Journal of Cardiac Failure
Volume 12, Issue 8 , Pages 601-607, October 2006

Cystatin C, Left Ventricular Hypertrophy, and Diastolic Dysfunction: Data From the Heart and Soul Study

  • Joachim H. Ix, MD

      Affiliations

    • From the Division of Nephrology, University of California San Francisco, San Francisco, California
    • Department of Medicine, University of California San Francisco, San Francisco, California
    • Corresponding Author InformationReprint 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.
  • ,
  • Michael G. Shlipak, MD, MPH

      Affiliations

    • Department of Medicine, University of California San Francisco, San Francisco, California
    • Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, California
    • Section of General Internal Medicine, VA Medical Center, San Francisco, California
  • ,
  • Glenn M. Chertow, MD, MPH

      Affiliations

    • From the Division of Nephrology, University of California San Francisco, San Francisco, California
    • Department of Medicine, University of California San Francisco, San Francisco, California
    • Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, California
  • ,
  • Sadia Ali, MD, MPH

      Affiliations

    • Section of General Internal Medicine, VA Medical Center, San Francisco, California
  • ,
  • Nelson B. Schiller, MD

      Affiliations

    • Department of Medicine, University of California San Francisco, San Francisco, California
    • Division of Cardiology, University of California San Francisco, San Francisco, California
  • ,
  • Mary A. Whooley, MD

      Affiliations

    • Department of Medicine, University of California San Francisco, San Francisco, California
    • Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, California
    • Section of General Internal Medicine, VA Medical Center, San Francisco, California

Received 1 May 2006; received in revised form 18 July 2006; accepted 25 July 2006.

San Francisco, California

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

Journal of Cardiac Failure
Volume 12, Issue 8 , Pages 601-607, October 2006