sustained\n AF<\/jats:styled-content>\n .\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1161\/jaha.114.000916","type":"journal-article","created":{"date-parts":[[2014,5,1]],"date-time":"2014-05-01T23:04:26Z","timestamp":1398985466000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":79,"title":["Predisposing Factors Associated With Development of Persistent Compared With Paroxysmal Atrial Fibrillation"],"prefix":"10.1161","volume":"3","author":[{"given":"Roopinder K.","family":"Sandhu","sequence":"first","affiliation":[{"name":"Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada"},{"name":"Division of Preventive Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Conen","sequence":"additional","affiliation":[{"name":"Division of Preventive Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston MA"},{"name":"Department of Medicine, University Hospital, Basel, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Usha B.","family":"Tedrow","sequence":"additional","affiliation":[{"name":"Division of Preventive Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston MA"},{"name":"Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kathryn C.","family":"Fitzgerald","sequence":"additional","affiliation":[{"name":"Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aruna D.","family":"Pradhan","sequence":"additional","affiliation":[{"name":"Division of Preventive Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston MA"},{"name":"Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul M","family":"Ridker","sequence":"additional","affiliation":[{"name":"Division of Preventive Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston MA"},{"name":"Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert J.","family":"Glynn","sequence":"additional","affiliation":[{"name":"Division of Preventive Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christine M.","family":"Albert","sequence":"additional","affiliation":[{"name":"Division of Preventive Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston MA"},{"name":"Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, 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