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NCT Number: NCT02127177

Long-term Effects of CPAP on Lipidemia and Hs-CRP Levels in OSA Patients

The increased risk of atherosclerotic morbidity and mortality in patients with obstructive sleep apnea (OSA) has been linked to hypertension, insulin resistance, dyslipidemia, and systemic inflammation. The relationship regarding obstructive sleep apnea (OSA) and lipidemia and systemic inflammation is far from conclusion for obesity as a strong confounding factor.

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Key information

Age range

45 year–75 year

Sex eligibility

All sexes

Study type

Interventional

Phase

Not applicable

Primary location

center of pulmonary vascular disease, Fuwai hospital

Beijing, 100037, China

About this study

Obstructive sleep apnea (OSA) is a common sleep disorder characterized by recurrent episodes of partial or complete obstruction of the upper airway during sleep, resulting in sleep fragmentation and oxyhemoglobin desaturation. OSA is recognized as an important public health problem in developed country, affecting 9 and 24% of middle-aged females and males, respectively. OSA, however, is not recognized as an abnormality for the majority and doesn't get more attention from most people in China. Increasing evidence now indicates that severe OSA is associated with increased cardiovascular morbidity and mortality, mainly due to acute myocardial infarction and stroke. Atherosclerosis is a key mechanism for these cardiovascular events. Numerous studies have explored the relationship between hypertension and OSA. And these studies confirms that OSA is an important identifiable cause of hypertension and a raised blood pressure has been shown to fall with effective continuous positive airway pressure (CPAP) treatment. Dyslipidemia, an established independent risk factor for coronary heart disease (CHD) and atherosclerosis, is common in patients with OSA. But there are limited interventional data on OSA and lipidemia, showing controversial results. Several studies9,10 have shown a direct relationship between OSA and lipid profiles, independently of obesity, while other studies have demonstrated that obesity, as a confounding factor, contributed to dyslipidemia among OSA patients.11,12 Taken together, adiposity is a strong confounding factor for interpretation of the causal relationship between dyslipidemia and OSA. Few studies have focused on nonobese patients.10,13 There are only a small number of randomized trials that have examined the effect of CPAP on fasting lipid profiles14,15 and none were specifically designed to evaluate the lipid profiles. Furthermore, most studies assessed the impact of CPAP on OSA-related lipids without statin therapy. In this way, it may be useful to avoid the disturb conditions due to statin treatment. But it is impractical to those patients with OSA and CHD. Since statins, in addition to decreasing hyperlipidemia levels, also inhibit inflammatory cytokines and play a critical role of plaque stabilization in CHD patients. Similarly, the condition existed in the examination of high-sensitivity C-reactive protein (hs-CRP) in CHD subjects with OSA. Therefore, the aims of the present study were (1) to establish whether CPAP therapy decreases lipid profiles and hs-CRP levels in nonobese patients with CHD and OSA, (2) to establish whether a relationship exists between the severity of OSA and levels of these circulating markers, and (3) to demonstrate a possible mechanism for the prevention of cardiovascular disease.

Who can participate

Healthy volunteers accepted: No

Only the study team can determine whether someone qualifies for participation.

Inclusion criteria

  • Participants diagnosed with a confirmation of CHD and moderate to severe

Exclusion criteria

  • A body mass index (BMI) ≥ 25 kg/m2
  • Established hypertension, diabetes mellitus, predominantly central sleep apnea, hypothyroidism
  • A history of smoking, chronic obstructive pulmonary disease, atopy, rhinitis, arthritis
  • Pharmacological treatment that could affect lipids and hs-CRP levels
  • Epworth Sleepiness Scale (ESS) ≥15
  • Diagnosed with malignant cancer with a life expectancy of less than 1 years
  • Severe psychiatric disease, sustained excessive alcohol use, New York Heart Association Class III-IV degree
  • Declined to participate or were unable to give informed consent.

Treatment and study plan

Continuous Positive Airway Pressure Ventilator

Device

CPAP group received fixed-level CPAP titration using an automated pressure setting device for one night. The optimal CPAP pressure for each patient in the CPAP group was set at the minimum pressure required to abolish snoring, obstructive respiratory events, and airflow limitation for 95% of the night, according to a previous validation by our study.

Other names: Continuous Positive Airway Pressure(CPAP)

Primary outcomes

  1. lipid profiles

    Time frame: baseline, Change from baseline lipids at 6 months,Change from baseline lipids at 12 months

    plasma fasting lipid profiles were measured at baseline, 6months,and 12months.

Secondary outcomes

  1. High-sensitivity C-reactive protein

    Time frame: baseline,Change from baseline high-sensitivity C-reactive protein at 6 months,Change from baseline high-sensitivity C-reactive protein at 12 months

    Fasting plasma high-sensitivity C-reactive protein was analyzed at baseline,6 months,and 12 months.

Sponsors and collaborators

Lead sponsor

Chinese Pulmonary Vascular Disease Research Group

Other

Registry information

Official study title

Long-term Effects of Continuous Positive Airway Pressure on Lipidemia and High-sensitivity C-reactive Protein Levels in Nonobese Patients With Coronary Heart Disease and Obstructive Sleep Apnea

Important dates

Study start
2010
Primary completion
2013
Study completion
2013
First posted
Apr 30, 2014
Registry last updated
Apr 30, 2014

OpenTrials presents study information sourced from ClinicalTrials.gov. The official registry record should be consulted for the latest information.

View the official ClinicalTrials.gov record (opens in a new tab)

This listing is for discovery and informational purposes only. It is not medical advice, does not guarantee that a study is recruiting, and does not determine eligibility. Contact the study team and a qualified healthcare professional when considering participation.

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