Impact of CPAP Therapy in Obstructive Sleep Apnea on Parameters of Nocturnal Pulse Wave Analysis

NCT ID: NCT01814462

Last Updated: 2018-10-30

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

COMPLETED

Clinical Phase

NA

Total Enrollment

314 participants

Study Classification

INTERVENTIONAL

Study Start Date

2013-03-04

Study Completion Date

2017-05-30

Brief Summary

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The present study aims to document and assess changes in single parameters of pulse wave analysis (ASI single parameters) as well as to evaluate ASI cardiovascular risk assessment before initiation of CPAP therapy and after 6 months of CPAP therapy in patients with obstructive sleep apnea.

Detailed Description

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Obstructive sleep apnea (OSA) is characterized by repeated occurrence of apneas or reduced inspiratory air flow due to obstructions of the upper airways (hypopneas). These recurring events are accompanied by intermittent hypoxemia and sympathetic activation, leading to hemodynamic oscillations including relevant variations of pulse wave and blood pressure. Thus, OSA is associated with cardiovascular diseases and was identified as an independent risk factor for hypertension.

Direct effects of obstructive respiratory events (obstructive apneas and hypopneas) include changes of the peripheral pulse wave. The latter can easily be measured by finger plethysmography, e.g. by using established pulse oximeters. Certain pulse wave characteristics and their reaction towards obstructive respiratory events may provide information on cardiovascular function and thereby help in individual cardiovascular risk assessment.

Recently, Grote et al. published a concept for cardiovascular risk assessment based on pulse oximetry and pulse wave analysis ("ASI" - Grote et al. 2011, CHEST). The algorithm described herein is able to differentiate between high and low risk patients according to ESH/ESC risk classification (high risk = 4 and 5, low risk 1-3). To that end, oxygen saturation as measured by pulse oximetry, reductions in pulse wave amplitude, pulse rate accelerations, pulse propagation time and cardiorespiratory coupling are taken into account to calculate a quantitative total risk.

A successful OSA therapy applying positive airway pressure (e.g. CPAP) normalizes sleep-related breathing disturbances and thus counterbalances hemodynamic oscillations. This presumably results in reduced cardiovascular risk and should be detectable by measurable changes in pulse wave. This study aims to evaluate these effects by analyzing the single pulse wave parameters, which are part of the ASI algorithm. At the same time, established risk factors as well as the objective therapy outcome will be documented from the established sleep medicine viewpoint.

Conditions

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Obstructive Sleep Apnea

Study Design

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Allocation Method

NA

Intervention Model

SINGLE_GROUP

Primary Study Purpose

BASIC_SCIENCE

Blinding Strategy

NONE

Study Groups

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6 months CPAP

Application of continuous positive airway pressure (CPAP) therapy as established per routine clinical treatment. Home use of therapy for a period of 6 months.

Group Type EXPERIMENTAL

6 months CPAP

Intervention Type DEVICE

Interventions

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6 months CPAP

Intervention Type DEVICE

Eligibility Criteria

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Inclusion Criteria

* Sleep-related breathing disorders with an apnea-hypopnea index ≥15/h and \<30% central respiratory events (OSA patients)
* Stable optimal medication according to European Society of Cardiology guidelines (if applicable)

Exclusion Criteria

* Prior exposure to positive airway pressure treatment
* Atrial fibrillation
* Facial anomalies or injuries inhibiting proper mask fit
* Pregnancy and/or lactation
* Acute life-threatening illness (e.g. instable angina pectoris, acute bronchial asthma, heart failure New York Heart Association stage IV, myocardial infarction, exacerbated Chronic obstructive pulmonary disease, malignant tumor requiring treatment)
* Drug or alcohol abuse
* Intake of hypnotics/sedatives
* Any medical, psychological or other condition impairing the patient's ability to provide informed consent
Minimum Eligible Age

18 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

No

Sponsors

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Wissenschaftliches Institut Bethanien e.V

OTHER

Sponsor Role lead

Responsible Party

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Responsibility Role SPONSOR

Locations

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Bethanien Hospital

Solingen, , Germany

Site Status

Countries

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Germany

References

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Grote L, Sommermeyer D, Zou D, Eder DN, Hedner J. Oximeter-based autonomic state indicator algorithm for cardiovascular risk assessment. Chest. 2011 Feb;139(2):253-259. doi: 10.1378/chest.09-3029. Epub 2010 Jul 29.

Reference Type BACKGROUND
PMID: 20671056 (View on PubMed)

Lavie P, Herer P, Hoffstein V. Obstructive sleep apnoea syndrome as a risk factor for hypertension: population study. BMJ. 2000 Feb 19;320(7233):479-82. doi: 10.1136/bmj.320.7233.479.

Reference Type BACKGROUND
PMID: 10678860 (View on PubMed)

Nieto FJ, Young TB, Lind BK, Shahar E, Samet JM, Redline S, D'Agostino RB, Newman AB, Lebowitz MD, Pickering TG. Association of sleep-disordered breathing, sleep apnea, and hypertension in a large community-based study. Sleep Heart Health Study. JAMA. 2000 Apr 12;283(14):1829-36. doi: 10.1001/jama.283.14.1829.

Reference Type BACKGROUND
PMID: 10770144 (View on PubMed)

Young T, Peppard P, Palta M, Hla KM, Finn L, Morgan B, Skatrud J. Population-based study of sleep-disordered breathing as a risk factor for hypertension. Arch Intern Med. 1997 Aug 11-25;157(15):1746-52.

Reference Type BACKGROUND
PMID: 9250236 (View on PubMed)

Grote L, Ploch T, Heitmann J, Knaack L, Penzel T, Peter JH. Sleep-related breathing disorder is an independent risk factor for systemic hypertension. Am J Respir Crit Care Med. 1999 Dec;160(6):1875-82. doi: 10.1164/ajrccm.160.6.9811054.

Reference Type BACKGROUND
PMID: 10588600 (View on PubMed)

Bixler EO, Vgontzas AN, Lin HM, Ten Have T, Leiby BE, Vela-Bueno A, Kales A. Association of hypertension and sleep-disordered breathing. Arch Intern Med. 2000 Aug 14-28;160(15):2289-95. doi: 10.1001/archinte.160.15.2289.

Reference Type BACKGROUND
PMID: 10927725 (View on PubMed)

Peppard PE, Young T, Palta M, Skatrud J. Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med. 2000 May 11;342(19):1378-84. doi: 10.1056/NEJM200005113421901.

Reference Type BACKGROUND
PMID: 10805822 (View on PubMed)

Parish JM, Somers VK. Obstructive sleep apnea and cardiovascular disease. Mayo Clin Proc. 2004 Aug;79(8):1036-46. doi: 10.4065/79.8.1036.

Reference Type BACKGROUND
PMID: 15301332 (View on PubMed)

Peker Y, Hedner J, Norum J, Kraiczi H, Carlson J. Increased incidence of cardiovascular disease in middle-aged men with obstructive sleep apnea: a 7-year follow-up. Am J Respir Crit Care Med. 2002 Jul 15;166(2):159-65. doi: 10.1164/rccm.2105124.

Reference Type BACKGROUND
PMID: 12119227 (View on PubMed)

O'Donnell CP, Ayuse T, King ED, Schwartz AR, Smith PL, Robotham JL. Airway obstruction during sleep increases blood pressure without arousal. J Appl Physiol (1985). 1996 Mar;80(3):773-81. doi: 10.1152/jappl.1996.80.3.773.

Reference Type BACKGROUND
PMID: 8964736 (View on PubMed)

Davies RJ, Belt PJ, Roberts SJ, Ali NJ, Stradling JR. Arterial blood pressure responses to graded transient arousal from sleep in normal humans. J Appl Physiol (1985). 1993 Mar;74(3):1123-30. doi: 10.1152/jappl.1993.74.3.1123.

Reference Type BACKGROUND
PMID: 8482650 (View on PubMed)

Buchner NJ, Sanner BM, Borgel J, Rump LC. Continuous positive airway pressure treatment of mild to moderate obstructive sleep apnea reduces cardiovascular risk. Am J Respir Crit Care Med. 2007 Dec 15;176(12):1274-80. doi: 10.1164/rccm.200611-1588OC. Epub 2007 Aug 2.

Reference Type BACKGROUND
PMID: 17673692 (View on PubMed)

Hui DS, Shang Q, Ko FW, Ng SS, Szeto CC, Ngai J, Tung AH, To KW, Chan TO, Yu CM. A prospective cohort study of the long-term effects of CPAP on carotid artery intima-media thickness in obstructive sleep apnea syndrome. Respir Res. 2012 Mar 16;13(1):22. doi: 10.1186/1465-9921-13-22.

Reference Type BACKGROUND
PMID: 22424053 (View on PubMed)

Other Identifiers

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WI_ASIC+CPAP_121/2012

Identifier Type: -

Identifier Source: org_study_id

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