Abstract
RationaleAdaptive servo-ventilation (ASV), a novel respiratory support therapy for sleep disorders, may improve cardiac function in heart failure (HF). However, the reasons that ASV improves cardiac function have not been fully studied especially in sympathetic nervous function (SNF). The purpose of the present study was to investigate the effects of ASV therapy on cardiac SNF in patients with HF. MethodsWe evaluated ASV therapeutic effects before and 6 months after ASV therapy in 9 HF patients [57.3 ± 17.3 years old, left ventricular ejection fraction (LVEF) 36.1 ± 16.7%]. We performed echocardiography, polysomnography, biomarkers, 11C-hydroxyephedrine (HED) PET as a presynaptic function marker and planar 123I-metaiodobenzylguanidine (MIBG) to evaluate washout rate. ResultsASV therapy reduced apnea-hypopnea index (AHI) and improved plasma brain natriuretic peptide (BNP) concentration. In 123I-MIBG imaging, the early heart/mediastinum (H/M) ratio increased after ASV therapy (2.19 ± 0.58 to 2.40 ± 0.67; P = 0.045). Washout rate did not change (23.8 ± 7.3% to 23.8 ± 8.8%; P = 0.122). Global 11C-HED retention index (RI) improved from 0.068 ± 0.033/s to 0.075 ± 0.034/s (P = 0.029). ConclusionsASV reduced AHI and improved BNP. ASV might initially improve presynaptic cardiac sympathetic nervous function in HF patients after 6 months of treatment.
Highlights
Sympathetic nervous function (SNF) is an important compensatory mechanism to maintain cardiovascular homeostasis in chronic heart failure (HF).[1,2] continuous activation of cardiac SNF induces myocardial remodeling through increased active oxygen uptake and alters the signal transduction system of the betaadrenergic receptor, resulting in increased long-term mortality in HF.[3]
apnea-hypopnea index (AHI) reflects the severity of sleep apnea disorders and AHI [ 15 is defined as sleep apnea.[26]
Our findings suggest that Adaptive servoventilation (ASV) improves cardiac SNF in HF patients, but we cannot draw any conclusions about their long-term prognosis
Summary
Sympathetic nervous function (SNF) is an important compensatory mechanism to maintain cardiovascular homeostasis in chronic heart failure (HF).[1,2] continuous activation of cardiac SNF induces myocardial remodeling through increased active oxygen uptake and alters the signal transduction system of the betaadrenergic receptor, resulting in increased long-term mortality in HF.[3]. ASV could convert rapid shallow breathing patterns to slow regular breathing patterns and prevent respiratory oscillations in HF patients, which could inhibit cardiac SNF.[14,15] the evaluation of cardiac SNF is essential to determining the therapeutic mechanisms behind ASV in HF
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