Cystatin C, Left Ventricular Hypertrophy, and Diastolic Dysfunction: Data From the Heart and Soul Study
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.
Key Words: Heart failure, Echocardiography, Kidney, Structure
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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.
PII: S1071-9164(06)00838-4
doi:10.1016/j.cardfail.2006.07.005
© 2006 Elsevier Inc. All rights reserved.
