Cardiac Biomarkers and Risk of Atrial Fibrillation in Chronic Kidney Disease: The CRIC Study
JournalJournal of the American Heart Association
PublisherAmerican Heart Association
MetadataShow full item record
AbstractBackground: 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.
Identifier to cite or link to this itemhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85071171058&doi=10.1161%2fJAHA.119.012200&partnerID=40&md5=479bdfe3d48e75c2c2040bcce464d7fe; http://hdl.handle.net/10713/10495