{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,23]],"date-time":"2026-01-23T22:51:22Z","timestamp":1769208682922,"version":"3.49.0"},"reference-count":57,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2019,4,2]]},"abstract":"\n Background<\/jats:title>\n \n Blacks harbor more cardiovascular risk factors than whites, but experience less atrial fibrillation (\n AF<\/jats:styled-content>\n ). Conversely, whites may have a lower risk of heart failure (\n CHF<\/jats:styled-content>\n ). N\u2010terminal pro\u2010B\u2010type natriuretic peptide (\n NT<\/jats:styled-content>\n \u2010pro\n BNP)<\/jats:styled-content>\n levels are higher in whites, predict incident\n AF<\/jats:styled-content>\n , and have diuretic effects in the setting of increased ventricular diastolic pressures, potentially providing a unifying explanation for these racial differences.\n <\/jats:p>\n <\/jats:sec>\n \n Methods and Results<\/jats:title>\n \n We used data from the CHS (Cardiovascular Health Study) to determine the degree to which baseline\n NT<\/jats:styled-content>\n \u2010pro\n BNP<\/jats:styled-content>\n levels mediate the relationships between race and incident\n AF<\/jats:styled-content>\n and\n CHF<\/jats:styled-content>\n by comparing beta estimates between models with and without\n NT<\/jats:styled-content>\n \u2010pro\n BNP<\/jats:styled-content>\n . The ARIC (Atherosclerosis Risk in Communities) study was used to assess reproducibility. Among 4731\n CHS<\/jats:styled-content>\n (770 black) and 12\u00a0418\n ARIC<\/jats:styled-content>\n (3091 black) participants, there were 1277 and 1253 incident\n AF<\/jats:styled-content>\n events, respectively. Whites had higher baseline\n NT<\/jats:styled-content>\n \u2010pro\n BNP<\/jats:styled-content>\n (\n CHS<\/jats:styled-content>\n : 40% higher than blacks; 95%\n CI<\/jats:styled-content>\n , 29\u201353;\n ARIC<\/jats:styled-content>\n : 39% higher; 95%\n CI<\/jats:styled-content>\n , 33\u201346) and had a greater risk of incident\n AF<\/jats:styled-content>\n compared with blacks (\n CHS<\/jats:styled-content>\n : adjusted hazard ratio, 1.60; 95%\n CI<\/jats:styled-content>\n , 1.31\u20131.93;\n ARIC<\/jats:styled-content>\n : hazard ratio, 1.93; 95%\n CI<\/jats:styled-content>\n , 1.57\u20132.27).\n NT<\/jats:styled-content>\n \u2010pro\n BNP<\/jats:styled-content>\n levels explained a significant proportion of the racial difference in\n AF<\/jats:styled-content>\n risk (\n CHS<\/jats:styled-content>\n : 36.2%; 95%\n CI<\/jats:styled-content>\n , 23.2\u201369.2%;\n ARIC<\/jats:styled-content>\n : 24.6%; 95%\n CI<\/jats:styled-content>\n , 14.8\u201339.6%). Contrary to our hypothesis, given an increased risk of\n CHF<\/jats:styled-content>\n among whites in\n CHS<\/jats:styled-content>\n (adjusted hazard ratio, 1.20; 95%\n CI<\/jats:styled-content>\n , 1.05\u20131.47) and the absence of a significant association between race and\n CHF<\/jats:styled-content>\n in\n ARIC<\/jats:styled-content>\n (adjusted hazard ratio, 1.07; 95%\n CI<\/jats:styled-content>\n , 0.94\u20131.23),\n CHF<\/jats:styled-content>\n \u2010related mediation analyses were not performed.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n A substantial portion of the relationship between race and\n AF<\/jats:styled-content>\n was statistically explained by baseline\n NT<\/jats:styled-content>\n \u2010pro\n BNP<\/jats:styled-content>\n levels. No consistent relationship between race and\n CHF<\/jats:styled-content>\n was observed.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1161\/jaha.118.010868","type":"journal-article","created":{"date-parts":[[2019,3,26]],"date-time":"2019-03-26T09:00:42Z","timestamp":1553590842000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":20,"title":["NT\u2010proBNP as a Mediator of the Racial Difference in Incident Atrial Fibrillation and Heart Failure"],"prefix":"10.1161","volume":"8","author":[{"given":"Isaac R.","family":"Whitman","sequence":"first","affiliation":[{"name":"Section\u00a0of Cardiac Electrophysiology Lewis Katz School of Medicine at Temple University Philadelphia Pennsylvania USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Eric","family":"Vittinghoff","sequence":"additional","affiliation":[{"name":"Department of Epidemiology and Biostatistics University of California, San Francisco San Francisco California USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christopher R.","family":"DeFilippi","sequence":"additional","affiliation":[{"name":"Division of Cardiology University of Maryland Baltimore Maryland USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John S.","family":"Gottdiener","sequence":"additional","affiliation":[{"name":"Division of Cardiology University of Maryland Baltimore Maryland USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alvaro","family":"Alonso","sequence":"additional","affiliation":[{"name":"Department of Epidemiology Rollins School of Public Health Emory University Atlanta Georgia USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bruce M.","family":"Psaty","sequence":"additional","affiliation":[{"name":"Cardiovascular Health Research Unit Departments of Medicine, Epidemiology, and Health Services University of Washington Seattle Washington USA"},{"name":"Kaiser Permanente Washington Health Research Institute Seattle Washington USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Susan R.","family":"Heckbert","sequence":"additional","affiliation":[{"name":"Department of Epidemiology University of Washington, School of Public Health Seattle Washington USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ron C.","family":"Hoogeveen","sequence":"additional","affiliation":[{"name":"Division of Atherosclerosis and Vascular Medicine Baylor College of Medicine Houston Texas USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dan E.","family":"Arking","sequence":"additional","affiliation":[{"name":"McKusick\u2010Nathans Institute of Genetic Medicine Johns Hopkins University Baltimore Maryland USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Elizabeth","family":"Selvin","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular and Clinical Epidemiology Johns Hopkins University Baltimore Maryland USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lin Y.","family":"Chen","sequence":"additional","affiliation":[{"name":"Cardiovascular Division University of Minnesota Minneapolis and Saint Paul, Minnesota USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thomas A.","family":"Dewland","sequence":"additional","affiliation":[{"name":"Knight Cardiovascular Institute Oregon Health & Science University Portland Oregon USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gregory M.","family":"Marcus","sequence":"additional","affiliation":[{"name":"Division of Cardiac Electrophysiology University of California, San Francisco San Francisco California USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIR.0000000000000558"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1161\/cir.0000000000000041"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9343(99)80348-9"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(09)60443-8"},{"key":"e_1_3_2_6_2","unstructured":"US Renal Data System USRDS 2009 Annual Data Report: Atlas of Chronic Kidney Disease and End\u2010Stage Renal Disease in the United States. 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