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Shahrokh Javaheri - One of the best experts on this subject based on the ideXlab platform.
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Central Sleep Apnea a brief review
Current Pulmonology Reports, 2019Co-Authors: Safwan M Badr, John D Dingell, Shahrokh JavaheriAbstract:The purpose of this review is to discuss the pathogenesis, clinical manifestations, diagnosis, and treatment, including areas of controversy and uncertainty. Central Apnea may be due to hypoventilation or to hypocapnia following hyperventilation. The occurrence of Central Apnea initiates a cascade of events that perpetuates breathing instability, recurrent Central Apnea, and upper airway narrowing. In fact, breathing instability and upper airway narrowing are key elements of Central and obstructive Apnea. Clinically, Central Apnea is noted in association with obstructive Sleep Apnea, heart failure, atrial fibrillation, cerebrovascular accident tetraplegia, and chronic opioid use. Management strategies for Central Apnea aim to eliminate abnormal respiratory events, stabilize Sleep, and alleviate the underlying clinical condition. Positive pressure therapy (PAP) remains a standard therapy for Central as well as obstructive Apnea. Other treatment options include adaptive servo-ventilation (ASV), supplemental oxygen, phrenic nerve stimulation, and pharmacologic therapy. However, ASV is contraindicated in patients with Central Sleep Apnea who had heart failure with reduced ejection fraction, owing to increased mortality in this population. There are several therapeutic options for Central Apnea. Randomized controlled studies are needed to ascertain the long-term effectiveness of individual, or combination, treatment modalities in different types of Central Apnea.
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sustained 12 month benefit of phrenic nerve stimulation for Central Sleep Apnea
American Journal of Cardiology, 2018Co-Authors: Maria Rosa Costanzo, Shahrokh Javaheri, Christoph Stellbrink, Ralph Augostini, Piotr Ponikowski, Lee R Goldberg, Richard Holcomb, Rami Khayat, Olaf Oldenburg, William T AbrahamAbstract:Transvenous phrenic nerve stimulation improved Sleep metrics and quality of life after 6 months versus control in the remedē System Pivotal Trial. This analysis explored the effectiveness of phrenic nerve stimulation in patients with Central Sleep Apnea after 12 months of therapy. Reproducibility of treatment effect was assessed in the former control group in whom the implanted device was initially inactive for the sixth month and subsequently activated when the randomized control assessments were complete. Patients with moderate-to-severe Central Sleep Apnea implanted with the remedē System were randomized to therapy activation at 1 month (treatment) or after 6 months (control). Sleep indices were assessed from baseline to 12 months in the treatment group and from 6 to 12 months in former controls. In the treatment group, a ≥50% reduction in Apnea-hypopnea index occurred in 60% of patients at 6 months (95% confidence interval [CI] 47% to 64%) and 67% (95% CI 53% to 78%) at 12 months. After 6 months of therapy, 55% of former controls (95% CI 43% to 67%) achieved ≥50%reduction in Apnea-hypopnea index. Patient Global Assessment was markedly ormoderately improved at 6 and 12 months in 60% of treatment patients.Improvements persisted at 12 months. A serious adverse event within 12 months occurred in 13 patients (9%). Phrenic nerve stimulation produced sustained improvements in Sleep indices and quality of life to at least 12 months in patients with Central Sleep Apnea. The similar improvement of former controls after 6 months of active therapy confirms benefits are reproducible and reliable.
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positive airway pressure therapy for hyperventilatory Central Sleep Apnea idiopathic heart failure cerebrovascular disease and high altitude
Sleep Medicine Clinics, 2017Co-Authors: Shahrokh Javaheri, Lee K BrownAbstract:Central Sleep Apnea (CSA) and Hunter-Cheyne-Stokes breathing (HCSB) are caused by failure of the pontomedullary pacemaker generating breathing rhythm. CSA/HCSB may complicate several disorders causing recurrent arousals and desaturations. Common causes of CSA in adults are congestive heart failure, stroke, and chronic use of opioids; opioids have hypoventilatory effects. Diagnosis and treatment of hyperventilatory CSA may improve quality of life, and, when associated with heart failure or cerebrovascular disease, reduce morbidity and perhaps mortality.
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design of the remedē system pivotal trial a prospective randomized study in the use of respiratory rhythm management to treat Central Sleep Apnea
Journal of Cardiac Failure, 2015Co-Authors: Maria Rosa Costanzo, Christoph Stellbrink, Ralph Augostini, Piotr Ponikowski, Lee R Goldberg, Shahrokh JavaheriAbstract:Abstract Background Central Sleep Apnea is common in patients with cardiovascular disease and worsens outcomes. There is a lack of established therapies for Central Sleep Apnea, and those available are limited by poor patient adherence and potentially adverse cardiovascular effects, at least in a subset of patients. The rem edē System (Respicardia, Minnetonka, Minnesota) is a new physiologic treatment that uses transvenous phrenic nerve stimulation to contract the diaphragm, thereby stabilizing gas exchange and restoring normal breathing throughout the Sleep period. Methods This is a prospective multicenter randomized trial with blinded end points evaluating the safety and efficacy of the rem edē System. Up to 173 patients with Central Sleep Apnea will be randomized 1:1 to rem edē System therapy initiated at 1 month after implantation (treatment) or to an implanted rem edē System that will remain inactive for 6 months (control). Primary efficacy end point is the percentage of patients who experience a reduction in Apnea-hypopnea index by a ≥50% at 6 months (responder analysis). Primary safety end point is freedom from serious adverse events through 12 months. Secondary end points include Sleep-disordered breathing parameters, Sleep architecture, Epworth Sleepiness Scale score, and Patient Global Assessment. Conclusions This is the 1st randomized controlled trial of the safety and efficacy of the rem edē System for the treatment of Central Sleep Apnea.
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Central Sleep Apnea
Comprehensive Physiology, 2013Co-Authors: Shahrokh Javaheri, Jerome A DempseyAbstract:Neurophysiologically, Central Apnea is due to a temporary failure in the pontomedullary pacemaker generating breathing rhythm. As a polysomnographic finding, Central Apneas occur in many pathophysiological conditions. Depending on the cause or mechanism, Central Apneas may not be clinically significant, for example, those that occur normally at Sleep onset. In contrast, Central Apneas occur in a number of disorders and result in pathophysiological consequences. Central Apneas occur commonly in high-altitude sojourn, disrupt Sleep, and cause desaturation. Central Sleep Apnea also occurs in number of disorders across all age groups and both genders. Common causes of Central Sleep Apnea in adults are congestive heart failure and chronic use of opioids to treat pain. Under such circumstances, diagnosis and treatment of Central Sleep Apnea may improve quality of life, morbidity, and perhaps mortality. The mechanisms of Central Sleep Apnea have been best studied in congestive heart failure and hypoxic conditions when there is increased CO2 sensitivity below eupnea resulting in lowering eupneic PCO2 below apneic threshold causing cessation of breathing until the PCO2 rises above the apneic threshold when breathing resumes. In many other disorders, the mechanism of Central Sleep Apnea (CSA) remains to be investigated.
T D Bradley - One of the best experts on this subject based on the ideXlab platform.
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rationale and design of the canadian continuous positive airway pressure trial for congestive heart failure patients with Central Sleep Apnea canpap
Canadian Journal of Cardiology, 2001Co-Authors: T D Bradley, Alexander G. Logan, John S Floras, Canpap InvestigatorsAbstract:BACKGROUND Cheyne-Stokes respiration with Central Sleep Apnea (CSR-CSA) is commonly observed in patients with congestive heart failure (CHF), in which it is an independent risk factor for death. Treating CSR-CSA may, therefore, improve outcomes in patients with CHF. OBJECTIVE The Canadian Continuous Positive Airway Pressure Trial for Congestive Heart Failure Patients with Central Sleep Apnea (CANPAP) is a multicentre, randomized, controlled clinical trial designed to test the hypothesis that treating CSR-CSA with continuous positive airway pressure (CPAP) will reduce the combined rate of all-cause mortality and cardiac transplantation in patients with CHF. Secondary outcomes include the severity of CSR-CSA, left ventricular volumes and function, submaximal exercise capacity, quality of life and hospital admissions. PATIENTS AND METHODS The aim is to enroll 408 patients with CHF (New York Heart Association class II to IV and left ventricular ejection fraction of less than 40%) and CSR-CSA over a five-year period. Patients are randomly assigned to either standard medical therapy for CHF or standard medical therapy plus CPAP. The trial has 80% power to detect a 35% between-group treatment difference for the all-cause mortality-cardiac transplantation rate. Substudies will assess the role of oximetry as a screening tool for detecting CSR-CSA in patients with CHF, and the effects of CPAP on cardiac arrhythmias and plasma concentrations of natriuretic peptides and catecholamines. CONCLUSIONS The CANPAP trial will help to define the role of CPAP better as a nonpharmacological intervention for the treatment of patients with CHF who have CSR-CSA.
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hypocapnia and increased ventilatory responsiveness in patients with idiopathic Central Sleep Apnea
American Journal of Respiratory and Critical Care Medicine, 1995Co-Authors: Ailiang Xie, B Wong, T D Bradley, R Rutherford, Fiona RankinAbstract:We previously demonstrated that Central Apneas during Sleep in patients with idiopathic Central Sleep Apnea (ICSA) are triggered by abrupt hyperventilation. In addition, baseline PCO2 at the time of augmented breaths which triggered Central Apneas was lower than for augmented breaths which did not trigger Apneas. These observations led us to hypothesize that patients with ICSA chronically hyperventilate maintaining their PCO2 close to the threshold for Apnea during Sleep owing to increased chemical respiratory drive. To test these hypotheses, we recorded transcutaneous PCO2 (PtcCO2) during overnight Sleep studies on nine consecutive patients with ICSA and nine sex-, age-, and body-mass-index-matched control subjects. Daytime PaCO2 as well as rebreathing and single breath ventilatory responses to CO2 were also measured. Compared with the control subjects, the patients had significantly lower mean PtcCO2 during Sleep (37.8 +/- 1.2 versus 42.7 +/- 10.9 mm Hg, p < 0.01) and lower PaCO2 while awake (35.1 +/- 1.3 versus 38.8 +/- 0.9 mm Hg, p < 0.05). Furthermore, patients with ICSA had significantly higher ventilatory responses to CO2 for both the rebreathing (3.14 +/- 0.34 versus 1.60 +/- 0.32 L/min/mm Hg, p < 0.005) and single breath methods (0.51 +/- 0.10 versus 0.25 +/- 0.04 L/min/mm Hg, p < 0.05). We conclude that: (1) patients with ICSA chronically hyperventilate awake and aSleep and (2) chronic hyperventilation is probably related to augmented Central and peripheral respiratory drive which predisposes to respiratory control system instability.
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effects of nasal cpap on sympathetic activity in patients with heart failure and Central Sleep Apnea
American Journal of Respiratory and Critical Care Medicine, 1995Co-Authors: Matthew T Naughton, R Rutherford, Fiona Rankin, D C Benard, Peter P Liu, T D BradleyAbstract:We hypothesized that (1) patients with congestive heart failure (CHF) and Cheyne-Stokes respiration with Central Sleep Apnea (CSR-CSA) would have greater nocturnal urinary and daytime plasma norepinephrine concentrations (UNE and PNE, respectively) than those without CSR-CSA because of Apneas, hypoxia and arousals from Sleep and (2) attenuation of CSR-CSA by nasal continuous positive airway pressure (NCPAP) would reduce UNE and PNE concentrations. Eighteen patients with and 17 without CSR-CSA (Non-CSR-CSA group) were studied. Left ventricular ejection fraction was similar in the two groups, but overnight UNE and awake PNE concentrations were greater in the CSR-CSA group (30.2 +/- 2.5 nmol/mmol creatinine and 3.32 +/- 0.29 nmol/L) than in the Non-CSR-CSA group (15.8 +/- 2.1 nmol/mmol creatinine, p < 0.005, and 2.06 +/- 0.56 nmol/L, p < 0.05, respectively). Patients with CSR-CSA were randomized to a control group or to nightly NCPAP for 1 mo. CSR-CSA was attenuated in the NCPAP but not in the control group. The NCPAP group experienced greater reductions in UNE and PNE concentrations (-12.5 +/- 3.3 nmol/mmol creatinine and -0.74 +/- 0.40 nmol/L) than did the control group (-1.3 +/- 2.8 nmol/mmol creatinine, p < 0.025 and 1.16 +/- 0.66 nmol/L, p < 0.025, respectively). In conclusion, in patients with CHF, CSR-CSA is associated with elevated sympathoneural activity, which can be reduced by NCPAP.
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interaction of hyperventilation and arousal in the pathogenesis of idiopathic Central Sleep Apnea
American Journal of Respiratory and Critical Care Medicine, 1994Co-Authors: Ailiang Xie, B Wong, Eliot A Phillipson, A S Slutsky, T D BradleyAbstract:Central Apneas during Sleep may arise as a result of reduction in PaCO2 below the Apnea threshold. We therefore hypothesized that hyperventilation and arousals from Sleep interact to cause hypocapnia and subsequent Central Apneas in patients with idiopathic Central Sleep Apnea (ICSA). Accordingly, the relationships among preapneic ventilation, arousal from Sleep, and the onset and duration of subsequent Central Apneas were examined during Stage 2 non-REM Sleep in eight patients with ICSA (mean +/- SEM, 45.4 +/- 4.7 Central Apneas and hypopneas/h of Sleep). During Stage 2 Sleep, all episodes of periodic breathing with Central Apneas were triggered by hyperventilation. Minute ventilation (VI) was greater (6.3 +/- 0.7 versus 5.4 +/- 0.8 L/min, p < 0.05) and mean transcutaneous PCO2 (PtcCO2) was lower (37.8 +/- 1.3 versus 38.9 +/- 1.6 mm Hg, p < 0.05) during periodic breathing than during stable breathing. VI during the ventilatory phase of the periodic breathing cycle increased progressively with increasing ...
Matthew T Naughton - One of the best experts on this subject based on the ideXlab platform.
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lateral Sleeping position reduces severity of Central Sleep Apnea cheyne stokes respiration
Sleep, 2006Co-Authors: Irene Szollosi, Teanau Roebuck, Matthew T Naughton, Bruce ThompsonAbstract:INTRODUCTION The influence of Sleeping position on obstructive Sleep Apnea severity is well established. However, in Central Sleep Apnea with Cheyne Stokes respiration (CSA-CSR) in which respiratory-control instability plays a major pathophysiologic role, the effect of position is less clear. STUDY OBJECTIVES To examine the influence of position on CSA-CSR severity as well as Central and mixed Apnea frequency. METHODS Polysomnograms with digitized video surveillance of 20 consecutive patients with heart failure and CSA-CSR were analyzed for total Apnea-hypopnea index, mean event duration, and mean oxygen desaturation according to Sleep stage and position. Position effects on mixed and Central Apnea index, mean Apnea duration, and mean desaturation were also examined in non-rapid eye movement Sleep. RESULTS Data are presented as mean +/- SEM unless otherwise indicated. Group age was 59.9 +/- 2.3 years, and total Apnea-hypopnea index was 26.4 +/- 3.0 events per hour. Compared with supine position, lateral position reduced the Apnea-hypopnea index in all Sleep stages (Stage 1, 54.7 +/- 4.2 events per hour vs 27.2 +/- 4.1 events per hour [p < .001]; Stage 2, 43.3 +/- 6.1 events per hour vs 14.4 +/- 3.6 events per hour [p < .001]; slow-wave Sleep, 15.9 +/- 6.4 events per hour vs 5.4 +/- 2.9 events per hour [p < .01]; rapid eye movement Sleep, 38.0 +/- 7.3 events per hour vs 11.0 +/- 3.0 events per hour [p < .001]). Lateral position attenuated Apnea and hypopnea associated desaturation (supine 4.7% +/- 0.3%, lateral 3.0% +/- 0.4%; p < .001) with no difference in event duration (supine 25.7 +/- 2.8 seconds, lateral 26.9 +/- 3.4 seconds; p = .921). Mixed Apneas were longer than Central (29.1 +/- 2.1 seconds and 19.3 +/- 1.1 seconds; p < .001) and produced greater desaturation (6.1% +/- 0.5% and 4.5% +/- 0.5%, p = .003). Lateral position decreased desaturation independent of Apnea type (supine 5.4% +/- 0.5%, lateral 3.9% < or = 0.4%; p = .003). CONCLUSIONS Lateral position attenuates severity of CSA-CSR. This effect is independent of postural effects on the upper airway and is likely to be due to changes in pulmonary oxygen stores. Further studies are required to investigate mechanisms involved.
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the effect of successful heart transplant treatment of heart failure on Central Sleep Apnea
Chest, 2003Co-Authors: Darren Mansfield, Peter Solin, Teanau Roebuck, Peter Bergin, David M Kaye, Matthew T NaughtonAbstract:Study objective Central Sleep Apnea (CSA) associated with Cheyne-Stokes respiration in patients with congestive heart failure (CHF) is thought to be an acquired pattern of respiratory control instability related, at least in part, to elevated sympathetic nervous system activity. The effect of restoring heart function to normal with heart transplantation in patients with CHF and CSA has only been reported within weeks of the transplant and with varying results. The purpose of the study was to evaluate the impact of successful heart transplant on sympathetic nervous system activity and CSA severity in patients with CHF. Design Controlled prospective trial. Setting University hospital. Patients Twenty-two patients with CHF (13 patients with CSA, and 9 patients with no Sleep-disordered breathing [SDB]). Interventions and measurements Polysomnography, left ventricular ejection fraction (LVEF), and overnight urinary norepinephrine excretion (UNE) were measured before and > 6 months after successful heart transplantation. Results In the CSA group, there was a fall in Apnea-hypopnea index (AHI) [mean ± SD, 28 ± 15 to 7 ± 6/h; p Conclusions We conclude that CSA may persist despite normalization of heart function and sympathetic nerve activity.
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raised sympathetic nerve activity in heart failure and Central Sleep Apnea is due to heart failure severity
Circulation, 2003Co-Authors: Darren Mansfield, Peter Solin, David M Kaye, Hanspeter Brunner La Rocca, Murray D Esler, Matthew T NaughtonAbstract:Background— Congestive heart failure (CHF) patients with Central Sleep Apnea (CHF-CSA) have elevated plasma norepinephrine (NE) compared with CHF patients without Apnea (CHF-N). Patients with CHF-CSA also demonstrate higher mean pulmonary artery pressure (PAP), which is suggestive of worse cardiac function. Whether CSA contributes to chronic elevation of sympathetic nerve activity or is associated with more severe CHF remains unknown. We measured awake total body and cardiac NE spillover and related these to measurements of cardiac hemodynamics and Apnea severity in CHF patients with CSA, with normal breathing, and with obstructive Sleep Apnea (CHF-OSA). Methods and Results— A total of 55 CHF patients underwent right heart catheterization and measurements of total body and cardiac NE spillover using NE radioisotope dilution methodology. After polysomnography, patients were grouped by Apnea type: 19 were CHF-N, 15 were CHF-OSA, and 21 were CHF-CSA. Compared with the CHF-N and CHF-OSA groups, the CHF-CSA gr...
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effects of nasal cpap on sympathetic activity in patients with heart failure and Central Sleep Apnea
American Journal of Respiratory and Critical Care Medicine, 1995Co-Authors: Matthew T Naughton, R Rutherford, Fiona Rankin, D C Benard, Peter P Liu, T D BradleyAbstract:We hypothesized that (1) patients with congestive heart failure (CHF) and Cheyne-Stokes respiration with Central Sleep Apnea (CSR-CSA) would have greater nocturnal urinary and daytime plasma norepinephrine concentrations (UNE and PNE, respectively) than those without CSR-CSA because of Apneas, hypoxia and arousals from Sleep and (2) attenuation of CSR-CSA by nasal continuous positive airway pressure (NCPAP) would reduce UNE and PNE concentrations. Eighteen patients with and 17 without CSR-CSA (Non-CSR-CSA group) were studied. Left ventricular ejection fraction was similar in the two groups, but overnight UNE and awake PNE concentrations were greater in the CSR-CSA group (30.2 +/- 2.5 nmol/mmol creatinine and 3.32 +/- 0.29 nmol/L) than in the Non-CSR-CSA group (15.8 +/- 2.1 nmol/mmol creatinine, p < 0.005, and 2.06 +/- 0.56 nmol/L, p < 0.05, respectively). Patients with CSR-CSA were randomized to a control group or to nightly NCPAP for 1 mo. CSR-CSA was attenuated in the NCPAP but not in the control group. The NCPAP group experienced greater reductions in UNE and PNE concentrations (-12.5 +/- 3.3 nmol/mmol creatinine and -0.74 +/- 0.40 nmol/L) than did the control group (-1.3 +/- 2.8 nmol/mmol creatinine, p < 0.025 and 1.16 +/- 0.66 nmol/L, p < 0.025, respectively). In conclusion, in patients with CHF, CSR-CSA is associated with elevated sympathoneural activity, which can be reduced by NCPAP.
Michael Pfeifer - One of the best experts on this subject based on the ideXlab platform.
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effects of dynamic bilevel positive airway pressure support on Central Sleep Apnea in men with heart failure
Chest, 2008Co-Authors: Michael Arzt, Friedrich C Blumberg, Roland Wensel, Sylvia Montalvan, Thomas Schichtl, Stephan Schroll, Stephan Budweiser, G A J Riegger, Michael PfeiferAbstract:Background Treatment with continuous positive airway pressure (CPAP) improves cardiac function in chronic heart failure (CHF) patients with Central Sleep Apnea (CSA)-Cheyne-Stokes respiration (CSR) by stabilizing ventilation, but frequently Central Apneas and hypopneas persist. Our objective was to test the hypothesis that flow-targeted dynamic bilevel positive airway pressure (BPAP) support (BiPAP autoSV; Respironics; Murrysville, PA) effectively suppresses CSR-CSA in CHF patients. Methods We studied 14 CHF patients with CSR-CSA (and residual CSA on positive airway pressure therapy) during 3 consecutive nights: (1) diagnostic polysomnography, (2) CPAP (n = 10) or BPAP (n = 4) titration, and (3) dynamic flow-targeted dynamic BPAP support with an expiratory positive airway pressure (EPAP) set to suppress obstructive respiratory events, and an inspiratory positive airway pressure (IPAP) dynamically ranging between 0 and 15 cm H 2 O above the EPAP. Results CPAP or BPAP significantly reduced the Apnea-hypopnea index (AHI) [mean ± SD, 46 ± 4 events/h to 22 ± 4 events/h; p = 0.001] compared to the first night without treatment. Flow-targeted dynamic BPAP support (mean EPAP, 6.5 ± 1.7 cm H 2 O; maximal IPAP, 21.9 ± 2.1 cm H 2 O) further reduced the AHI to 4 ± 1/h of Sleep compared to the untreated (p Conclusion Flow-targeted dynamic BPAP support effectively suppresses CSR-CSA in patients with CHF and is well tolerated.
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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
Circulation, 2007Co-Authors: Michael Arzt, Alexander G. Logan, Frédéric Sériès, Debra Morrison, Kathleen A. Ferguson, Israel Belenkie, Michael Pfeifer, John S Floras, John R Kimoff, John A. FleethamAbstract: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 tra...
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Continuous positive airway pressure for Central Sleep Apnea and heart failure.
The New England journal of medicine, 2005Co-Authors: T. Douglas Bradley, Alexander G. Logan, R. John Kimoff, Frédéric Sériès, Debra Morrison, Kathleen A. Ferguson, Israel Belenkie, Michael Pfeifer, John A. Fleetham, Patrick J. HanlyAbstract:Background The Canadian Continuous Positive Airway Pressure for Patients with Central Sleep Apnea and Heart Failure trial tested the hypothesis that continuous positive airway pressure (CPAP) would...
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enhanced ventilatory response to exercise in patients with chronic heart failure and Central Sleep Apnea
Circulation, 2003Co-Authors: Michael Arzt, Martina Harth, Andreas Luchner, Frank Muders, Stephan R Holmer, Friedrich C Blumberg, Gunter A J Riegger, Michael PfeiferAbstract:Background— In patients with chronic heart failure (CHF), Central Sleep Apnea (CSA) and enhanced ventilatory response (Ve/Vco2 slope) to exercise are common. Both breathing disorders alone indicate poor prognosis in CHF. Although augmented chemosensitivity to co2 is thought to be one important underlying mechanism for both breathing disorders, it is unclear whether both breathing disorders are related closely in patients with CHF. Methods and Results— We investigated 20 CHF patients with clinically important CSA (Apnea-hypopnea-index (AHI), number of episodes per hour ≥15) and 10 CHF patients without CSA. Patients with and without CSA did not differ with respect to exercise capacity (peak Vo2, 63.4±3.4% versus 60.8±4.4% of predicted value; P=0.746) and left ventricular ejection fraction (LVEF, 31±2% versus 31±3%; P=0.948). The AHI was not correlated with exercise capacity (peak Vo2, percent of predicted value; P=0.260) and LVEF (percent, P=0.886). In contrast, the positive correlation of the Ve/Vco2...
Douglas T Bradley - One of the best experts on this subject based on the ideXlab platform.
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nocturnal rostral fluid shift a unifying concept for the pathogenesis of obstructive and Central Sleep Apnea in men with heart failure
Circulation, 2010Co-Authors: Dai Yumino, Stefania Redolfi, Stephanie Smith, Susanna Mak, Gary E. Newton, Pimon Ruttanaumpawan, Douglas T BradleyAbstract:Background— Obstructive Sleep Apnea (OSA) and Central Sleep Apnea are common in patients with heart failure. We hypothesized that in such patients, severity of OSA is related to overnight rostral leg fluid displacement and increase in neck circumference, severity of Central Sleep Apnea is related to overnight rostral fluid displacement and to Sleep Pco2, and continuous positive airway pressure alleviates OSA in association with prevention of fluid accumulation in the neck. Methods and Results— In 57 patients with heart failure (ejection fraction ≤45%), we measured change in leg fluid volume and neck circumference before and after polysomnography, and we measured transcutaneous Pco2 during polysomnography. Patients were divided into an obstructive-dominant group (≥50% of Apneas and hypopneas obstructive) and a Central-dominant group (>50% of events Central). Patients with OSA received continuous positive airway pressure. In obstructive-dominant patients, there were inverse relationships between overnight c...
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association between atrial fibrillation and Central Sleep Apnea
Sleep, 2005Co-Authors: Richard S T Leung, Douglas T Bradley, Matthias A Huber, Thomas Rogge, Nimrod Maimon, Kuoliang ChiuAbstract:Background: We previously described an association between atrial fibrillation and Central Sleep Apnea in a group of patients with congestive heart failure. We hypothesized that the prevalence of atrial fibrillation might also be increased in patients with Central Sleep Apnea in the absence of other cardiac disease. Methods and Results: We compared the prevalence of atrial fibrillation in a series of 60 consecutive patients with idiopathic Central Sleep Apnea (Apnea-hypopnea index > 10 events per hour, > 50% Central events) with that in 60 patients with obstructive Sleep Apnea (Apnea-hypopnea index > 10, > 50% obstructive events) and 60 patients without Sleep Apnea (Apnea-hypopnea index < 10), matched for age, sex, and body mass index. Subjects with a history of congestive heart failure, coronary artery disease, or stroke were excluded from the study. The prevalence of atrial fibrillation among patients with idiopathic Central Sleep Apnea was found to be significantly higher than the prevalence among patients with obstructive Sleep Apnea or no Sleep Apnea (27%, 1.7%, and 3.3%, respectively, P<.001). However, hypertension was most common and oxygen desaturation most extreme among patients with obstructive Sleep Apnea. Conclusions: We conclude that there is a markedly increased prevalence of atrial fibrillation among patients with idiopathic Central Sleep Apnea in the absence of congestive heart failure. Moreover, the high prevalence of atrial fibrillation among patients with idiopathic Central Sleep Apnea is not explainable by the presence of hypertension or nocturnal oxygen desaturation, since both of these were more strongly associated with obstructive Sleep aonea.
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Sleep Apnea and heart failure part ii Central Sleep Apnea
Circulation, 2003Co-Authors: Douglas T Bradley, John S FlorasAbstract:In the first part of this 2-part review, we provided a synopsis of the cardiovascular effects of normal Sleep and an overview of the diagnostic, pathophysiological, and therapeutic implications of obstructive Sleep Apnea (OSA) in the setting of heart failure (HF). In this second part, we turn our attention to Central Sleep Apnea (CSA), commonly referred to as Cheyne-Stokes respiration. This breathing disorder has a strikingly higher prevalence in patients with HF as compared with the general population with normal left ventricular function, and when present appears to have adverse prognostic implications. Our objective in Part II of this review is to provide a broad perspective of the pathophysiological and clinical significance of CSA in HF. CSA associated with Cheyne-Stokes respiration is a form of periodic breathing in which Central Apneas and hypopneas alternate with periods of hyperventilation that have a waxing-waning pattern of tidal volume. Figure 1 illustrates the proposed mechanisms that underlie periodic oscillations in ventilation in HF. Unlike OSA, CSA likely arises as a consequence of HF. Thus, the presence of CSA may alert the physician to the necessity of intensifying HF therapy. The current debate is whether CSA is simply a reflection of severely compromised cardiac function with elevated left ventricular filling pressures, or whether, for the same degree of cardiac dysfunction, CSA exerts unique and independent pathological effects on the failing myocardium. Although there are not yet sufficient data to resolve this controversy within the confines of this review, we will discuss evidence on both sides of this issue. Figure 1. Pathophysiology of Central Sleep Apnea in heart failure (HF). HF leads to increased left ventricular (LV) filling pressure. The resulting pulmonary congestion activates lung vagal irritant receptors, which stimulate hyperventilation and hypocapnia. Superimposed arousals cause further abrupt increases in ventilation and drive PaCO2 …