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Schlafbezogene Atmungsstörungen und kardiale Arrhythmien
Abstract
Schlafbezogene Atmungsstörungen sind eine häufige und klinisch relevante Komorbidität bei Patienten mit Herzrhythmusstörungen. Eine erhöhte Inzidenz ebenso wie ein vorzeitiges Wiederauftreten von Vorhofflimmern nach elektrischer Kardioversion oder Katheterablation gilt bei Patienten mit unbehandelter schlafbezogener Atmungsstörung als gesichert. Bei herzinsuffizienten Patienten scheint es zu häufigerem und vorzeitigem Auftreten lebensbedrohlicher Arrhythmien zu kommen. Die obstruktive, schlafbezogene Atmungsstörung (OSA) gilt als Risikofaktor für den plötzlichen Herztod, der hier gehäuft während des Schlafes auftritt. Während erste Studien positive Effekte auf die Arrhythmieneigung bei Patienten mit OSA unter kontinuierlicher Überdruckbeatmung nachweisen konnten, stehen randomisierte Studien für die positive Beeinflussung von Arrhythmien bei Patienten mit Cheyne-Stokes-Atmung noch aus.
Abstract
Sleep-disordered breathing is a highly prevalent and clinically relevant co-morbidity in patients with heart rhythm disorders. An increased incidence of atrial fibrillation as well as a premature reoccurrence of atrial fibrillation following electrical cardioversion or catheter ablation has previously been demonstrated. Patients with chronic heart failure seem to face an increased risk for malignant arrhythmic events. Furthermore, in patients with obstructive sleep apnea sudden cardiac death occurs more frequently during sleeping hours. Preliminary data suggest beneficial effects on arrhythmia occurrence in patients with obstructive sleep apnea (OSA) undergoing continuous positive airway pressure. However, as in patients with Cheyne-Stokes respiration, randomized, controlled trial results for ventilation therapy are still lacking.
... Therefore, the number of patients for whom treatment is indicated is likely to rise in parallel with the current aging demographic [2,3]. In cardiac patients, OSA is associated with the development and recurrence of arrhythmias, even after specific antiarrhythmic therapy [4]. ...
Purpose of Review
Sleep-disordered breathing (SDB) is an independent risk factor for cardiovascular disease. SDB-related changes in the autonomic nervous system (ANS) and the association between obstructive sleep apnea and atrial fibrillation (Afib) have been extensively researched. SDB has also been associated with occurrence of ventricular arrhythmias. We evaluated the effects of SDB on the ANS and its relationship with ventricular and supraventricular arrhythmias.
Recent Findings
The ANS is an important regulator of the cardiovascular system and contributes to the development of cardiovascular diseases including hypertension and coronary artery disease. SDB has an important influence on the ANS and contributes to electromechanical remodeling of the left atrium via a number of mechanisms, increasing susceptibility to Afib. There is evidence that these mechanisms also affect the ventricular myocardium and therefore lead to ventricular arrhythmias. Effective treatment of SDB reduces the rate of Afib recurrence and seems to reduce ventricular arrhythmogenicity.
Summary
SDB has an important impact on the ANS and therefore plays a major role in the development of cardiac arrhythmias. Although SDB screening of patients with Afib is recommended by current guidelines, SDB remains underdiagnosed. Additional research is needed to clarify the role of SDB and its treatment in ventricular arrhythmias.
The preliminary evidence supports an association between obstructive sleep apnoea (OSA), disturbed cardiac repolarization, and consequent cardiac dysrhythmias. The aim of the current trial was to assess the effects of continuous positive airway pressure (CPAP) therapy withdrawal on the measures of cardiac repolarization in patients with OSA.
Forty-one OSA patients established on CPAP treatment were randomized to either CPAP withdrawal (subtherapeutic CPAP) or continue therapeutic CPAP for 2 weeks. Polysomnography was performed, and indices of cardiac repolarization (QT(c), TpTe(c) intervals) and dispersion of repolarization (TpTe/QT ratio) were derived from 12-lead electrocardiography (ECG) at baseline and 2 weeks. Continuous positive airway pressure withdrawal led to a recurrence of OSA. Compared with therapeutic CPAP, subtherapeutic CPAP for 2 weeks was associated with a significant increase in the length of the QT(c) and TpTe(c) intervals (mean difference between groups 21.4 ms, 95% CI 11.3-1.6 ms, P < 0.001 and 14.4 ms, 95% CI 7.2-21.5 ms, P < 0.001, respectively) and in the TpTe/QT ratio (mean difference between groups 0.02, 95% CI 0.00-0.03, P = 0.020). There was a statistically significant correlation between the change in apnoea/hypopnoea index (AHI) from baseline, and both the change in the QT(c) interval and the TpTe(c) interval (r = 0.60, 95% CI 0.36-0.77, P < 0.001 and r = 0.45, 95% CI 0.17-0.67, P = 0.003, n = 41, respectively).
Continuous positive airway pressure withdrawal is associated with the prolongation of the QT(c) and TpTe(c) intervals and TpTe/QT ratio, which may provide a possible mechanistic link between OSA, cardiac dysrhythmias, and thus sudden cardiac death.
Heart block during sleep has been described in up to 10% of patients with obstructive sleep apnoea. The aim of this study was to determine the relationship between sleep stage, oxygen desaturation and apnoea-associated bradyarrhythmias as well as the effect of nasal continuous positive airway pressure (nCPAP)/nasal bi-level positive airway pressure (nBiPAP) therapy on these arrhythmias in patients without electrophysiological abnormalities. Sixteen patients (14 males and two females, mean age 49.6+/-10.4 yrs) with sleep apnoea and nocturnal heart block underwent polysomnography after exclusion of electrophysiological abnormalities of the sinus node function and atrioventricular (AV) conduction system by invasive electrophysiological evaluation. During sleep, 651 episodes of heart block were recorded, 572 (87.9%) occurred during rapid eye movement (REM) sleep and 79 (12.1%) during nonrapid eye movement (NREM) sleep stages 1 and 2. During REM sleep, the frequency of heart block was significantly higher than during NREM sleep: 0.69+/-0.99 versus 0.02+/-0.04 episodes of heart block x min(-1) of the respective sleep stage (p<0.001). During apnoeas or hypopnoeas, 609 bradyarrhythmias (93.5%) occurred with a desaturation of at least 4%. With nCPAP/ nBiPAP therapy, apnoea/hypopnoea index (AHI) decreased from 75.5+/-39.6 x h(-1) to 3.0+/-6.6 x h(-1) (p<0.01) and the number of arrhythmias from 651 to 72 (p<0.01). We conclude that: 1) 87.9% of apnoea-associated bradyarrhythmias occur during rapid eye movement sleep; 2) the vast majority of heart block episodes occur during a desaturation of at least 4% without a previously described threshold value of 72%; and 3) nasal continuous positive airway pressure or nasal bi-level positive airway pressure is the therapy of choice in patients with apnoea-associated bradyarrhythmias.
Obstructive sleep apnea (OSA), the most common form of sleep-disordered breathing, is prevalent and frequently underdiagnosed in our community. Although presenting with predominantly respiratory symptoms, the most serious complications from OSA are cardiovascular, including arrhythmias, disease of the sinus node and conducting system, and sudden cardiac death. The acute and chronic effects of OSA on the cardiovascular system, which include major effects on autonomic function during sleep and wakefulness, are potent contributors to the development and persistence of cardiac arrhythmias. Although large randomized studies are currently lacking, treatment of OSA may be an important primary or additional therapy to supplement the use of drugs or devices in the treatment of cardiac arrhythmias.
Obstructive sleep apnea (OSA) is more common in patients with atrial fibrillation (AFib). Recently, an additional association between central sleep apnea/Cheyne-Stokes respiration (CSA/CSR) and AFib has been described. The aim of this study was to investigate the prevalence and type of sleep-disordered breathing in patients with AFib and normal systolic left ventricular function.
150 patients (110 men and 40 women, aged 66.1 +/- 1.7 years) underwent cardiorespiratory polygraphy, capillary blood gas analysis, measurement of NT-proBNP, and echocardiography to determine the diameter of the left atrium (LAD) and the peak systolic pulmonary artery pressure (PAP).
Sleep-disordered breathing was documented in 74% of all patients with AFib (43% had OSA and 31% had CSA/CSR). Patients with CSA/CSR had a higher PAP, a higher apnea-hypopnea index, a greater LAD, and a lower capillary blood pCO(2) than patients with OSA.
Patients with AFib were found to have not only a high prevalence of obstructive sleep apnea, as has been described previously, but also a high prevalence of CSA/CSR. It remains unknown whether CSA/CSR is more common in AFib because of diastolic dysfunction or whether phenomena associated with CSA/CSR predispose to AFib. Further research on this question is needed.
Rates of cardiac arrhythmias increase with age and may be associated with clinically significant morbidity. We studied the association between sleep-disordered breathing (SDB) with nocturnal atrial fibrillation or flutter (AF) and complex ventricular ectopy (CVE) in older men.
A total of 2911 participants in the Outcomes of Sleep Disorders in Older Men Study underwent unattended polysomnography. Nocturnal AF and CVE were ascertained by electrocardiogram-specific analysis of the polysomnographic data. Exposures were (1) SDB defined by respiratory disturbance index (RDI) quartile (a major index including all apneas and hypopneas), and ancillary definitions incorporating (2) obstructive events, obstructive sleep apnea (OSA; Obstructive Apnea Hypopnea Index quartile), or (3) central events, central sleep apnea (CSA; Central Apnea Index category), and (4) hypoxia (percentage of sleep time with <90% arterial oxygen percent saturation). Multivariable logistic regression analyses were performed.
An increasing RDI quartile was associated with increased odds of AF and CVE (P values for trend, .01 and <.001, respectively). The highest RDI quartile was associated with increased odds of AF (odds ratio [OR], 2.15; 95% confidence interval [CI], 1.19-3.89) and CVE (OR, 1.43; 95% CI, 1.12-1.82) compared with the lowest quartile. An increasing OSA quartile was significantly associated with increasing CVE (P value for trend, .01) but not AF. Central sleep apnea was more strongly associated with AF (OR, 2.69; 95% CI, 1.61-4.47) than CVE (OR, 1.27; 95% CI, 0.97-1.66). Hypoxia level was associated with CVE (P value for trend, <.001); those in the highest hypoxia category had an increased odds of CVE (OR, 1.62; 95% CI, 1.23-2.14) compared with the lowest quartile.
In this large cohort of older men, increasing severity of SDB was associated with a progressive increase in odds of AF and CVE. When SDB was characterized according to central or obstructive subtypes, CVE was associated most strongly with OSA and hypoxia, whereas AF was most strongly associated with CSA, suggesting that different sleep-related stresses may contribute to atrial and ventricular arrhythmogenesis in older men.
In the early days of sleep research it was thought that heart block (second and third degree atrioventricular block), sinus arrest, or sinoatrial block were frequent findings in patients with sleep apnoea. Tilkian and co-workers1 reported that more than 50% of patients with sleep apnoea develop episodes of heart block during sleep. In 400 patients studied by Guilleminault et al 2 bradycardic arrhythmias were reported in almost 18% of the patients and later studies found heart block in 9–13% of patients with sleep apnoea.3 4 Due to ventricular asystoles of up to 13 seconds in duration it was hypothesised that heart block might lead to an increased mortality risk in these patients.2 A recent publication challenged previous results in that no increased prevalence of bradycardic arrhythmias was seen in patients with sleep apnoea compared with those without sleep apnoea.5
To examine these seemingly discrepant results further we performed Holter monitoring in 239 consecutive patients diagnosed as having sleep apnoea (apnoea/hypopnoea index >10/h) using a validated ambulatory recording device based on the measurement of heart rate, Sao 2, snoring sound, and body position. Episodes of second and third degree atrioventricular (AV) block and/or sinus arrest of more than two seconds in duration occurred in 17 of the 239 patients.6 There was no significant difference in age between patients with and without heart block (mean (SD) 50.7 (12.8) versus 52.1 (9.8) years), but those with heart block were significantly more obese (38.7 (7.3) versus 30.7 (4.6)).
Twelve of the 17 patients (70.6%) had arterial hypertension, seven (41.1%) suffered from heart failure (NYHA II–III), and four (23.5%) had pulmonary hypertension. None of the patients reported a myocardial infarction in their medical history, and in only one (5.9%) exercise testing showed signs of coronary heart disease. Ten …
In previous analyses of the occurrence of central (CSA) and obstructive sleep apnea (OSA) in patients with congestive heart failure (CHF), only men were studied and risk factors for these disorders were not well characterized. We therefore analyzed risk factors for CSA and OSA in 450 consecutive patients with CHF (382 male, 68 female) referred to our sleep laboratory. Risk factors for CSA were male gender (odds ratio [OR] 3.50; 95% confidence interval [CI], 1.39 to 8.84), atrial fibrillation (OR 4.13; 95% CI 1.53 to 11. 14), age > 60 yr (OR 2.37; 95% CI 1.35 to 4.15), and hypocapnia (PCO(2 )< 38 mm Hg during wakefulness) (OR 4.33; 95% CI 2.50 to 7. 52). Risk factors for OSA differed by gender: in men, only body mass index (BMI) was significantly associated with OSA (OR for a BMI > 35 kg/m(2), 6.10; 95% CI 2.86 to 13.00); whereas, in women, age was the only important risk factor (OR for age > 60 yr, 6.04; 95% CI 1.75 to 20.0). We conclude that historical information, supplemented by a few simple laboratory tests may enable physicians to risk stratify CHF patients for the presence of CSA or OSA, and the need for diagnostic polysomnography for such patients. Sin DD, Fitzgerald F, Parker JD, Newton G, Floras JS, Bradley TD. Risk factors for central and obstructive sleep apnea in 450 men and women with congestive heart failure.
The aim of this study was to examine the influence of sleep-related breathing disorders (SBDs) on the occurrence of ventricular arrhythmias in patients with reduced left ventricular ejection fraction (LVEF), and life-threatening ventricular tachyarrhythmias treated with an implantable cardioverter-defibrillator.
Thirty-eight patients with LVEF of 36 +/- 13% (mean +/- SD) underwent a sleep study. When an apnea-hypopnea index (AHI) > 10/h occurred, SBD was diagnosed.
In patients with SBDs, ventricular arrhythmias (couplets, triplets, short runs) were recorded simultaneously by Holter ECG and differentiated in episodes with and without disordered breathing. An apnea-associated arrhythmia index (AI) was defined as the number of ventricular arrhythmias occurring simultaneous to disordered breathing. Accordingly, a nonapnea-associated arrhythmia index (NAI) was calculated as the number of ventricular arrhythmias during normal breathing. SBDs were diagnosed in 14 patients: Cheyne-Stokes respiration (CSR) [n = 8; AHI, 32.1 +/- 25.0/h], and obstructive sleep apnea (OSA) [n = 6; AHI, 34.1 +/- 14.6/h]. Four patients in the OSA group and four patients in the CSR group had ventricular arrhythmias during sleep, revealed by Holter ECG. In these eight patients, the AI was significantly higher than the NAI (20.9 +/- 18.8/h vs 4.9 +/- 3.3/h, respectively).
These data show that ventricular arrhythmias occurred significantly more often in association with disordered breathing in patients at high risk for arrhythmias and reduced LVEF.
Obstructive sleep apnoea (OSA) elicits a number of cardiovascular perturbations that could lead acutely or chronically to increased ventricular ectopy in patients with heart failure (HF). We tested the hypothesis that treatment of OSA with continuous positive airway pressure (CPAP) in patients with HF would reduce the frequency of ventricular premature beats (VPBs) during sleep in association with reduced sympathetic nervous system activity.
Following optimisation of medical treatment, 18 HF patients with OSA and >10 VPBs per hour of sleep were randomised to a control group (n = 8) or a treatment group who received CPAP (n = 10). The frequency of VPBs and urinary norepinephrine (noradrenaline) concentrations during total sleep time were determined at baseline and after 1 month.
Control patients did not experience any significant changes in apnoea-hypopnoea index (AHI), mean nocturnal O(2) saturation, or the frequency of VPBs. In contrast, there was a significant reduction in AHI (p<0.001), an increase in minimum O(2) saturation (p = 0.05), a reduction in urinary norepinephrine concentrations (p = 0.009), and a 58% reduction in the frequency of VPBs during total sleep (from mean (SE) 170 (65) to 70 (28) per hour, p = 0.011) after 1 month of CPAP treatment.
In patients with HF, treatment of co-existing OSA by CPAP reduces the frequency of VPBs during sleep. These data suggest that reductions in VPBs and other ventricular arrhythmias through treatment of OSA might improve the prognosis in patients with HF.
The results of 24-hour continuous electrocardiographic monitoring of 23 patients with documented sleep apnea syndrome were reviewed to evaluate the prevalence of cardiac arrhythmias and conduction disturbances in this disorder. During sleep, marked sinus arrhythmia (more than 30 beats/min variation) was found in 18 patients. Extreme sinus bradycardia (heart rate less than 30 beats/min) and sinus pauses (more than 1.8 sec) were found in only two patients. First-degree and type I second-degree atrioventricular block were found in another patient. There was a decrease in grade of ventricular ectopy from wakefulness to sleep. These data suggest that the prevalence of serious arrhythmias and conduction disturbances during sleep in patients with the sleep apnea syndrome is much lower than previously reported.
Background
The risk of sudden death from cardiac causes in the general population peaks from 6 a.m. to noon and has a nadir from midnight to 6 a.m. Obstructive sleep apnea is highly prevalent and associated with neurohormonal and electrophysiological abnormalities that may increase the risk of sudden death from cardiac causes, especially during sleep.
Methods
We reviewed polysomnograms and the death certificates of 112 Minnesota residents who had undergone polysomnography and had died suddenly from cardiac causes between July 1987 and July 2003. For four intervals of the day, we compared the rates of sudden death from cardiac causes among people with obstructive sleep apnea and the following: the rates among people without obstructive sleep apnea, the rates in the general population, and the expectations according to chance. For each interval, we assessed the median apnea–hypopnea index and the relative risk of sudden death from cardiac causes. We similarly analyzed sudden death from cardiac causes during three time intervals that correlate with usual sleep–wake cycles.
Results
From midnight to 6 a.m., sudden death from cardiac causes occurred in 46 percent of people with obstructive sleep apnea, as compared with 21 percent of people without obstructive sleep apnea (P=0.01), 16 percent of the general population (P<0.001), and the 25 percent expected by chance (P<0.001). People with sudden death from cardiac causes from midnight to 6 a.m. had a significantly higher apnea–hypopnea index than those with sudden death from cardiac causes during other intervals, and the apnea–hypopnea index correlated directly with the relative risk of sudden death from cardiac causes from midnight to 6 a.m. For people with obstructive sleep apnea, the relative risk of sudden death from cardiac causes from midnight to 6 a.m. was 2.57 (95 percent confidence interval, 1.87 to 3.52). The analysis of usual sleep–wake cycles showed similar results.
Conclusions
People with obstructive sleep apnea have a peak in sudden death from cardiac causes during the sleeping hours, which contrasts strikingly with the nadir of sudden death from cardiac causes during this period in people without obstructive sleep apnea and in the general population.
This study aimed to investigate whether adequate treatment of Cheyne-Stokes respiration (CSR) reduces the risk of arrhythmic events in patients with chronic heart failure (CHF).
A cohort of 403 registry patients with CHF (LVEF≤45%, NYHA-class≥2) and implanted cardioverter-defibrillator devices (ICD) was studied. They underwent overnight polygraphy, with 221 having mild or no CSR (apnea-hypopnea index [AHI]<15/h), and 182 having moderate to severe CSR (AHI>15/h). Latter ones were offered therapy with adaptive servoventilation (ASV), which 96 patients accepted and 86 rejected. During follow-up (21± 15 months) defibrillator therapies were recorded in addition to clinical and physiologic measures of heart failure severity.
Event-free survival from (a) appropriate cardioverter-defibrillator therapies and (b) appropriately monitored ventricular arrhythmias was shorter in the untreated CSR group compared to the treated CSR and the no CSR group. Stepwise Cox proportional hazard regression analysis showed untreated CSR (a: hazard ratio [HR] 1.99, 95% confidence interval [CI] 1.46-2.72, P < 0.001; b: HR 2.19, 95%CI 1.42-3.37, P < 0.001), but not treated CSR (a: HR 1.06, 95%CI 0.74-1.50; P = 0.77; b: HR 1.21, 95%CI 0.75-1.93, P = 0.43) was an independent risk factor. The treated CSR group showed improvements in cardiac function and respiratory stability compared to the untreated CSR group.
This study demonstrates a decrease of appropriate defibrillator therapies by ASV treated CSR in patients with CHF and ICD. A reduced exposure to hyperventilation, hypoxia, and improvement in indices of CHF severity and neurohumoral disarrangements are potential causative mechanisms.
Objectives:
This study sought to identify the risk of sudden cardiac death (SCD) associated with obstructive sleep apnea (OSA).
Background:
Risk stratification for SCD, a major cause of mortality, is difficult. OSA is linked to cardiovascular disease and arrhythmias and has been shown to increase the risk of nocturnal SCD. It is unknown if OSA independently increases the risk of SCD.
Methods:
We included 10,701 consecutive adults undergoing their first diagnostic polysomnogram between July 1987 and July 2003. During follow-up up to 15 years, we assessed incident resuscitated or fatal SCD in relation to the presence of OSA, physiological data including the apnea-hypopnea index (AHI), and nocturnal oxygen saturation (O2sat) parameters, and relevant comorbidities.
Results:
During an average follow-up of 5.3 years, 142 patients had resuscitated or fatal SCD (annual rate 0.27%). In multivariate analysis, independent risk factors for SCD were age, hypertension, coronary artery disease, cardiomyopathy or heart failure, ventricular ectopy or nonsustained ventricular tachycardia, and lowest nocturnal O2sat (per 10% decrease, hazard ratio [HR]: 1.14; p = 0.029). SCD was best predicted by age >60 years (HR: 5.53), apnea-hypopnea index >20 (HR: 1.60), mean nocturnal O2sat <93% (HR: 2.93), and lowest nocturnal O2sat <78% (HR: 2.60; all p < 0.0001).
Conclusions:
In a population of 10,701 adults referred for polysomnography, OSA predicted incident SCD, and the magnitude of risk was predicted by multiple parameters characterizing OSA severity. Nocturnal hypoxemia, an important pathophysiological feature of OSA, strongly predicted SCD independently of well-established risk factors. These findings implicate OSA, a prevalent condition, as a novel risk factor for SCD.
Objectives:
The aim of this study was to examine the effect of continuous positive airway pressure (CPAP) therapy on atrial fibrillation (AF) recurrence in patients with obstructive sleep apnea (OSA) undergoing pulmonary vein isolation (PVI).
Background:
OSA is a predictor of AF recurrence following PVI. However, the impact of CPAP therapy on PVI outcome in patients with OSA is poorly known.
Methods:
Among 426 patients who underwent PVI between 2007 and 2010, 62 patients had a polysomnography-confirmed diagnosis of OSA. While 32 patients were "CPAP users" the remaining 30 patients were "CPAP nonusers." The recurrence of any atrial tachyarrhythmia, use of antiarrhythmic drugs, and need for repeat ablations were compared between the groups during a follow-up period of 12 months. Additionally, the outcome of patients with OSA was compared to a group of patients from the same PVI cohort without OSA.
Results:
CPAP therapy resulted in higher AF-free survival rate (71.9% vs. 36.7%; p = 0.01) and AF-free survival off antiarrhythmic drugs or repeat ablation following PVI (65.6% vs. 33.3%; p = 0.02). AF recurrence rate of CPAP-treated patients was similar to a group of patients without OSA (HR: 0.7, p = 0.46). AF recurrence following PVI in CPAP nonuser patients was significantly higher (HR: 2.4, p < 0.02) and similar to that of OSA patients managed medically without ablation (HR: 2.1, p = 0.68).
Conclusions:
CPAP is an important therapy in OSA patients undergoing PVI that improves arrhythmia free survival. PVI offers limited value to OSA patients not treated with CPAP.
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.
Advanced heart failure (HF) is associated with severe sleep-disordered breathing (SDB). In addition, most patients with HF are treated with an implantable cardioverter-defibrillator (ICD) for primary prevention of sudden cardiac death. The incidence of ICD therapy in such a patient cohort with SDB has never been investigated. The present study sought to determine the effect of SDB on the incidence of appropriate and inappropriate ICD therapy in patients with a categorical primary prevention ICD indication. A total of 133 consecutive ICD patients with New York Heart Association class II-III HF and depressed left ventricular function (≤35%) with no history of ventricular arrhythmia underwent a sleep study before ICD implantation and were followed for 24 ± 8 months, prospectively. A relevant SDB was defined as an apnea-hypopnea index of ≥10 events/hour. Of these 133 patients, 82 (62%) had SDB. Overweight (body mass index >29.1 vs 24.7 kg/m(2); p <0.001) was identified as the only independent risk factor for SDB. Appropriate ICD therapy intervention was significantly greater among patients with SDB than among patients without SDB (54% vs 34%, p = 0.03). Inappropriate ICD therapy intervention was documented more often in patients with SDB (n = 24 [29%] vs 7 [14%]; p = 0.04). An apnea-hypopnea index >10 events/hour was an independent predictor of appropriate ICD therapy on multivariate analysis (odds ratio 2.5, 95% confidence interval 1.8 to 4.04; p = 0.01). In conclusion, the present study is the first trial exploring the effect of SDB on the incidence of appropriate and inappropriate ICD therapy in patients with HF with a primary prevention indication. These results indicate that a preimplantation sleep study will identify patients with HF prone to receive appropriate and inappropriate ICD therapy.
Background:
Recent studies have suggested an emerging link between obstructive sleep apnea (OSA) and atrial fibrillation (AF). Patients with OSA are less likely to remain in sinus rhythm after radiofrequency catheter ablation of AF.
Objective:
To evaluate the efficacy of appropriate treatment with continuous positive airway pressure (CPAP) on recurrences of AF after ablation.
Methods:
This study prospectively included 153 patients (128 men; 60 ± 9 years) who underwent extensive encircling pulmonary vein isolation for drug refractory AF. The standard overnight polysomnographic evaluation was performed 1 week after ablation, and the total duration and the number of central or obstructive sleep apnea or hypopnea episodes were examined.
Results:
Of 153 patients, 116 patients were identified as having OSA. Data regarding the use of CPAP and recurrences of AF were obtained in 82 patients. The remaining 34 patients with OSA were defined as the no-CPAP group. Polysomnography revealed no sleep-disordered breathing in 37 patients. During a mean follow-up period of 18.8 ± 10.3 months, 51 (33%) patients experienced AF recurrences after ablation. A Cox regression analysis revealed that the left atrial volume (hazard ratio [HR] 1.11; 95% confidence interval [CI] 1.01-1.23; P<.05), concomitant OSA (HR 2.61; 95% CI 1.12-6.09; P<.05), and usage of CPAP therapy (HR 0.41; 95% CI 0.22-0.76; P<.01) were associated with AF recurrences during the follow-up period.
Conclusions:
Patients with untreated OSA have a higher recurrence of AF after ablation. Appropriate treatment with CPAP in patients with OSA is associated with a lower recurrence of AF.
AimsTo assess the prognostic significance of screening for sleep-disordered breathing in patients with implantable cardioverter-defibrillator (ICD) with regard to appropriate ICD therapy and total mortality.Methods and resultsOvernight sleep studies were performed in 204 ICD recipients not known to have sleep apnoea and with no history of daytime sleepiness. Sleep-disordered breathing was diagnosed in the presence of an apnoea-hypopnea index of five or more events per hour. Seventy patients (34%) had no sleep apnoea, 105 patients (51%) had central sleep apnoea, and 29 patients (14%) had obstructive sleep apnoea. During 38 ± 26 months follow-up, 80 patients (39%) received appropriate ICD therapy for ventricular tachycardia (VT) or ventricular fibrillation (VF), and 54 patients (26%) died. On multivariate Cox regression analysis, age, left ventricular (LV) end-diastolic diameter, secondary prevention ICD indication, use of diuretics, and absence of aldosterone antagonist therapy but not sleep apnoea were associated with appropriate ICD therapy for VT or VF. In addition, multivariate Cox analysis identified age and LV ejection fraction but not sleep apnoea as predictors of total mortality.Conclusion
Undiagnosed sleep-disordered breathing is common in ICD recipients. The presence and severity of previously unknown sleep apnoea in ICD recipients, however, does not appear to be an independent predictor of appropriate ICD therapy or morality during follow-up.
Background
The clinical yield of cavotricuspid isthmus (CTI) radiofrequency ablation of atrial flutter (AF) is limited by a high incidence of atrial fibrillation (AFib) in the long term. Among other acknowledged variables, the association of obstructive sleep apnea (OSA) could favor incomplete arrhythmia control in this setting. We assessed the impact of CPAP in reducing the occurrence of AFib after CTI ablation.
Methods
Consecutive patients with AF who were undergoing CTI ablation were screened for OSA. Relationship of the following variables with the occurrence of AFib during follow-up (12 months) was investigated: CPAP initiation, hypertension, BMI, underlying structural heart disease, left atrial diameter, and AFib documentation prior to ablation.
Results
We prospectively included 56 patients (mean age: 66 (± 11) years; 12 female patients), of whom 46 (82%) had OSA and 25 (45%) had severe OSA. Twenty-one patients (38%) had AFib during follow-up after CTI ablation. Both freedom from AFib prior to ablation and CPAP initiation in those patients without previously documented AFib at inclusion were associated with a reduction of AFib episodes during follow-up (P = .019 and P = .025, respectively). Inversely, CPAP was not protective from AFib recurrence when this arrhythmia was documented prior to ablation (P = .25).
Conclusions
OSA is a prevalent condition in patients with AF. Treatment with CPAP is associated with a lower incidence of newly diagnosed AFib after CTI ablation. Screening for OSA in patients with AF appears to be a reasonable clinical strategy.
In patients with atrial fibrillation (AF) undergoing pulmonary vein isolation, cryoballoon technique (cryoPVI) has been adopted in many centers. This study aimed to evaluate predictors of AF recurrence including impact of sleep-disordered breathing (SDB).
In 82 patients consecutively assigned to cryoPVI cardiorespiratory screening for SDB, assessment of medical history, ECG, echocardiography, standard laboratory measurement, and blood gas analysis were performed prior to intervention. After a 3-month blanking period, a 7-day Holter ECG was performed at 3, 6 and then every 6 months to determine AF recurrence. Seventy-five patients (69 paroxysmal AF, 6 persistent AF, 22 female, age 60 ± 9 years) completed at least 6-month follow-up. Median follow-up of 12 months (interquartile range 6-18 months) confirmed maintenance of sinus rhythm in 69.4% of these patients. Stepwise forward regression model revealed moderate to severe SDB (cut-off apnea-hypopnea-index (AHI) ≥ 15 per hour; Hazard Ratio (HR) 2.95, P = 0.04), early recurrence of AF (HR 8.74, P < 0.001), persistent AF (HR 7.16, P < 0.001), preprocedural class III-antiarrhythmic drug treatment (HR 3.63, P = 0.02), but not SDB per se (AHI ≥ 5 per hour) as independent predictors for AF recurrence.
Moderate to severe SDB is a treatable condition that independently predicts AF recurrence in patients undergoing cryoPVI. Screening for SDB and adequate treatment may improve long-term success of cryoPVI.
Increased prevalence of cardiac arrhythmias has been reported in patients with severe obstructive sleep apnea (OSA), but this may not be generalizable to patients from the general population with a milder form of the condition. The aim of this study was to assess the association between cardiac arrhythmias and OSA of mainly mild and moderate severity. In total, 486 subjects (mean age 49 years, 55% men) recruited from a population-based study in Norway underwent polysomnography for OSA assessment and Holter recordings for arrhythmia assessment. Of these, 271 patients were diagnosed with OSA (apnea-hypopnea index [AHI] ≥5, median AHI 16.8, quartiles 1 to 3 8.9 to 32.6). Mean nadir oxygen saturations were 82% and 89% in patients with and without OSA, respectively. Ventricular premature complexes (≥5/hour) were more prevalent in subjects with OSA compared to subjects without OSA (median AHI 1.4, quartiles 1 to 3 0.5 to 3.0) during the night (12.2% vs 4.7%, p = 0.005) and day (14% vs 5.1%, p = 0.002). In multivariate analysis after adjusting for relevant confounders, AHI was independently associated with an increased prevalence of ventricular premature complexes at night (odds ratio per 1-U increase of log-transformed AHI 1.5, 95% confidence interval 1.1 to 2.0, p = 0.008) and during the day (odds ratio 1.37, 95% confidence interval 1.0 to 1.8, p = 0.035). In conclusion, the prevalence of ventricular premature complexes is increased in middle-aged patients with mainly mild or moderate OSA, suggesting an association between OSA and ventricular arrhythmias even in mild OSA.
The association between obstructive sleep apnea (OSA) and atrial fibrillation (AF) is strong and is now well established. However, studies on the role of OSA on AF recurrence after catheter ablation have yielded conflicting results. The aim of the present study was to investigate the role of OSA on AF recurrence after catheter-based pulmonary vein isolation. We performed a data search on the PubMed, Web of Science, and the Cochrane databases for studies published by August 2010. In addition, we manually searched the conference proceedings of the European Society of Cardiology, American College of Cardiology, and American Heart Association for related abstracts. After the initial search returned 402 reports, we identified 6 studies with a total of 3,995 patients that met our inclusion criteria. Overall, patients with OSA have a 25% greater risk of AF recurrence after catheter ablation than those without OSA (risk ratio 1.25, 95% confidence interval 1.08 to 1.45, p = 0.003). Subgroup analysis showed that OSA diagnosed using polysomnography is a strong predictor of AF recurrence (risk ratio 1.40, 95% confidence interval 1.16 to 1.68, p = 0.0004) but not when OSA was diagnosed using the Berlin questionnaire (risk ratio 1.07, 95% confidence interval 0.91 to 1.27, p = 0.39). In conclusion, patients with OSA have significantly greater AF recurrence rates after pulmonary vein isolation. In addition to other factors, a diagnosis of OSA merits special consideration when evaluating patients for catheter-based AF ablation.
Obstructive sleep apnea (OSA) causes negative tracheal pressure (NTP) and is associated with atrial fibrillation (AF).
This study aimed to determine the mechanism of atrial electrophysiological changes during tracheal occlusion with or without applied NTP and to evaluate the role of vagal activation, Na(+)/H(+)exchanger (NHE), and ATP-dependent potassium channels (K(ATP)).
Seventeen closed-chest pigs were anesthetized with urethane, and an endotracheal tube was placed to apply NTP (up to -100 mbar), comparable to clinically observed OSA in patients by a negative pressure device for a time period of 2 minutes. Right atrial refractory periods (AERP) and AF inducibility were measured transvenously by a monophasic action potential recording and stimulation catheter.
All tracheal occlusions with and without applied NTP resulted in comparable increases in blood pressure and hypoxemia. NTP shortened AERP (157.0 ± 2.8 to 102.1 ± 6.2 ms; P <.0001) and enhanced AF inducibility during AERP measurements from 0% at baseline to 90% (P <.00001) during NTP. Release of NTP resulted in a prompt restoration of sinus rhythm, and AERP returned to normal. NTP-induced AERP shortening and AF inducibility were prevented by atropine or vagotomy. Neither the NHE blocker cariporide nor the K(ATP) channel blocker glibenclamide abolished NTP-induced AERP shortening. By contrast, tracheal occlusion without applied NTP caused comparable changes in blood gases but did not induce AERP shortening or AF inducibility.
NTP during obstructive events is a strong trigger for AF compared with changes in blood gases alone. NTP caused AERP shortening and increased susceptibility to AF mainly by enhanced vagal activation. AERP shortening was not prevented by K(ATP) channel blockade or NHE blockade.
In patients with cardiac disease growing interests have been centered on concomitant co-morbidities such as sleep disordered breathing (SDB). Obstructive sleep apnoea (OSA) as well as Cheyne-Stokes Respiration (CSR) have been recognized as relevant co-morbidities that are highly prevalent and associated with an impaired prognosis. As a known consequence from recurrent hypoxaemias and an increased sympathetic activity, SDB promotes structural myocardial changes and potentially triggers cardiac arrhythmias. Several investigations thus reported an increasing frequency of cardiac arrhythmias among patients with either OSA or CSR. Sufficiently suppressing SDB by adequate therapies seems to ameliorate its arrhythmogenic impact. However, especially for CSR data from randomized, controlled trial are urgently awaited to definitely answer this question.
© Georg Thieme Verlag KG Stuttgart · New York.
Sleep-disordered breathing (SDB) has been associated with various benign cardiac arrhythmias occurring during sleep.
The purpose of this study was to demonstrate that SDB contributes to the development of life-threatening ventricular arrhythmias in patients with an established arrhythmic substrate.
We prospectively studied the association between SDB and timing of life-threatening ventricular arrhythmic events in 45 patients with an implantable cardioverter-defibrillator (ICD). SDB was defined as an apnea-hypopnea index (AHI) >10 events/hour based on an overnight sleep study. The primary outcome measure was appropriate ICD therapy, defined as antitachycardia pacing or shock for ventricular tachycardia or ventricular fibrillation during 1-year follow-up.
SDB was present in 26 (57.8%) patients. Appropriate ICD therapies were higher among patients with SDB (73% vs 47%, P = .02). Logistic regression identified SDB as a predictor of any appropriate ICD therapy (odds ratio 4.4, 95% confidence interval 1.4-15.3, P = .01). The risk for ventricular arrhythmias was higher in patients with SDB solely due to an increase in events occurring between midnight and 6 AM (odds ratio 5.6, 95% confidence interval 2.0-15.6, P = .001) with no discernible effect on appropriate ICD therapy during nonsleeping hours (odds ratio 0.7, 95% confidence interval 0.2-2.3, P = .61).
Patients with an ICD and SDB have a striking increase in the onset of life-threatening ventricular arrhythmic events during sleeping hours. These findings provide a rationale for SDB screening in patients with appropriate ICD therapy if device interrogation reveals a predominance of nocturnal onset of arrhythmias.
The aim of this first large-scale long-term study was to investigate whether obstructive sleep apnoea (OSA) and/or central sleep apnoea (CSA) are associated with an increased risk of malignant cardiac arrhythmias in patients with congestive heart failure (CHF).
Of 472 CHF patients who were screened for sleep disordered breathing (SDB) 6 months after implantation of a cardiac resynchronization device with cardioverter-defibrillator, 283 remained untreated [170 with mild or no sleep disordered breathing (mnSDB) and 113 patients declined ventilation therapy] and were included into this study. During follow-up (48 months), data on appropriately monitored ventricular arrhythmias as well as appropriate cardioverter-defibrillator therapies were obtained from 255 of these patients (90.1%). Time period to first monitored ventricular arrhythmias and to first appropriate cardioverter-defibrillator therapy were significantly shorter in patients with either CSA or OSA. Forward stepwise Cox models revealed an independent correlation for CSA and OSA regarding monitored ventricular arrhythmias [apnoea-hypopnoea index (AHI) ≥5 h(-1): CSA HR 2.15, 95% CI 1.40-3.30, P < 0.001; OSA HR 1.69, 95% CI 1.64-1.75, P = 0.001; AHI ≥15 h(-1): CSA HR 2.06, 95% CI 1.40-3.05, P < 0.001; OSA HR 1.69, 95% CI 1.14-2.51, P = 0.02] and appropriate cardioverter-defibrillator therapies (AHI ≥5 h(-1): CSA HR 3.24, 95% CI 1.86-5.64, P < 0.001; OSA HR 2.07, 95% CI 1.14-3.77, P = 0.02; AHI ≥15 h(-1): CSA HR 3.41, 95% CI 2.10-5.54, P < 0.001; OSA HR 2.10, 95% CI 1.17-3.78, P = 0.01).
In patients with CHF, CSA and OSA are independently associated with an increased risk for ventricular arrhythmias and appropriate cardioverter-defibrillator therapies.
Obstructive sleep apnea (OSA) may be associated with pulmonary vein antrum isolation (PVAI) failure. The aim of the present study was to investigate if treatment with continuous positive airway pressure (CPAP) improved PVAI success rates.
From January 2004 to December 2007, 3000 consecutive patients underwent PVAI. Patients were screened for OSA and CPAP use. Six hundred forty (21.3%) patients had OSA. Patients with OSA had more procedural failures (P=0.024) and hematomas (P<0.001). Eight percent of the non-OSA paroxysmal atrial fibrillation patients had nonpulmonary vein antrum triggers (non-PV triggers) and posterior wall firing versus 20% of the OSA group (P<0.001). Nineteen percent of the non-OSA nonparoxysmal atrial fibrillation population had non-PV triggers versus 31% in the OSA group (P=0.001). At the end of the follow-up period (32±14 months), 79% of the non-CPAP and 68% of the CPAP group were free of atrial fibrillation (P=0.003). Not using CPAP in addition to having non-PV triggers strongly predicted procedural failure (hazard ratio, 8.81; P<0.001).
OSA was an independent predictor for PVAI failure. Treatment with CPAP improved PVAI success rates. Patients not treated with CPAP in addition to having higher prevalence of non-PV triggers were 8 times more likely to fail the procedure.
Obstructive sleep apnea is highly prevalent in patients with cardiovascular disease and has detrimental effects on systolic and diastolic function of the ventricles. In this research, the changes in strain (S) and strain rate (SR) during the performance of the Mueller maneuver (MM) in an effort to better understand how negative intrathoracic pressures affect ventricular mechanics.
The MM was performed to maintain a target intrathoracic pressure of -40 mm Hg. Echocardiography was used to measure various parameters of cardiac structure and function. Myocardial deformation measurements were performed using tissue speckle tracking. Twenty-four healthy subjects (9 women; mean age, 30+/-6 years) were studied. Global left ventricular longitudinal S in systole and SR in early filling were significantly decreased during the MM (S: baseline, -17.0+/-1.6%; MM, -14.5+/-2.2%; P<0.0001, SR: baseline, 1.09+/-0.20 s(-1); MM, 0.92+/-0.21 s(-1); P=0.01). Global right ventricular longitudinal S was also significantly decreased during the MM (baseline, -22.0+/-3.1%; MM, -17.2+/-2.5%; P<0.0001), as was global right ventricular longitudinal systolic SR (baseline, -1.34+/-0.35 s(-1); MM, -1.02+/-0.21 s(-1); P=0.0006).
Left ventricular and right ventricular longitudinal deformation are significantly reduced during the MM. These results suggest that negative intrathoracic pressure during apnea may contribute to changes in myocardial mechanics. These results could help explain the observed changes in left ventricular and right ventricular mechanics in patients with obstructive sleep apnea.
The purpose of this study was to determine the relationship between obstructive sleep apnea (OSA) and cardiovascular disorders in a large Japanese population, and to assess the efficacy of continuous positive airway pressure (CPAP) in the treatment of OSA-associated arrhythmias. The study population comprised 1394 Japanese subjects (1086 men and 308 women) who were divided into four groups on the basis of polysomnography (PSG) analysis as follows: the no sleep apnea (N-SA) group (n = 44, apnea-hypopnea index [AHI] < 5), the mild OSA (Mi-OSA) group (n = 197, 5 < AHI < 15), the moderate OSA (Mo) group (n = 368, 15 < AHI < 30), and severe OSA (SOSA) group (n = 785, AHI < 30). The following baseline characteristics were significantly associated with OSA: age (P < 0.001), gender (P < 0.001), body mass index (P < 0.001), hypertension (P < 0.001), diabetes (P = 0.009), and hyperlipidemia (P = 0.013). In the OSA group, PSG revealed the predominance of paroxysmal atrial fibrillation (PAF) (P = 0.051), premature atrial complex short run (P < 0.005), premature ventricular complex (PVC, P = 0.004), sinus bradycardia (P = 0.036), and sinus pause (arrest >2 s, P < 0.001) during the PSG recording. A total of 316 patients from the group underwent CPAP titration and were then re-evaluated. Continuous positive airway pressure therapy significantly reduced the occurrences of PAF (P < 0.001), PVC (P = 0.016), sinus bradycardia (P = 0.001), and sinus pause (P = 0.004). The results of this study demonstrate a significant relationship between OSA and several cardiac disorders, and also demonstrate the efficacy of CPAP in preventing OSA-associated arrhythmias in a large population of Japanese patients.
Implantable cardioverter defibrillators (ICDs) are increasingly employed in patients affected by congestive heart failure (CHF) and sleep disordered breathing (SDB) is frequent in this population.
To investigate SDB prevalence and influence on appropriate ICD discharges in CHF patients.
A total of 22 consecutive ICD patients with systolic CHF (left ventricular ejection fraction [LVEF]< 45%) were studied by polysomnography.
A total of 17 (77.2%) showed SDB (apnea-hypopnea index [AHI]_ 10 events/hour). After controlling for LVEF and New York Heart Association (NYHA) class, AHI and severity of hypoxia during sleep results correlated to appropriate ICD discharges (r = 0.718; P < .001, r = - 0.619; P = .003, respectively).
Sleep disordered breathing is frequent in ICD recipients due to left systolic ventricular dysfunction and may increase the risk of ventricular arrhythmia and appropriate ICD discharges.
Chronic atrial fibrillation (AF) as a precursor of stroke was assessed over 24 years of follow-up of the general population sample at Framingham, Massachusetts. Persons with chronic established AF, with or without rheumatic heart disease (RHD), are at greatly increased risk of stroke, and the stroke is probably due to embolism. Chronic AF in the absence of RHD is associated with more than a fivefold increase in stroke indicence, while AF with RHD has a 17-fold increase. Stroke occurrence increased as duration of AF increased, with no evidence of a particularly vulnerable period. Chronic idiopathic AF is an important precursor of cerebral embolism. Controlled trials of anticoagulants or antiarrhythmic agents in persons with chronic AF may demonstrate if strokes can be prevented in this highly susceptible group.
In the Cardiac Arrhythmia Suppression Trial, designed to test the hypothesis that suppression of ventricular ectopy after a myocardial infarction reduces the incidence of sudden death, patients in whom ventricular ectopy could be suppressed with encainide, flecainide, or moricizine were randomly assigned to receive either active drug or placebo. The use of encainide and flecainide was discontinued because of excess mortality. We examined the mortality and morbidity after randomization to encainide or flecainide or their respective placebo.
Of 1498 patients, 857 were assigned to receive encainide or its placebo (432 to active drug and 425 to placebo) and 641 were assigned to receive flecainide or its placebo (323 to active drug and 318 to placebo). After a mean follow-up of 10 months, 89 patients had died: 59 of arrhythmia (43 receiving drug vs. 16 receiving placebo; P = 0.0004), 22 of nonarrhythmic cardiac causes (17 receiving drug vs. 5 receiving placebo; P = 0.01), and 8 of noncardiac causes (3 receiving drug vs. 5 receiving placebo). Almost all cardiac deaths not due to arrhythmia were attributed to acute myocardial infarction with shock (11 patients receiving drug and 3 receiving placebo) or to chronic congestive heart failure (4 receiving drug and 2 receiving placebo). There were no differences between the patients receiving active drug and those receiving placebo in the incidence of nonlethal disqualifying ventricular tachycardia, proarrhythmia, syncope, need for a permanent pacemaker, congestive heart failure, recurrent myocardial infarction, angina, or need for coronary-artery bypass grafting or angioplasty.
There was an excess of deaths due to arrhythmia and deaths due to shock after acute recurrent myocardial infarction in patients treated with encainide or flecainide. Nonlethal events, however, were equally distributed between the active-drug and placebo groups. The mechanisms underlying the excess mortality during treatment with encainide or flecainide remain unknown.
Patients with obstructive sleep apnea are considered to be at increased risk of sudden, presumably arrhythmia-related death during sleep. The present study was undertaken to determine the relationship between ventricular ectopy and the severity of oxyhemoglobin desaturation in these patients. Thirty-one male patients with obstructive sleep apnea (mean age, 55 +/- 11 years) underwent overnight polysomnography. Arterial oxyhemoglobin saturation (SaO2) was monitored by ear oximetry, and premature ventricular complexes (PVC) were detected using electrocardiographic leads CC5 and CM5. The data were recorded on electromagnetic tape for subsequent computer-assisted analysis to obtain PVC frequency as a function of decile levels of SaO2. Total sleep time averaged 333 +/- 75 minutes, the apnea index was 44 +/- 26 per hour, and the hypopnea index was 18 +/- 24 per hour. Premature ventricular complexes were observed in 23 (74 percent) of the subjects. By analysis of variance, no significant relationship was found between PVC frequency and decile levels of SaO2 for saturations greater than 60 percent; however, in the 16 subjects with SaO2 below 60 percent, a significant increase in PVC frequency was detected with decreasing SaO2 (p less than 0.01). Ventricular bigeminy was observed with SaO2 below 60 percent in three of these 16 subjects. From these results, we conclude that patients with obstructive sleep apnea are at relatively low risk of developing ventricular arrhythmias provided SaO2 remains greater than 60 percent, while those with SaO2 below 60 percent are at increased risk and should be managed accordingly.
This report presents the first study of cardiac arrhythmias and conduction disturbance in a large group (400 patients) with sleep apnea syndrome studied between 1974 and 1979 with 24-hour Holter electrocardiography and a simultaneously recorded polygraph during late afternoon or nocturnal sleep. Of the 400, 193 patients (48%) had cardiac arrhythmias during the recorded night. The mean number of apneic events, age, weight and lowest oxygen saturation during sleep were not significantly different in those with arrhythmias. The most significant abnormalities were unsustained ventricular tachycardia in 8 patients, sinus arrest that lasted for 2.5 to 13 seconds in 43 patients, and second-degree atrioventricular conduction block in 31. Seventy-five had frequent (greater than 2 beats/min) premature ventricular contractions during sleep. Fifty patients with significant arrhythmias had a tracheostomy and were monitored again after surgery. No arrhythmia was present in these patients except for premature ventricular contractions.
The results of 24-hour continuous electrocardiographic monitoring of 23 patients with documented sleep apnea syndrome were reviewed to evaluate the prevelance of cardiac arrhythmias and conduction disturbances in this disorder. During sleep, marked sinus arrhythmia (more than 30 beats/min variation) was found in 18 patients. Extreme sinus bradycardia (heart rate less than 30 beats/min) and sinus pauses (more than 1.8 sec) were found in only two patients. First-degree and type I second-degree atrioventricular block were found in another patient. There was a decrease in grade of ventricular ectopy from wakefulness to sleep. These data suggest that the prevalence of serious arrhythmias and conduction disturbances during sleep in patients with the sleep apnea syndrome is much lower than previously reported.
Sinus arrest and atrioventricular (AV) block have been demonstrated in as much as 30% of patients with sleep apnea (SA). The reversal of heart block after tracheostomy has been shown. Nasal continuous positive airway pressure (nCPAP) now is widely used as the treatment of SA, but little data are available on the effect of nCPAP on heart block in patients with SA. During a 17-mo period 239 patients were found to have SA in an ambulatory study. Heart block was identified in 17 (16 male, one female) of these patients. Standard polysomnography and two-channel long-term ECG before and during nCPAP therapy were performed in order to assess the effect of nCPAP on SA and heart block. Mean age of the 17 patients was 50.7 yr (range, 27 to 78 yr), mean respiratory disturbance index (RDI) was 90/h (SD +/- 36.1) before nCPAP and 6/h (SD +/- 6.2) on the second treatment night. The number of episodes of heart block during sleep decreased significantly (p < 0.001) from 1,575 before therapy to 165 during nCPAP. In 12 patients (70.6%) heart block was totally prevented by nCPAP. In another three patients, there was a 71 to 97% reduction in the number of episodes of heart block on the second treatment night, and in two of them a complete reversal occurred thereafter. Two patients exhibited an increase in block frequency during nCPAP, which was reversed after 4 wk of nCPAP in one but persisted in the other.(ABSTRACT TRUNCATED AT 250 WORDS)
Patients with heart failure and systolic dysfunction may develop disordered breathing during sleep. Repeated episodes of apnea and hypopnea may result in desaturation and arousals, which could adversely affect left ventricular function. The purpose of this study was to determine the short-term effects of continuous positive airway pressure (CPAP) on sleep-disordered breathing and its consequences in heart failure patients.
The author prospectively studied 29 male patients whose initial polysomnograms showed 15 or more episodes of apnea and hypopnea per hour (apnea-hypopnea index, AHI). Twenty-one patients had predominately central and 8 patients obstructive sleep apnea. All were treated with CPAP during the subsequent night. In 16 patients, CPAP resulted in virtual elimination of disordered breathing. In these patients, the mean AHI (36+/-12 [SD] versus 4+/-3 per hour, P=0.0001), arousal index due to disordered breathing (16+/-9 versus 2+/-2 per hour, P=0.0001), and percent of total sleep time below saturation of 90% (20+/-23% to 0.3+/-0.7%, P=0.0001) decreased, and lowest saturation (76+/-8% versus 90+/-3%, P=0.0001) increased with CPAP. In 13 patients who did not respond to CPAP, these values did not change significantly. In patients whose sleep apnea responded to CPAP, the number of hourly episodes of nocturnal premature ventricular contractions (66+/-117 versus 18+/-20, P=0.055) and couplets (3.2+/-6 versus 0.2+/-0.21, P=0.031) decreased. In contrast, in patients whose sleep apnea did not respond to CPAP, ventricular arrhythmias did not change significantly.
In 55% of patients with heart failure and sleep apnea, first-night nasal CPAP eliminates disordered breathing and reduces ventricular irritability.
Twenty-nine patients in whom severe bradyarrhythmias occurred exclusively during obstructive sleep apnea and in whom advanced sinus node disease or atrioventricular conduction system dysfunction had been excluded by invasive electrophysiologic evaluation were prospectively followed on nasal continuous positive airway pressure. During 54 +/- 10 months follow-up, no syncope and no sudden deaths were observed, suggesting that patients with sleep apnea-associated bradyarrhythmias and a normal electrophysiologic study appear to have a favorable prognosis with continuous positive airway pressure.
Sudden cardiac death (SCD) is a major clinical and public health problem.
United States (US) vital statistics mortality data from 1989 to 1998 were analyzed. SCD is defined as deaths occurring out of the hospital or in the emergency room or as "dead on arrival" with an underlying cause of death reported as a cardiac disease (ICD-9 code 390 to 398, 402, or 404 to 429). Death rates were calculated for residents of the US aged >/=35 years and standardized to the 2000 US population. Of 719 456 cardiac deaths among adults aged >/=35 years in 1998, 456 076 (63%) were defined as SCD. Among decedents aged 35 to 44 years, 74% of cardiac deaths were SCD. Of all SCDs in 1998, coronary heart disease (ICD-9 codes 410 to 414) was the underlying cause on 62% of death certificates. Death rates for SCD increased with age and were higher in men than women, although there was no difference at age >/=85 years. The black population had higher death rates for SCD than white, American Indian/Alaska Native, or Asian/Pacific Islander populations. The Hispanic population had lower death rates for SCD than the non-Hispanic population. From 1989 to 1998, SCD, as the proportion of all cardiac deaths, increased 12.4% (56.3% to 63.9%), and age-adjusted SCD rates declined 11.7% in men and 5.8% in women. During the same time, age-specific death rates for SCD increased 21% among women aged 35 to 44 years.
SCD remains an important public health problem in the US. The increase in death rates for SCD among younger women warrants additional investigation.
We tested the hypothesis that patients with untreated obstructive sleep apnea (OSA) would be at increased risk for recurrence of atrial fibrillation (AF) after cardioversion.
We prospectively obtained data on history, echocardiogram, ECG, body mass index, hypertension, diabetes, NYHA functional class, ejection fraction, left atrial appendage velocity, and medications in patients with AF/atrial flutter referred for DC cardioversion. Forty-three individuals were identified as having OSA on the basis of a previous sleep study. Data regarding the use of continuous positive airway pressure (CPAP) and recurrence of AF were obtained for 39 of these patients. Follow-up data were also obtained in 79 randomly selected postcardioversion patients (controls) who did not have any previous sleep study. Twenty-seven of the 39 OSA patients either were not receiving any CPAP therapy (n=25) or were using CPAP inappropriately (n=2). Recurrence of AF at 12 months in these 27 patients was 82%, higher than the 42% recurrence in the treated OSA group (n=12, P=0.013) and the 53% recurrence (n=79, P=0.009) in the 79 control patients. Of the 25 OSA patients who had not been treated at all, the nocturnal fall in oxygen saturation was greater (P=0.034) in those who had recurrence of AF (n=20) than in those without recurrence (n=5).
Patients with untreated OSA have a higher recurrence of AF after cardioversion than patients without a polysomnographic diagnosis of sleep apnea. Appropriate treatment with CPAP in OSA patients is associated with lower recurrence of AF.
In this new era of insertable loop recorders, we studied obstructive sleep apnoea-hypopnoea syndrome (OSAHS) patients in order to evaluate their arrhythmias and the beneficial effect of Continuous Positive Airway Pressure treatment (CPAP), over a long-term period.
We enrolled 23 patients (16 men, 50 +/- 11 years) with moderate and severe OSAHS. In all patients, an insertable loop recorder capable of monitoring the heart rhythm for 16 months was implanted. Cardiac pauses >3 s and bradycardic episodes <40 bpm during a 2-month period before, and for 14 months after, the CPAP application, were noted. In each period, the patients underwent two 24-h Holter recordings. Before treatment, 11 patients (47%) revealed severe cardiac rhythm disturbances, mostly nocturnal. Holter recordings showed disturbances in only 3 (13%) patients (P=0.039), those in whom the insertable loop device had recorded frequent episodes. Eight weeks after the initiation of treatment, the total number of the recorded episodes tended to decrease while, during the last 6 months of the follow-up, no episodes were recorded.
Approximately half of OSAHS patients evidence severe cardiac rhythm disturbances, which are significantly reduced by CPAP. Holter recordings seem unable to precisely describe the incidence of severe brady-arrhythmias and the effect of treatment.
Obstructive sleep apnea (OSA) is associated with recurrent atrial fibrillation (AF) after electrocardioversion. OSA is highly prevalent in patients who are male, obese, and/or hypertensive, but its prevalence in patients with AF is unknown.
We prospectively studied consecutive patients undergoing electrocardioversion for AF (n=151) and consecutive patients without past or current AF referred to a general cardiology practice (n=312). OSA was diagnosed with the Berlin questionnaire, which is validated to identify patients with OSA. We also assessed its accuracy compared with polysomnography in a sample of the study population. Groups were compared with the 2-tailed t, Wilcoxon, and chi2 tests. Logistic regression modeled the association of AF and OSA after adjustment for relevant covariates. Patients in each group had similar age, gender, body mass index, and rates of diabetes, hypertension, and congestive heart failure. The questionnaire performed with 0.86 sensitivity, 0.89 specificity, and 0.97 positive predictive value in our sample. The proportion of patients with OSA was significantly higher in the AF group than in the general cardiology group (49% versus 32%, P=0.0004). The adjusted odds ratio for the association between AF and OSA was 2.19 (95% CI 1.40 to 3.42, P=0.0006).
The novel finding of this study is that a strong association exists between OSA and AF, such that OSA is strikingly more prevalent in patients with AF than in high-risk patients with multiple other cardiovascular diseases. The coinciding epidemics of obesity and AF underscore the clinical importance of these results.
The risk of sudden death from cardiac causes in the general population peaks from 6 a.m. to noon and has a nadir from midnight to 6 a.m. Obstructive sleep apnea is highly prevalent and associated with neurohormonal and electrophysiological abnormalities that may increase the risk of sudden death from cardiac causes, especially during sleep.
We reviewed polysomnograms and the death certificates of 112 Minnesota residents who had undergone polysomnography and had died suddenly from cardiac causes between July 1987 and July 2003. For four intervals of the day, we compared the rates of sudden death from cardiac causes among people with obstructive sleep apnea and the following: the rates among people without obstructive sleep apnea, the rates in the general population, and the expectations according to chance. For each interval, we assessed the median apnea-hypopnea index and the relative risk of sudden death from cardiac causes. We similarly analyzed sudden death from cardiac causes during three time intervals that correlate with usual sleep-wake cycles.
From midnight to 6 a.m., sudden death from cardiac causes occurred in 46 percent of people with obstructive sleep apnea, as compared with 21 percent of people without obstructive sleep apnea (P=0.01), 16 percent of the general population (P<0.001), and the 25 percent expected by chance (P<0.001). People with sudden death from cardiac causes from midnight to 6 a.m. had a significantly higher apnea-hypopnea index than those with sudden death from cardiac causes during other intervals, and the apnea-hypopnea index correlated directly with the relative risk of sudden death from cardiac causes from midnight to 6 a.m. For people with obstructive sleep apnea, the relative risk of sudden death from cardiac causes from midnight to 6 a.m. was 2.57 (95 percent confidence interval, 1.87 to 3.52). The analysis of usual sleep-wake cycles showed similar results.
People with obstructive sleep apnea have a peak in sudden death from cardiac causes during the sleeping hours, which contrasts strikingly with the nadir of sudden death from cardiac causes during this period in people without obstructive sleep apnea and in the general population.