Journal of Cardiac Failure
Volume 13, Issue 9 , Pages 738-743, November 2007

In Patients With Heart Failure Elevated Soluble TNF-Receptor 1 Is Associated With Higher Risk of Depression

  • Alec J. Moorman, MD

      Affiliations

    • Department of Internal Medicine, Division of Cardiology, and Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, Washington
    • ,
  • Dariush Mozaffarian, MD, DrPH

      Affiliations

    • Harvard School of Public Health, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts
    • ,
  • Charles W. Wilkinson, PhD

      Affiliations

    • Geriatric Research, Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, and Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, Washington
    • ,
  • Richard L. Lawler, BS

      Affiliations

    • Gastroenterology/Hepatology Section, Fred Hutchinson Cancer Research Center, Seattle, Washington
    • ,
  • George B. McDonald, MD

      Affiliations

    • Gastroenterology/Hepatology Section, Fred Hutchinson Cancer Research Center, Seattle, Washington
    • ,
  • Barbara A. Crane, RN

      Affiliations

    • Department of Internal Medicine, Division of Cardiology, and Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, Washington
    • ,
  • John A. Spertus, MD, MPH

      Affiliations

    • Mid America Heart Institute and the University of Missouri–Kansas City, Kansas City, Missouri
    • ,
  • Joan E. Russo, PhD

      Affiliations

    • Department of Internal Medicine, Division of Cardiology, and Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, Washington
    • ,
  • April S. Stempien-Otero, MD

      Affiliations

    • Department of Internal Medicine, Division of Cardiology, and Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, Washington
    • ,
  • Mark D. Sullivan, MD, PhD

      Affiliations

    • Department of Internal Medicine, Division of Cardiology, and Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, Washington
    • ,
  • Wayne C. Levy, MD

      Affiliations

    • Department of Internal Medicine, Division of Cardiology, and Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, Washington
    • Corresponding Author InformationReprint requests: Wayne C. Levy, University of Washington, Box 356422, 1959 NE Pacific Street, Seattle, WA 98195.

Received 27 January 2007; received in revised form 13 May 2007; accepted 4 June 2007.

Abstract 

Background

Pro-inflammatory cytokines may contribute to the development and progression of heart failure (HF) and are also implicated in depressive disorders. In this cross-sectional study, we investigated whether systemic inflammation, as assessed by circulating levels of inflammatory cytokines, was associated with comorbid depression in patients with heart failure.

Methods and Results

Baseline clinical variables, depression status, and inflammatory marker levels were measured in 129 ambulatory HF patients. We hypothesized that pro-inflammatory cytokines, specifically tumor necrosis factor (TNF)-α, interleukin (IL)-1, and IL-6, would be elevated in HF patients with comorbid depression. In unadjusted analyses, levels of soluble TNF-α receptor1 (sTNFr1) were significantly higher among depressed (1.6 ng/mL), compared with nondepressed (1.1 ng/mL), HF patients (P = .01). After multivariate adjustment, compared with patients in the lowest quartile of sTNFr1 levels, those in the highest quartile had an adjusted near 5-fold higher risk of depression (OR 4.6, 95% CI 1.2–17.3; P for trend .008). The subgroup of patients on antidepressants but not currently depressed had a trend toward higher levels of sTNFr1, suggesting that antidepressants may not lower cytokine levels even when adequately treating depressive symptoms. IL-1β and IL-6 levels were not significantly different among depressed versus nondepressed HF patients.

Conclusions

In this cross-sectional analysis, HF patients with comorbid depression, compared with nondepressed HF patients, had higher levels of sTNFr1 and trend toward higher levels of sTNFr1 even when adequately treated for depression.

Key Words: Heart failure, depression, cytokines, inflammation

To access this article, please choose from the options below

Login to an existing account or Register a new account.

  • Purchase this article for 31.50 USD (You must login/register to purchase this article)

    Online access for 24 hours. The PDF version can be downloaded as your permanent record.

  • Subscribe to this title

    Get unlimited online access to this article and all other articles in this title 24/7 for one year.

  • Claim access now

    For current subscribers with Society Membership or Account Number.

  • Visit SciVerse ScienceDirect to see if you have access via your institution.
 

 Supported in part by a Charles A. Dana Foundation Grant, Dana Foundation, New York, NY; and in part by an American Heart Association Grant 9970185N to Dr. Sullivan. A portion of this work was conducted through the Clinical Research Center Facility at the University of Washington and supported by Grant M01-RR-00037 from the National Institutes of Health, Bethesda, MD. Dr. McDonald's Cytokine Analysis Laboratory was supported by Grant CA18029 from the National Institutes of Health, Bethesda, MD.

PII: S1071-9164(07)00471-X

doi:10.1016/j.cardfail.2007.06.301

Journal of Cardiac Failure
Volume 13, Issue 9 , Pages 738-743, November 2007

Article Tools