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Purpose: Sleep-disordered breathing (SDB) is highly prevalent in patients with heart failure and reduced left ventricular ejection fraction (HF-REF). SDB is classified as predominant obstructive (OSA) or central (CSA) and may alter sleep duration, sleep quality, and quality of life. This study describes sleep quality and duration in well-characterized cohorts of these patients., Methods: Two hundred fifty consecutive patients with HF-REF (NYHA class ≥II, ejection fraction ≤45%) underwent cardiac and pulmonary examination, plus full attended in-hospital overnight polysomnography (PSG). PSG recordings were performed according to current recommendations and underwent independent, blinded analysis at a core laboratory., Results: Patients with HF-REF and CSA were older and had more impaired cardiac function compared to those with OSA. With respect to sleep parameters, patients with CSA spent more time in bed than those with OSA (468 ± 52 vs 454 ± 46 min, p = 0.021) while sleep efficiency was lower (67 ± 14 vs 72 ± 13% of total sleep time (TST), p = 0.008). In addition, CSA patients spent more time awake after sleep onset (101 ± 61 vs 71 ± 46 min, p = 0.001) and had more stage N1 (light) sleep (33 ± 19 vs 28 ± 16% of TST, p = 0.017). Overall, the proportion of sleep spent in N3 (slow-wave/deep) sleep in HF-REF patients with SDB was low (4.1 ± 6.3% of TST) compared with healthy adults., Conclusions: HF-REF patients with CSA compared to OSA have worse sleep efficiency and quality. This could result in less restorative sleep, changes in sympathovagal balance, and impaired resetting of important reflexes, which might contribute to worse cardiovascular outcomes in HF-REF patients with SDB.

Sleep-disordered breathing (SDB) is associated with an increased risk of cardiovascular events. Previous studies showed that severe SDB has a negative impact on myocardial salvage and progression of left ventricular dysfunction after acute myocardial infarction (AMI). This study investigated the frequency of SDB and the effects of SDB on left ventricular function after AMI. This retrospective study enrolled all patients with AMI who had undergone cardiorespiratory polygraphy for SDB diagnosis. The apnea-hypopnea index was used as a standard metric of SDB severity. SDB was classified as mild (apnea-hypopnea index >5 to <15 per h), moderate (≥15 to <30 per h) or severe (apnea-hypopnea index ≥30 per h). According to the majority of events, SDB was classified as predominant obstructive sleep apnea, central sleep apnea or mixed sleep apnea (mixed SDB). A total of 223 patients with AMI (112 with ST elevation and 111 without ST elevation; 63.2 ± 11.2 years, 82% male, left ventricular ejection fraction 49 ± 12%) were enrolled. SDB was present in 85.6%, and was moderate-to-severe in 63.2%; 40.8% had obstructive sleep apnea, 41.7% had central sleep apnea and 3.1% had mixed SDB. Left ventricular ejection fraction was lower in patients with AMI with severe SDB (45 ± 14%) versus those without SDB (57 ± 7%; P < 0.005). In addition, lower left ventricular ejection fraction (≤45%) was associated with increased frequency (apnea-hypopnea index ≥5 per h in 96%) and severity (apnea-hypopnea index ≥30 per h in 48%) of SDB in general and a higher percentage of central sleep apnea (57%) in particular. SDB is highly frequent in patients with AMI. SDB severity appeared to be linked to impaired left ventricular function, especially in patients with central sleep apnea., (© 2017 European Sleep Research Society.)

Competing Interests: Disclosure The authors report no conflicts of interest in this work.

Heart failure (HF) treatment remains complex and challenging, with current recommendations aiming at consideration and treatment of comorbidities in patients with HF. Sleep-disordered breathing (SDB) and arrhythmia come into play, as both are associated with quality of life deterioration, and morbidity and mortality increase in patients with HF. Interactions of these diseases are versatile and may appear intransparent in daily practice. Nevertheless, because of their importance for patients' condition and prognosis, SDB and arrhythmia individually, but also through interaction on one another, necessitate attention, following the fact that treatment is requested and desired considering latest research findings and outcomes., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Sleep disordered breathing (SDB) (obstructive sleep apnea, central sleep apnea/Cheyne-Stokes respiration or the combination of both) is highly prevalent in patients with a wide variety of cardiovascular diseases including hypertension, arrhythmia, coronary artery disease, myocardial infarction and stroke (reviewed previously in the September issue of this journal). Its close association with outcomes in chronic heart failure with reduced ejection fraction (HF-REF) suggests that it may be a potential treatment target. Herein, we provide an update on SDB and its treatment in HF-REF.

Aim: This study investigated the prognostic value of sleep-disordered breathing (SDB) in a large cohort of patients with heart failure with reduced left ventricular function (HF-REF), with focus on the role of nocturnal hypoxaemia., Methods: This single-centre prospective cohort study enrolled patients with chronic stable HF-REF (NYHA ≥II) receiving guideline-based treatment. Unattended in-hospital polygraphy was performed to determine the apnoea-hypopnoea index (AHI). Pulse oximetry was used to determine hypoxaemic burden [time with oxygen saturation <90% (T90)], and all-cause mortality was recorded., Results: Complete data were available for 963 of 1249 patients. At baseline, 58% of patients had moderate-to-severe SDB. The median follow-up was 7.35 years; 480 of 963 (49.8%) patients died. Mortality rate (per 100 person-years) was 8.1 [95% confidence interval (CI) 7.0-9.4] in patients with no or mild SDB, but 12.2 (95% CI 10.9-13.7) in moderate-to-severe SDB. Apnoea-hypopnoea index was significantly associated with time to death from any cause in a simple Cox model [hazard ratio (HR) 1.011, P < 0.001], but was no longer significant after adjustment for confounding factors (HR 1.005, P = 0.085). T90 was significantly (P < 0.001) associated with time to death from any cause even after adjustment for confounding factors. The risk of death increased by 16.1% (95% CI 8.6-24.2) per hour of T90. Five-year survival probabilities for patients in T90 quartiles 1, 2, 3, and 4 were 70, 63, 60, and 50%, respectively., Conclusion: Hypoxaemic burden was a robust and independent predictor of all-cause mortality in chronic stable HF-REF patients. Whether or not targeting nocturnal hypoxaemia is associated with beneficial effects on mortality in HF-REF patients remains to be determined., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2015. For permissions please email: journals.permissions@oup.com.)

Aims: Sleep-disordered breathing (SDB), in particular obstructive sleep apnoea, is associated with an increased risk of onset or recurrence of atrial fibrillation (AF) and atrial flutter. This prospective study investigated the relationship between restoration of sinus rhythm and SDB in patients with AF or atrial flutter., Methods and Results: 138 consecutive patients (age 67.8 ± 10.3 years, 67.4 % male) with AF (86.2 %) or atrial flutter (13.8 %) were enrolled and underwent multichannel cardiorespiratory polygraphy the night before and immediately after electrical cardioversion (CV). None of the patients was treated with ventilation therapy before or during the study. Overall prevalence of SDB [apnoea-hypopnoea index (AHI) ≥5/h] was 92 % and prevalence of moderate-to-severe SDB (AHI) ≥15/h was 64 %. Within the first night after CV, AHI decreased from 23.4 ± 16.3 to 16.3 ± 11.5/h, p < 0.001. This was due to a significant decrease in central respiratory events, with a total reduction of patients showing central sleep apnoea (n = 53 at baseline vs n = 23 immediately after CV; p < 0.001)., Conclusions: In conclusion, SDB represents a highly prevalent comorbidity in patients with atrial arrhythmias. Through cardioversion, an immediate reduction of SDB can be detected due to a significant reduction in central respiratory events.

Objectives: This randomized, controlled trial aimed to investigate whether acute improvement of pulmonary congestion would reduce the severity of Cheyne-Stokes respiration (CSR) in patients with chronic heart failure (CHF)., Methods: Twenty-one consecutive patients with CHF and CSR (apnea-hypopnea index [AHI] ≥15/h) underwent right heart catheterization with titration of intravenous (IV) glyceryltrinitrate (GTN) to a maximum tolerable dosage and inhalation of iloprost 10 μg/mL after a washout phase. Maximum tolerable dosages of GTN and iloprost were randomly applied during full cardiorespiratory polysomnography within two split-night procedures and compared with IV or inhaled sodium chloride (NaCl) 0.9 %, respectively., Results: GTN (6.2 ± 1.5 mg/h) and iloprost significantly lowered \mean pulmonary artery pressure (20.1 ± 9.0 to 11.6 ± 4.2 mmHg, p < 0.001 and 16.9 ± 7.9 to 14.2 ± 6.4 mmHg, p < 0.01, respectively). Pulmonary capillary wedge pressure was only reduced by GTN (14.0 ± 5.6 to 7.2 ± 3.9 mmHg, p < 0.001), and there was no significant change in the cardiac index. Sleep studies revealed no significant improvement in markers of CSR severity, including AHI, central apnea index, and CSR cycle length following GTN or iloprost treatment. Significant decreases in blood pressure, mean oxygen saturation, and S3 sleep were documented during GTN infusion., Conclusions: Acute improvement of pulmonary congestion by GTN had no immediate impact on CSR severity. Future investigations must therefore include longer treatment periods and treatment regimens that have positive, rather than negative, additional effects on peripheral and central chemoreceptors and sleep structure., Trial Registration: German Clinical Trial Registry-ID:DRKS00000467 ( www.germanctr.de ).

Obstructive sleep apnoea and central sleep apnoea/Cheyne-Stokes respiration are collectively referred to as sleep-disordered breathing (SDB). Rapidly accumulating evidence suggests that both forms of SDB, and often a combination of both, are highly prevalent in patients with a wide variety of cardiovascular diseases, including hypertension, heart failure, arrhythmias, coronary artery disease, acute coronary syndrome and stroke. The presence of SDB in these patients is independently associated with worse cardiac function and exercise tolerance, recurrent arrhythmias, infarct expansion, decreased quality of life and increased mortality. Recent data suggest positive effects of positive airway pressure (PAP) therapy on quality of life and cardiovascular function. In addition, ongoing clinical trials may soon provide first definitive data on PAP therapy of SDB on hard outcomes such as mortality. This review presents current data highlighting links between SDB and a variety of cardiovascular conditions, the importance of recognising and diagnosing SDB in patients with cardiovascular disease, and the effects of effective SDB treatment on cardiovascular endpoints.

Over the past few years sleep-disordered breathing has been identified as an important factor in arrhythmogenesis and a potential target of therapy to prevent cardiac arrhythmias in selected patients. In this review we highlight the role of obstructive sleep apnea and Cheyne-Stokes respiration in the pathophysiology of arrhythmias, address their clinical effect in supraventricular and ventricular tachyarrhythmias, and in conduction disturbances, and address the role of current treatment options for sleep-disordered breathing in the primary and secondary prevention of arrhythmic events., (Copyright © 2015 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.)

Study Objectives: This study investigated the implications of the revised scoring rules of the American Academy of Sleep Medicine (AASM) in patients with heart failure (HF) with Cheyne-Stokes respiration (CSR)., Methods: Ninety-one patients (NYHA ≥II, LVEF ≤45 %; age 73.6 ± 11.3 years old; 81 male subjects) with documented CSR underwent 8 h of cardiorespiratory polygraphy recordings. Those were analyzed by a single scorer strictly applying the 2007 recommended, 2007 alternative, and the 2012 scoring rules., Results: Compared with the AASM 2007 recommended rules, apnea-hypopnea index (AHI) and hypopnea index (HI) increased significantly when the 2007 alternative and 2012 rules were applied (AHI 34.1 ± 13.5/h vs 37.6 ± 13.2/h vs 38.3 ± 13.2/h, respectively; HI 10.2 ± 9.4/h vs 13.7 ± 10.7/h vs 14.4 ± 11.0/h, respectively; all p < 0.001). Duration of CSR increased significantly with the alternate versus recommended 2007 rules (182.2 ± 117.0 vs 170.1 ± 115.0 min; p ≤ 0.001); there was a significant decrease in CSR duration for the 2012 versus 2007 alternative rules (182.2 ± 117.0 vs 166.7 ± 115.4 min; p ≤ 0.001)., Conclusion: AHI was higher using the AASM 2012 scoring rules due to a less strict definition of hypopnea. Data on the prognostic effects of CSR in patients with HF and the benefits of treatment are mostly based on the AASM 2007 recommended rules, so differences between these and the newer version need to be taken into account.

Objective: In patients with heart failure (HF), Cheyne-Stokes respiration (CSR) is characterized by chronic hyperventilation (HV) with low arterial partial pressure of carbon dioxide (pCO2). It is still unclear whether this HV represents a compensatory response to HF or an independent comorbidity. This study investigated the hemodynamic effects of HV in HF patients and volunteers., Methods: A total of 15 volunteers [13 male, 25 ± 4 years, brain natriuretic peptide (BNP) <49 pg/mL, left ventricular rejection fraction (LVEF) >55 %) and 20 HF patients with reduced LVEF (15 male, 67.7 ± 12 years, NYHA class 2.6 ± 0.6, BNP 790 ± 818 pg/mL, LVEF 32.4 ± 7.3 %) were enrolled. Hemodynamics was monitored noninvasively in volunteers (TaskForce Monitor, CNSystems) and invasively in HF patients., Results: During HV, the transcutaneous CO2 pressure in volunteers decreased from 38.7 ± 2.5 to 28.6 ± 3.3 mmHg (p < 0.001) and pCO2 in HF patients decreased from 33.6 ± 3.7 to 22.2 ± 3.2 mmHg (p < 0.001). There was a significant increase in cardiac output (CO) in both volunteers (6.2 ± 1.3-7.5 ± 1.3 L/min, p < 0.001) and HF patients (4.4 ± 1.3-5.0 ± 1.3 L/min), mainly as a result of an increase in heart rate (67.4 ± 7.6-82.8 ± 10.9/min, p < 0.001; and 77.2 ± 17.7-86.2 ± 22.4/min, p < 0.001, respectively); stroke volume (SV) was unchanged in volunteers (93.7 ± 19.6-93.8 ± 21.4 mL) and only slightly increased in HF patients (64.4 ± 28.7-68.5 ± 23.2 mL)., Conclusions: CSR with associated HV may be a compensatory mechanism in patients with a failing heart. This compensatory mechanism includes an increase in heart rate, which might be deleterious in the long run.

Sleep-disordered breathing (SDB) has so far been a neglected comorbidity in patients with cardiac arrhythmias. Recently however, several studies have revealed a correlation between SDB and malignant ventricular arrhythmias. This review article is intended to provide the reader with an update on the pathophysiological association between SDB and ventricular arrhythmias, available clinical data, and therapeutic options.

Purpose: Supraventricular tachyarrhythmias are a major cause of inappropriate defibrillator shocks. Sleep-disordered breathing (SDB) is a known risk factor for atrial fibrillation (AF). We hypothesized that Cheyne-Stokes respiration (CSA) and obstructive sleep apnea (OSA) have an impact on inappropriate defibrillator discharges in patients witch chronic heart failure (CHF) and cardiac resynchronization therapy with defibrillator (CRT-D)., Methods: In this study, 172 patients with CHF (LVEF ≤ 45 %, NYHA-class ≥ 2) and CRT-D underwent overnight polygraphy; 54 had no SDB (apnea-hypopnea index < 5/h), 59 had OSA, and 59 had CSA. During follow-up (36 months), inappropriate defibrillator shocks were documented., Results: In all, 17 patients had inappropriate defibrillator shocks (9.9 %; eight oversensing due to lead fractures, five caused by atrial fibrillation, four because of sinus tachycardia). Mean event-free survival time was 33.5 ± 1.2 months in the CSA group, 35.2 ± 0.7 months in the OSA group, and 32.1 ± 1.5 months in the no SDB group, respectively (CSA vs. no SDB p = 0.63; OSA vs. no SDB p = 0.31; CSA vs. OSA p = 0.45). Stepwise Cox proportional hazard regression analysis revealed an independent association for age (per year: hazard ratio 0.90, 95 % confidence interval 0.85-0.96, p < 0.001), but not for any kind of SDB., Conclusions: SDB was not associated with inappropriate defibrillator shocks. We assume this is due to the low incidenceand low proportion of inappropriate therapies in response to AF.

Sleep-disordered breathing (SDB) is of growing interest in cardiology because SDB is a highly prevalent comorbidity in patients with a variety of cardiovascular diseases. The prevalence of SDB is particularly high in patients with cardiac dysrhythmias and/or heart failure. In this setting, many patients now have implantable cardiac devices, such as pacemakers, implantable cardioverter-defibrillators or implanted cardiac resynchronisation therapy devices (CRT). Treatment of SDB using implantable cardiac devices has been studied previously, with atrial pacing and CRT being shown not to bring about satisfactory results in SDB care. The latest generations of these devices have the capacity to determine transthoracic impedance, to detect and quantify breathing efforts and to identify SDB. The capability of implantable cardiac devices to detect SDB is of potential importance for patients with cardiovascular disease, allowing screening for SDB, monitoring of the course of SDB in relation to cardiac status, and documenting of the effects of treatment.

Purpose: Using pulse transit time (PTT) and an ECG appears to be a promising alternative for invasive or noninvasive monitoring of blood pressure (BP). This study assessed the validity of PTT for BP monitoring in clinical practice., Methods: Twenty-nine patients with chronic heart failure (HF; 27 male, 70.5 ± 9.9 years) and nocturnal Cheyne-Stokes respiration were noninvasively ventilated for one hour using adaptive servoventilation (ASV) therapy (PaceWave, ResMed). BP was measured using two devices (oscillometrically via Task Force Monitor, CNSystems and PTT via SOMNOscreen, Somnomedics) at least every 7 min for 30 min before, during, and after ASV., Results: Mean systolic BP was 118.1 ± 14.4 mmHg vs. 115.9 ± 14.1 mmHg for oscillometric method vs PTT, respectively. Corresponding values for diastolic BP were 72.3 ± 10.3 mmHg and 69.4 ± 11.1 mmHg. While clinically comparable, differences between the two methods were statistically significant (p < 0.05). The difference between the two methods showed an increasing trend over time. A total of 18.5 % of PTT-based measurements could not be analyzed. The direction of a change in BP was opposite for PTT vs oscillometry for 17.0 % and 32.8 % of systolic and diastolic BP measurements, respectively., Conclusions: When monitoring BP in HF patients, overall BP monitoring using PTT is comparable to oscillometry for a period of 2 h (including a 1-h ASV phase). However, PTT shows a tendency to underestimate BP over time and during ASV.

Pacemaker apnea scan algorithms are able to screen for sleep apnea. We investigated whether these systems were able to accurately detect sleep-disordered breathing (SDB) in two patients from an outpatient clinic. The first patient suffered from ischemic heart failure and severe central sleep apnea (CSA) and underwent adaptive servoventilation therapy (ASV). The second patient suffered from dilated cardiomyopathy and moderate obstructive sleep apnea (OSA). Pacemaker read-outs did not match polysomnography (PSG) recordings well and overestimated the apnea-hypopnea index. However, ASV therapy-induced SDB improvements were adequately recognized by the apnea scan of the Boston Scientific INVIVE® cardiac resynchronization therapy pacemaker. Detection of obstructive respiratory events using impedance-based technology may underestimate the number of events, as frustrane breathing efforts induce impedance changes without significant airflow. By contrast, in the second case, apnea scan overestimated the number of total events and of obstructive events, perhaps owing to a very sensitive but less specific hypopnea definition and detection within the diagnostic algorithm of the device. These two cases show that a pacemaker apnea scan is able to reflect SDB, but PSG precision is not met by far. The device scan revealed the decline of SDB through ASV therapy for CSA in one patient, but not for OSA in the second case. To achieve reliable monitoring of SDB, further technical developments and clinical studies are necessary.

Background: Manifestation of central sleep apnea (CSA) with Cheyne-Stokes respiration is of major prognostic impact in chronic heart failure (CHF). Inflammatory processes have been linked to a progression of cardiovascular diseases, including heart failure. While an association of C-reactive protein (CRP) levels to obstructive sleep apnea has been documented before, there is a lack of information regarding variation of CRP levels in patients with CSA., Objectives: The objective of this study was to investigate a potential association of CRP levels to CSA severity in CHF patients., Methods: High sensitivity CRP levels were analyzed in 966 patients with CHF (BMI 26.3 ± 4.6, New York Heart Association class 2.6 ± 0.5, left ventricular ejection fraction 29.4 ± 7.9%, N-terminal pro-brain natriuretic peptide, NT-proBNP, level 2,209 ± 3,315 pg/ml) without sleep-disordered breathing (SDB; Apnea-Hypopnea Index, AHI, <5/h) or various degrees of CSA, documented by in-hospital cardiorespiratory polygraphy or polysomnography., Results: The CRP concentration in CHF patients was 0.550 ± 0.794 mg/dl in patients without SDB (AHI 0-4/h, n = 403) versus 0.488 ± 0.708 mg/dl in patients with mild CSA (AHI 5-14/h, n = 123, p = n.s.) and 0.660 ± 0.963 mg/dl in patients with moderate CSA (AHI 15-29/h, n = 160, p = n.s.). In patients with severe CSA (AHI ≥ 30/h, n = 280), significantly higher CRP concentrations were documented (0.893 ± 1.384 mg/dl, p < 0.05). Stepwise regression analysis revealed AHI, NT-proBNP and heart rate to be independently associated with elevated CRP levels., Conclusion: Severe CSA in CHF patients is associated with elevated levels of CRP, a systemic marker of inflammation and cardiovascular risk. This might explain in part the negative prognostic impact of CSA in these patients., (Copyright © 2013 S. Karger AG, Basel.)

Background: We examined the prevalence of sleep-disordered breathing (SDB) in patients with severe aortic valve stenosis (AS) and the impact of transfemoral aortic valve implantation (TAVI) on SDB., Methods: 79 patients underwent cardiorespiratory polygraphy (PG) before TAVI (CoreValve™), 62 of them a second PG after the procedure., Results: Forty-nine (62 %) patients had obstructive sleep apnea (OSA), 25 (32 %) central sleep apnea (CSA), and 5 (6 %) presented without significant SDB (apnea-hypopnea index (AHI) < 5/h). Among the 62 patients evaluated before and after TAVI, 36 (58 %) had OSA, 22 (36 %) CSA, and 4 patients (7 %) no SDB. AHI was significantly higher in CSA patients than in OSA patients (34.5 ± 18.3 vs. 18.0 ± 12.6/h, p < 0.001). Successful TAVI had a significant impact on CSA but not on OSA: CSA patients with optimal TAVI results experienced a significant reduction in central respiratory events (AHI 39.6 ± 19.6-23.1 ± 16.0/h, p = 0.035), while no changes were detected in OSA patients (AHI 18.8 ± 13.0-20.25 ± 13.4/h, p = 0.376). In contrast, in patients who developed at least moderate periprosthetic aortic regurgitation (AR > I), CSA increased significantly (AHI 26.3 ± 13.2-39.2 ± 18.4/h, p = 0.036), whereas no acute change was seen in patients with OSA (AHI 10.5 ± 7.8-12.5 ± 5.0/h, p = 0.5)., Conclusion: OSA and CSA are prevalent in more than 90 % of patients undergoing TAVI for severe aortic valve stenosis. Successful TAVI had no significant impact on OSA but improved CSA. In case of an acute change from pressure overload (aortic stenosis) to acute volume overload (aortic regurgitation after TAVI), central, but not obstructive, sleep apnea deteriorated.

Objective: 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)., Methods: 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., Results: 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., Conclusion: 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., (© 2013 Wiley Periodicals, Inc.)

This review illustrates the importance of sleep disordered breathing in evolution and progression of atrial fibrillation. While in early years associations were mainly attributed to the impact of hypoxemia and hypertension, nowadays multiple, additional pathways have been investigated or are currently under investigation. Sleep disordered breathing has been shown to have a direct impact on mechanical and electrical remodeling. In addition hypercapnia and negative intrathoracic pressure seem to alter atrial electrophysiology. Finally, impacts on inflammation and metabolic dysregulation display the complex interplay between breathing disorders and evolution and progression of atrial fibrillation.

This study investigated the effect of heart failure on respiratory patterns in patients with obstructive sleep apnoea (OSA). 39 patients with established OSA (apnoea/hypopnoea index (AHI) >10 events·h(-1)) and either with heart failure (New York Heart Association (NYHA) class II and III, left ventricular-ejection fraction (LVEF) ≤40%; n=26, age mean ± SD 67 ± 9 years) or without heart failure (LVEF ≥50%, N-terminal pro-brain naturic peptide <400 pg·mL(-1); n=13, age 73 ± 6 years) underwent simultaneous right- and left-heart catheterisation within 12 h of cardiorespiratory polygraphy recording. Respiratory patterns of OSA were significantly longer in OSA patients with heart failure versus without heart failure, including mean ± SD cycle length (46.0 ± 10.0 versus 37.8 ± 10.6 s; p=0.024), ventilation length (25.4 ± 6.3 versus 21.3 ± 7.1 s; p=0.044), apnoea length (20.5 ± 4.9 versus 16.5 ± 3.9 s; p=0.013), time-to-peak ventilation (10.6 ± 3.0 versus 8.3 ± 2.5 sc; p=0.021) and circulatory delay (28.5 ± 7.5 versus 22.6 ± 3.7 s; p=0.005). Positive and robust correlations were found between some of these parameters and the degree of congestion in heart failure: cycle length (r=0.53; p=0.006), ventilation length (r=0.55; p=0.004) and time-to-peak ventilation (r=0.47; p=0.015) all increased with a rise in pulmonary capillary wedge pressure. Respiratory patterns in OSA appear to be dependent on cardiac function, with an increase in event lengths as cardiac function decreases. In patients with heart failure, some of these events correlate with the degree of pulmonary congestion.

Sleep-disordered breathing (SDB) has a prognostic impact in patients with cardiac diseases. We included 257 patients with preserved left ventricular function and angiographically proven coronary artery disease (CAD). All patients underwent cardiorespiratory polygraphy. In 251 patients high-sensitive C-reactive protein and fibrinogen were measured. SDB was documented in 188 patients (apnea-hypopnea-index [AHI] 16.4+/- 1.9/h): 58 patients presented central sleep apnea (CSA) and 130 patients obstructive sleep apnea (OSA). All patients (73%) with SDB had higher blood fibrinogen levels than those without SDB (p = 0.01). We found 197 patients with CRP-values below the cut-off of 0.5 mg/dl (group 1) and 54 patients with no active infection but CRP>0.5 mg/dl (group 2). Severity of SDB was significantly higher in group 2 (p = 0.01). SDB has a high prevalence in CAD patients and seems to be associated with chronic inflammation, which may be linked to CAD progression and/or acute coronary events.