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Original Research: Sleep Disorders |

Leptin Deficiency Promotes Central Sleep Apnea in Patients With Heart FailureLeptin Predicts Central Sleep Apnea

Ivan Cundrle, Jr, MD; Virend K. Somers, MD, PhD, FCCP; Prachi Singh, PhD; Bruce D. Johnson, PhD; Christopher G. Scott, MS; Christelle van der Walt, RPSGT; Lyle J. Olson, MD
Author and Funding Information

From the Department of Anesthesiology and Intensive Care (Dr Cundrle), International Clinical Research Center, St. Anne’s University Hospital, Brno, Czech Republic; and the Division of Cardiovascular Diseases (Drs Somers, Singh, Johnson, and Olson and Ms van der Walt) and the Department of Biomedical Statistics and Informatics (Mr Scott), Mayo Clinic, Rochester, MN.

Correspondence to: Lyle J. Olson, MD, Cardiovascular Diseases, Mayo Clinic, 200 First St SW, Rochester, MN 55905; e-mail: olson.lyle@mayo.edu


Funding/Support: Dr Cundrle was supported by the European Regional Development Fund, Project FNUSA-ICRC [CZ.1.05/1.1.00/02.0123], the European Social Fund, and the State Budget of the Czech Republic. This work was further supported by the Mayo Foundation; the American Heart Association [Grant 04-50103Z]; the National Heart, Lung, and Blood Institute [Grant HL65176]; the National Center for Research Resources, a component of the National Institutes of Health [Grant 1ULI RR024150]; and the National Institutes of Health Roadmap for Medical Research.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2014;145(1):72-78. doi:10.1378/chest.12-2914
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Background:  Leptin-deficient animals hyperventilate. Leptin expression by adipocytes is attenuated by atrial natriuretic peptide (ANP). Increased circulating natriuretic peptides (NPs) are associated with an increased risk of central sleep apnea (CSA). This study tested whether serum leptin concentration is inversely correlated to NP concentration and decreased in patients with heart failure (HF) and CSA.

Methods:  Subjects with HF (N = 29) were studied by measuring leptin, NPs, CO2 chemosensitivity (Δminute ventilation [V. e]/Δpartial pressure of end-tidal CO2 [Petco2]), and ventilatory efficiency (V. e/CO2 output [V. co2]) and were classified as CSA or no sleep-disordered breathing by polysomnography. CSA was defined as a central apnea-hypopnea index ≥ 15. The Student t test, Mann-Whitney U test, and logistic regression were used for analysis, and data were summarized as mean ± SD; P < .05 was considered significant.

Results:  Subjects with CSA had higher ANP and brain natriuretic peptide (BNP) concentrations (P < .05), ΔV. e/ΔPetco2 (2.39 ± 1.03 L/min/mm Hg vs 1.54 ± 0.35 L/min/mm Hg, P = .01), and V. e/V. co2 (43 ± 9 vs 34 ± 7, P < .01) and lower leptin concentrations (8 ± 10.7 ng/mL vs 17.1 ± 8.8 ng/mL, P < .01). Logistic regression analysis (adjusted for age, sex, and BMI) demonstrated leptin (OR = 0.07; 95% CI, 0.01-0.71; P = .04) and BNP (OR = 4.45; 95% CI, 1.1-17.9; P = .05) to be independently associated with CSA.

Conclusions:  In patients with HF and CSA, leptin concentration is low and is inversely related to NP concentration. Counterregulatory interactions of leptin and NP may be important in ventilatory control in HF.

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