Michael Arzt

Suppression of Central Sleep Apnea by Continuous Positive Airway Pressure and Transplant-Free Survival in Heart Failure A Post Hoc Analysis of the Canadian Continuous Positive Airway Pressure for Patients With Central Sleep Apnea and Heart Failure Trial (CANPAP)

Background— In the main analysis of the Canadian Continuous Positive Airway Pressure (CPAP) for Patients with Central Sleep Apnea (CSA) and Heart Failure Trial (CANPAP), CPAP had no effect on heart transplant–free survival; however, CPAP only reduced the mean apnea-hypopnea index to 19 events per hour of sleep, which remained above the trial inclusion threshold of 15. This stratified analysis of CANPAP tested the hypothesis that suppression of CSA below this threshold by CPAP would improve left ventricular ejection fraction and heart transplant–free survival. Methods and Results— Of the 258 heart failure patients with CSA in CANPAP, 110 of the 130 randomized to the control group and 100 of the 128 randomized to CPAP had sleep studies 3 months later. CPAP patients were divided post hoc into those whose apnea-hypopnea index was or was not reduced below 15 at this time (CPAP-CSA suppressed, n=57, and CPAP-CSA unsuppressed, n=43, respectively). Their changes in left ventricular ejection fraction and heart transplant–free survival were compared with those in the control group. Despite similar CPAP pressure and hours of use in the 2 groups, CPAP-CSA–suppressed subjects experienced a greater increase in left ventricular ejection fraction at 3 months (P=0.001) and significantly better transplant-free survival (hazard ratio [95% confidence interval] 0.371 [0.142 to 0.967], P=0.043) than control subjects, whereas the CPAP-CSA–unsuppressed group did not (for left ventricular ejection fraction, P=0.984, and for transplant-free survival, hazard ratio 1.463 [95% confidence interval 0.751 to 2.850], P=0.260). Conclusions— These results suggest that in heart failure patients, CPAP might improve both left ventricular ejection fraction and heart transplant–free survival if CSA is suppressed soon after its initiation.

Alterations in upper airway cross-sectional area in response to lower body positive pressure in healthy subjects

Background: Fluid accumulation in the neck during recumbency might narrow the upper airway (UA) and thereby contribute to its collapse in patients with obstructive sleep apnoea (OSA). It is hypothesised that acute fluid shifts from the legs to the upper body in healthy subjects would increase neck circumference and reduce the cross-sectional area of the UA (UA-XSA). Methods: In 27 healthy non-obese subjects of mean (SE) age 39 (3) years and body mass index 23.2 (0.6) kg/m2 studied while supine, leg fluid volume was measured using bioelectrical impedance, neck circumference using a mercury strain gauge and mean UA-XSA between the velum and the glottis using acoustic pharyngometry at end expiration. Measurements were made at baseline after which subjects were randomly assigned to a 5 min time control period or to a 5 min application of lower body positive pressure (LBPP) at 40 mm Hg by anti-shock trousers, separated by a 15 min washout period. Subjects then crossed over to the opposite arm of the study. Results: Compared with control, application of LBPP significantly reduced leg fluid volume (p<0.001) and increased neck circumference (p<0.001), both at 1 min and 5 min, and reduced UA-XSA after both 1 min (−0.15 cm2; 95% CI −0.23 to −0.09, p<0.001) and 5 min (−0.20 cm2; 95% CI −0.33 to −0.09, p<0.001). Conclusion: In healthy subjects, displacement of fluid from the legs by LBPP causes distension of the neck and narrowing of the UA lumen. Fluid displacement from the lower to the upper body while recumbent may contribute to pharyngeal narrowing and obstruction to airflow in patients with OSA. This may have particular pathological significance in oedematous states such as heart and renal failure.

Prognostic impact of sleep disordered breathing and its treatment in heart failure: an observational study

Sleep disordered breathing (SDB) may contribute to disease progression in patients with chronic heart failure (CHF). The objective of this observational study was to evaluate whether SDB is a risk factor for mortality in CHF patients and whether this risk can be attenuated by treatment with positive airway pressure (PAP).

Dissociation of Obstructive Sleep Apnea From Hypersomnolence and Obesity in Patients With Stroke

Background and Purpose— Obstructive sleep apnea (OSA) is seldom considered in the diagnostic investigation in the poststroke period although it is a stroke risk factor and has adverse prognostic implications after stroke. One reason might be that widely used clinical criteria for detection of OSA in the general community are not applicable in patients with stroke. We hypothesized that patients with stroke report less sleepiness and are less obese than subjects from a community sample with the same severity of OSA. Methods— We performed polysomnography in 96 consecutive patients with stroke admitted to a stroke rehabilitation unit and in a community sample of 1093 subjects without a history of stroke. We compared the degrees of subjective sleepiness assessed by the Epworth Sleepiness Scale and body mass index between the 2 samples according to OSA categories assessed by the frequency of apneas and hypopneas per hour of sleep (<5, no OSA; 5 to <15 mild OSA; and ≥15, moderate to severe OSA). Results— Compared with the community sample, patients with stroke with OSA had significantly lower Epworth Sleepiness Scale scores and body mass index for mild OSA (Epworth Sleepiness Scale 9.3±0.3 versus 5.6±0.5, P<0.001 and body mass index 33.1±0.5 versus 28.5±1.1, P<0.048) and for moderate to severe OSA (Epworth Sleepiness Scale 9.7±0.4 versus 7.1±0.9, P=0.043 and body mass index 36.4±0.8 versus 27.2±0.8 kg/m2, P<0.025). Conclusions— For a given severity of OSA, patients with stroke had less daytime sleepiness and lower body mass index than subjects without stroke. These factors may make the diagnosis of OSA elusive in the poststroke period and preclude many such patients from the potential benefits of OSA therapy.

Sleep Apnea is an Independent Correlate of Erectile and Sexual Dysfunction

INTRODUCTION Obstructive sleep apnea (OSA) has been linked with erectile dysfunction (ED), but it is unknown whether this association is maintained in the presence of other risk factors for ED. AIM The aim of this study was to evaluate the relationship between ED/sexual dysfunction and polysomnographic measures of sleep apnea in patients with known risk factors for ED. METHODS Prospective cross-sectional analysis of 401 male patients undergoing in-lab polysomnography for suspected OSA. Erectile (EF) and sexual function were assessed by the 15-item International Index of Erectile Function (IIEF-15) questionnaire. MAIN OUTCOME MEASURES Severity of OSA via apnea-hypopnea index (AHI) and mean/lowest nocturnal oxygen saturation (SaO(2)). The IIEF-15 including the sexual domains: EF, intercourse satisfaction, orgasmic function, sexual desire, and overall satisfaction. RESULTS OSA (AHI > 5/h) was diagnosed in 92% of patients. ED (EF subdomain < or = 25) was present in 69% of patients with, and 34% of patients without OSA (P < 0.001). Multivariate stepwise regression analyses including known risk factors for ED, such as age, obesity, coronary heart disease, peripheral occlusive disease, hypertension, diabetes, prostate surgery, and beta-blocker treatment, and measures of sleep apnea identified mean nocturnal SaO(2) as independently associated with ED (P = 0.002; mean [95% CI] normalized slope 0.126 [0.047; 0.205]). Age (P < 0.001), peripheral occlusive disease (P = 0.001), prostate surgery (P = 0.018), and hypertension (P = 0.021) were confirmed as risk factors for ED, but did not abolish the sleep apnea-associated risk. Similar results were obtained for sexual dysfunction. Logistic regression analysis using the diagnosis of ED (EF subdomain < or = 25) as binary dependent variable confirmed that mean nocturnal SaO(2) (P = 0.012), as well as age (P < 0.001) were independently associated with ED. CONCLUSIONS ED and overall sexual dysfunction were highly prevalent in patients with suspected OSA. Irrespective of known risk factors, mean nocturnal SaO(2) was an additional, independent correlate of these dysfunctions, suggesting that OSA-related intermittent nocturnal hypoxemia specifically contributes to their development.

Impact of right ventricular reserve on exercise capacity and survival in patients with pulmonary hypertension.

Pulmonary hypertension is a clinical syndrome characterized by a progressive increase in pulmonary vascular resistance leading to right ventricular failure and death. Pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH) are key subgroups of this disorder with comparable clinical and pathological findings. Resting pulmonary haemodynamics correlate only moderately with functional parameters and do not predict prognosis in these patients sufficiently accurately. We therefore correlated exercise haemodynamics with peak oxygen uptake (peakVO2) and determined their prognostic significance.

Shift in sleep apnoea type in heart failure patients in the CANPAP trial

In patients with heart failure (HF), the predominant type of sleep apnoea can change over time in association with alterations in circulation time. The aim of this study was to determine whether, in some patients with HF, a spontaneous shift from mainly central (>50% central events) to mainly obstructive (>50% obstructive events) sleep apnoea (CSA and OSA, respectively) over time coincides with improvement in left ventricular ejection fraction (LVEF). Therefore, sleep studies and LVEFs of HF patients with CSA from the control arm of the Canadian Continuous Positive Airway Pressure for Patients with Central Sleep Apnea and Heart Failure (CANPAP) trial were examined to determine whether some converted to mainly OSA and, if so, whether this was associated with an increase in LVEF. Of 98 patients with follow-up sleep studies and LVEFs, 18 converted spontaneously to predominantly OSA. Compared with those in the nonconversion group, those in the conversion group had a significantly greater increase in the LVEF (2.8% versus -0.07%) and a significantly greater fall in the lung-to-ear circulation time (-7.6 s versus 0.6 s). In patients with HF, spontaneous conversion from predominantly CSA to OSA is associated with an improvement in left ventricular systolic function. Future studies will be necessary to further examine this relationship.

Auto-servoventilation in heart failure with sleep apnoea: a randomised controlled trial

We tested the hypotheses that in patients with congestive heart failure (CHF) and sleep disordered breathing (SDB) auto-servoventilation (ASV) improves cardiac function and quality of life. Between March 2007 and September 2009, patients with stable CHF (left ventricular ejection fraction (LVEF) ≤40%) and SDB (apnoea/hypopnoea index ≥20 events·h−1) were randomised to receive either ASV (BiPAP ASV (Philips Respironics, Murrysville, PA, USA), n=37) and optimal medical management, or optimal medical management alone (n=35). Outcomes were assessed at baseline and 12 weeks. The apnoea/hypopnoea index assessed with polysomnography scored in one core laboratory was significantly more reduced in the ASV group (-39±16 versus -1±13 events·h−1; p<0.001) with an average use of 4.5±3.0 h·day−1. Both groups showed similar improvements of the primary end-point LVEF (+3.4±5 versus +3.5±6%; p=0.915) assessed with echocardiography. In the ASV group, reduction of N-terminal pro-brain natriuretic peptide (NT-proBNP) was significantly greater (-360±569 versus +135±625 ng·mL−1; p=0.010). No differences were observed between the groups in subjective quality of life. In patients with CHF and SDB, ASV reduced NT-proBNP levels, but improvement of LVEF or quality of life was not greater than in the control group. The data support that such patients can be randomised in large-scale, long-term trials of positive airway pressure therapy versus control to determine effects on cardiovascular outcome. Patients with heart failure and sleep apnoea can be randomised in long-term trials of positive airway pressure therapy http://ow.ly/nQnVg

Impact of noninvasive home ventilation on long‐term survival in chronic hypercapnic COPD: a prospective observational study

Aims:  The long‐term benefit from noninvasive ventilation (NIV) in chronic hypercapnic chronic obstructive pulmonary disease (COPD) remains uncertain.

Prevalence and treatment of central sleep apnoea emerging after initiation of continuous positive airway pressure in patients with obstructive sleep apnoea without evidence of heart failure

BackgroundThis study aimed to assess the prevalence of complex sleep apnoea (CompSA), defined as central sleep apnoea (CSA) emerging after the initiation of continuous positive airway pressure (CPAP) therapy for obstructive sleep apnoea (OSA), in patients with normal brain natriuretic peptide (BNP) levels, along with assessing the prevalence of CSA persisting in such patients after the onset of CPAP therapy. We hypothesised that the prevalence of CompSA and persistent CSA after CPAP initiation would be low in patients with OSA and normal BNP levels.Material and methodsBetween April 2004 and July 2007, CPAP was initiated for all patients with OSA for two nights using a standardised protocol. The prevalence of CompSA syndrome (CompSAS) and persisting CSA [central apnoea index (CAI) >5/h and apnoea–hypopnoea index (AHI) >15/h with >50% central events during CPAP therapy] was prospectively assessed in patients with normal BNP levels. Patients with CompSAS or persisting CSA upon CPAP treatment received adaptive servoventilation (ASV).ResultsOf 1,776 patients with OSA receiving CPAP, 28 patients (1.57%) had CSA at the time of CPAP therapy and normal BNP levels. Additionally, 10 patients had CompSAS (0.56%) and 18 patients (1.01%) had persisting CSA. In patients with CompSA or persisting CSA, the AHI was significantly lower with CPAP therapy than at the time of diagnosis (34 ± 15/h vs. 47 ± 20/h, p = 0.005). The CAI increased from 10 ± 10/h to 18/h ± 13/h (p = 0.009) upon initiation of CPAP therapy. ASV reduced the AHI to 6 ± 12/h (p < 0.001) during the first night of use.ConclusionThe prevalence of CompSA or persisting CSA in patients with OSA and normal BNP levels who are receiving CPAP therapy is low (1.57%). ASV is an effective treatment for these patients.