<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/NCT01686269</url>
  </required_header>
  <id_info>
    <org_study_id>FEMH-95-C-018</org_study_id>
    <nct_id>NCT01686269</nct_id>
  </id_info>
  <brief_title>Endothelial Progenitor Cells</brief_title>
  <official_title>Mobilization of Endothelial Progenitor Cells in Patients With Coronary Artery Bypass Surgery</official_title>
  <sponsors>
    <lead_sponsor>
      <agency>Far Eastern Memorial Hospital</agency>
      <agency_class>Other</agency_class>
    </lead_sponsor>
  </sponsors>
  <source>Far Eastern Memorial Hospital</source>
  <oversight_info>
    <has_dmc>Yes</has_dmc>
  </oversight_info>
  <brief_summary>
    <textblock>
      Vascular stenosis as a result of neointimal hyperplasia is a major clinical problem that has&#xD;
      an impact on multiple and diverse disciplines, including cardiology (coronary restenosis),&#xD;
      cardiothoracic and vascular surgery (saphenous vein and polytetrafluoroethylene [PTFE] graft&#xD;
      failure), neurology (carotid stenosis), nephrology (dialysis access dysfunction), and&#xD;
      transplant medicine (chronic allograft rejection in hearts and kidneys). [1] In marked&#xD;
      contrast to the deleterious effects of smooth muscle progenitor cells on neointimal&#xD;
      hyperplasia, circulating endothelial progenitor cells (EPCs) are believed to play an&#xD;
      important role in vascular repair and in the inhibition of neointimal hyperplasia. [2]&#xD;
      Endothelial progenitor cells (EPCs) circulate in adult peripheral blood and contribute to&#xD;
      neovascularization. Satoshi et al. have demonstrated that lineage-committed EPCs and&#xD;
      CD34-positive mononuclear cells, their putative precursors, are mobilized during an acute&#xD;
      ischemic event in humans. [3] Reduced levels of circulating EPCs independently predict&#xD;
      atherosclerotic disease progression, thus supporting an important role for endogenous&#xD;
      vascular repair to modulate the clinical course of coronary artery disease. [4] These&#xD;
      observations prompt the hypothesis that circulating EPCs may provide an endogenous repair&#xD;
      mechanism to counteract surgery-induced endothelial cell injury and to replace dysfunctional&#xD;
      endothelium perioperatively. Therefore, the investigators examined whether levels of&#xD;
      circulating EPCs correlate with time course and outcomes of coronary artery bypass surgery to&#xD;
      establish a clinical role of endogenous endothelial repair mediated by circulating EPCs.&#xD;
    </textblock>
  </brief_summary>
  <overall_status>Unknown status</overall_status>
  <last_known_status>Recruiting</last_known_status>
  <start_date>March 2007</start_date>
  <phase>N/A</phase>
  <study_type>Interventional</study_type>
  <has_expanded_access>No</has_expanded_access>
  <study_design_info>
    <allocation>Non-Randomized</allocation>
    <intervention_model>Single Group Assignment</intervention_model>
    <primary_purpose>Diagnostic</primary_purpose>
    <masking>None (Open Label)</masking>
  </study_design_info>
  <enrollment type="Anticipated">50</enrollment>
  <condition>Coronary Artery Disease</condition>
  <intervention>
    <intervention_type>Procedure</intervention_type>
    <intervention_name>blood collecting</intervention_name>
  </intervention>
  <eligibility>
    <criteria>
      <textblock>
        Inclusion Criteria:&#xD;
&#xD;
          -  age from 18 to 85 years&#xD;
&#xD;
          -  signed written informed consent&#xD;
&#xD;
          -  angiographically documented coronary artery disease and indicated for coronary artery&#xD;
             bypass surgery&#xD;
&#xD;
        Exclusion Criteria:&#xD;
&#xD;
          -  clinical or biochemical evidence for the presence of concomitant inflammatory disease&#xD;
&#xD;
          -  chronic renal insufficiency (serum creatinine &gt; 1.4 mmol/L)&#xD;
&#xD;
          -  impaired left ventricular ejection fraction (&lt; 45%)&#xD;
&#xD;
          -  autoimmune or malignant disease&#xD;
&#xD;
          -  thrombocytopenia (&lt; 100 000/L)&#xD;
&#xD;
          -  anemia (hemoglobin &lt; 8.5 g/dL)&#xD;
&#xD;
          -  inability to understand the consent form&#xD;
&#xD;
          -  previous coronary bypass surgery&#xD;
&#xD;
          -  severe peripheral arterial occlusive disease or atrial fibrillation&#xD;
      </textblock>
    </criteria>
    <gender>All</gender>
    <minimum_age>18 Years</minimum_age>
    <maximum_age>85 Years</maximum_age>
    <healthy_volunteers>No</healthy_volunteers>
  </eligibility>
  <overall_official>
    <last_name>Kuan-Ming Chiu, MD</last_name>
    <role>Study Director</role>
    <affiliation>Far Eastern Memorial Hospital</affiliation>
  </overall_official>
  <overall_contact>
    <last_name>Kuan-MIng Chiu, MD</last_name>
    <phone>886-2-89667000</phone>
    <email>kmchius@yahoo.com.tw</email>
  </overall_contact>
  <location>
    <facility>
      <name>Far Eastern Memorial Hospital</name>
      <address>
        <city>Taipei</city>
        <zip>220</zip>
        <country>Taiwan</country>
      </address>
    </facility>
    <status>Recruiting</status>
    <contact>
      <last_name>Kuan-Ming Chiu, MD</last_name>
      <phone>886-2-89667000</phone>
      <email>kmchius@yahoo.com.tw</email>
    </contact>
    <investigator>
      <last_name>Kuan-Ming Chiu, MD</last_name>
      <role>Principal Investigator</role>
    </investigator>
  </location>
  <location_countries>
    <country>Taiwan</country>
  </location_countries>
  <verification_date>January 2007</verification_date>
  <study_first_submitted>February 6, 2009</study_first_submitted>
  <study_first_submitted_qc>September 12, 2012</study_first_submitted_qc>
  <study_first_posted type="Estimate">September 18, 2012</study_first_posted>
  <last_update_submitted>September 12, 2012</last_update_submitted>
  <last_update_submitted_qc>September 12, 2012</last_update_submitted_qc>
  <last_update_posted type="Estimate">September 18, 2012</last_update_posted>
  <keyword>Endothelial progenitor cell</keyword>
  <keyword>coronary artery bypass</keyword>
  <condition_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Coronary Artery Disease</mesh_term>
  </condition_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/NCT01686269
org study id: FEMH-95-C-018
nct id: NCT01686269
lead sponsor: 
has dmc: Yes
Vascular stenosis as a result of neointimal hyperplasia is a major clinical problem that has
      an impact on multiple and diverse disciplines, including cardiology (coronary restenosis),
      cardiothoracic and vascular surgery (saphenous vein and polytetrafluoroethylene [PTFE] graft
      failure), neurology (carotid stenosis), nephrology (dialysis access dysfunction), and
      transplant medicine (chronic allograft rejection in hearts and kidneys). [1] In marked
      contrast to the deleterious effects of smooth muscle progenitor cells on neointimal
      hyperplasia, circulating endothelial progenitor cells (EPCs) are believed to play an
      important role in vascular repair and in the inhibition of neointimal hyperplasia. [2]
      Endothelial progenitor cells (EPCs) circulate in adult peripheral blood and contribute to
      neovascularization. Satoshi et al. have demonstrated that lineage-committed EPCs and
      CD34-positive mononuclear cells, their putative precursors, are mobilized during an acute
      ischemic event in humans. [3] Reduced levels of circulating EPCs independently predict
      atherosclerotic disease progression, thus supporting an important role for endogenous
      vascular repair to modulate the clinical course of coronary artery disease. [4] These
      observations prompt the hypothesis that circulating EPCs may provide an endogenous repair
      mechanism to counteract surgery-induced endothelial cell injury and to replace dysfunctional
      endothelium perioperatively. Therefore, the investigators examined whether levels of
      circulating EPCs correlate with time course and outcomes of coronary artery bypass surgery to
      establish a clinical role of endogenous endothelial repair mediated by circulating EPCs.
allocation: Non-Randomized
intervention model: Single Group Assignment
primary purpose: Diagnostic
masking: None (Open Label)
intervention type: Procedure
intervention name: blood collecting
criteria: 
gender: All
minimum age: 18 Years
maximum age: 85 Years
healthy volunteers: No
last name: Kuan-Ming Chiu, MD
role: Study Director
affiliation: Far Eastern Memorial Hospital
last name: Kuan-MIng Chiu, MD
phone: 886-2-89667000
email: kmchius@yahoo.com.tw
facility: 
status: Recruiting
contact: 
investigator: 
country: Taiwan
mesh term: Coronary Artery Disease