Diagnosis and Treatment of Sleep Apnea in the Acute Exacerbation of Heart Failure - Full Text View

Purpose

Congestive heart failure affects 2.3 percent of the population (approximately 4,900,000) with an incidence of 10 per 1,000 of the population after the age of 65 (1). The admission rate for patients with heart failure is on the rise, so is the mortality associated with it and its national annual bill, now exceeding $21 billion (1). Obstructive Sleep Apnea (OSA) is present in 11-37 percent of patients with heart failure (2,3), and tends to increase in severity when the heart failure is less controlled (4, 5). Therefore, the actual prevalence of OSA in patients hospitalized with acute heart failure is likely higher. There is now evidence that treatment of OSA with nasal Continuous Positive Pressure (nCPAP) in outpatients with stable heart failure improves left ventricular ejection fraction, and quality of life (6), and confers a reduction in fatal and non-fatal cardiovascular events (7). However, there has not been any evaluation of the role of diagnosis and treatment of OSA in patients hospitalized with acute heart failure. This uncertainty about the true prevalence and role of OSA in exacerbations of heart failure, and the role of its treatment in the acute setting may explain why aggressive diagnostic and therapeutic strategy for OSA in patients admitted to the hospital with acute heart failure is not part of the standard clinical practice in acute care centers. Given the rising admission rate, and mortality associated with heart failure, an evaluation of the role of OSA and its treatment in this patient population is highly significant.

Condition	Intervention
Sleep Apnea Heart Failure	Device: auto adjusting bi-level positive airway pressure device

Study Type:	Interventional
Study Design:	Allocation: Randomized Endpoint Classification: Efficacy Study Intervention Model: Parallel Assignment Masking: Open Label Primary Purpose: Treatment
Official Title:	The Role of Diagnosis and Treatment of Sleep Apnea in the Acute Exacerbation of Heart Failure

Resource links provided by NLM:

MedlinePlus related topics: Heart Failure Sleep Apnea

U.S. FDA Resources

Further study details as provided by Ohio State University:

Primary Outcome Measures:

Left Ventricular Ejection Fraction Improvement [ Time Frame: baseline and again after three nights in hospital ] [ Designated as safety issue: No ]
Left ventricular function was assessed using doppler ultrasound. Positive increase in left ventricular function from baseline to 3 nights post treatment indicates potential beneficial impact of treatment on heart function.

Enrollment:	54
Study Start Date:	August 2006
Study Completion Date:	August 2008
Primary Completion Date:	August 2008 (Final data collection date for primary outcome measure)

Arms	Assigned Interventions
Experimental: Device Provided with an auto adjusting bi-level positive airway pressure device	Device: auto adjusting bi-level positive airway pressure device auto adjusting bi-level positive airway pressure device is provided for treatment of obstructive sleep apnea. Other Names: APAP CPAP
No Intervention: Control No device

Detailed Description:

OSA is associated with large negative swings in the intrathoracic pressure, significant increase in the sympathetic nerve activity and repetitive surges in blood pressure, along with episodic hypoxia and hypercapnea (8, 9). These autonomic and respiratory changes may increase the cardiac muscle workload, cardiac dysrrhythmia, and exacerbate ischemia (10,11,12). Treatment with continuous positive airway pressure (CPAP) is the most successful therapeutic modality available for obstructive sleep apnea. It is still not clear whether establishing the diagnosis of OSA and initiating treatment with CPAP while still in the hospital carries any benefit in the management of patients with acute heart failure. This study will evaluate the effect of work up and treatment of OSA on the outcome of patients hospitalized with acute congestive heart failure (CHF).

Eligibility

Ages Eligible for Study:	21 Years to 80 Years
Genders Eligible for Study:	Both
Accepts Healthy Volunteers:	No

Criteria

.Inclusion Criteria:

Able to provide an informed consent
Speaks English
Older than 21
Heart Failure
Positive for OSA

Exclusion Criteria:

CSA
Already on CPAP
Hemodynamic instability
Acute respiratory failure
Neurological defect
Dialysis

Contacts and Locations

Please refer to this study by its ClinicalTrials.gov identifier: NCT00701038

Sponsors and Collaborators

Rami Khayat

Investigators

Principal Investigator:

Rami N Khayat, MD

Ohio State University

More Information

Publications:

Javaheri S, Parker TJ, Liming JD, Corbett WS, Nishiyama H, Wexler L, Roselle GA. Sleep apnea in 81 ambulatory male patients with stable heart failure. Types and their prevalences, consequences, and presentations. Circulation. 1998 Jun 2;97(21):2154-9.

Sin DD, Fitzgerald F, Parker JD, Newton G, Floras JS, Bradley TD. Risk factors for central and obstructive sleep apnea in 450 men and women with congestive heart failure. Am J Respir Crit Care Med. 1999 Oct;160(4):1101-6.

Skinner MA, Choudhury MS, Homan SD, Cowan JO, Wilkins GT, Taylor DR. Accuracy of monitoring for sleep-related breathing disorders in the coronary care unit. Chest. 2005 Jan;127(1):66-71.

Solin P, Bergin P, Richardson M, Kaye DM, Walters EH, Naughton MT. Influence of pulmonary capillary wedge pressure on central apnea in heart failure. Circulation. 1999 Mar 30;99(12):1574-9.

Mansfield DR, Gollogly NC, Kaye DM, Richardson M, Bergin P, Naughton MT. Controlled trial of continuous positive airway pressure in obstructive sleep apnea and heart failure. Am J Respir Crit Care Med. 2004 Feb 1;169(3):361-6. Epub 2003 Nov 3.

Marin JM, Carrizo SJ, Vicente E, Agusti AG. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet. 2005 Mar 19-25;365(9464):1046-53.

Katragadda S, Xie A, Puleo D, Skatrud JB, Morgan BJ. Neural mechanism of the pressor response to obstructive and nonobstructive apnea. J Appl Physiol. 1997 Dec;83(6):2048-54.

Morgan BJ, Denahan T, Ebert TJ. Neurocirculatory consequences of negative intrathoracic pressure vs. asphyxia during voluntary apnea. J Appl Physiol. 1993 Jun;74(6):2969-75.

Magder SA, Lichtenstein S, Adelman AG. Effect of negative pleural pressure on left ventricular hemodynamics. Am J Cardiol. 1983 Sep 1;52(5):588-93.

Stoohs R, Guilleminault C. Cardiovascular changes associated with obstructive sleep apnea syndrome. J Appl Physiol. 1992 Feb;72(2):583-9.

Hanly P, Sasson Z, Zuberi N, Lunn K. ST-segment depression during sleep in obstructive sleep apnea. Am J Cardiol. 1993 Jun 1;71(15):1341-5.

Roebuck T, Solin P, Kaye DM, Bergin P, Bailey M, Naughton MT. Increased long-term mortality in heart failure due to sleep apnoea is not yet proven. Eur Respir J. 2004 May;23(5):735-40.

Additional publications automatically indexed to this study by ClinicalTrials.gov Identifier (NCT Number):

Khayat RN, Abraham WT, Patt B, Pu M, Jarjoura D. In-hospital treatment of obstructive sleep apnea during decompensation of heart failure. Chest. 2009 Oct;136(4):991-7. Epub 2009 Jun 30.

Responsible Party:	Rami Khayat, Associate Professor-Clinical, The Ohio State University
ClinicalTrials.gov Identifier:	NCT00701038 History of Changes
Other Study ID Numbers:	2005H0186
Study First Received:	June 17, 2008
Results First Received:	August 12, 2011
Last Updated:	January 29, 2013
Health Authority:	United States: Institutional Review Board

Keywords provided by Ohio State University:

Sleep apnea,
obstructive sleep apnea,
heart failure,
CHF

Additional relevant MeSH terms:

Apnea
Heart Failure
Sleep Apnea Syndromes
Respiration Disorders
Respiratory Tract Diseases
Signs and Symptoms, Respiratory
Signs and Symptoms

Heart Diseases
Cardiovascular Diseases
Sleep Disorders, Intrinsic
Dyssomnias
Sleep Disorders
Nervous System Diseases

ClinicalTrials.gov processed this record on June 13, 2013