Cystatin C, Left Ventricular Hypertrophy, and Diastolic Dysfunction: Data From the Heart and Soul Study
Received 1 May 2006; received in revised form 18 July 2006; accepted 25 July 2006.
Abstract
Background
Impaired kidney function, as measured by serum cystatin C, is associated with risk of incident heart failure. Whether cystatin C is associated with preclinical cardiac structural abnormalities is unknown. We evaluate whether cystatin C is associated with left ventricular hypertrophy, diastolic dysfunction, and systolic dysfunction among 818 outpatients with coronary artery disease who were free of clinical heart failure.
Methods and Results
The 818 study participants were categorized into quartiles based on serum cystatin C concentrations, with ≤0.91 mg/L constituting the lowest quartile (I) and ≥1.28 mg/L constituting the highest (IV). Left ventricular hypertrophy (left ventricular mass index >90 g/m2 by truncated ellipsoid method), diastolic dysfunction (impaired relaxation, pseudo-normal, or restrictive filling patterns) and systolic dysfunction (left ventricular ejection fraction ≤50%) were determined by echocardiography. Left ventricular hypertrophy was present in 68% of participants in quartile IV, compared with 44% of those in quartile I (adjusted odds ratio [OR] 2.17; 95% confidence interval [CI] 1.34 to 3.52; P = .002). Diastolic dysfunction was present in 52% of participants in quartile IV, compared with 24% of those in quartile I (adjusted OR 1.79; 95% CI 1.04 to 3.11; P = .04). Systolic dysfunction was present in 12% of those in quartile IV, compared with 6% of those in quartile I (adjusted OR 1.83; 95% CI 0.75 to 4.46; P = .15).
Conclusion
Higher cystatin C concentrations are strongly associated with left ventricular hypertrophy and diastolic dysfunction in outpatients with coronary artery disease and without heart failure.
1From the Division of Nephrology, University of California San Francisco, San Francisco, California
2Department of Medicine, University of California San Francisco, San Francisco, California
3Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, California
5Division of Cardiology, University of California San Francisco, San Francisco, California
4Section of General Internal Medicine, VA Medical Center, San Francisco, California
Reprint requests: Joachim H. Ix, MD, Division of Nephrology, Department of Medicine, Box 0532, HSE 672, University of California, San Francisco, San Francisco, CA 94143–0532.
Supported by grants from the UCSF Academic Senate, the American Heart Association Fellow to Faculty Award (J.H.I.), and the Department of Veterans Affairs, the American Federation for Aging Research, the Robert Wood Johnson Foundation, the Ischemia Research and Education Foundation, and Dade Behring, Inc (M.A.W.). This study was supported by a research grant from Dade Behring, Inc. Dade Behring, Inc. played no role in the design, analysis, or preparation of the manuscript.
Previously presented in abstract form at the American Heart Association 46th Annual Council on Epidemiology and Prevention, Phoenix, Arizona, March 3, 2006.
All decisions regarding this manuscript were made by a guest editor.
ABSTRACT