Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2026
Autonomic effects of simulated periodic breathing in patients with chronic heart failure on contemporary guideline-directed therapy.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Gentile Francesco, Stumpp Lars, Sciarrone Paolo, Navari Alessandro, Degl'Innocenti Eleonora, D'Alesio Giacomo, Borrelli Chiara, Montuoro Sabrina, Floras John, Macefiled Vaughan G, Oddo Calogero Maria, Passino Claudio, Emdin Michele, Giannoni Alberto
Аннотация
PURPOSE: The aim of this study was to evaluate sympathetic responses to experimentally induced periodic breathing/Cheyne-Stokes respiration (PB/CSR)-like patterns in optimally treated patients with chronic heart failure (CHF) compared with matched healthy controls.
METHODS: Muscle sympathetic nerve activity (MSNA) was recorded in 22 patients with systolic CHF (63 ± 9 years; left ventricular ejection fraction 31 ± 8%) and 10 age- and sex-matched healthy controls during spontaneous breathing and during two experimental protocols designed to reproduce PB/CSR-like oscillations: a short-cycle protocol (five cycles of 30-s apnea/30-s recovery breathing) and a long-cycle protocol (five cycles of 30-s apnea/60-s recovery breathing).
RESULTS: At baseline, MSNA was comparable between patients with CHF and controls, whereas heart rate variability indices were reduced in CHF. Compared with spontaneous breathing, simulated PB/CSR-averaging apnea and recovery phases-was associated with modest reductions in MSNA, with no significant differences between protocols or groups (p > 0.05). Both maneuvers elicited reproducible oscillatory patterns in MSNA, characterized by increases during apnea and decreases during recovery breathing, consistent with PB/CSR-like entrainment. However, patients with CHF exhibited weaker and more temporally dispersed coupling between MSNA and cardiorespiratory variables compared with controls.
CONCLUSIONS: In optimally treated CHF, baseline sympathetic activity is comparable to that of healthy controls, and PB/CSR-like breathing primarily induces phase-locked oscillatory modulation of MSNA rather than sustained sympathetic activation. Impaired autonomic-hemodynamic coupling may represent a key mechanism underlying the clinical relevance of abnormal breathing patterns in CHF.
METHODS: Muscle sympathetic nerve activity (MSNA) was recorded in 22 patients with systolic CHF (63 ± 9 years; left ventricular ejection fraction 31 ± 8%) and 10 age- and sex-matched healthy controls during spontaneous breathing and during two experimental protocols designed to reproduce PB/CSR-like oscillations: a short-cycle protocol (five cycles of 30-s apnea/30-s recovery breathing) and a long-cycle protocol (five cycles of 30-s apnea/60-s recovery breathing).
RESULTS: At baseline, MSNA was comparable between patients with CHF and controls, whereas heart rate variability indices were reduced in CHF. Compared with spontaneous breathing, simulated PB/CSR-averaging apnea and recovery phases-was associated with modest reductions in MSNA, with no significant differences between protocols or groups (p > 0.05). Both maneuvers elicited reproducible oscillatory patterns in MSNA, characterized by increases during apnea and decreases during recovery breathing, consistent with PB/CSR-like entrainment. However, patients with CHF exhibited weaker and more temporally dispersed coupling between MSNA and cardiorespiratory variables compared with controls.
CONCLUSIONS: In optimally treated CHF, baseline sympathetic activity is comparable to that of healthy controls, and PB/CSR-like breathing primarily induces phase-locked oscillatory modulation of MSNA rather than sustained sympathetic activation. Impaired autonomic-hemodynamic coupling may represent a key mechanism underlying the clinical relevance of abnormal breathing patterns in CHF.