Soft cervical collar in obstructive sleep apnoea: a pilot study.

In severe obstructive sleep apnoea, a soft cervical collar was well tolerated at night in 10 patients with no changes in polygraphy results. With the same design, a randomised controlled trial would need 246 inclusions for conclusive results. https://bit.ly/2KiU3j1.

Death in patients with adaptive servo-ventilation for sleep apnea and no specific SERVE-HF profile: A case series study.

PURPOSE: The SERVE-HF study reported a risk of cardiovascular death associated with adaptive servo-ventilation (ASV) for central sleep apnea in patients with chronic heart failure with reduced left ventricular ejection fraction (LVEF). Therefore, we adopted in May 2015 a safety procedure in our 32 patients with ASV since 2006. It led to ASV removal in four patients due to ≤45% LVEF. At the end of the procedure we noted eight cases of death. This high 25% mortality rate led us to study these cases. METHODS: The study population was derived from our database of patient follow-up from the sleep unit of our cardiovascular department. RESULTS: All deceased patients but one had cardiac disorders but only one matched the SERVE-HF patient profile. ASV was due to predominant central (n = 4) or mixed (n = 4) sleep apnea. Six patients died prior to our procedure including two patients who died several months after ASV cessation, one from ventricular fibrillation and one from respiratory infection. The cases with ongoing ASV consisted in one case of end-stage heart failure with asystole, two cases of cancer and one case of suicide. Two patients died after their safety procedure with no contra-indications to ASV and before study completion in all the patients, one from cancer and one from pulmonary and renal disorders. CONCLUSIONS: In this series, no relationship became apparent between sleep apnea or ASV and death. Cardiovascular deaths were not predominant. Further study will be required to clarify the risks associated with ASV in patients with cardiovascular disease.

Nocturnal oxygen therapy in patients with chronic heart failure and sleep apnea: a systematic review.

Chronic heart failure (CHF) is a public health problem which affects >2% of the adult population, with high morbidity, mortality, and financial cost. Sleep apnea, prevalent in >50% of patients with CHF, can aggravate vital prognosis due to worsening of heart failure. It is considered that a decrease in the apnea-hypopnea load may improve outcomes for those patients. Nocturnal non invasive ventilation can be proposed to treat sleep apnea in this situation, there being few alternatives. The present review concerns the use of nocturnal oxygen therapy (NOT) in patients suffering from both CHF and sleep apnea. The interest of NOT in this situation lies in its ability to reduce the central apnea-hypopnea index and to improve nocturnal oximetry disorders related to sleep apnea. Impact on cardiac contractility, patient tolerance, side effects, and costs of NOT are also approached as well as the underlying mechanisms of NOT. In addition, the results of the SERVE-HF trial have shown an increased death rate in patients with CHF and central sleep apnea and who were treated with adaptive servo-ventilation versus control patients. This may lead to renewed interest in NOT in those patients.

Short- and long-term effects of nocturnal oxygen therapy on sleep apnea in chronic heart failure.

PURPOSE: This paper studies the short- and long-term effects of nocturnal oxygen therapy (NOT) on sleep apnea in chronic heart failure (CHF). METHODS: We enrolled 51 adults in New York Heart Association (NYHA) heart failure functional classes II or III, ≤45 % left ventricular ejection fraction (LVEF), in a randomized, open, single-center study. Nocturnal cardiorespiratory polygraphy showed sleep apnea [apnea-hypopnea index (AHI) ≥15 events/h] in 33 patients, of whom 19 were randomly assigned to NOT, 3.0 l/min, and 14 to no NOT. The NOT group underwent follow-up polygraphy at 24 h and 6 months, and the no NOT group a single follow-up polygraphy at 6 months. RESULTS: No significant difference was observed between baseline and 6 months in the no NOT group. In the NOT group, AHI decreased from 36.8 ± 2.6 events/h at baseline to 20.8 ± 3.0 at 24 h and to 18.3 ± 2.4 at 6 months (both P < 0.0001 vs. baseline), due to central AHI changes from 23.3 ± 2.8 events/h at baseline to 8.3 ± 1.6 at 24 h and to 6.1 ± 1.4 at 6 months (both P < 0.0001 vs. baseline). Oxygen desaturation index (ODI) decreased from 33.0 ± 5.2 events/h at baseline to 7.5 ± 0.5 at 24 h and 9.3 ± 2.6 at 6 months (both P < 0.0001 vs. baseline). NOT had no significant effect on obstructive and mixed AHI, quality of life (QOL), NYHA class, and LVEF up to 6 months of follow-up. CONCLUSIONS: NOT decreased central AHI and ODI significantly within 24 h and up to 6 months in CHF patients with sleep apnea, without significantly modifying obstructive and mixed AHI, QOL, and ventricular function.

Overdrive ventricular pacing in pacemaker recipients with permanent atrial fibrillation and sleep apnea.

STUDY OBJECTIVES: Cardiac pacing is ineffective in obstructive sleep apnea (SA), but it can alleviate central SA/Cheyne-Stokes respiration (CSA) in patients with heart failure (HF). We examined whether overnight overdrive ventricular pacing (OVP) has an effect on SA in pacemaker recipients with permanent atrial fibrillation (AF). METHODS: An apnea-hypopnea index (AHI) ≥ 15 was confirmed in 28/38 patients screened by finger pulse oximetry during overnight ventricular pacing at a backup rate of 40 bpm (BUV40). These patients (23 men, 77.9 ± 7.6 y, BMI 27.6 ± 5.1 kg/m(2)) were randomly assigned to 2 consecutive nocturnal ventilation polygraphies with BUV40 versus OVP at 20 bpm above the mean nocturnal heart rate observed during screening. RESULTS: During BUV40 versus OVP, (1) mean heart rate was 49 ± 8 versus 71 ± 8 bpm (p < 0.0001) and percent ventricular pacing 36% ± 38% versus 96% ± 6% (p < 0.0001); (2) AHI was 35.4 ± 11.9 versus 32.5 ± 15.5 (p = ns), central AHI 23.9 ± 11.8 versus 19.1 ± 12.7 (p < 0.001), and obstructive AHI 11.6 ± 13.1 versus 13.5 ± 15.9 (p = ns). In 15/28 patients without HF, mean left ventricular ejection fraction (LVEF) was 51% ± 17%, AHI was 37.6 ± 11.0 during BUV40 and 39.0 ± 11.5 during OVP, versus 32.8 ± 12.9 and 24.9 ± 16.5 in 13/28 patients with HF (p = 0.02) and mean LVEF 35% ± 15% (p = 0.01). Between the 2 subgroups, (1) central AHI was 23.6 ± 12.4 during BUV40 and 21.5 ± 14.0 during OVP versus 24.1 ± 11.6 and 16.2 ± 10.7 (p = 0.05); (2) obstructive AHI was 14.0 ± 13.7 during BUV40 and 17.6 ± 16.5 during OVP versus 8.8 ± 12.3 and 8.7 ± 14.3 (p = ns). CONCLUSIONS: The prevalence of SA, predominantly central, was high in our pacemaker recipients with permanent AF. In those with HF, a single overnight OVP resulted in modest improvement in central events.

Sleep apnoea in patients with heart failure: part II: therapy.

Nasal continuous positive airway pressure (CPAP) is generally recommended for the treatment of obstructive sleep apnoea. CPAP lowers the cardiovascular morbidity and mortality associated with severe obstructive sleep apnoea. At least 50% of patients presenting with chronic heart failure (HF) have sleep apnoea; a subset of these patients may have obstructive sleep apnoea and may derive a survival benefit from CPAP. However, this population is also prone to developing central sleep apnoea, Cheyne-Stokes respiration or both (CSA/CSR), for which CPAP lowers the apnoea-hypopnoea index only partially and for which the overall effect of CPAP on survival remains to be determined, particularly as it has been observed to increase the mortality rate in subsets of patients. Other treatments may prove effective in patients with chronic HF and CSA/CSR, although none, thus far, has been found to confer a survival benefit. New ventilatory modes include bi-level positive airway pressure and automated adaptive servoventilation, the latter being most effective against CSA/CSR. Measures that can alleviate CSA/CSR indirectly include beta-adrenergic blockers and renin-angiotensin-aldosterone system inhibitors, nocturnal supplemental oxygen and cardiac resynchronization therapy (CRT). The effects of theophylline, acetazolamide and nocturnal CO(2) have also been studied. The second part of this review describes the applications and effects of therapies that are available for sleep apnoea in patients with chronic HF.

Sleep apnoea in patients with heart failure. Part I: diagnosis, definitions, prevalence, pathophysiology and haemodynamic consequences.

Sleep disorder specialists manage 90% of patients suffering from obstructive sleep apnoea, which affects 10% of the general population. From another perspective, cardiovascular disease specialists are particularly challenged by sleep apnoea, since it affects a large proportion of their patients and its complications are largely cardiovascular. At least 50% of patients with chronic heart failure (HF) suffer from sleep apnoea, predominantly central and/or Cheyne-Stokes respiration as opposed to obstructive sleep apnoea. While its effect on survival remains uncertain, sleep apnoea promotes the progression of chronic HF and is a predictor of poor prognosis. After screening by cardiologists, patients presenting with chronic HF and sleep apnoea should be referred to a sleep disorder specialist for diagnostic confirmation and treatment. In Part I of this review, we describe the diagnostic steps recommended when sleep apnoea is suspected in patients with chronic HF. We also review the definitions of abnormal sleep-related respiratory events and the prevalence, pathophysiology and haemodynamic consequences of sleep apnoea in this patient population.

Prevalence of positive carotid sinus massage and related risk of syncope in patients with Alzheimer's disease.

AIMS: The prevalence of positive carotid sinus massage (CSM) in asymptomatic elderly persons and related risk of syncope are poorly known. METHODS AND RESULTS: We examined the ability of CSM to predict the risk of profound bradycardia or syncope in 30 patients with Alzheimer's disease (AD) and no history of syncope, before treatment with cholinesterase inhibitors. Carotid sinus massage was repeated at 1, 2 and 8 months after onset of cholinergic therapy. The long-term incidence of syncope was observed over a 20-month follow-up. Among the study patients (mean age = 80 +/- 6 years, 83% women), 10 had positive CSM, with prolonged ventricular standstill in two of them (6.7%). The response to CSM was not predictive of an increased risk in bradycardia-mediated syncope, though syncope occurred in three patients during long-term follow-up, related to orthostatic hypotension in one and to undetermined causes in the others. Cholinergic therapy in all patients, or drugs that slow cardiac conduction, administered to 40% of the responders to CSM and 45% of the non-responders, or the presence of a bundle branch block did not affect the response to CSM or incidence of syncope. CONCLUSIONS: A positive CSM was (i) observed in 30% of elderly persons with AD and no history of syncope, and (ii) not predictive of an increased risk of bradycardia-mediated syncope.

[Arrhythmias in sleep apnea syndrome]. / Troubles du rythme cardiaque dans le syndrome d'apnée du sommeil.

Arrhythmias are more frequent in patients with sleep apnea syndrome. Bradycardias predominate. In the absence of controlled studies, it is difficult to link arrhythmias to sleep apnea syndrome or to the disease accompanying it (coronary disease, hypertension, etc.). Continuous positive airway pressure (CPAP) reduces arrhythmias significantly.

Cardiovascular effects and risk of syncope related to donepezil in patients with Alzheimer's disease.

BACKGROUND: When otherwise unexplained, syncope in patients with Alzheimer's disease may be attributed to bradycardia caused by cholinesterase inhibitors. We studied prospectively the clinical events and cardiovascular changes occurring during treatment with donepezil in patients with Alzheimer's disease. METHODS: Consecutive patients presenting with mild-to-moderate Alzheimer's disease were included in the study. Their clinical characteristics, blood pressure, heart rate and electrocardiogram were recorded before (baseline) and during treatment with donepezil. The drug was administered at a dosage of 5 mg/day for 1 month and 10 mg/day for the following 7 months, as tolerated. We compared the baseline observations with those made at 1, 2 and 8 months of donepezil treatment. We also examined the effects of negatively chronotropic or dromotropic drugs concomitantly administered with donepezil. RESULTS: Thirty patients were included in the study, of whom 43% were taking negatively chronotropic or dromotropic drugs. The first month of therapy (donepezil 5 mg/day) was completed by 26 patients. During the 7-month high-dosage phase (10 mg/day), four patients dropped out of the study; thus, 22 patients completed the full 8 months of the study. The mean heart rate was 66 +/- 8 beats/min at baseline in the overall study population. This decreased significantly to 62 +/- 9, 61 +/- 7 and 62 +/- 8 beats/min at the 1, 2 and 8 month timepoints, respectively (all p = 0.002 vs baseline). Among patients not receiving negatively chronotropic or dromotropic drugs, heart rate decreased significantly over the course of the study (from 67 +/- 8 beats/min at baseline to 62 +/- 8 beats/min at 1 month, 62 +/- 7 beats/min at 2 months and 62 +/- 8 beats/min at 8 months [all p = 0.005 vs baseline]). There was no significant change in heart rate in patients who were receiving negatively chronotropic or dromotropic drugs. The PR interval increased over the course of the study in all patient groups, but these changes were only statistically significant in the group of patients who were not taking negatively chronotropic or dromotropic drugs (155 +/- 23ms at baseline vs 158 +/- 21, 160 +/- 22 and 163 +/- 24ms at the 1, 2 and 8 month timepoints; all p = 0.02 vs baseline). One patient developed syncope due to orthostatic hypotension; there were no cases of bradycardia-induced syncope. Gastrointestinal manifestations were reported in ten of the study patients. Abdominal pain and vomiting were the reasons for study termination in five of the eight patients who did not complete the trial. CONCLUSION: A donepezil-induced decrease in heart rate and increase in PR interval were observed only in patients with Alzheimer's disease who were not treated with negatively chronotropic or dromotropic drugs. These changes were not associated with bradycardia-induced syncope.

Causes of syncope in patients with Alzheimer's disease treated with donepezil.

INTRODUCTION: Treatment of Alzheimer's disease (AD) with cholinesterase inhibitors carries a theoretical risk of precipitating bradycardia. Though syncope occurs in patients with AD, its aetiology is unclear. The aim of this study was to determine the causes of syncope in patients with AD who were treated with donepezil and hospitalised for evaluation of syncope. METHODS: We studied 16 consecutive patients (12 women, 4 men) with AD aged 80 +/- 4 years who were hospitalised for evaluation of syncope. All patients underwent staged evaluation, ranging from physical examination to electrophysiological testing. RESULTS: The mean dose of donepezil administered was 7.8 mg/day, and the mean duration of donepezil treatment at the time of syncope was 12 +/- 8 months. A cause of syncope was identified in 69% of patients. Carotid sinus syndrome was observed in three patients, complete atrioventricular block in two patients, sinus node dysfunction in two patients, severe orthostatic hypotension in two patients and paroxysmal atrial fibrillation in one patient. A brain tumour was discovered in one patient. No cause of syncope was found in 31% of patients despite comprehensive investigation. Repetition of the investigations after discontinuation of donepezil was noncontributory. CONCLUSION: In patients with AD treated with donepezil, a noninvasive evaluation identified a probable cause of syncope in over two-thirds of patients. Cardiovascular abnormalities were predominant. Noninvasive evaluation is recommended before discontinuing treatment with cholinesterase inhibitors in patients with AD and unexplained syncope.

Death during polysomnography of a patient with cheyne-stokes respiration, respiratory acidosis, and chronic heart failure.

A patient with chronic heart failure and chronic respiratory failure (CRF) underwent ambulatory polysomnography at home. She was found dead on the morning after the recording. The tracings confirmed severe sleep apnea syndrome. After 8 h of incessant Cheyne-Stokes respiration during sleep, respiratory arrest occurred, followed 7 min later by asystole. This report illustrates a case of respiratory drive failure during sleep as the mode of death in a patient with heart failure, sleep apnea syndrome, and CRF.

Suicide by self-removal of a pacemaker.

A 70-year-old man extracted his own pacemaker and subclavian port used for delivery of chemotherapy, both implanted 2 weeks earlier. The patient died of septicemia within 6 days. This fatal outcome illustrates the risks of complications associated with severe psychiatric disorders after implantation of prosthetic devices.

Sleep apnea: a new indication for cardiac pacing?

In the general adult population, prevalence of sleep apnea syndrome reaches 4% in men and 2% in women. Continuous positive airway pressure is the most efficient treatment. At the present time, although severe atrial bradycardias could occur during sleep apnea episodes, cardiac pacing has not been demonstrated as an efficient treatment for those bradycardias. Treating sleep apnea generally reduces the number of bradyarrhythmias. However, recent studies reported a beneficial effect of atrial pacing on the sleep apnea burden. The mechanisms rely on two phenomena: first to counteract nocturnal hypervagotonia, and second to treat heart failure. By increasing the heart rate, cardiac output improves, which mitigates pulmonary subedema. Consequently, stimulation of the pulmonary afferent vagal fibers is diminished, which reduces central sleep apnea incidence. During nocturnal hypervagotonia, snoring and obstructive apnea episodes are increased, mainly due to an excessive muscular relaxation of the upper airway area inducing cyclical substantial decreases in the airway caliper. In patients with a low heart rate, atrial pacing can counteract hypervagotonia by enhancing the sympathetic tone and modifying the degree of vigilance. Accordingly, in the near future, sleep apnea treatment might potentially rely on atrial pacing in bradycardic patients with hypervagotonia (with or without heart failure). The role of the physician would then be not only to diagnose sleep apnea, but also to identify potential responders to cardiac pacing.

Benefit of atrial pacing in sleep apnea syndrome.

BACKGROUND: Many patients with sleep apnea syndrome have nocturnal bradycardia, paroxysmal tachyarrhythmias, or both, which can be prevented by permanent atrial pacing. We evaluated the effect of using cardiac pacing to increase the heart rate during sleep in patients with sleep apnea syndrome. METHODS: We studied 15 patients (11 men and 4 women; mean [+/-SD] age, 69+/-9 years) with central or obstructive sleep apnea who had received permanent atrial-synchronous ventricular pacemakers for symptomatic sinus bradycardia. All patients underwent three polysomnographic evaluations on consecutive nights, the first night for base-line evaluation and then, in random order, one night in spontaneous rhythm and one in dual-chamber pacing mode with atrial overdrive (basic rate, 15 beats per minute faster than the mean nocturnal sinus rate). The total duration and number of episodes of central or obstructive sleep apnea or hypopnea were analyzed and compared. RESULTS: The mean 24-hour sinus rate during spontaneous rhythm was 57 +/- 5 beats per minute at base line, as compared with 72 +/- 3 beats per minute with atrial overdrive pacing (P<0.001). The total duration of sleep was 321 +/- 49 minutes in spontaneous rhythm, as compared with 331 +/- 46 minutes with atrial overdrive pacing (P=0.48). The hypopnea index (the total number of episodes of hypopnea divided by the number of hours of sleep) was reduced from 9 +/- 4 in spontaneous rhythm to 3 +/-3 with atrial overdrive pacing (P<0.001). For both apnea and hypopnea, the value for the index was 28 +/- 22 in spontaneous rhythm, as compared with 11 +/- 14 with atrial overdrive pacing (P<0.001). CONCLUSIONS: In patients with sleep apnea syndrome, atrial overdrive pacing significantly reduces the number of episodes of central or obstructive sleep apnea without reducing the total sleep time.