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Volume 16, Issue 1, Pages 55-60 (January 2010)


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Impaired Kidney Function and Atrial Fibrillation in Elderly Subjects

Rajat Deo, MD1Corresponding Author Informationemail address, Ronit Katz, DPhil2, Bryan Kestenbaum, MD3, Linda Fried, MD, MPH4, Mark J. Sarnak, MD5, Bruce M. Psaty, MD, PhD6, David S. Siscovick, MD, MPH6, Michael G. Shlipak, MD, MPH7

Received 30 May 2009; received in revised form 29 June 2009; accepted 1 July 2009. published online 04 September 2009.

Abstract 

Background

Impaired kidney function is associated with increased risk for cardiovascular events. We evaluated whether kidney function is associated with atrial fibrillation (AF) risk in elderly persons.

Methods and Results

Subjects were participants in the Cardiovascular Health Study (CHS), a population-based cohort of ambulatory elderly. Measures of kidney function were cystatin C and creatinine-based estimated glomerular filtration rate (eGFR). Among the 4663 participants, 342 (7%) had AF at baseline and 579 (13%) developed incident AF during follow-up (mean 7.4 years). In unadjusted analyses, cystatin C quartiles were strongly associated with prevalent AF with a nearly 3-fold odds in the highest quartile compared with the lowest (HR=1.19, 95% CI [0.80-1.76] in quartile 2; HR=2.00, 95% CI [1.38-2.88] in quartile 3; and HR=2.87, 95% CI [2.03-4.07] in quartile 4). This increased risk for prevalent AF remained significant after multivariate adjustment. The risk for incident AF increased across cystatin C quartiles in the unadjusted analysis (HR=1.37, 95% CI [1.07-1.75] in quartile 2; HR=1.43, 95% CI [1.11-1.84] in quartile 3; and HR=1.88, 95% CI [1.47-2.41] in quartile 4); however, after multivariate adjustment, these findings were no longer significant. An estimated GFR <60 mL·min·1.73m2 was associated with prevalent and incident AF in unadjusted, but not multivariate analyses.

Conclusions

Impaired kidney function, as measured by cystatin C, is an independent marker of prevalent AF; however, neither cystatin C nor eGFR are predictors of incident AF.

1 Division of Cardiology, University of Pennsylvania, Philadelphia, PA

2 Collaborative Health Studies Coordinating Center, University of Washington, Seattle, WA

3 Division of Nephrology, Department of Medicine, University of Washington, Veterans Affairs Puget Sound Health Care System, Seattle, WA

4 The Renal-Electrolyte Division, University of Pittsburgh School of Medicine, and the Renal Section, VA Pittsburgh Healthcare System, Pittsburgh, PA

5 Division of Nephrology, Department of Internal Medicine, Tufts-New England Medical Center, Boston, MA

6 Cardiovascular Health Research Unit, University of Washington, Seattle, WA

7 General Internal Medicine Section, Veterans Affairs Medical Center, San Francisco, CA; Departments of Medicine, Epidemiology and Biostatistics, University of California, San Francisco, CA

Corresponding Author InformationReprint requests: Rajat Deo, MD, Division of Cardiology, University of Pennsylvania, 3400 Spruce Street / 9 Founders Cardiology, Philadelphia, PA 19104. Phone: (215) 615-5455; Fax: (215) 662-2879.

 Supported by contracts N01-HC-35129, N01-HC-45133, N01-HC-75150, N01-HC-85079 through N01-HC-85086, N01 HC-15103, N01 HC-55222, and U01 HL080295 from the National Heart, Lung, and Blood Institute, with additional contribution from the National Institute of Neurological Disorders and Stroke.

PII: S1071-9164(09)00653-8

doi:10.1016/j.cardfail.2009.07.002


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