Treatment of sleep apnea in chronic heart failure patients with auto-servo ventilation improves sleep fragmentation: a randomized controlled trial

Background: Impaired sleep efficiency is independently associated with worse prognosis in patients with chronic heart failure (CHF). Therefore, a test was conducted on whether auto-servo ventilation (ASV, biphasic positive airway pressure [BiPAP]-ASV, Philips Respironics) reduces sleep fragmentation and improves sleep efficiency in CHF patients with central sleep apnea (CSA) or obstructive sleep apnea (OSA). Methods: In this multicenter, randomized, parallel group trial, a study was conducted on 63 CHF patients (age 64 +/- 10 years; left ventricular ejection fraction 29 +/- 7%) with CSA or OSA (apnea-hypopnea Index, AHI 47 +/- 18/h; 46% CSA) referred to sleep laboratories of the four participating centers. Participants were randomized to either ASV (n = 32) or optimal medical treatment alone (control, n = 31). Results: Polysomnography (PSG) and actigraphy at home (home) with centralized blinded scoring were obtained at baseline and 12 weeks. ASV significantly reduced sleep fragmentation (total arousal indexpsc: -16.4 +/- 20.6 vs.-0.6 13.2/h, p = 0.001; sleep fragmentation index(home):-7.6 +/- 15.6 versus 4.3 +/- 13.9/h, p = 0.003, respectively) and significantly increased sleep efficiency assessed by actigraphy (SEhome) compared to controls (2.3 +/- 10.1 vs.-2.1 +/- 6.9%, p = 0.002). Effects of ASV on sleep fragmentation and efficiency were similar in patients suffering from OSA and CSA. Conclusions: At home, ASV treatment modestly improves sleep fragmentation as well as sleep efficiency in CHF patients having either CSA or OSA. (C) 2015 Elsevier B.V. All rights reserved

Schlafapnoe

In 2017 the German Sleep Society (Deutsche Gesellschaft fur Schlafforschung und Schlafmedizin, DGSM) published the new S3 guideline "Nonrestorative Sleep/Sleep Disorders, chapter Sleep-Related Breathing Disorders in Adults. Sleep apnea contributes to an increased morbidity and mortality in patients with cardiovascular diseases, e.g. coronary heart disease, heart failure and diabetes mellitus and is associated with an increased perioperative risk. It is also an important comorbidity in respiratory, neurologic and oncologic diseases. Treatment of sleep apnea can improve daytime sleepiness, quality of life und reduce blood pressure. In patients with atrial fibrillation, obstructive sleep apnea treatment should be optimized to improve treatment results. In addition to CPAP (continuous positive airway pressure) therapy and mandibular advancement devices, there are new therapies (e.g. hypoglossal nerve stimulation). Telemonitoring can help to improved therapy adherence. Nevertheless, in a current study CPAP could not prevent cardiovascular events in patients with moderate-to-severe obstructive sleep apnea and established cardiovascular disease. Patients with predominantly central sleep apnea and systolic hear failure (left ventricular ejection fraction 45%) had an increased cardiovascular mortality when treated with adaptive servoventilation. Therefore, ASV is contraindicated in this small group of patients. Further studies are ongoing

Adaptive servo-ventilation therapy of central sleep apnoea and its effect on sleep quality

Poor sleep quality is common in patients with chronic heart failure (CHF). This study tested the hypothesis that adaptive servo-ventilation (ASV) therapy in CHF patients whose central sleep apnoea (CSA) was not suppressed by continuous positive airway pressure (CPAP) (CPAP-non-responders) would improve sleep quality compared to CPAP-responders receiving ongoing CPAP therapy. Eighty-two patients with CHF (65 +/- A 9 years, left ventricular ejection fraction 35 +/- A 16 %) and CSA [apnoea-hypopnoea index (AHI) a parts per thousand yen15/h] were retrospectively studied. Within an average of 47 days, patients were reevaluated on CPAP therapy and stratified according to their suppression of CSA: 34 were CPAP-non-responders switched to ASV therapy the following day and 48 were CPAP-responders who continued on CPAP therapy. Polysomnographic parameters were assessed in the diagnostic night and on the last night of PAP therapy (CPAP or ASV) before the patient was discharged with the final pressure settings. Compared with the CPAP group, the ASV group had significantly greater reductions from baseline in AHI (-37 +/- A 15/h vs -28 +/- A 18/h, p = 0.02), arousal index (-12.7 +/- A 13.6/h vs -6.8 +/- A 12.5/h, p = 0.04) and sleep stage N1 (-9 +/- A 14 % vs -2 +/- A 12 %, p = 0.03). In addition, the ASV group gained significantly more rapid eye movement (REM) sleep compared with the CPAP group (+5 +/- A 9 % vs +1 +/- A 9 %, p = 0.02). CPAP therapy is effective in reducing AHI in a significant proportion of CHF patients with reduced ejection fraction and CSA. Treatment of CSA with ASV in CHF patients reduces sleep fragmentation and improves sleep structure to a significantly greater extent than changes seen in responders to CPAP therapy

Effects of continuous positive airway pressure therapy on daytime and nighttime arterial blood pressure in patients with severe obstructive sleep apnea and endothelial dysfunction

Purpose A nocturnal non-dipping or rise in blood pressure (BP) is associated with poor cardiovascular outcome. This study aimed to test whether continuous positive airway pressure (CPAP) therapy can reduce nocturnal BP and normalize the 24-h BP profile in patients with severe obstructive sleep apnea (OSA) and erectile dysfunction as a surrogate for endothelial dysfunction (ED). Patients and methods Eighteen consecutive patients with OSA and ED on stable antihypertensive medication (age 55.8 +/- 9.5 years, body mass index 35.5 +/- 3.8 kg/m(2), apnea-hypopnoea index 66.1 +/- 27.4/h) were treated with CPAP for 6 months (average daily use 5.8 +/- 2.3 h). Twenty-four hour BP recordings were performed using a portable monitoring device. Rising was defined as an increase, whereas non-dipping was defined as a fall in nocturnal BP of less than 10% compared to daytime values. Serum noradrenaline levels as markers of sympathetic activity were measured at baseline and at 6 month follow up. Results Compared to baseline, nocturnal systolic and diastolic BP were significantly reduced after CPAP therapy (128.5 +/- 14 to 122.9 +/- 11 mmHg,p = 0.036; 76.2 +/- 9 to 70.5 +/- 5 mmHg,p = 0.007). The frequency of non-dipping and rising nocturnal systolic BP, as well as mean nocturnal heart rate, was reduced after CPAP treatment (73 to 27%,p = 0.039;20 to 7%,p = 0.625; from 81.5 +/- 10 to 74.8 +/- 8 beats per minutep = 0.043). Serum levels of noradrenaline were significantly lower after CPAP therapy (398 +/- 195 ng/l vs. 303 +/- 135 ng/l,p = 0.032). Conclusion In patients with severe OSA and clinically apparent ED, CPAP therapy was associated with a decrease in nocturnal BP and serum noradrenaline levels, as well as a normalization of the 24-h BP profile

Rationale and design of the randomised Treatment of sleep apnoea Early After Myocardial infarction with Adaptive Servo-Ventilation trial (TEAM-ASV I)

Aims In acute myocardial infarction (AMI), impaired myocardial salvage and large infarct size result in residual heart failure, which is one of the most important predictors of morbidity and mortality after AMI. Sleep-disordered breathing (SDB) is associated with reduced myocardial salvage index (MSI) within the first 3 months after AMI. Adaptive servo-ventilation (ASV) can effectively treat both types of SDB (central and obstructive sleep apnoea). The Treatment of sleep apnoea Early After Myocardial infarction with Adaptive Servo-Ventilation trial (TEAM-ASV I) will investigate the effects of ASV therapy, added to percutaneous coronary intervention (PCI) and optimal medical management of AMI, on myocardial salvage after AMI. Methods/design TEAM ASV-I is a multicentre, randomised, parallel-group, open-label trial with blinded assessment of PCI outcomes. Patients with first AMI and successful PCI within 24 h after symptom onset and SDB (apnoea-hypopnoea index >= 15/h) will be randomised (1:1 ratio) to PCI and optimal medical therapy alone (control) or plus ASV (with stratification of randomisation by infarct location; left anterior descending (LAD) or no LAD lesion). The primary outcome is the MSI, assessed by cardiac magnetic resonance imaging. Key secondary outcomes are change of infarct size, left ventricular ejection fraction and B-type natriuretic peptide levels and disease-specific symptom burden at 12 weeks. Conclusion TEAM ASV-I will help to determine whether treatment of SDB with ASV in the acute phase after myocardial infarction contributes to more myocardial salvage and healing

Obstructive sleep apnoea is associated with the development of diastolic dysfunction after myocardial infarction with preserved ejection fraction

Background Left ventricular diastolic dysfunction is a predictor of adverse outcome after acute myocardial infarction (AMI). We aimed to test if sleep-disordered breathing (SDB) contributes to the development of diastolic dysfunction in patients with preserved left ventricular ejection fraction after AMI. Method Patients with AMI, percutaneous coronary intervention and an ejection fraction ≥50% were included in this sub-analysis of a prospective observational study. Patients with AMI (n = 41) underwent cardiovascular magnetic resonance imaging (volume–time curve analysis) to define diastolic function by means of the normalised peak filling rate [nPFR; (end diastolic volume/second)]. In patients with AMI, the nPFR was assessed within <5 days and three months after AMI. Patients with AMI were stratified in patients with (apnoea-hypopnoea index, AHI ≥15/h) and without (AHI <15/h) SDB as assessed by polysomnography. Results At the time of AMI, the nPFR was similar between patients with and without SDB (2.90 ± 0.54 vs. 3.03 ± 1.20, p = 0.662). Within three months after AMI, diastolic function was significantly lower in patients with SDB than in patients without SDB (ΔnPFR: −0.83 ± 0.14 vs. 0.03 ± 0.14; p < 0.001; ANCOVA, adjusted for baseline nPFR). In contrast to central AHI, obstructive AHI was associated with a lower nPFR three months after AMI, after accounting for established risk factors for diastolic dysfunction [multiple linear regression analysis, B (95%CI): −0.036 (−0.063 to −0.009), p = 0.011]. Conclusion Our data indicate that obstructive sleep apnoea impairs diastolic function early after myocardial infarction

The impact of epicardial adipose tissue in patients with acute myocardial infarction

Aims Epicardial adipose tissue (EAT) has been linked to impaired reperfusion success after percutaneous coronary intervention (PCI). Whether EAT predicts myocardial damage in the early phase after acute myocardial infarction (MI) is unclear. Therefore, we investigated whether EAT in patients with acute MI is associated with more microvascular obstruction (MVO), greater ST-deviation, larger infarct size and reduced myocardial salvage index (MSI). Methods and results This retrospective analysis of a prospective observational study including patients with acute MI (n = 54) undergoing PCI and 12 healthy matched controls. EAT, infarct size and MSI were analyzed with cardiac magnetic resonance imaging, conducted 3–5 days and 12 weeks after MI. Patients with acute MI showed higher EAT volume than healthy controls (46 [25.;75. percentile: 37;59] vs. 24 [15;29] ml, p < 0.001). The high EAT group (above median) showed significantly more MVO (2.22 [0.00;5.38] vs. 0.0 [0.00;2.18] %, p = 0.004), greater ST-deviation (0.38 [0.22;0.55] vs. 0.15 [0.03;0.20] mV×10−1, p = 0.008), larger infarct size at 12 weeks (23 [17;29] vs. 10 [4;16] %, p < 0.001) and lower MSI (40 [37;54] vs. 66 [49;88] %, p < 0.001) after PCI than the low EAT group. After accounting for demographic characteristics, body-mass index, heart volume, infarct location, TIMI-flow grade as well as apnea–hypopnea index, EAT was associated with infarct size at 12 weeks (B = 0.38 [0.11;0.64], p = 0.006), but not with MSI. Conclusions Patients with acute MI showed higher volume of EAT than healthy individuals. High EAT was linked to more MVO and greater ST-deviation. EAT was associated with infarct size, but not with MSI

Association of sleep-disordered breathing and disturbed cardiac repolarization in patients with ST-segment elevation myocardial infarction

OBJECTIVE In patients with ST-segment elevation myocardial infarction (STEMI), disturbed cardiac repolarization before percutaneous coronary intervention (PCI) is a risk factor for malignant ventricular arrhythmia. We tested the hypothesis that sleep-disordered breathing (SDB) in patients with STEMI is associated with disturbed cardiac repolarization. METHODS Thirty-three patients with STEMI who underwent PCI were prospectively enrolled. To assess cardiac repolarization, the heart-rate corrected interval from the peak of the T wave to the end of the T wave (TpTec) and QTc intervals were assessed with 12-lead electrocardiography before PCI, within 24 h after PCI, and 12 weeks after PCI. SDB defined as an apnea-hypopnea index (AHI) ≥15 per hour was diagnosed by polysomnography. RESULTS Before PCI, patients with SDB had a significantly prolonged TpTec interval compared to patients without SDB (133 vs 104 ms, p = 0.035). Within 24 h after PCI, the TpTec interval was 107 vs 92 ms (p = 0.178). QTc intervals showed a similar pattern (pre-PCI: 443 vs 423 ms, p = 0.199; post-PCI: 458 vs 432 ms, p = 0.115). In multiple linear regression analyses, AHI was significantly associated with prolonged TpTec intervals (pre-PCI: B-coefficient = 1.11, 95% confidence interval (CI) 0.48-1.74, p = 0.001; post-PCI: B = 0.97, 95% CI 0.29-1.65, p = 0.007), prolonged QTc intervals (pre-PCI: B = 1.05, 95% CI 0.20-1.91, p = 0.018; post-PCI: B = 1.37, 95% CI 0.51-2.24, p = 0.003), and higher TpTe/QT-ratios (pre-PCI: B = 0.16, 95% CI 0.05-0.27, p = 0.007; post-PCI: B = 0.13, 95% CI < 0.01-0.25, p = 0.036), independent of known risk factors for cardiac arrhythmia. CONCLUSION In patients with STEMI, SDB was significantly associated with disturbed cardiac repolarization before and after PCI, independent of known risk factors. These findings suggest that SDB may contribute to the risk of developing malignant ventricular arrhythmia

Obstructive sleep apnoea but not central sleep apnoea is associated with left ventricular remodelling after acute myocardial infarction

Obejctive Obstructive sleep apnoea (OSA) increases left ventricular transmural pressure more than central sleep apnoea (CSA) owing to negative intrathoracic pressure swings. We tested the hypothesis that the severity of OSA, and not CSA, is therefore associated with spheric cardiac remodelling after acute myocardial infarction. Methods This sub-analysis of a prospective observational study included 24 patients with acute myocardial infarction who underwent primary percutaneous coronary intervention. Spheric remodelling, calculated according to the sphericity index, was assessed by cardiac magnetic resonance imaging at baseline and 12 weeks after acute myocardial infarction. OSA and CSA [apnoea-hypopnoea index (AHI) >= 5/hour] were diagnosed by polysomnography. Results Within 12 weeks after acute myocardial infarction, patients with OSA exhibited a significant increase in systolic sphericity index compared to patients without sleep-disordered breathing (no SDB) and patients with CSA (OSA vs. CSA vs. no SDB: 0.05 +/- 0.04 vs. 0.01 +/- 0.04 vs. - 0.03 +/- 0.03,p = 0.002). In contrast to CSA, the severity of OSA was associated with an increase in systolic sphericity index after accounting for TIMI-flow before percutaneous coronary intervention, infarct size, pain-to-balloon-time and systolic blood pressure [OSA: B (95% CI) 0.443 (0.021; 0.816),p = 0.040; CSA: 0.193 (- 0.134; 0.300),p = 0.385]. Conclusion In contrast to CSA and no SDB, OSA is associated with spheric cardiac remodelling within the first 12 weeks after acute myocardial infarction. Data suggest that OSA-related negative intrathoracic pressure swings may contribute to this remodelling after acute myocardial infaction. [GRAPHICS]

CPAP therapy improves erectile function in patients with severe obstructive sleep apnea

Objectives: Erectile dysfunction (ED) is highly prevalent in obstructive sleep apnea (OSA), however, the effect of continuous positive airway pressure (CPAP) therapy on erectile function has not yet been thoroughly investigated in these patients. Methods: Ninety-four men with severe OSA (ie, with an apnea-hypopnea-index >= 30/h of sleep) were prospectively evaluated for the presence and severity of ED before and after 6-12 months of CPAP therapy. The abbreviated version of the International Index of Erectile Function, (the IIEF-5) was used to rate erectile function. Furthermore, all study participants responded to standard questionnaires of daytime sleepiness (Epworth Sleepiness Scale), quality of life (WHO Wellbeing 5 questionnaire) and depression (Major Depression Inventory). Results: ED as defined by an IIEF-5 score of <= 21 was present in 64 patients (68.1%). CPAP treatment significantly improved erectile function in those patients suffering from moderate and severe ED. Additionally, a trend for a correlation between the improvement of erectile function under CPAP and the hours of its use was observed. Finally, this effect was associated with larger improvements of quality of life in affected patients. Conclusions: ED is very frequent in men with severe OSA and can at least partly be reversed by long-term CPAP therapy in most seriously affected patients. The beneficial effect on erectile function may depend on CPAP compliance and is accompanied by improvements of quality of life. Randomized controlled trials are needed to confirm these findings. (c) 2018 Elsevier B.V. All rights reserved