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Journal of Cardiology Cases logoLink to Journal of Cardiology Cases
. 2025 Jun 21;32(3):130–133. doi: 10.1016/j.jccase.2025.06.005

Impacts of atrial fibrillation on sleep-disordered breathing: Insights from two heart failure cases

Naoya Kataoka 1, Teruhiko Imamura 1,, Koichiro Kinugawa 1
PMCID: PMC12432507  PMID: 40948950

Abstract

Respiratory stability time (RST) has been proposed as an index for assessing heart failure-related sleep-disordered breathing. This case report examines the impact of catheter ablation for atrial fibrillation (AF) on RST and its relationship with heart failure. Two patients were analyzed: one with preserved ejection fraction (Case 1) and one with reduced ejection fraction (Case 2). In Case 1, RST improved significantly following ablation, accompanied by a decrease in plasma B-type natriuretic peptide levels. In contrast, while B-type natriuretic peptide levels decreased post-ablation in Case 2, RST showed minimal change, suggesting that the hemodynamic effects of restoring sinus rhythm had a lesser impact on respiratory stability. These findings indicate that the contribution of AF to the worsening of sleep-disordered breathing in heart failure differs between preserved and reduced ejection fraction. Further investigation of the association between RST and AF may offer valuable insights into the complex relationship between AF and heart failure.

Learning objective

This case report is the first to demonstrate changes in nocturnal respiratory dysfunction after catheter ablation for atrial fibrillation in heart failure. Quantitative assessment of respiratory stability may help elucidate the role of atrial fibrillation in heart failure.

Keywords: Atrial fibrillation, Catheter ablation, Sleep-disordered breathing, Respiratory stability time, Heart failure

Introduction

Sleep-disordered breathing has been recognized not only as the predominant form of respiratory dysfunction in patients with chronic heart failure but also as a contributor to arrhythmias, particularly atrial fibrillation (AF). This is thought to occur through mechanisms involving intermittent hypoxia, carbon dioxide and acid-base alterations, and hyperactivation of the sympathetic nervous system [1,2]. As a result, sleep-disordered breathing, heart failure, and AF are intricately intertwined, influencing each other, while the causal relationships between them remain unclear.

Asanoi and colleagues previously introduced a novel index, termed ‘respiratory stability time (RST),’ for assessing sleep-disordered breathing using a device (PARAMAOUNT BED Co., Ltd., Tokyo, Japan) equipped with sensors to detect thoracic movements associated with respiration and software with an algorithm to calculate RST (Fig. 1) [3]. Detailed parameters obtained from RST devices are provided in the Online Materials. Sleep-disordered breathing in heart failure with reduced ejection fraction, commonly presenting as Cheyne–Stokes respiration, is characterized by periodic breathing, resulting in a broad frequency distribution in the frequency analysis of chest wall motion. Based on this theory, the RST value is high when the breathing state is stable and low when periodic breathing is more pronounced. Several clinical studies have reported its utility in evaluating heart failure exacerbations requiring hospitalization and in predicting the prognosis of heart failure cohorts [4,5]. However, analyses of RST in patients with AF and the acute changes in RST after conversion to sinus rhythm have yet to be established.

Fig. 1.

Fig. 1

The concept of respiratory stability time (RST) monitoring system.

Herein, we present two cases of catheter ablation for AF in patients with heart failure. The changes in RST following the procedure provide new insights into the impact of AF on hemodynamics in patients with heart failure, as well as the differences between those with reduced and preserved ejection fraction.

Case reports

Case 1: preserved ejection fraction

Before hospitalization

A 70-year-old male with a body mass index of 21.2 kg/m2 and a history of long-standing AF, diagnosed three years earlier and treated with dabigatran 75 mg (2 capsules twice daily), was referred to our hospital. He had been taking amlodipine 5 mg daily for hypertension for approximately 10 years. There was no prior diagnosis of sleep apnea, and family members had never reported significant snoring. Until recently, he had no significant symptoms; however, since approximately six months, he began experiencing dyspnea on exertion, which led to his referral to our hospital. Echocardiographic evaluation revealed a left atrial diameter of 36 mm, a left ventricular end-diastolic dimension of 41 mm, a left ventricular end-systolic dimension of 31 mm, and a left ventricular ejection fraction of 63 %. The patient was subsequently diagnosed with heart failure with preserved ejection fraction. Therefore, we decided to proceed with catheter ablation for AF to restore sinus rhythm.

After hospitalization

On the day of hospitalization, the electrocardiogram revealed AF, and the chest X-ray showed slight cardiomegaly with a cardiothoracic ratio of 47.5 % (Fig. 2A). Laboratory data revealed a serum creatinine level of 1.14 mg/dL. The RST device was initiated on the day of hospitalization, and chest wall motion cycles associated with respiration during nighttime were recorded two days prior to catheter ablation. On the third day of hospitalization, pulsed-field ablation for AF was performed utilizing the PulseSelect™ system (Medtronic Inc., Minneapolis, MN, USA). The procedure successfully restored the patient from AF to sinus rhythm. Following the procedure, the symptom of dyspnea resolved, accompanied by a reduction in the cardiothoracic ratio (Fig. 2A). The RST was 20 s with an ultra-low frequency rate of 24.3 % on the day of hospitalization and 16 s with a rate of 34.5 % on the second day. Following the procedure, B-type natriuretic peptide levels decreased from 166.5 pg/mL to 61.8 pg/mL, RST improved to 96 s, and the ultra-low frequency rate declined to 2.2 % (Fig. 2A).

Fig. 2.

Fig. 2

Trends in respiratory stability time (RST), Ultra-Low Frequency Rate, and B-Type Natriuretic Peptide. Panel A represents Case 1, while Panel B represents Case 2. In both cases, B-type natriuretic peptide levels decreased following the restoration of sinus rhythm. However, RST increased in Case 1, whereas no significant change was observed in Case 2. The numerical values in chest X-rays indicate the cardiothoracic ratio.

Case 2: reduced ejection fraction

Before hospitalization

A 79-year-old male with persistent AF, diagnosed four months previously, was referred to our hospital. Similar to Case 1, he had no prior diagnosis of sleep apnea. He had severe aortic stenosis with regurgitation and underwent aortic valve replacement 10 years previously. His left ventricular ejection fraction declined from 42 % to 30 % postoperatively. Seven years previously, he underwent implantation of a cardiac resynchronization therapy device for advanced atrioventricular block with reduced ejection fraction. Approximately one year previously, he experienced an acute myocardial infarction due to embolism in the left anterior descending artery. During a device check, asymptomatic paroxysmal AF was detected, and he was diagnosed with coronary artery embolism due to AF. Warfarin 1.75 mg daily was initiated; however, rhythm control for AF was not pursued. As a result, his AF became persistent four months previously. Serum N-terminal pro B-type natriuretic peptide levels increased from 1500 to 4000 pg/mL and remained elevated, leading to worsening heart failure, which prompted his referral to our department. Echocardiographic evaluation revealed a left atrial diameter of 41 mm, a left ventricular end-diastolic dimension of 55 mm, a left ventricular end-systolic dimension of 45 mm, and a left ventricular ejection fraction of 40 %. We determined that AF contributed to the worsening of the heart failure condition and decided to proceed with AF ablation.

After hospitalization

On the day of hospitalization, the electrocardiogram revealed AF concomitant with biventricular pacing, exhibiting nearly 100 % pacing capture due to atrioventricular conduction disorder (Fig. 2B). The chest X-ray showed a cardiothoracic ratio of 49.5 % accompanied by mild pulmonary congestion. On the third day of hospitalization, pulsed-field ablation was performed using the PulseSelect™ system. Following the procedure, the cardiac rhythm was successfully restored to sinus rhythm; however, the cardiothoracic ratio did not decrease, which differed from Case 1 (Fig. 2B). The RST was 23 s with an ultra-low frequency rate of 36.8 % on the day of hospitalization and 13 s with a rate of 59.0 % on the second day. Although plasma B-type natriuretic peptide levels decreased from 654.5 pg/mL to 143.6 pg/mL after the procedure, the RST remained approximately unchanged at 15 s, and the ultra-low frequency rate remained 21 % (Fig. 2B).

Discussion

These case reports represent the first human data on RST changes before and after AF ablation. In a patient with preserved ejection fraction (Case 1), RST improved post-procedure alongside a decrease in B-type natriuretic peptide. However, in a patient with reduced ejection fraction requiring cardiac resynchronization therapy (Case 2), B-type natriuretic peptide decreased immediately, but RST remained unchanged.

Possible factors to cause RST fluctuation in heart failure with AF

AF is a well-established contributor to the progression of heart failure, regardless of whether ejection fraction is preserved or reduced [6]. Since RST was originally developed as a monitoring index for heart failure, it can be inferred that RST values in heart failure patients are closely associated with AF. Sleep-disordered breathing in heart failure is influenced by three factors: elevation of left ventricular filling pressure leading to pulmonary edema, respiratory center dysfunction due to cerebral tissue hypoperfusion associated with low cardiac output, and overactivation of chemosensitivity in the brain [7]. The acute effects of AF primarily affect hemodynamics, leading to an increase in left atrial pressure due to the loss of the atrial kick. Therefore, the first factor among the three components mentioned above is likely to be the key factor in the association between the acute changes in RST and AF.

Mechanisms underlying the differences between Case 1 and Case 2

Fig. 3 illustrates potential pressure-volume loops in heart failure with AF. In cases with elevated B-type natriuretic peptide levels associated with AF, left ventricular filling pressure is expected to be elevated, accompanied by the absence of the a-wave loop, indicating an increase in left atrial pressure (Fig. 3, central panel). After catheter ablation for AF, left atrial pressure in cases with preserved ejection fraction will decrease rapidly to near-normal levels, with the a-wave regaining (Fig. 3, left panel). Consequently, the RST will immediately increase to levels observed in healthy individuals. However, in cases with reduced ejection fraction, left atrial pressure may remain elevated due to a high v-wave (Fig. 3, right panel). Subsequently, even if B-type natriuretic peptide levels decrease numerically following the restoration of sinus rhythm, pulmonary congestion does not improve rapidly, and the RST remains low. It is well established that AF itself leads to elevated levels of natriuretic peptides, making it challenging to diagnose heart failure in the presence of concomitant AF [8].

Fig. 3.

Fig. 3

A hypothesis for respiratory stability time (RST) changes using the left atrial pressure-volume loop. Possible pressure-volume loops in heart failure with preserved ejection fraction (left panel) or reduced ejection fraction (right panel). The central panel illustrates the state of elevated left atrial pressure in the presence of atrial fibrillation (AF), indicating worsening heart failure.

EF, ejection fraction; SR, sinus rhythm.

The changes in ultra-low frequency rates provide valuable insights. The ultra-low frequency component increases with the exacerbation of central sleep-disordered breathing, typically presenting as Cheyne-Stokes respiration in cases of severely reduced ejection fraction [3]. Cheyne-Stokes respiration is thought to be primarily influenced by cerebral tissue hypoperfusion and overactivation of chemosensitivity, rather than by an elevation in left atrial pressure [9]. Notably, while the trend of daily changes in ultra-low frequency rates was similar between the two cases, the rates were consistently higher in Case 2 compared to Case 1 (Fig. 2, black lines). These findings suggest that the ultra-low frequency components of periodic breathing during sleep are primarily influenced by cardiac output, rather than by acute hemodynamic changes associated with left heart pressure.

Limitations

Firstly, as neither right heart catheterization nor echocardiographic assessment was performed following the ablation, it cannot be definitively concluded whether the observed changes in RST were attributable to hemodynamic alterations. Secondly, the relationship between RST and data obtained from polysomnography has not been fully elucidated in previous studies; therefore, this issue should be addressed in future investigations [5]. Furthermore, it remains unclear whether low-frequency components improve following AF ablation in patients with heart failure with reduced ejection fraction, and whether such improvements occur concurrently with changes in ejection fraction or exhibit a temporal delay. In addition, it is uncertain whether RST values ultimately show improvement. These questions warrant further research.

Conclusion

We present two cases of catheter ablation for AF in heart failure, one with preserved ejection fraction showing improvement in RST following the procedure, and another with reduced ejection fraction demonstrating no change in RST. The quantitative evaluation of sleep-disordered breathing may offer valuable insights into the relationship between AF and heart failure.

Patient permission/consent statement

Written informed consent was obtained from the patients.

Declaration of competing interest

None.

Footnotes

Appendix A

Supplementary data to this article can be found online at https://doi.org/10.1016/j.jccase.2025.06.005.

Appendix A. Supplementary data

Supplementary material

mmc1.docx (18KB, docx)

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Supplementary Materials

Supplementary material

mmc1.docx (18KB, docx)

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