<clinical_study>
  <!-- This xml conforms to an XML Schema at:
    https://clinicaltrials.gov/ct2/html/images/info/public.xsd -->
  <required_header>
    <download_date>ClinicalTrials.gov processed this data on September 20, 2023</download_date>
    <link_text>Link to the current ClinicalTrials.gov record.</link_text>
    <url>https://clinicaltrials.gov/ct2/show/NCT01699126</url>
  </required_header>
  <id_info>
    <org_study_id>98-2167B</org_study_id>
    <nct_id>NCT01699126</nct_id>
  </id_info>
  <brief_title>The Endothelium Dysfunction in Patients of Obstructive Sleep Apnea Syndrome</brief_title>
  <official_title>The Endothelium Dysfunction in Patients of Obstructive Sleep Apnea Syndrome</official_title>
  <sponsors>
    <lead_sponsor>
      <agency>Chang Gung Memorial Hospital</agency>
      <agency_class>Other</agency_class>
    </lead_sponsor>
  </sponsors>
  <source>Chang Gung Memorial Hospital</source>
  <oversight_info>
    <has_dmc>Yes</has_dmc>
  </oversight_info>
  <brief_summary>
    <textblock>
      study Hypothesis: We hypothesize that CPAP could effectively improve the endothelial&#xD;
      dysfunction by anti-inflammatory effect in patients of OSA,and compare to the effect of&#xD;
      statin.&#xD;
    </textblock>
  </brief_summary>
  <detailed_description>
    <textblock>
      Obstructive sleep apnea is a prevalent disorder that affect 2-4% adults in general&#xD;
      population. Cardiovascular and Neurocognitive complication were the most common and severe&#xD;
      consequence noted in patients of OSA. Endothelial dysfunction is the early pathologic changes&#xD;
      in the vascular wall that precede to the clinical cardiovascular events. Endothelial&#xD;
      dysfunction with the deficit of vascular relaxation will induce the development of&#xD;
      hypertension. Endothelial dysfunction predict the occurrence of ischemic heart disease and&#xD;
      cardiovascular events as stroke. The development of endothelial dysfunction significantly&#xD;
      remark the early sign of the development of cardiovascular diseases.&#xD;
&#xD;
      Inflammation trigger by oxygen radical in the vascular system were the major pathogenesis of&#xD;
      the endothelial dysfunction. Intermittent hypoxia in the patients of OSA during repeated&#xD;
      apnea at night will increase the oxygen radicals therefore trigger the cascade of&#xD;
      inflammation process. The inflammatory process could be mediated by the activation of the&#xD;
      transcription factors such as NF-KB, AP-1 or from the pathway of HIF-1 cascade. Inflammatory&#xD;
      cytokine such as HsCRP inducted by the activation of NF-KB and AP-1 will induce the&#xD;
      interaction of monocytes and lymphocytes to further injury to the endothelium of vascular&#xD;
      wall. TGF-B secreted by lymphocyte will create the remodeling by fibroblast which result in&#xD;
      the thickening of vascular wall. Another pathway by VEGF, endothelin 1, or other protein&#xD;
      modulated by HIF-1 is also proposed directly injure to the endothelium that cause the&#xD;
      following cardiovascular events.&#xD;
&#xD;
      CPAP treatment for OSA were shown to lowering the severity of blood pressure and&#xD;
      cardiovascular events in some reports. Although the effect for blood pressure lowering is&#xD;
      still controversial, Most reports actually showed marginal effect on reducing BP to 2 mmHg by&#xD;
      CPAP. There is still part of OSA patients with hypertension not responding to CPAP&#xD;
      treatment.Besides of the effect of CPAP treatment, the compliance of CPAP is still a major&#xD;
      concerning in the treatment of OSA. 60% of patients were reported to continue used CPAP in&#xD;
      the well-supported sleep center in USA. Even the CPAP is covered by reimbursement in USA, the&#xD;
      low compliance of CPAP impede the treatment of cardiovascular complication of OSA. To improve&#xD;
      the control of the cardiovascular consequence of OSA, a convenient and well-tolerated&#xD;
      intervention is mandatory. Statin, a powerful lipid-lowering medication, is found to have a&#xD;
      significant anti-inflammatory effect in several reports. Statin is even suggested in the&#xD;
      population of normal cholesterol to prevent the development of cardiovascular event. Statins&#xD;
      exert cholesterol-independent, anti-inflammatory and immunomodulatory effects. Pleiotropic&#xD;
      effects are typically mediated by HMG-CoA reductase inhibition, are dose dependent and occur&#xD;
      rapidly after initiation of statin treatment. In order to evaluate and explore a safe and&#xD;
      convenient method in the control of the cardiovascular complication of OSA, we conduct this&#xD;
      study.&#xD;
    </textblock>
  </detailed_description>
  <overall_status>Completed</overall_status>
  <start_date>May 2010</start_date>
  <completion_date type="Actual">August 2013</completion_date>
  <primary_completion_date type="Actual">February 2013</primary_completion_date>
  <phase>Phase 4</phase>
  <study_type>Interventional</study_type>
  <has_expanded_access>No</has_expanded_access>
  <study_design_info>
    <allocation>Randomized</allocation>
    <intervention_model>Parallel Assignment</intervention_model>
    <primary_purpose>Treatment</primary_purpose>
    <masking>None (Open Label)</masking>
  </study_design_info>
  <primary_outcome>
    <measure>Flow-Mediated dilatation test(FMD)</measure>
    <time_frame>6 months</time_frame>
    <description>FMD is the most sensitive physical marker of endothelial function, we measure the FMD changes after treatment</description>
  </primary_outcome>
  <secondary_outcome>
    <measure>Blood pressure</measure>
    <time_frame>6 months</time_frame>
    <description>Hypertension is the most common cardiovascular disease and prevalent in general population. Many factors including age, obesity, DM, atherosclerosis, OSA….etc will trigger hypertension and exacerbate disease condition. There are more and more evidences showing that OSA play an independent role in hypertension therapy.OSA with CPAP therapy had been proved to reduce blood pressure in many papers especially in resisted hypertension.&#xD;
However, during OSA therapy, we found that not all OSA patients with CPAP therapy will achieve the additional goal of blood pressure reduction. Therefore, we hypothesize that there is responder and non-responder in OSA patients with hypertension to CPAP therapy. To clarify the character of responder of OSA patients with hypertension and further investigate the mechanism between OSA and hypertension, we aim to conduct this study:</description>
  </secondary_outcome>
  <other_outcome>
    <measure>Hs-CRP</measure>
    <time_frame>6 months</time_frame>
    <description>Endothelial dysfunction is supposed to be mediated by inflammation process after hypoxia. Hs-CRP is the most sensitive marker to evaluate the inflammation level.</description>
  </other_outcome>
  <other_outcome>
    <measure>Inflammatory markers</measure>
    <time_frame>6 months</time_frame>
    <description>Inflammation after hypoxia is suggested to be the pathogenesis of endothelial dysfunction. We will measure the inflammatory markers after treatment.</description>
  </other_outcome>
  <number_of_arms>4</number_of_arms>
  <enrollment type="Actual">46</enrollment>
  <condition>Sleep Apnea, Obstructive</condition>
  <arm_group>
    <arm_group_label>CPAP, Hypertension</arm_group_label>
    <arm_group_type>Experimental</arm_group_type>
    <description>evaluate the effect on FMD, blood pressure and inflammation after CPAP on OSA</description>
  </arm_group>
  <arm_group>
    <arm_group_label>CPAP and statin, Hypertension</arm_group_label>
    <arm_group_type>Active Comparator</arm_group_type>
    <description>evaluate the effect on FMD, blood pressure and inflammation after CPAP plus statin on OSA patients</description>
  </arm_group>
  <arm_group>
    <arm_group_label>OSA, statin, Hypertension</arm_group_label>
    <arm_group_type>Active Comparator</arm_group_type>
    <description>evaluate the effect on FMD, blood pressure and inflammation after statin treatment on OSA</description>
  </arm_group>
  <arm_group>
    <arm_group_label>Placebo</arm_group_label>
    <arm_group_type>No Intervention</arm_group_type>
    <description>We will also measure the FMD, blood pressure and inflammation on patients with only life style modification as in all other patients</description>
  </arm_group>
  <intervention>
    <intervention_type>Device</intervention_type>
    <intervention_name>CPAP</intervention_name>
    <description>Continuous Positive Airway Pressure is the routine treatment of OSA, patients will be randomly assigned into CPAP treatment group</description>
    <arm_group_label>CPAP and statin, Hypertension</arm_group_label>
    <arm_group_label>CPAP, Hypertension</arm_group_label>
  </intervention>
  <intervention>
    <intervention_type>Drug</intervention_type>
    <intervention_name>Statin</intervention_name>
    <description>Statin is an lipid lowering medication with anti-inflammatory effect.</description>
    <arm_group_label>CPAP and statin, Hypertension</arm_group_label>
    <arm_group_label>OSA, statin, Hypertension</arm_group_label>
    <other_name>rosuvastatin</other_name>
  </intervention>
  <eligibility>
    <criteria>
      <textblock>
        Inclusion Criteria:&#xD;
&#xD;
        - 1.OSA with AHI&gt;30 2.Male patients with hypertension 3.LDL over 130 mg/dL without any&#xD;
        lipid-lowering drug therapy in recent 6 months 4.Signed inform consent and cooperative&#xD;
&#xD;
        Exclusion Criteria:&#xD;
&#xD;
        - 1.Non-cooperative 2.Can't sign inform consent. 3.Had proven major cardiovascular&#xD;
        complication such as AMI, CVA. 4.Major chronic disorders and inflammatory disorders: such&#xD;
        as DM, ESRD, COPD or rheumatoid arthritis. 5.Under anti-inflammatory medication: such as&#xD;
        aspirin, NSAID, steroids, theophylline etc. 6.Acute of chronic infection 1 weeks between&#xD;
        blood drawing period will be discarded 7.Study medication will be discontinued among&#xD;
        subjects who develop myopathy (CK ≥10 times ULN and muscle aches or weakness) or a&#xD;
        persistent elevation in ALT (≥3 times ULN on 2 consecutive tests).&#xD;
      </textblock>
    </criteria>
    <gender>All</gender>
    <minimum_age>18 Years</minimum_age>
    <maximum_age>N/A</maximum_age>
    <healthy_volunteers>No</healthy_volunteers>
  </eligibility>
  <overall_official>
    <last_name>WAN-CHING Ho, M.D.</last_name>
    <role>Principal Investigator</role>
    <affiliation>Taiwan Society of Cardiology</affiliation>
  </overall_official>
  <location>
    <facility>
      <name>Chang Gang Memorial Hospital</name>
      <address>
        <city>Taoyuan</city>
        <zip>333</zip>
        <country>Taiwan</country>
      </address>
    </facility>
  </location>
  <location_countries>
    <country>Taiwan</country>
  </location_countries>
  <results_reference>
    <citation>Luthje L, Andreas S. Obstructive sleep apnea and coronary artery disease. Sleep Med Rev. 2008 Feb;12(1):19-31. doi: 10.1016/j.smrv.2007.08.002. Epub 2007 Nov 1.</citation>
    <PMID>17936040</PMID>
  </results_reference>
  <results_reference>
    <citation>Bradley TD, Floras JS. Obstructive sleep apnoea and its cardiovascular consequences. Lancet. 2009 Jan 3;373(9657):82-93. doi: 10.1016/S0140-6736(08)61622-0. Epub 2008 Dec 26.</citation>
    <PMID>19101028</PMID>
  </results_reference>
  <results_reference>
    <citation>Atkeson A, Yeh SY, Malhotra A, Jelic S. Endothelial function in obstructive sleep apnea. Prog Cardiovasc Dis. 2009 Mar-Apr;51(5):351-62. doi: 10.1016/j.pcad.2008.08.002.</citation>
    <PMID>19249441</PMID>
  </results_reference>
  <results_reference>
    <citation>Jelic S, Padeletti M, Kawut SM, Higgins C, Canfield SM, Onat D, Colombo PC, Basner RC, Factor P, LeJemtel TH. Inflammation, oxidative stress, and repair capacity of the vascular endothelium in obstructive sleep apnea. Circulation. 2008 Apr 29;117(17):2270-8. doi: 10.1161/CIRCULATIONAHA.107.741512. Epub 2008 Apr 14.</citation>
    <PMID>18413499</PMID>
  </results_reference>
  <results_reference>
    <citation>Gozal D, Kheirandish-Gozal L. Cardiovascular morbidity in obstructive sleep apnea: oxidative stress, inflammation, and much more. Am J Respir Crit Care Med. 2008 Feb 15;177(4):369-75. doi: 10.1164/rccm.200608-1190PP. Epub 2007 Nov 1.</citation>
    <PMID>17975198</PMID>
  </results_reference>
  <results_reference>
    <citation>Gilmartin GS, Tamisier R, Curley M, Weiss JW. Ventilatory, hemodynamic, sympathetic nervous system, and vascular reactivity changes after recurrent nocturnal sustained hypoxia in humans. Am J Physiol Heart Circ Physiol. 2008 Aug;295(2):H778-85. doi: 10.1152/ajpheart.00653.2007. Epub 2008 Jun 6.</citation>
    <PMID>18539753</PMID>
  </results_reference>
  <results_reference>
    <citation>Iturriaga R, Rey S, Del Rio R. Cardiovascular and ventilatory acclimatization induced by chronic intermittent hypoxia: a role for the carotid body in the pathophysiology of sleep apnea. Biol Res. 2005;38(4):335-40. doi: 10.4067/s0716-97602005000400004.</citation>
    <PMID>16579514</PMID>
  </results_reference>
  <results_reference>
    <citation>Williams B. The year in hypertension. J Am Coll Cardiol. 2008 May 6;51(18):1803-17. doi: 10.1016/j.jacc.2008.03.010. No abstract available.</citation>
    <PMID>18452788</PMID>
  </results_reference>
  <results_reference>
    <citation>Campos-Rodriguez F. Screening for sleep apnea in patients with resistant hypertension. Am J Hypertens. 2008 Jul;21(7):728. doi: 10.1038/ajh.2008.193. No abstract available.</citation>
    <PMID>18584016</PMID>
  </results_reference>
  <results_reference>
    <citation>Haentjens P, Van Meerhaeghe A, Moscariello A, De Weerdt S, Poppe K, Dupont A, Velkeniers B. The impact of continuous positive airway pressure on blood pressure in patients with obstructive sleep apnea syndrome: evidence from a meta-analysis of placebo-controlled randomized trials. Arch Intern Med. 2007 Apr 23;167(8):757-64. doi: 10.1001/archinte.167.8.757.</citation>
    <PMID>17452537</PMID>
  </results_reference>
  <results_reference>
    <citation>Phillips CL, Yee B, Yang Q, Villaneuva AT, Hedner J, Berend N, Grunstein R. Effects of continuous positive airway pressure treatment and withdrawal in patients with obstructive sleep apnea on arterial stiffness and central BP. Chest. 2008 Jul;134(1):94-100. doi: 10.1378/chest.07-3121. Epub 2008 Mar 17.</citation>
    <PMID>18347202</PMID>
  </results_reference>
  <verification_date>January 2018</verification_date>
  <study_first_submitted>August 30, 2012</study_first_submitted>
  <study_first_submitted_qc>October 1, 2012</study_first_submitted_qc>
  <study_first_posted type="Estimate">October 3, 2012</study_first_posted>
  <last_update_submitted>January 30, 2018</last_update_submitted>
  <last_update_submitted_qc>January 30, 2018</last_update_submitted_qc>
  <last_update_posted type="Actual">February 1, 2018</last_update_posted>
  <responsible_party>
    <responsible_party_type>Sponsor</responsible_party_type>
  </responsible_party>
  <keyword>Obstructive Sleep Apnea</keyword>
  <keyword>CPAP</keyword>
  <keyword>Endothelium dysfunction</keyword>
  <keyword>Hypertension</keyword>
  <condition_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Apnea</mesh_term>
    <mesh_term>Sleep Apnea Syndromes</mesh_term>
    <mesh_term>Sleep Apnea, Obstructive</mesh_term>
  </condition_browse>
  <intervention_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Rosuvastatin Calcium</mesh_term>
  </intervention_browse>
  <!-- Results have not yet been posted for this study                                          -->
</clinical_study>


download date: ClinicalTrials.gov processed this data on September 20, 2023
link text: Link to the current ClinicalTrials.gov record.
url: https://clinicaltrials.gov/ct2/show/NCT01699126
org study id: 98-2167B
nct id: NCT01699126
lead sponsor: 
has dmc: Yes
study Hypothesis: We hypothesize that CPAP could effectively improve the endothelial
      dysfunction by anti-inflammatory effect in patients of OSA,and compare to the effect of
      statin.
Obstructive sleep apnea is a prevalent disorder that affect 2-4% adults in general
      population. Cardiovascular and Neurocognitive complication were the most common and severe
      consequence noted in patients of OSA. Endothelial dysfunction is the early pathologic changes
      in the vascular wall that precede to the clinical cardiovascular events. Endothelial
      dysfunction with the deficit of vascular relaxation will induce the development of
      hypertension. Endothelial dysfunction predict the occurrence of ischemic heart disease and
      cardiovascular events as stroke. The development of endothelial dysfunction significantly
      remark the early sign of the development of cardiovascular diseases.

      Inflammation trigger by oxygen radical in the vascular system were the major pathogenesis of
      the endothelial dysfunction. Intermittent hypoxia in the patients of OSA during repeated
      apnea at night will increase the oxygen radicals therefore trigger the cascade of
      inflammation process. The inflammatory process could be mediated by the activation of the
      transcription factors such as NF-KB, AP-1 or from the pathway of HIF-1 cascade. Inflammatory
      cytokine such as HsCRP inducted by the activation of NF-KB and AP-1 will induce the
      interaction of monocytes and lymphocytes to further injury to the endothelium of vascular
      wall. TGF-B secreted by lymphocyte will create the remodeling by fibroblast which result in
      the thickening of vascular wall. Another pathway by VEGF, endothelin 1, or other protein
      modulated by HIF-1 is also proposed directly injure to the endothelium that cause the
      following cardiovascular events.

      CPAP treatment for OSA were shown to lowering the severity of blood pressure and
      cardiovascular events in some reports. Although the effect for blood pressure lowering is
      still controversial, Most reports actually showed marginal effect on reducing BP to 2 mmHg by
      CPAP. There is still part of OSA patients with hypertension not responding to CPAP
      treatment.Besides of the effect of CPAP treatment, the compliance of CPAP is still a major
      concerning in the treatment of OSA. 60% of patients were reported to continue used CPAP in
      the well-supported sleep center in USA. Even the CPAP is covered by reimbursement in USA, the
      low compliance of CPAP impede the treatment of cardiovascular complication of OSA. To improve
      the control of the cardiovascular consequence of OSA, a convenient and well-tolerated
      intervention is mandatory. Statin, a powerful lipid-lowering medication, is found to have a
      significant anti-inflammatory effect in several reports. Statin is even suggested in the
      population of normal cholesterol to prevent the development of cardiovascular event. Statins
      exert cholesterol-independent, anti-inflammatory and immunomodulatory effects. Pleiotropic
      effects are typically mediated by HMG-CoA reductase inhibition, are dose dependent and occur
      rapidly after initiation of statin treatment. In order to evaluate and explore a safe and
      convenient method in the control of the cardiovascular complication of OSA, we conduct this
      study.
allocation: Randomized
intervention model: Parallel Assignment
primary purpose: Treatment
masking: None (Open Label)
measure: Flow-Mediated dilatation test(FMD)
time frame: 6 months
description: FMD is the most sensitive physical marker of endothelial function, we measure the FMD changes after treatment
measure: Blood pressure
time frame: 6 months
description: Hypertension is the most common cardiovascular disease and prevalent in general population. Many factors including age, obesity, DM, atherosclerosis, OSA….etc will trigger hypertension and exacerbate disease condition. There are more and more evidences showing that OSA play an independent role in hypertension therapy.OSA with CPAP therapy had been proved to reduce blood pressure in many papers especially in resisted hypertension.
However, during OSA therapy, we found that not all OSA patients with CPAP therapy will achieve the additional goal of blood pressure reduction. Therefore, we hypothesize that there is responder and non-responder in OSA patients with hypertension to CPAP therapy. To clarify the character of responder of OSA patients with hypertension and further investigate the mechanism between OSA and hypertension, we aim to conduct this study:
measure: Hs-CRP
time frame: 6 months
description: Endothelial dysfunction is supposed to be mediated by inflammation process after hypoxia. Hs-CRP is the most sensitive marker to evaluate the inflammation level.
measure: Inflammatory markers
time frame: 6 months
description: Inflammation after hypoxia is suggested to be the pathogenesis of endothelial dysfunction. We will measure the inflammatory markers after treatment.
arm group label: CPAP, Hypertension
arm group type: Experimental
description: evaluate the effect on FMD, blood pressure and inflammation after CPAP on OSA
arm group label: CPAP and statin, Hypertension
arm group type: Active Comparator
description: evaluate the effect on FMD, blood pressure and inflammation after CPAP plus statin on OSA patients
arm group label: OSA, statin, Hypertension
arm group type: Active Comparator
description: evaluate the effect on FMD, blood pressure and inflammation after statin treatment on OSA
arm group label: Placebo
arm group type: No Intervention
description: We will also measure the FMD, blood pressure and inflammation on patients with only life style modification as in all other patients
intervention type: Device
intervention name: CPAP
description: Continuous Positive Airway Pressure is the routine treatment of OSA, patients will be randomly assigned into CPAP treatment group
arm group label: CPAP and statin, Hypertension
arm group label: CPAP, Hypertension
intervention type: Drug
intervention name: Statin
description: Statin is an lipid lowering medication with anti-inflammatory effect.
arm group label: CPAP and statin, Hypertension
arm group label: OSA, statin, Hypertension
other name: rosuvastatin
criteria: 
gender: All
minimum age: 18 Years
maximum age: N/A
healthy volunteers: No
last name: WAN-CHING Ho, M.D.
role: Principal Investigator
affiliation: Taiwan Society of Cardiology
facility: 
country: Taiwan
citation: Luthje L, Andreas S. Obstructive sleep apnea and coronary artery disease. Sleep Med Rev. 2008 Feb;12(1):19-31. doi: 10.1016/j.smrv.2007.08.002. Epub 2007 Nov 1.
PMID: 17936040
citation: Bradley TD, Floras JS. Obstructive sleep apnoea and its cardiovascular consequences. Lancet. 2009 Jan 3;373(9657):82-93. doi: 10.1016/S0140-6736(08)61622-0. Epub 2008 Dec 26.
PMID: 19101028
citation: Atkeson A, Yeh SY, Malhotra A, Jelic S. Endothelial function in obstructive sleep apnea. Prog Cardiovasc Dis. 2009 Mar-Apr;51(5):351-62. doi: 10.1016/j.pcad.2008.08.002.
PMID: 19249441
citation: Jelic S, Padeletti M, Kawut SM, Higgins C, Canfield SM, Onat D, Colombo PC, Basner RC, Factor P, LeJemtel TH. Inflammation, oxidative stress, and repair capacity of the vascular endothelium in obstructive sleep apnea. Circulation. 2008 Apr 29;117(17):2270-8. doi: 10.1161/CIRCULATIONAHA.107.741512. Epub 2008 Apr 14.
PMID: 18413499
citation: Gozal D, Kheirandish-Gozal L. Cardiovascular morbidity in obstructive sleep apnea: oxidative stress, inflammation, and much more. Am J Respir Crit Care Med. 2008 Feb 15;177(4):369-75. doi: 10.1164/rccm.200608-1190PP. Epub 2007 Nov 1.
PMID: 17975198
citation: Gilmartin GS, Tamisier R, Curley M, Weiss JW. Ventilatory, hemodynamic, sympathetic nervous system, and vascular reactivity changes after recurrent nocturnal sustained hypoxia in humans. Am J Physiol Heart Circ Physiol. 2008 Aug;295(2):H778-85. doi: 10.1152/ajpheart.00653.2007. Epub 2008 Jun 6.
PMID: 18539753
citation: Iturriaga R, Rey S, Del Rio R. Cardiovascular and ventilatory acclimatization induced by chronic intermittent hypoxia: a role for the carotid body in the pathophysiology of sleep apnea. Biol Res. 2005;38(4):335-40. doi: 10.4067/s0716-97602005000400004.
PMID: 16579514
citation: Williams B. The year in hypertension. J Am Coll Cardiol. 2008 May 6;51(18):1803-17. doi: 10.1016/j.jacc.2008.03.010. No abstract available.
PMID: 18452788
citation: Campos-Rodriguez F. Screening for sleep apnea in patients with resistant hypertension. Am J Hypertens. 2008 Jul;21(7):728. doi: 10.1038/ajh.2008.193. No abstract available.
PMID: 18584016
citation: Haentjens P, Van Meerhaeghe A, Moscariello A, De Weerdt S, Poppe K, Dupont A, Velkeniers B. The impact of continuous positive airway pressure on blood pressure in patients with obstructive sleep apnea syndrome: evidence from a meta-analysis of placebo-controlled randomized trials. Arch Intern Med. 2007 Apr 23;167(8):757-64. doi: 10.1001/archinte.167.8.757.
PMID: 17452537
citation: Phillips CL, Yee B, Yang Q, Villaneuva AT, Hedner J, Berend N, Grunstein R. Effects of continuous positive airway pressure treatment and withdrawal in patients with obstructive sleep apnea on arterial stiffness and central BP. Chest. 2008 Jul;134(1):94-100. doi: 10.1378/chest.07-3121. Epub 2008 Mar 17.
PMID: 18347202
responsible party type: Sponsor
mesh term: Apnea
mesh term: Sleep Apnea Syndromes
mesh term: Sleep Apnea, Obstructive
mesh term: Rosuvastatin Calcium