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Purpose <p>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.</p> Methods <p>Muscle sympathetic nerve activity (MSNA) was recorded in 22 patients with systolic CHF (63 ± 9&#xa0;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).</p> Results <p>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 (<i>p</i> &gt; 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.</p> Conclusions <p>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.</p> Graphical abstract <p></p>

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Autonomic effects of simulated periodic breathing in patients with chronic heart failure on contemporary guideline-directed therapy

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月20日

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  • Francesco Gentile,
  • Lars Stumpp,
  • Paolo Sciarrone,
  • Alessandro Navari,
  • Eleonora Degl’Innocenti,
  • Giacomo D’Alesio,
  • Chiara Borrelli,
  • Sabrina Montuoro,
  • John Floras,
  • Vaughan G. Macefiled,
  • Calogero Maria Oddo,
  • Claudio Passino,
  • Michele Emdin,
  • Alberto Giannoni

摘要

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.

Graphical abstract