TY - JOUR
T1 - Cardiac Biomarkers and Risk of Atrial Fibrillation in Chronic Kidney Disease
T2 - The CRIC Study
AU - on behalf of the CRIC Study Investigators
AU - Lamprea-Montealegre, Julio A.
AU - Zelnick, Leila R.
AU - Shlipak, Michael G.
AU - Floyd, James S.
AU - Anderson, Amanda H.
AU - He, Jiang
AU - Christenson, Rob
AU - Seliger, Stephen L.
AU - Soliman, Elsayed Z.
AU - Deo, Rajat
AU - Ky, Bonnie
AU - Feldman, Harold I.
AU - Kusek, John W.
AU - deFilippi, Christopher R.
AU - Wolf, Myles S.
AU - Shafi, Tariq
AU - Go, Alan S.
AU - Bansal, Nisha
AU - Appel, Lawrence J.
AU - Lash, James P.
AU - Rao, Panduranga S.
AU - Rahman, Mahboob
AU - Townsend, Raymond R.
N1 - Funding Information:
This study was also supported by R01 DK103612 (Bansal) and R01 01DK104730 (Anderson). This research was supported in part by an unrestricted gift from the Northwest Kidney Centers to the Kidney Research Institute. Roche Diagnostics provided partial funding for the NT‐proBNP and hsTnT assays. Funding for the CRIC Study was obtained under a cooperative agreement from National Institute of Diabetes and Digestive and Kidney Diseases (U01DK060990, U01DK060984, U01DK061022, U01DK061021, U01DK061028, U01DK060980, U01DK060963, and U01DK060902). In addition, this work was supported in part by: the Perelman School of Medicine at the University of Pennsylvania Clinical and Translational Science Award NIH/NCATS UL1TR000003, Johns Hopkins University UL1 TR‐000424, University of Maryland GCRC M01 RR‐16500, Clinical and Translational Science Collaborative of Cleveland, UL1TR000439 from the National Center for Advancing Translational Sciences (NCATS) component of the National Institutes of Health and NIH Roadmap for Medical Research, Michigan Institute for Clinical and Health Research (MICHR) UL1TR000433, University of Illinois at Chicago CTSA UL1RR029879, Tulane COBRE for Clinical and Translational Research in Cardiometabolic Diseases P20 GM109036, Kaiser Permanente NIH/NCRR UCSF‐CTSI UL1 RR‐024131.
Funding Information:
Dr Seliger has received research funding from Roche Diagnostics and Critical Diagnostics. The remaining authors have no disclosures to report.
Funding Information:
Dr Lamprea‐Montealegre is recipient of a postdoctoral research fellowship from the American Heart Association (AHA 18POST34030003).
Publisher Copyright:
© 2019 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.
PY - 2019/8/6
Y1 - 2019/8/6
N2 - Background: We tested associations of cardiac biomarkers of myocardial stretch, injury, inflammation, and fibrosis with the risk of incident atrial fibrillation (AF) in a prospective study of chronic kidney disease patients. Methods and Results: The study sample was 3053 participants with chronic kidney disease in the multicenter CRIC (Chronic Renal Insufficiency Cohort) study who were not identified as having AF at baseline. Cardiac biomarkers, measured at baseline, were NT-proBNP (N-terminal pro-B-type natriuretic peptide), high-sensitivity troponin T, galectin-3, growth differentiation factor-15, and soluble ST-2. Incident AF (“AF event”) was defined as a hospitalization for AF. During a median follow-up of 8 years, 279 (9%) participants developed a new AF event. In adjusted models, higher baseline log-transformed NT-proBNP (N-terminal pro-B-type natriuretic peptide) was associated with incident AF (adjusted hazard ratio [HR] per SD higher concentration: 2.11; 95% CI, 1.75, 2.55), as was log-high-sensitivity troponin T (HR 1.42; 95% CI, 1.20, 1.68). These associations showed a dose–response relationship in categorical analyses. Although log-soluble ST-2 was associated with AF risk in continuous models (HR per SD higher concentration 1.35; 95% CI, 1.16, 1.58), this association was not consistent in categorical analyses. Log-galectin-3 (HR 1.05; 95% CI, 0.91, 1.22) and log-growth differentiation factor-15 (HR 1.16; 95% CI, 0.96, 1.40) were not significantly associated with incident AF. Conclusions: We found strong associations between higher NT-proBNP (N-terminal pro-B-type natriuretic peptide) and high-sensitivity troponin T concentrations, and the risk of incident AF in a large cohort of participants with chronic kidney disease. Increased atrial myocardial stretch and myocardial cell injury may be implicated in the high burden of AF in patients with chronic kidney disease.
AB - Background: We tested associations of cardiac biomarkers of myocardial stretch, injury, inflammation, and fibrosis with the risk of incident atrial fibrillation (AF) in a prospective study of chronic kidney disease patients. Methods and Results: The study sample was 3053 participants with chronic kidney disease in the multicenter CRIC (Chronic Renal Insufficiency Cohort) study who were not identified as having AF at baseline. Cardiac biomarkers, measured at baseline, were NT-proBNP (N-terminal pro-B-type natriuretic peptide), high-sensitivity troponin T, galectin-3, growth differentiation factor-15, and soluble ST-2. Incident AF (“AF event”) was defined as a hospitalization for AF. During a median follow-up of 8 years, 279 (9%) participants developed a new AF event. In adjusted models, higher baseline log-transformed NT-proBNP (N-terminal pro-B-type natriuretic peptide) was associated with incident AF (adjusted hazard ratio [HR] per SD higher concentration: 2.11; 95% CI, 1.75, 2.55), as was log-high-sensitivity troponin T (HR 1.42; 95% CI, 1.20, 1.68). These associations showed a dose–response relationship in categorical analyses. Although log-soluble ST-2 was associated with AF risk in continuous models (HR per SD higher concentration 1.35; 95% CI, 1.16, 1.58), this association was not consistent in categorical analyses. Log-galectin-3 (HR 1.05; 95% CI, 0.91, 1.22) and log-growth differentiation factor-15 (HR 1.16; 95% CI, 0.96, 1.40) were not significantly associated with incident AF. Conclusions: We found strong associations between higher NT-proBNP (N-terminal pro-B-type natriuretic peptide) and high-sensitivity troponin T concentrations, and the risk of incident AF in a large cohort of participants with chronic kidney disease. Increased atrial myocardial stretch and myocardial cell injury may be implicated in the high burden of AF in patients with chronic kidney disease.
KW - atrial fibrillation
KW - biomarker
KW - chronic kidney disease
UR - http://www.scopus.com/inward/record.url?scp=85071171058&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85071171058&partnerID=8YFLogxK
U2 - 10.1161/JAHA.119.012200
DO - 10.1161/JAHA.119.012200
M3 - Article
C2 - 31379242
AN - SCOPUS:85071171058
VL - 8
JO - Journal of the American Heart Association
JF - Journal of the American Heart Association
SN - 2047-9980
IS - 15
M1 - e012200
ER -