TY - JOUR
T1 - Leptin deficiency promotes central sleep apnea in patients with heart failure
AU - Cundrle, Ivan
AU - Somers, Virend K.
AU - Singh, Prachi
AU - Johnson, Bruce D.
AU - Scott, Christopher G.
AU - Van Der Walt, Christelle
AU - Olson, Lyle J.
N1 - Funding Information:
Financial/nonfinancial disclosures: The authors have reported to CHEST the following conflicts of interest: Dr Somers has served as a consultant for ResMed; Cardiac Concepts, Inc; GlaxoSmithKline; Sunovian Pharmaceuticals Inc; Deshum Medical; Respicardia; and Medtronic, Inc; and has been a principal investigator or coinvestigator on research grants funded by The Respironics Charitable Foundation, The ResMed Foundation, and the Sorin Corporation. Drs Cundrle, Singh, Johnson, and Olson; Mr Scott; and Ms van der Walt have reported that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.
Funding Information:
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.
PY - 2014/1
Y1 - 2014/1
N2 - 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 [VE]/Δpartial pressure of end-tidal CO2 [PETCO 2]), and ventilatory efficiency (VE/CO2 output [VCO 2]) 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), ΔVE/ ΔPETCO2 (2.39 ± 1.03 L/min/mm Hg vs 1.54 ± 0.35 L/min/mm Hg, P = .01), and VE/VCO2 (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.
AB - 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 [VE]/Δpartial pressure of end-tidal CO2 [PETCO 2]), and ventilatory efficiency (VE/CO2 output [VCO 2]) 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), ΔVE/ ΔPETCO2 (2.39 ± 1.03 L/min/mm Hg vs 1.54 ± 0.35 L/min/mm Hg, P = .01), and VE/VCO2 (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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U2 - 10.1378/chest.12-2914
DO - 10.1378/chest.12-2914
M3 - Article
C2 - 24030529
AN - SCOPUS:84892658216
SN - 0012-3692
VL - 145
SP - 72
EP - 78
JO - Chest
JF - Chest
IS - 1
ER -