Obstructive Sleep Apnea (OSA) in Pulmonary Arterial Hypertension (PAH)

Obstructive Sleep Apnea Clinical Trial

Official title:

Effect of Pulmonary Arterial Hypertension Treatment on Obstructive Sleep Apnea

Clinical Trial Details — Status: Terminated

Administrative data

• NCT number: NCT01835080
• Other study ID #: 12.038
• Status: Terminated
• Start date: April 2013
• Est. completion date: March 2014

Study information

• Verified date: June 2014
• Source: Inova Health Care Services
• Contact: n/a
• Is FDA regulated: No
• Study type: Observational

Clinical Trial Summary

The purpose of this study is to determine whether pulmonary arterial hypertension can worsen or even cause sleep apnea. It is hypothesized that if pulmonary arterial hypertension does indeed worsen or cause sleep apnea, then the treatment should first focus on the underlying pulmonary arterial hypertension instead of the sleep apnea.

To determine if a person has sleep apnea, they will undergo one overnight polysomnogram (sleep study). If it is found that they have mild to moderate sleep apnea, then the subject will be invited to continue in the study and their pulmonary arterial hypertension will be treated by their managing primary physician. After the subject has had treatment for their pulmonary arterial hypertension, the study center will have them return for a follow up sleep study to learn the effects of pulmonary arterial hypertension treatment management on their sleep apnea, 12-24 weeks after the first sleep study.

Description:

Pulmonary Arterial Hypertension (PAH) is associated with fluid retention. Currently, the treatment paradigm for newly diagnosed PAH patients includes evaluation for Obstructive Sleep Apnea (OSA). The investigators propose that untreated or sub-optimally managed PAH patients have significant fluid retention which redistributes to the upper body during sleep and exacerbates or even mimics OSA. The investigators hypothesize that treatment of PAH patients with vasodilators and diuretics to optimize fluid balance will attenuate or even resolve OSA prior to the initiation of specific therapy for OSA (CPAP).

Recruitment information / eligibility

• Status: Terminated
• Enrollment: 2
• Est. completion date: March 2014
• Est. primary completion date: March 2014
• Accepts healthy volunteers: Accepts Healthy Volunteers
• Gender: All
• Age group: 18 Years and older

Eligibility

Inclusion Criteria:

• • Diagnosis of Group 1 PAH

• Either lack of treatment for PAH or sub-optimally treated PAH as defined by NYHA FC 3 or 4

• Age 18 or older

• Ability to give consent

• Ability to undergo overnight polysomnogram

• Previously diagnosed OSA not on therapy

Exclusion Criteria:

• Age younger than 18

• Pregnancy

• Previously diagnosed OSA and receiving therapy

• Inability to undergo overnight polysomnography in laboratory

Related Conditions & MeSH terms

• Apnea
• Familial Primary Pulmonary Hypertension
• Hypertension
• Obstructive Sleep Apnea
• Pulmonary Arterial Hypertension
• Sleep Apnea Syndromes
• Sleep Apnea, Obstructive

Locations

Country	Name	City	State
United States	Inova Heart and Vascular Institute/Inova Fairfax Hospital	Falls Church	Virginia

Sponsors (4)

Lead Sponsor	Collaborator
Inova Health Care Services	Brown University, George Washington University, Tufts University

Country where clinical trial is conducted

United States, 

References & Publications (11)

Atwood CW Jr, McCrory D, Garcia JG, Abman SH, Ahearn GS; American College of Chest Physicians. Pulmonary artery hypertension and sleep-disordered breathing: ACCP evidence-based clinical practice guidelines. Chest. 2004 Jul;126(1 Suppl):72S-77S. Review. — View Citation

Badesch DB, Raskob GE, Elliott CG, Krichman AM, Farber HW, Frost AE, Barst RJ, Benza RL, Liou TG, Turner M, Giles S, Feldkircher K, Miller DP, McGoon MD. Pulmonary arterial hypertension: baseline characteristics from the REVEAL Registry. Chest. 2010 Feb;137(2):376-87. doi: 10.1378/chest.09-1140. Epub 2009 Oct 16. — View Citation

Bady E, Achkar A, Pascal S, Orvoen-Frija E, Laaban JP. Pulmonary arterial hypertension in patients with sleep apnoea syndrome. Thorax. 2000 Nov;55(11):934-9. — View Citation

Brown LM, Chen H, Halpern S, Taichman D, McGoon MD, Farber HW, Frost AE, Liou TG, Turner M, Feldkircher K, Miller DP, Elliott CG. Delay in recognition of pulmonary arterial hypertension: factors identified from the REVEAL Registry. Chest. 2011 Jul;140(1):19-26. doi: 10.1378/chest.10-1166. Epub 2011 Mar 10. — View Citation

Elias RM, Bradley TD, Kasai T, Motwani SS, Chan CT. Rostral overnight fluid shift in end-stage renal disease: relationship with obstructive sleep apnea. Nephrol Dial Transplant. 2012 Apr;27(4):1569-73. doi: 10.1093/ndt/gfr605. Epub 2011 Nov 5. — View Citation

Friedman O, Bradley TD, Chan CT, Parkes R, Logan AG. Relationship between overnight rostral fluid shift and obstructive sleep apnea in drug-resistant hypertension. Hypertension. 2010 Dec;56(6):1077-82. doi: 10.1161/HYPERTENSIONAHA.110.154427. Epub 2010 Nov 8. — View Citation

Jafari B, Mohsenin V. Overnight rostral fluid shift in obstructive sleep apnea: does it affect the severity of sleep-disordered breathing? Chest. 2011 Oct;140(4):991-997. doi: 10.1378/chest.11-0044. Epub 2011 Mar 24. — View Citation

Proceedings of the 4th World Symposium on Pulmonary Hypertension, February 2008, Dana Point, California, USA. J Am Coll Cardiol. 2009 Jun 30;54(1 Suppl):S1-117. — View Citation

Redolfi S, Arnulf I, Pottier M, Bradley TD, Similowski T. Effects of venous compression of the legs on overnight rostral fluid shift and obstructive sleep apnea. Respir Physiol Neurobiol. 2011 Mar 15;175(3):390-3. doi: 10.1016/j.resp.2011.01.001. Epub 2011 Jan 8. — View Citation

Redolfi S, Arnulf I, Pottier M, Lajou J, Koskas I, Bradley TD, Similowski T. Attenuation of obstructive sleep apnea by compression stockings in subjects with venous insufficiency. Am J Respir Crit Care Med. 2011 Nov 1;184(9):1062-6. doi: 10.1164/rccm.201102-0350OC. — View Citation

Ulrich S, Fischler M, Speich R, Bloch KE. Sleep-related breathing disorders in patients with pulmonary hypertension. Chest. 2008 Jun;133(6):1375-1380. doi: 10.1378/chest.07-3035. Epub 2008 Mar 13. — View Citation

* Note: There are 11 references in all — Click here to view all references

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Primary endpoint is a decrease in Respiratory Disturbance Index (RDI) by 10 events/hour	All patients will undergo a sleep study (polysomnogram) before their PAH is treated (or treated optimally) and each patient will have a repeat sleep study at 12- 24 weeks after their PAH treatment is optimally managed by their primary managing physician. These sleep studies will be centrally scored to determine whether a decrease in RDI of at least 10 events/hour has been met.	12-24 weeks
Secondary	Decrease in neck circumference by 0.9 cm	All subjects will be assessed for decrease in neck circumference by 0.9 cm	12-24 weeks
Secondary	Decrease in ankle circumference by 0.8 cm	All subjects will be assessed for decrease in ankle circumference by 0.8 cm	12-24 weeks
Secondary	improvement in Epworth Sleepiness Scale	All subjects will be assessed for improvement in Epworth Sleepiness Scale	12-24 weeks
Secondary	improvement in Arousal Index	All subjects will be assessed for improvement in Arousal Index	12-24 weeks