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Background <p>Obstructive sleep apnoea (OSA) may lead to heart rhythm abnormalities including bradycardia. Our aim was to ascertain clinical and echocardiographic parameters in patients with OSA in whom severe bradycardia was detected in an outpatient setting, as well as to evaluate the efficacy of CPAP therapy on heart rate normalization at the early stages of treatment.</p> Methods <p>Fifteen patients mild, moderate or severe OSA and concomitant bradycardia were enrolled. A standard non-invasive diagnostic assessment protocol was followed, including blood tests and echocardiography. The 24-hour Holter ECG was performed to confirm the presence of bradycardia and determine its subtype. Then CPAP therapy was commenced. Throughout the hospitalisation, continued cardiac monitoring was used in all patients, and 3–4 days following CPAP therapy commencement, a follow-up 24-hour Holter ECG was performed.</p> Results <p>Out of 15 patients observed, 3 patients did not consent to CPAP therapy, and one patient had to undergo emergency pacemaker implantation before he was started on CPAP. A complete resolution of bradycardia and cardiac conduction abnormalities was achieved in the remaining 11 patients by day 4. of treatment. The mean lowest recorded HR was 52.7&#xa0;bpm as compared to 33.9&#xa0;bpm before CPAP therapy commencement (<i>p</i> &lt; 0.0002). Sinus pauses exceeding 2.5s were not detected in any of those patients.</p> Conclusion <p>OSA may be comorbid with and precipitate severe bradycardia. CPAP therapy enabled rapid resolution of bradycardia in more than 80% of our cohort, which may potentially prevent pacemaker implantation provided they remain compliant.</p>

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Severe bradycardia in patients with obstructive sleep apnoea and good early response to CPAP

  • 期刊论文

  • 发表日期：

    2025年1月27日

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  • Justyna Tyfel-Paluszek,
  • Aleksandra Kułaga,
  • Aleksandra Mikunda,
  • Łukasz Pominkiewicz,
  • Jacek Łach,
  • Wojciech Płazak

摘要

Background

Obstructive sleep apnoea (OSA) may lead to heart rhythm abnormalities including bradycardia. Our aim was to ascertain clinical and echocardiographic parameters in patients with OSA in whom severe bradycardia was detected in an outpatient setting, as well as to evaluate the efficacy of CPAP therapy on heart rate normalization at the early stages of treatment.

Methods

Fifteen patients mild, moderate or severe OSA and concomitant bradycardia were enrolled. A standard non-invasive diagnostic assessment protocol was followed, including blood tests and echocardiography. The 24-hour Holter ECG was performed to confirm the presence of bradycardia and determine its subtype. Then CPAP therapy was commenced. Throughout the hospitalisation, continued cardiac monitoring was used in all patients, and 3–4 days following CPAP therapy commencement, a follow-up 24-hour Holter ECG was performed.

Results

Out of 15 patients observed, 3 patients did not consent to CPAP therapy, and one patient had to undergo emergency pacemaker implantation before he was started on CPAP. A complete resolution of bradycardia and cardiac conduction abnormalities was achieved in the remaining 11 patients by day 4. of treatment. The mean lowest recorded HR was 52.7 bpm as compared to 33.9 bpm before CPAP therapy commencement (p < 0.0002). Sinus pauses exceeding 2.5s were not detected in any of those patients.

Conclusion

OSA may be comorbid with and precipitate severe bradycardia. CPAP therapy enabled rapid resolution of bradycardia in more than 80% of our cohort, which may potentially prevent pacemaker implantation provided they remain compliant.