Overdrive atrial pacing does not improve obstructive sleep apnoea syndrome.

The aim of this study was to assess the ability of overdrive atrial pacing to reduce sleep apnoea severity. A total of 17 unselected patients (12 males; mean+/-SD age 71+/-10 yrs; body mass index 27+/-3 kg x m(-2)) who had received permanent atrial-synchronous ventricular pacemakers for symptomatic bradyarrhythmias and not known to have central or obstructive sleep apnoea syndrome (OSAS) were studied. Using a crossover study design, patients were or were not in pacing mode with atrial overdrive (15 beats x min(-1) faster than mean baseline nocturnal cardiac frequency) for 1 month. Patients were paced only during sleep periods, identified by a specific algorithm included in the pacemaker. Patients underwent three overnight polysomnographic evaluations 1 month apart. The first was performed for baseline evaluation. The patients were then randomly assigned to either 1 night in spontaneous rhythm or to 1 night in pacing mode with atrial overdrive. Two patients refused to continue the study after the first polysomnographic evaluation. OSAS was highly prevalent in this population: 10 of the 15 (67%) patients exhibited an apnoea-hypopnoea index of >30 events x h(-1). The nocturnal spontaneous rhythm was 59+/-7 beats x min(-1) at baseline, compared to 75+/-10 beats x min(-1) with atrial overdrive pacing. The apnoea-hypopnoea index was 46+/-29 events x h(-1) in spontaneous rhythm, compared to 50+/-24 events x h(-1) with atrial overdrive pacing. Overdrive pacing changed none of the respiratory indices, or sleep fragmentation or sleep structure parameters. In conclusion, atrial overdrive pacing has no significant effect on obstructive sleep apnoea.     

Analysis of interaction of acute atrial overdrive pacing with sleep-related breathing disorder

Dose-related effects of atrial overdrive pacing (AOP) on sleep-related breathing disorder (SRBD) were studied. Fourteen patients with pacemakers with moderate to severe SRBD (mean screening apnea-hypopnea index [AHI] 35.2 +/- 21.9 events/hour) were randomized to 3 levels of pacing (50, 10, and 20 beats/min greater than the mean nocturnal heart rate) and studied by polysomnography, observing for changes in AHI. At the 2 AOP levels, no significant change was observed in the primary end point of reduction in AHI. Additionally, there was no observed impact on secondary end points of the study. Cyclic variation of heart rate was progressively abolished with higher levels of AOP without affecting AHI. Large variations were observed between the screening and control studies in SRBD indexes in a number of patients. In conclusion, AOP demonstrated no benefit to predominantly obstructive SRBD disorder of at least moderate severity.     

稳定期慢性充血性心力衰竭患者睡眠呼吸障碍

目的了解稳定期、已得到良好治疗的慢性充血性心力衰竭(心衰)患者的睡眠呼吸障碍的发生情况及睡眠呼吸障碍对心衰的影响.方法应用多导睡眠监护仪(Polywin1000,RespironicsInc.)对稳定期充血性心衰患者进行监测.结果病人分为两组,Ⅰ组(21例)A-H指数≤15,Ⅱ组(15例,占41.7%)A-H指数》15.Ⅱ组A-H指数为16.8～78.8,平均42.6±15.5,其中阻塞性AHI为11.1±8.4,而中枢性AHI为31.5±9.6.同时,Ⅱ组有着显著多的醒觉指数,为36.8±21.3(Ⅰ组为19.4±11.2),这直接与呼吸暂停及低通气指数有关,并与睡眠中最低血氧饱和度[Ⅱ组(76.7±4.6)%,Ⅰ组(86.5±2.8)%、更低的左心室射血分数[Ⅱ组(24.2±8.8)%,Ⅰ组(31.5±10.6)%]有关.结论稳定期慢性充血性心衰患者有着很高的严重的睡眠呼吸障碍的发生率,主要为伴中枢性睡眠呼吸暂停的周期性呼吸.睡眠呼吸障碍的发生与严重的夜间氧合血红蛋白饱和度的下降及过多的觉醒有关.严重的未经治疗的睡眠呼吸障碍可能影响左心室功能,并能加剧充血性心衰患者的死亡.     

Prevalence of sleep-disordered breathing in elderly patients with cardiac pacemaker: a case-control study

Objective To investigate the prevalence of sleep-disordered breathing in elderly patients with permanent cardiac pacemaker implantation due to bradyarrhythmias, and the relationship between pacing mode and patients' sleep apnea-hypopnea index. Methods Forty-four elderly patients (>60 years) with cardiac pacemaker and their 44 controls matched for gender, age, body mass index and cardiovascular morbidity were studied using polysomnography or portable sleep monitoring device. Results Prevalence of sleep-disordered breathing (apnea-hypopnea index≥5/h) was 44.7% and the mean apnea-hypopnea index was 8.2±4.1/h in the cardiac pacemaker group , which were significantly higher than those in control subjects (25% and 4. 6±2.4/h, respectively, P<0.01 and P<0.05). The mean apnea-hypopnea index of patients with DDD or AAI pacemaker was significantly lower than that of patients with VVI pacemaker. Conclusions Sleep-disordered breathing was more common in patients who had their cardiac pacemaker implanted due to bradyarrhythmias than in their matched controls. Compared with VVI pacing, DDD or AAI pacing may be more beneficial to patients with bradyarrhythmias and sleep-disordered breathing.(J Geriatr Cardiol 2005,2(2): 114-117).     

Does atrial overdrive pacing prevent paroxysmal atrial fibrillation in paced patients?

The role of atrial overdrive pacing for the suppression of paroxysmal atrial fibrillation remains unclear. To investigate this we have performed a randomised study evaluating the role of an increased atrial base rate in suppressing this arrhythmia in patients implanted with a permanent pacemaker (Chorum ELA) for sick sinus syndrome with previous documented paroxysmal atrial fibrillation. Twenty-seven patients (mean age, 69; 15 female) were randomised to two 3-month single-blinded crossover periods of DDDR pacing. The pacemaker was set with a base rate of 60 bpm (normal) during one period and at 10 bpm (overdrive) above the average heart rate during the other, mean (S.D.) 75+/-7 beats/min (range, 70-96). The fallback algorithm of the pacemaker was activated to record the number and duration of paroxysmal atrial fibrillation episodes. During the overdrive period there was a significant increase in the total duration of atrial pacing (normal 60+/-26% vs. overdrive 72+/-28%, P<0.001). However there was no significant difference in the number of paroxysmal atrial fibrillation episodes (normal 43+/-109 vs. overdrive 43+/-106, P=ns), or their total duration (normal 42+/-108 h vs. overdrive 99+/-254 h, P=ns). In conclusion, atrial overdrive pacing, achieved by increasing the atrial base rate, has no incremental benefit in the suppression of paroxysmal atrial fibrillation when compared to rate responsive pacing with a base rate of 60 bpm.     

Dual-site atrial pacing for atrial fibrillation in patients without bradycardia.

Atrial pacing has been shown to delay the onset of atrial fibrillation (AF) when compared with ventricular pacing in patients with sick sinus syndrome. The role for pacing in the control of AF in patients without bradycardia is uncertain. We performed a randomized, crossover, single-blinded study in 22 patients (14 women, aged 63 +/- 10 years) with paroxysmal AF refractory to treatment with oral sotalol (202 +/- 68 mg/day) and no bradycardic indication for pacing. All patients received a dual-chamber pacemaker with 2 atrial pacing leads positioned at the high right atrium and coronary sinus ostium, respectively. Patients were randomized in a crossover fashion to be paced for 12 weeks, either with high right atrial (RA) pacing at 30 beats/min ("Off") or dual-site RA pacing with an overdrive algorithm that maintained atrial pacing at a rate slightly above the sinus rate ("On"). Treatment on resulted in a significantly higher percentage of atrial pacing and a reduction in atrial ectopic frequency than the treatment off period. The time to the first clinical AF recurrence was prolonged (15 +/- 17 to 50 +/- 35 days, p = 0.006), and total AF burden was reduced (45 +/- 34% vs 22 +/- 29%, p = 0.04) in the on-treatment phase. However, there was no difference in AF checklist symptom scores or overall quality-of-life measures. Dual-site RA pacing with continued sinus overdrive prolonged the time to AF recurrence and decreased AF burden in patients with paroxysmal AF. The absence of a major impact on symptom control suggests that pacing should be used as an adjunctive therapy with other treatment modalities for AF.     

Comparison of atrial overdrive pacing with and without extrastimuli for termination of atrial flutter.

Atrial overdrive pacing has been successfully used to terminate atrial flutter. This study compared the efficacy of atrial extrastimuli following a rapid pacing train to overdrive pacing without atrial extrastimuli for the termination of atrial flutter. Patients were randomized to treatments of short or long burst atrial overdrive pacing or atrial overdrive pacing followed by atrial extrastimuli in a crossover study design. A total of 22 patients (73%) had successful conversion of atrial flutter to sinus rhythm. The success rates in patients exposed to each therapy, including crossover therapies, were 62% with the atrial extrastimuli method, 8% with the short burst pacing method, and 8% with the long burst pacing method (p less than 0.001). Transient atrial fibrillation developed in 15 patients and in 9 of these this arrhythmia preceded conversion to sinus rhythm. Sustained atrial fibrillation was induced in 3 additional patients but never with the atrial extrastimuli method. In conclusion, the method of delivering atrial extrastimuli after a rapid pacing train is highly efficacious for the termination of atrial flutter. Furthermore, this method is more effective than atrial overdrive pacing methods delivered at the same pacing cycle length. These observations have important implications for the programming of antitachycardia pacemakers.     

Morning levels of C-reactive protein in children with obstructive sleep-disordered breathing

Obstructive sleep-disordered breathing is associated with cardiovascular disease in adults, and elevated C-reactive protein (CRP) has been proposed as a link between the two disorders. We hypothesized that children with sleep-disordered breathing have higher CRP values than do control subjects. CRP was measured in 39 children (mean age +/- SD: 6.9 +/- 3.2 years) without snoring (controls) and in 102 children (6.2 +/- 2.2 years) with habitual snoring who underwent polysomnography. No significant differences were found in mean CRP values between control subjects (0.12 +/- 0.16 mg/dl; n = 39) and snorers with an apnea-hypopnea index of less than 1 episode/hour (0.15 +/- 0.26; n = 18), snorers with an index of 1 or more and less than 5 (0.15 +/- 0.26; n = 54), and snorers with an index of 5 or more (0.22 +/- 0.43; n = 30; p > 0.05). There was no correlation between CRP or log-transformed CRP values and apnea-hypopnea index, respiratory movement/arousal index, Sa(O(2)) nadir, oxygen desaturation (>/= 4%) of hemoglobin index, or percentage of sleep time with saturation less than 95% (p > 0.05). Thus, findings of higher CRP values in adults with sleep-disordered breathing and correlations of these values with polysomnography indices were not confirmed in children.     

Sleep-disordered breathing in patients with idiopathic cardiomyopathy.

BACKGROUND: Sleep-disordered breathing may adversely affect heart function, and thereby contribute to the progression of heart failure. A study was undertaken in patients with idiopathic cardiomyopathy to document the characteristics of sleep-disordered breathing. METHODS AND RESULTS: Thirty-five patients with a diagnosis of idiopathic cardiomyopathy, comprising 20 patients with dilated cardiomyopathy (DCM) and 15 patients with hypertrophic cardiomyopathy (HCM), underwent overnight polysomnography. Of these 35, 16 (80%) of the DCM patients and 7 (47%) of the HCM patients had sleep-disordered breathing. Central sleep apnea-hypopnea syndrome (CSAHS) was seen in 10 DCM patients, but not in the HCM patients, and obstructive sleep apnea-hypopnea syndrome (OSAHS) was seen in 6 DCM patients and 7 HCM patients. CSAHS was seen in DCM patients with a low left ventricular ejection fraction. HCM patients with OSAHS had a significantly greater body mass index (BMI) than those without OSAHS and CSAHS (27.6 +/- 3.8 vs 22.0 +/- 4.0 kg/m2, p<0.05). DCM patients with OSAHS had a larger BMI than those with CSAHS (29.3 +/- 5.8 vs 24.2 +/- 4.0 kg/m2, p<0.05) and those without OSAHS and CSAHS (29.3 +/- 5.8 vs 21.3 +/- 3.1 kg/m2, p<0.05). CONCLUSIONS: Sleep-disordered breathing is common in patients with idiopathic cardiomyopathy; half of DCM patients had CSAHS, which was closely associated with obesity.     

Physiologic pacing in patients with obstructive sleep apnea: a prospective, randomized crossover trial.

OBJECTIVES: This study was designed to assess the impact of prevention of bradycardia with physiologic pacing on the severity of obstructive sleep apnea. BACKGROUND: Apneic episodes during sleep are associated with slowing of the heart rate during apnea and tachycardia with subsequent arousal. Patients with permanent pacemakers may have reduced episodes of sleep apnea when their pacemaker rate is set faster than their spontaneous nocturnal heart rate. METHODS: We conducted a prospective, randomized, single-blind crossover trial of temporary atrial pacing in obstructive sleep apnea to reduce the apnea hypopnea index (AHI). Fifteen patients (age 60 +/- 13 years, 12 men) with moderate to severe obstructive sleep apnea (AHI 34 +/- 14) underwent insertion of an externalized atrial permanent pacing system via the left subclavian vein. Patients underwent overnight respiratory sleep studies in hospital, during atrial pacing at 75 beats/min, and with pacing turned off. The order of pacing mode was randomized, with crossover the subsequent night to the other mode. Patients were blinded to pacing mode, and the analysis of sleep recordings was blind to pacing mode. RESULTS: Pacing was tolerated without complications in all patients. Overnight physiologic pacing did not affect the AHI (pacing 39 +/- 21/h vs. control 42 +/- 21/h, p = 0.23, 95% confidence interval -9.3 to 2.5 for difference), desaturation time (pacing 3.8 +/- 6.0% vs. control 3.5 +/- 4.3%, p = 0.70), or the minimum SaO(2) (pacing 75 +/- 10% vs. control 77 +/- 11%, p = 0.38). There was a borderline significant reduction in circulatory time with pacing (pacing 23.4 +/- 3.2 s vs. control 25.5 +/- 4.4 s, p = 0.09). CONCLUSIONS: Temporary atrial pacing does not appear to improve respiratory manifestations of obstructive sleep apnea. Permanent atrial pacing in this patient population does not appear to be justified.     

Association of nocturnal arrhythmias with sleep-disordered breathing: The Sleep Heart Health Study

RATIONALE: Sleep-disordered breathing recurrent intermittent hypoxia and sympathetic nervous system activity surges provide the milieu for cardiac arrhythmia development. OBJECTIVE: We postulate that the prevalence of nocturnal cardiac arrhythmias is higher among subjects with than without sleep-disordered breathing. METHODS: The prevalence of arrhythmias was compared in two samples of participants from the Sleep Heart Health Study frequency-matched on age, sex, race/ethnicity, and body mass index: (1) 228 subjects with sleep-disordered breathing (respiratory disturbance index>or=30) and (2) 338 subjects without sleep-disordered breathing (respiratory disturbance index<5). RESULTS: Atrial fibrillation, nonsustained ventricular tachycardia, and complex ventricular ectopy (nonsustained ventricular tachycardia or bigeminy or trigeminy or quadrigeminy) were more common in subjects with sleep-disordered breathing compared with those without sleep-disordered breathing: 4.8 versus 0.9% (p=0.003) for atrial fibrillation; 5.3 versus 1.2% (p=0.004) for nonsustained ventricular tachycardia; 25.0 versus 14.5% (p=0.002) for complex ventricular ectopy. Compared with those without sleep-disordered breathing and adjusting for age, sex, body mass index, and prevalent coronary heart disease, individuals with sleep-disordered breathing had four times the odds of atrial fibrillation (odds ratio [OR], 4.02; 95% confidence interval [CI], 1.03-15.74), three times the odds of nonsustained ventricular tachycardia (OR, 3.40; 95% CI, 1.03-11.20), and almost twice the odds of complex ventricular ectopy (OR, 1.74; 95% CI, 1.11-2.74). A significant relation was also observed between sleep-disordered breathing and ventricular ectopic beats/h (p<0.0003) considered as a continuous outcome. CONCLUSIONS: Individuals with severe sleep-disordered breathing have two- to fourfold higher odds of complex arrhythmias than those without sleep-disordered breathing even after adjustment for potential confounders.     

Temporary atrial epicardial pacing as prophylaxis against atrial fibrillation after heart surgery: a meta-analysis

INTRODUCTION: Recent studies have reported the use of temporary epicardial atrial pacing as prophylaxis for postoperative atrial fibrillation (AF). The aim of this study was to assess the effect of pacing therapies for prevention of postoperative AF using meta-analysis. METHODS AND RESULTS: Using a computerized MEDLINE search, eight pacing prophylaxis trials with 776 patients were included in the meta-analysis. Trials compared control patients to patients randomized to right atrial, left atrial, or biatrial pacing used in conjunction with either fixed high-rate pacing or overdrive pacing. Overdrive biatrial pacing (OR 2.6, CI 1.4-4.8), overdrive right atrial pacing (OR 1.8, CI 1.1-2.7), and fixed high-rate biatrial pacing (OR 2.5, CI 1.3-5.1) demonstrated a significant antiarrhythmic effect for prevention of AF after open heart surgery. Furthermore, studies investigating overdrive left atrial pacing and fixed high-rate right atrial pacing have been underpowered to assess efficacy. CONCLUSION: Biatrial overdrive and fixed high-rate pacing and right atrial fixed high-rate pacing reduced the risk of new-onset AF after open heart surgery, and the relative risk reduction is approximately 2.5-fold. These results imply that various pacing algorithms are useful as a nonpharmacologic method to prevent postoperative AF.     

The effect of oxygen on respiration and sleep in patients with congestive heart failure

STUDY OBJECTIVE: To determine the effect of supplemental oxygen on Cheyne-Stokes respiration, nocturnal oxygen saturation (SaO2), and sleep in male patients with severe, stable congestive heart failure. DESIGN: Randomized, single-blind, placebo-controlled crossover study. SETTING: Patients referred from outpatient cardiology clinics of two teaching hospitals. PATIENTS: Sequential sample of nine outpatients with severe, stable congestive heart failure. INTERVENTIONS: For each patient, sleep studies (after an adaptation night) from two consecutive randomized nights were compared; one study was done while the patient breathed compressed air and the other while the patient breathed oxygen (O2). Compressed air and oxygen were both administered through nasal cannulae at 2 to 3 L/min. MEASUREMENTS AND MAIN RESULTS: Cheyne-Stokes respiration, defined as periodic breathing with apnea or hypopnea, was found in all patients. Low-flow oxygen significantly reduced the duration of Cheyne-Stokes respiration (50.7% +/- 12.0% to 24.2% +/- 5.4% total sleep time), mainly during stage 1 NREM (non-rapid eye movement) sleep (21.3% +/- 7.1% to 6.7% +/- 2.3% total sleep time) with no significant change during stage 2 sleep, slow-wave sleep, or REM (rapid eye movement) sleep. Although patients had normal SaO2 (96.0% +/- 1.7%) while awake, severe sleep hypoxemia was common; breathing oxygen reduced the amount of time that SaO2 was less than 90% from 22.3% +/- 8.0% to 2.41% +/- 1.93% of total sleep time. Sleep, disrupted to a variable extent in all patients, improved with oxygen therapy: There was an increase in total sleep time from 275.3 min +/- 36.6 to 324.6 min +/- 23.3; a reduction in the proportion of stage 1 sleep (27.6% +/- 5.8% total sleep time to 15.2% +/- 2.6% total sleep time); and a reduction in the number of arousals (30.4/h +/- 8.0 to 13.8/h +/- 1.9). The apnea-hypopnea index was reduced from 30.0 +/- 4.7 to 18.9 +/- 2.4 with oxygen breathing. CONCLUSION: In severe, stable congestive heart failure, nocturnal oxygen therapy reduces Cheyne-Stokes respiration, corrects hypoxemia, and consolidates sleep by reducing arousals caused by the hyperpneic phase of Cheyne-Stokes respiration. Correction of nocturnal hypoxemia and sleep disruption may improve the clinical status of these patients.     

Long-term outcome of paced and nonpaced patients with severe carotid sinus syndrome.

The natural history of patients with severe carotid sinus syndrome, and the efficacy of permanent pacemaker treatment are not clearly known. A randomized treatment/nontreatment prospective study was performed in 60 patients affected by carotid sinus syndrome whose symptoms were judged to involve risk of major trauma or interfered with their daily activity. They were randomly assigned to 2 groups: 28 patients to no therapy (nonpacing group), and 32 to VVI (n = 18) or DDD (n = 14) pacemaker implant (pacing group). Syncope recurred in 16 patients (57%) of the nopacing group (mean follow-up 36 +/- 10 months) and in only 3 (9%) of the pacing group (mean follow-up 34 +/- 10 months) (p = 0.0002); moreover, 19 (68%) in the nonpacing group needed a secondary pacemaker implant because of the severity of symptoms. The actuarial rate of absence of syncopal recurrence after 1, 2, 3 and 4 years was 64, 54, 38 and 38%, respectively, for the nonpacing group, and 100, 97, 93 and 84%, respectively, for the pacing group (p = 0.0001). The actuarial rate of absence of minor symptoms after 1, 2, 3 and 4 years was 21, 14, 7 and 7%, respectively, for the nonpacing group and 66, 43, 27 and 27%, respectively, for the pacing group (p = 0.002). Reproducibility of carotid sinus reflex was tested after 15 +/- 8 months in 54 patients; an abnormal response to carotid sinus massage persisted in all 54. In conclusion, symptoms recur in most patients with untreated carotid sinus syndrome, and pacing is a useful therapy for preventing recurrences.     

Effect of atrial overdrive pacing on pulmonary vein focal discharge in patients with atrial fibrillation.

AIMS: Recently, it has been shown that atrial fibrillation may be caused by spontaneously discharging foci located predominantly in the pulmonary veins. However, the effect of atrial overdrive pacing on these pulmonary vein foci has not been studied. METHODS AND RESULTS: In 58 patients with drug refractory paroxysmal or persistent atrial fibrillation we performed radiofrequency catheter ablation of arrhythmogenic triggers inside the pulmonary veins and/or an ostial pulmonary vein isolation with conventional mapping and ablation technology. Continuous bigeminal pattern of discharge from one or more arrhythmogenic pulmonary veins was recorded in 14 patients. Atrial overdrive pacing resulted in suppression of pulmonary vein 'focus' activity in all patients. The longest mean atrial pacing cycle length resulting in overdrive suppression was 587+/-114 ms. Independent of pacing rate and duration, bigeminal pulmonary vein focus activity reemerged 2.5+/-3.7s after cessation of pacing. Overdrive suppression of the pulmonary vein focus was incomplete in 9 pacing attempts, and resulted in induction of atrial fibrillation from the same vein in 3 of 31 pacing manoeuvres. At 2 years follow-up 79% of these patients were free of atrial fibrillation, 55% without antiarrhythmic drugs, 24% on previously ineffective antiarrhythmic drug therapy. CONCLUSION: Stable pulmonary vein 'focus' activity in patients with atrial fibrillation can be suppressed by atrial overdrive pacing. However, 'proarrhythmic' effects of atrial overdrive pacing, such as induction of atrial fibrillation, were also seen.     

Association of sleep-disordered breathing and the occurrence of stroke

RATIONALE: Sleep-disordered breathing has been linked to stroke in previous studies. However, these studies either used surrogate markers of sleep-disordered breathing or could not, due to cross-sectional design, address the temporal relationship between sleep-disordered breathing and stroke. OBJECTIVES: To determine whether sleep-disordered breathing increases the risk for stroke. METHODS: We performed cross-sectional and longitudinal analyses on 1,475 and 1,189 subjects, respectively, from the general population. Sleep-disordered breathing was defined by the apnea-hypopnea index (frequency of apneas and hypopneas per hour of sleep) obtained by attended polysomnography. The protocol, including polysomnography, risk factors for stroke, and a history of physician-diagnosed stroke, was repeated at 4-yr intervals. MEASUREMENTS AND MAIN RESULTS: In the cross-sectional analysis, subjects with an apnea-hypopnea index of 20 or greater had increased odds for stroke (odds ratio, 4.33; 95% confidence interval, 1.32-14.24; p = 0.02) compared with those without sleep-disordered breathing (apnea-hypopnea index, <5) after adjustment for known confounding factors. In the prospective analysis, sleep-disordered breathing with an apnea-hypopnea index of 20 or greater was associated with an increased risk of suffering a first-ever stroke over the next 4 yr (unadjusted odds ratio, 4.31; 95% confidence interval, 1.31-14.15; p = 0.02). However, after adjustment for age, sex, and body mass index, the odds ratio was still elevated, but was no longer significant (3.08; 95% confidence interval, 0.74-12.81; p = 0.12). CONCLUSIONS: These data demonstrate a strong association between moderate to severe sleep-disordered breathing and prevalent stroke, independent of confounding factors. They also provide the first prospective evidence that sleep-disordered breathing precedes stroke and may contribute to the development of stroke.     

Atrial overdrive pacing compared to CPAP in patients with obstructive sleep apnoea syndrome.

AIMS: Obstructive sleep apnoea (OSA) is associated with oxygen desaturation, blood pressure increase, and neurohumoral activation, resulting in possible detrimental effects on the cardiovascular system. Continuous positive airway pressure (CPAP) is the therapy of choice for OSA. In a recent study, nocturnal atrial overdrive pacing (pacing) reduced the severity of sleep apnoea in pacemaker patients. We compared the effects of CPAP with those of pacing in patients with OSA but without pacemaker indication or clinical signs of heart failure. METHODS AND RESULTS: Ten patients with OSA on CPAP therapy were studied for three nights by polysomnography. During the nights that followed a night without any treatment (baseline), the patients were treated with CPAP or pacing in a random order. Pacing was performed with a temporary pacing lead. The pacing frequency was 15 b.p.m. higher than the baseline heart rate. The apnoea-hypopnoea index was 41.0 h(-1) (12.0-66.6) at baseline and was significantly lower during CPAP [2.2 h(-1) (0.3-12.4)] compared with pacing [39.1 h(-1) (8.2-78.5)]. Furthermore, duration and quality of sleep were significantly improved during CPAP when compared with pacing. CONCLUSION: Nocturnal atrial overdrive pacing is no alternative therapeutic strategy to CPAP for the treatment of OSA in patients without clinical signs of heart failure and without conventional indication for anti-bradycardia pacing.     

Comparative effects of permanent biventricular and right-univentricular pacing in heart failure patients with chronic atrial fibrillation.

BACKGROUND: One third of chronic heart failure patients have major intraventricular conduction and uncoordinated ventricular contraction. Non-controlled studies suggest that biventricular pacing may improve haemodynamics and well-being by reducing ventricular asynchrony. The aim of this trial was to assess the clinical efficacy and safety of this new therapy in patients with chronic atrial fibrillation. METHODS: Fifty nine NYHA class III patients with left ventricular systolic dysfunction, chronic atrial fibrillation, slow ventricular rate necessitating permanent ventricular pacing, and a wide QRS complex (paced width >or=200 ms), were implanted with transvenous biventricular-VVIR pacemakers. This single-blind, randomized, controlled, crossover study compared the patients' parameters, as monitored during two 3-month treatment periods of conventional right-univentricular vs biventricular pacing. The primary end-point was the 6-min walked distance, secondary end-points were peak oxygen uptake, quality-of-life, hospitalizations, patients' preferred study period and mortality. RESULTS: Because of a higher than expected drop-out rate (42%), only 37 patients completed both crossover phases. In the intention-to-treat analysis, we did not observe a significant difference. However, in the patients with effective therapy the mean walked distance increased by 9.3% with biventricular pacing (374+/-108 vs 342+/-103 m in univentricular;P =0.05). Peak oxygen uptake increased by 13% (P=0.04). Hospitalizations decreased by 70% and 85% of the patients preferred the biventricular pacing period (P<0.001). CONCLUSION: As compared with conventional VVIR pacing, effective biventricular pacing seems to improve exercise tolerance in NYHA class III heart failure patients with chronic atrial fibrillation and wide paced-QRS complexes. Further randomized controlled studies are required to definitively validate this therapy in such patients.     

Systemic hypertension in snorers with and without sleep apnea.

To investigate the impact of sleep-disordered breathing events on daytime hypertension (HT) in patients with increased upper airway resistance during sleep, we studied 191 male snorers aged 49.9 +/- 0.8 years. In 116 of them, an apnea-hypopnea index (AHI) above 10--defined as the presence of obstructive sleep apnea (OSA)--was found; the other 75 subjects had an AHI lower than 10 and were classified as habitual snorers (HSN). Prevalence of HT was not different between OSA (56 of 116 = 48 percent) and HSN (33 of 75 = 44 percent) and there was also no difference in systolic, diastolic, and mean blood pressures between the two groups. Hypertensive OSA patients had higher body mass index (BMI) than normotensive OSA subjects (31.4 +/- 0.7 vs 29.4 +/- 0.6; p less than 0.05), but there was no difference in age, AHI, and nocturnal oxygenation parameters. The same was true for the HSN group, with hypertensive subjects being more obese than normotensive subjects (BMI: 30 +/- 0.8 vs 27.3 +/- 0.8; p less than 0.05), but no difference in age and polysomnographic features. Discriminant analysis with HT as the classification variable and age, BMI, AHI, mean, and lowest nocturnal oxyhemoglobin saturation as independent variables, revealed an independent influence on HT only for BMI (F-prob = 0.001). Thus, our results stand against the hypothesis of a causal relationship between sleep-disordered breathing events and daytime hypertension. We conclude that the high prevalence of HT in male snorers is more directly linked to obesity than to sleep apnea, but an independent effect of snoring per se cannot be excluded.     

Nocturnal myocardial ischemic events and sleep-disordered breathing in patients with coronary artery disease

Objective To investigate the occurrence of nocturnal myocardial ischemia and its relationship with sleep-disordered breathing(apneas and oxygen desaturations)in patients with angina pectoris undergoing coronary an-giography.Methods Eighty-two men and 14 women referred for consideration of coronary intervention wererandomly selected.Observation by an overnight sleep monitor and Holter recording were performed to studysleep-disordered breathing(oxyhemoglobin desaturations≥4% and apnea-hypopneas),heart rates,and ST-seg-ment depressions(≥1mm,≥1 min).Results Nocturnal ST-segment depressions occurred in 37% of thepatients.ST-segment depression within 2 min after an apnea-hypopnea or desaturation occurred in 17% of thepatients.This temporal association was seen in 21% of the patients with nocturnal ST-segment depressions,morefrequendy in men(P<0.05)and more frequently in those with severe disordered breathing(P<0.05).Mostof these ST-segment depressions were preceded by a series of breathing events:repeated apnea-hypopneas or de-saturations or both in 73% of the patients.Conclusions Episodes of nocturnal myocardial ischemia are com-mon in patients with angina pectoris.A temporal relationship between sleep-disordered breathing and myocardialischemia was present in some of our patients,and occurs more frequently in men and in those with severely dis-ordered breathing.(J Geriatr Cardiol 2004;1(2):90-94.)