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

Primary Purpose

Obstructive Sleep Apnea

Status
Completed
Phase
Not Applicable
Locations
Germany
Study Type
Interventional
Intervention
6 months CPAP
Sponsored by
Wissenschaftliches Institut Bethanien e.V
About
Eligibility
Locations
Arms
Outcomes
Full info

About this trial

This is an interventional basic science trial for Obstructive Sleep Apnea focused on measuring Obstructive Sleep Apnea, Pulse wave analysis

Eligibility Criteria

18 Years - undefined (Adult, Older Adult)All SexesDoes not accept healthy volunteers

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

Sites / Locations

  • Bethanien Hospital

Arms of the Study

Arm 1

Arm Type

Experimental

Arm Label

6 months CPAP

Arm Description

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

Outcomes

Primary Outcome Measures

Change in pulse wave attenuation index
The pulse wave attenuation index represents the number of decreases of the pulse wave amplitude >10% and <30% compared with baseline (a moving median value of 20 samples surrounding the observed sample). This number is given as attenuations per hour. The difference from baseline (without therapy) to 6 months (on CPAP therapy) is calculated.

Secondary Outcome Measures

Change in mean pulse propagation time
The pulse propagation time represents the time interval between the systolic and dicrotic notch of the pulse wave form. The mean pulse propagation time of a complete recording is documented. The difference from baseline (without therapy) to 6 months (on CPAP therapy) is calculated.
Change in mean respiration-related pulse oscillation
The respiration-related pulse oscillation is calculated by measuring the breathing-associated oscillation (respiratory sinus arrhythmia in the frequency band between 0.15 and 0.4 Hz) from the pulse rate signal in the time domain. The mean respiration-related pulse oscillation value of a complete recording is documented. The difference from baseline (without therapy) to 6 months (on CPAP therapy) is calculated.
Change in pulse rate acceleration index
The pulse rate acceleration index represents the number of pulse rate increases ≥10% from baseline (a moving median value of 20 samples surrounding the observed sample). This number is given as increases per hour. The difference from baseline (without therapy) to 6 months (on CPAP therapy) is calculated.
Change in hypoxia index
The hypoxia index represents the number of oxygen desaturation events per hour. A desaturation event is defined as a ≥2% drop of saturation of each sample compared with a 90 seconds time window of the upcoming SpO2 signal. The difference from baseline (without therapy) to 6 months (on CPAP therapy) is calculated.
Change in ASI cardiovascular risk score
The ASI algorithm described by Grote et al. (2011) combines several single parameters from pulse wave analysis to calculate an overall cardiovascular risk score. The difference from baseline (without therapy) to 6 months (on CPAP therapy) is calculated.

Full Information

First Posted
March 11, 2013
Last Updated
October 26, 2018
Sponsor
Wissenschaftliches Institut Bethanien e.V
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1. Study Identification

Unique Protocol Identification Number
NCT01814462
Brief Title
Impact of CPAP Therapy in Obstructive Sleep Apnea on Parameters of Nocturnal Pulse Wave Analysis
Official Title
Impact of CPAP Therapy in Obstructive Sleep Apnea on Parameters of Nocturnal Pulse Wave Analysis
Study Type
Interventional

2. Study Status

Record Verification Date
October 2018
Overall Recruitment Status
Completed
Study Start Date
March 4, 2013 (Actual)
Primary Completion Date
May 30, 2017 (Actual)
Study Completion Date
May 30, 2017 (Actual)

3. Sponsor/Collaborators

Responsible Party, by Official Title
Sponsor
Name of the Sponsor
Wissenschaftliches Institut Bethanien e.V

4. Oversight

Data Monitoring Committee
No

5. Study Description

Brief Summary
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
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.

6. Conditions and Keywords

Primary Disease or Condition Being Studied in the Trial, or the Focus of the Study
Obstructive Sleep Apnea
Keywords
Obstructive Sleep Apnea, Pulse wave analysis

7. Study Design

Primary Purpose
Basic Science
Study Phase
Not Applicable
Interventional Study Model
Single Group Assignment
Masking
None (Open Label)
Allocation
N/A
Enrollment
314 (Actual)

8. Arms, Groups, and Interventions

Arm Title
6 months CPAP
Arm Type
Experimental
Arm Description
Application of continuous positive airway pressure (CPAP) therapy as established per routine clinical treatment. Home use of therapy for a period of 6 months.
Intervention Type
Device
Intervention Name(s)
6 months CPAP
Primary Outcome Measure Information:
Title
Change in pulse wave attenuation index
Description
The pulse wave attenuation index represents the number of decreases of the pulse wave amplitude >10% and <30% compared with baseline (a moving median value of 20 samples surrounding the observed sample). This number is given as attenuations per hour. The difference from baseline (without therapy) to 6 months (on CPAP therapy) is calculated.
Time Frame
6 months
Secondary Outcome Measure Information:
Title
Change in mean pulse propagation time
Description
The pulse propagation time represents the time interval between the systolic and dicrotic notch of the pulse wave form. The mean pulse propagation time of a complete recording is documented. The difference from baseline (without therapy) to 6 months (on CPAP therapy) is calculated.
Time Frame
6 months
Title
Change in mean respiration-related pulse oscillation
Description
The respiration-related pulse oscillation is calculated by measuring the breathing-associated oscillation (respiratory sinus arrhythmia in the frequency band between 0.15 and 0.4 Hz) from the pulse rate signal in the time domain. The mean respiration-related pulse oscillation value of a complete recording is documented. The difference from baseline (without therapy) to 6 months (on CPAP therapy) is calculated.
Time Frame
6 months
Title
Change in pulse rate acceleration index
Description
The pulse rate acceleration index represents the number of pulse rate increases ≥10% from baseline (a moving median value of 20 samples surrounding the observed sample). This number is given as increases per hour. The difference from baseline (without therapy) to 6 months (on CPAP therapy) is calculated.
Time Frame
6 months
Title
Change in hypoxia index
Description
The hypoxia index represents the number of oxygen desaturation events per hour. A desaturation event is defined as a ≥2% drop of saturation of each sample compared with a 90 seconds time window of the upcoming SpO2 signal. The difference from baseline (without therapy) to 6 months (on CPAP therapy) is calculated.
Time Frame
6 months
Title
Change in ASI cardiovascular risk score
Description
The ASI algorithm described by Grote et al. (2011) combines several single parameters from pulse wave analysis to calculate an overall cardiovascular risk score. The difference from baseline (without therapy) to 6 months (on CPAP therapy) is calculated.
Time Frame
6 months

10. Eligibility

Sex
All
Minimum Age & Unit of Time
18 Years
Accepts Healthy Volunteers
No
Eligibility Criteria
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
Facility Information:
Facility Name
Bethanien Hospital
City
Solingen
ZIP/Postal Code
42699
Country
Germany

12. IPD Sharing Statement

Citations:
PubMed Identifier
20671056
Citation
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.
Results Reference
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PubMed Identifier
10678860
Citation
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.
Results Reference
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PubMed Identifier
10770144
Citation
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. Erratum In: JAMA 2002 Oct 23-30;288(16):1985.
Results Reference
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PubMed Identifier
9250236
Citation
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.
Results Reference
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PubMed Identifier
10588600
Citation
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.
Results Reference
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PubMed Identifier
10927725
Citation
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.
Results Reference
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PubMed Identifier
10805822
Citation
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.
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PubMed Identifier
15301332
Citation
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.
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Citation
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.
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Impact of CPAP Therapy in Obstructive Sleep Apnea on Parameters of Nocturnal Pulse Wave Analysis

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