Cross-Sectional Relationship Between Atrial Conduction Delay and Arterial Stiffness in Patients with Obstructive Sleep Apnea.

Aim: Prolonged P-wave duration (PWD), which indicates atrial conduction delay, is a potent precursor of atrial fibrillation (AF) that may be induced by obstructive sleep apnea (OSA). The cardio-ankle vascular index (CAVI), which is an arterial stiffness parameter, is elevated in patients with OSA; moreover, an increased CAVI is associated with atrial conduction delay through left atrium enlargement in association with left ventricular diastolic dysfunction. We aimed to examine the relationship between the CAVI and PWD in patients with OSA. Methods: We included patients with a sinus rhythm who underwent overnight polysomnography. We measured the PWD and CAVI on standard 12-lead electrocardiograms; further, we analyzed the relationship between PWD and CAVI. Results: We analyzed data from 300 participants (men, 89.0%; mean age, 52.3 ± 13.1 years; and body mass index, 26.2 ± 3.9 kg/m2). The mean PWD was 104.4 ± 10.4 ms while the mean CAVI was 7.5 ± 1.5. PWD was significantly correlated with CAVI (r = 0.478, p < 0.001); additionally, PWD and CAVI were directly associated with OSA severity (p = 0.002 and p = 0.002, respectively). Multivariate regression analysis revealed an independent significant correlation of PWD and CAVI with OSA severity. Conclusion: In patients with OSA, an increase in arterial stiffness is associated with atrial conduction delay.

Effects of obstructive sleep apnea and its treatment on signal-averaged P-wave duration in men.

BACKGROUND: Prolonged P-wave duration, indicating atrial conduction delay, is a potent precursor of atrial fibrillation. Obstructive sleep apnea (OSA) is a risk factor for atrial fibrillation development. We investigated the association of P-wave duration with OSA and its treatment. METHODS AND RESULTS: We enrolled 80 consecutive men with normal sinus rhythms who underwent polysomnography, had no history of atrial fibrillation or ischemic heart disease, and no evidence of heart failure. Signal-averaged P-wave duration (SAPWD) was measured in all participants. Multivariable regression analysis showed that age, hypertension, and log-transformed apnea-hypopnea index were significantly and independently correlated with SAPWD. SAPWD was repeatedly measured after 1 month of continuous positive airway pressure (CPAP) therapy in 62 patients with moderate-to-severe OSA. As controls, 18 patients with moderate-to-severe OSA were enrolled. Their SAPWD was also measured at baseline and after 1 month without CPAP therapy. No significant change in SAPWD was found between baseline and after 1 month in the controls. However, SAPWD was significantly shortened after 1 month of CPAP therapy (from 137.5±8.6 to 129.7±8.5 ms; P<0.001), and the SAPWD change was significantly different in patients with CPAP therapy compared with controls (P<0.001). In addition, the SAPWD change in patients with CPAP therapy correlated inversely with nightly CPAP usage (r=-0.52; P<0.001). CONCLUSIONS: OSA severity was significantly associated with prolonged SAPWD. CPAP therapy significantly shortened SAPWD in patients with moderate-to-severe OSA. Thus, OSA may cause atrial conduction disturbances, leading to an increased risk of atrial fibrillation development, which may be modifiable by alleviating OSA with CPAP therapy.

Relationship between atrial conduction delay and obstructive sleep apnea.

Prolonged P-wave duration, indicating atrial conduction delay, is a marker of left atrial abnormality and is reported as a potent precursor of atrial fibrillation (AF). Several studies have shown that obstructive sleep apnea (OSA) is associated with AF. We evaluated the relationship between OSA and prolonged P-wave duration. Consecutive subjects who underwent overnight polysomnography and showed a normal sinus rhythm, had no history of AF or ischemic heart disease, and showed no evidence of heart failure were enrolled. Apnea-hypopnea index (AHI) is defined as the number of apnea and hypopnea events per hour of sleep. P-wave duration was determined on the basis of the mean duration of three consecutive beats in lead II from a digitally stored electrocardiogram. A total of 250 subjects (middle-aged, predominantly male, mildly obese, with a mean P-wave duration of 106 ms) were enrolled. In addition to age, male gender, body mass index (BMI), hypertension, dyslipidemia, and uric acid and creatinine levels, AHI (r = 0.56; P < 0.001) had significant univariable relationship with P-wave duration. Multivariate regression analysis showed that age, BMI, male gender, and AHI (partial correlation coefficient, 0.47; P < 0.001) were significantly independently correlated to P-wave duration. Severity of OSA is significantly associated with delayed atrial conduction time. Obstructive sleep apnea may lead to progression of atrial remodeling as an AF substrate.

Adaptive servo-ventilation in cardiac function and neurohormonal status in patients with heart failure and central sleep apnea nonresponsive to continuous positive airway pressure.

OBJECTIVES: The aim of this study was to investigate whether effective suppression of central sleep apnea (CSA) by adaptive servo-ventilation (ASV) improves underlying cardiac dysfunction among patients with heart failure (HF) in whom CSA was not effectively suppressed by continuous positive airway pressure (CPAP). BACKGROUND: The presence of CSA in HF is associated with a poor prognosis, whereas CPAP treatment improves HF. However, in a large-scale trial, CPAP failed to improve survival, probably due to insufficient CSA suppression. Recently, ASV was reported as the most effective alternative to CSA suppression. However, the effects of sufficient CSA suppression by ASV on cardiac function are unknown. METHODS: Patients with New York Heart Association class ≥II HF, left ventricular ejection fraction <50%, and CSA that was unsuppressed (defined as an apnea-hypopnea index ≥15) despite ≥3 months of CPAP were randomly assigned to receive ASV in either CPAP mode or ASV mode. RESULTS: Of 23 patients enrolled, 12 were assigned to the ASV-mode group and 11 were assigned to the CPAP-mode group. Three months after randomization, the ASV mode was significantly more effective in suppressing the apnea-hypopnea index (from 25.0 ± 6.9 events/h to 2.0 ± 1.4 events/h; p < 0.001) compared to the CPAP mode. Compliance was signi-ficantly greater with the ASV mode than with the CPAP mode. Improvement in left ventricular ejection fraction was greater with the ASV mode (32.0 ± 7.9% to 37.8 ± 9.1%; p < 0.001) than with the CPAP mode. CONCLUSIONS: Patients with HF and unsuppressed CSA despite receiving CPAP may receive additional benefit by having CPAP replaced with ASV. Additionally, effective suppression of CSA may improve cardiac function in HF patients.

Conversion from predominant central sleep apnea to obstructive sleep apnea following valvuloplasty in a patient with mitral regurgitation.

A few reports have shown that cardiac valve repair may improve central sleep apnea (CSA) in patients with valvular heart disease. It has been suggested that such improvements are associated with the improvement of cardiac function. We report the case of a 67-year-old man with mitral regurgitation, whose CSA converted to predominant obstructive sleep apnea following mitral valvuloplasty in association with a shortening of lung-to-finger circulation time.

Evaluation of the apnea-hypopnea index determined by the S8 auto-CPAP, a continuous positive airway pressure device, in patients with obstructive sleep apnea-hypopnea syndrome.

OBJECTIVE: Continuous positive airway pressure (CPAP) has been established as an effective treatment for obstructive sleep apnea-hypopnea syndrome (OSAHS). Recently, several auto-CPAP devices that can detect upper airway obstructive events and provide information about residual events while patients are on CPAP have come into clinical use. The purpose of this study was to compare the apnea-hypopnea index (AHI) determined by the S8 auto-CPAP device with the AHI derived by polysomnography in patients with OSAHS. METHOD: Consecutive patients with OSAHS titrated on S8 auto-CPAP were included. The correlation between AHI determined by manual scoring (AHI-PSG) and by S8 (AHIS8) during an overnight in-hospital polysomnogram with the patient on CPAP was assessed. Furthermore, the apnea index (Al) and the hypopnea index (HI) were evaluated separately. RESULTS: Seventy patients with OSAHS (94% men) were enrolled. The mean AHI on the diagnostic study was 51.9 +/- 2.4. During the titration, this device markedly suppressed the respiratory events (AHI-PSG, 4.2 +/- 0.4; AI, 1.9 +/- 0.3; HI, 2.3 +/- 0.3). On the other hand, the AHI-S8 was 9.9 +/- 0.6 (AI-S8, 2.4 +/- 0.3; HI-S8, 7.5 +/- 0.4). There was a strong correlation between the overall AHI-PSG and the AHI-S8 (r = 0.85, p < 0.001), with a stronger correlation in the apnea component AI-PSG and the AI-S8 (r = 0.93, p < 0.001), whereas there was a weaker correlation between the HI-PSG and the HI-S8 (r = 0.67, p <0.001). CONCLUSIONS: Using the same airflow signals as those of the CPAP device, a strong correlation between the AHI-PSG and the AHI-S8 was observed. However, the correlation was weakened when the analysis was limited to the HI.

Establishment of the cardio-ankle vascular index in patients with obstructive sleep apnea.

BACKGROUND: An arterial stiffness parameter, the cardio-ankle vascular index (CAVI), has been developed. CAVI is adjusted for BP and can be used to measure arterial stiffness with little influence of BP. The purpose of this study was to evaluate the reproducibility, validity, and clinical usefulness of CAVI among patients with obstructive sleep apnea (OSA), who often have elevated BP during measurement. METHODS: Overall, 543 consecutive patients with OSA were studied. CAVI was automatically calculated from the pulse volume record, BP, and the vascular length from the heart to the ankle. First, CAVI was measured three times on different days in 25 patients to evaluate its reproducibility. Second, the correlation between CAVI and BP was assessed. Third, patients were classified into two groups (mild OSA or moderate-to-severe OSA), and the CAVIs of these groups were compared. Fourth, the correlation between CAVI and carotid intima-media thickness (IMT) was also assessed in 74 patients. RESULTS: The mean coefficient of variation was 2.8. CAVI demonstrated weak or no correlations with BP (with systolic BP, r = 0.184; with diastolic BP, r = 0.223). Patients with moderate-to-severe OSA (n = 469) had a significantly greater CAVI than patients with mild OSA (p = 0.034). CAVI was positively correlated with IMT (r = 0.487). CONCLUSIONS: The measurement of CAVI demonstrated good reproducibility and was not affected by the BP during measurement. Additionally, CAVI was positively correlated with another arteriosclerosis indicator. CAVI was higher in patients with more severe OSA and is regarded as a clinically useful index for the progression of vascular damage.

Advanced atrioventricular block induced by obstructive sleep apnea before oxygen desaturation.

We report a patient with transient advanced atrioventricular (AV) block induced by obstructive sleep apnea (OSA). This 54-year-old man was diagnosed as having severe OSA and AV block with ventricular asystole for more than 6 s during overnight polysomnography, which occurred just from the onset of OSA before oxygen desaturation had occurred. An electrophysiological study revealed normal AV conduction system function and normal His-Purkinje system function. The resolution of OSA with continuous positive airway pressure therapy improved the advanced AV block. Therefore, the bradyarrhythmia was determined to be an OSA-induced AV block that occurred before oxygen desaturation.

Atrioventricular block during the phasic events of REM sleep in a patient with severe obstructive sleep apnea syndrome.

Patients with obstructive sleep apnea syndrome (OSAS) sometimes have atrioventricular (AV) block during sleep. However, significant resolution of such AV block with treatment for OSAS has been reported. On the other hand, during rapid eye movement (REM) sleep, conduction disturbances not associated with the apnea event can be observed, particularly in young healthy subjects. We report the case of a 67-year-old man with severe OSAS and 2:1 AV block that occurred only during the phasic events of REM sleep; continuous positive airway pressure (CPAP) treatment did not result in resolution of the AV block. No specific abnormalities were found on cardiac evaluation. Based on the analysis of overnight heart rate variability, CPAP treatment resulted in a markedly reduced ratio of low-frequency to high-frequency power and an increased high-frequency power, though high-frequency power was not increased during REM sleep on CPAP.