The Impact of Rosiglitazone on Regression of Atherosclerosis

This study has suspended participant recruitment.
(no fund)
Sponsor:
Collaborator:
National Science Council, Taiwan
Information provided by:
National Taiwan University Hospital
ClinicalTrials.gov Identifier:
NCT00166803
First received: September 11, 2005
Last updated: January 2, 2009
Last verified: December 2008

September 11, 2005
January 2, 2009
June 2005
November 2008   (final data collection date for primary outcome measure)
Vulnerable plaque analyses by PET: Define plaque location and activity at baseline, and compare with the follow-up scans site by site. [ Time Frame: 12 w ] [ Designated as safety issue: Yes ]
Vulnerable plaque analyses by PET: Define plaque location and activity at baseline, and compare with the follow-up scans site by site.
Complete list of historical versions of study NCT00166803 on ClinicalTrials.gov Archive Site
  • 1.Glycemic control after active treatment. (Fasting glucose level, HbA1c) [ Time Frame: 12 w ] [ Designated as safety issue: Yes ]
  • 2.Biomarkers:hs-CRP, MMP-1, MCP-1. [ Time Frame: 12 w ] [ Designated as safety issue: Yes ]
  • 1.Glycemic control after active treatment. (Fasting glucose level, HbA1c)
  • 2.Biomarkers:hs-CRP, MMP-1, MCP-1.
Not Provided
Not Provided
 
The Impact of Rosiglitazone on Regression of Atherosclerosis
The Impact of Rosiglitazone on Regression of Atherosclerosis: A Serial 18F-Fluorodeoxyglucose Positron Emission Tomography Study

Cardiovascular events are the leading cause of death in developed countries worldwide, including Taiwan. The disruption of atherosclerotic plaques and the subsequent formation of thrombi are currently recognized as the major cause of morbidity and mortality of cardiovascular diseases. Therefore, early detection of vulnerable plaques is clinically important for risk stratification and also to provide early treatment. Several imaging approaches have been adapted to detect vulnerable plaques, however, most of them are based on morphologic characteristics of atheroma. We hypothesize that PPARγ-induced plaque regression could be monitored clinically by use of 18FDG PET/CT approach, which could assess the inflammatory activity, and can be detected noninvasively earlier than previously reported.

The early detection of vulnerable plaques is clinically important for risk stratification and also to provide early treatment.Inflammation is important in the both pathogenesis and outcome of atherosclerosis. Plaques containing numerous inflammatory cells, particular macrophages, have a high risk of rupture. Diabetes is a major risk factor for the development of atherosclerosis. The discovery of the peroxisome proliferator-activated receptor γ (PPARγ) gene led to the hope of favorably influencing the insulin resistance syndrome. The administration of PPARγ agonists have been shown to reduce insulin resistance, to reduce the expression of leptin, to lower plasma free fatty acid level and to lower blood pressure. Moreover, beyond the glucose effect, PPARγ agonists may theoretically affect atherosclerosis also through the inhibition of inflammatory cytokines secreted from the macrophage, such as IL-6, IL-1β, TNF-α, etc. These evidences highlight the possibility of PPARγ agonists could be have great impact on plaque regression.

18FDG is a glucose analogue that is taken up by cells in proportion to their metabolic activity. Several papers have reported the potential roles of metabolic imaging in the assessment of inflammatory vascular diseases, especially in large vessels. However, PET has limited spatial resolution. Recently, a combined PET/CT is emerged as a promising modality which could provide both anatomical and functional information. We hypothesize that PPARγ agonists-induced plaque regression could be monitored clinically by use of 18FDG PET/CT approach, and providing information of early efficacy PPARγ treatment caused by stabilization of vulnerable plaque without affecting the lumen size.

Interventional
Not Provided
Allocation: Randomized
Endpoint Classification: Efficacy Study
Intervention Model: Parallel Assignment
Masking: Open Label
Primary Purpose: Treatment
Diabetes Mellitus, Atherosclerosis
Drug: Rosiglitazone
Rosiglitazone , 4 mg daily
Not Provided
Not Provided

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Suspended
60
Not Provided
November 2008   (final data collection date for primary outcome measure)

Inclusion Criteria:

  1. Type II DM patients who are aged 50 to 80 year-old with HbA1c between 7.0 to 10.0 %
  2. Under ≤ 2 kinds of anti-diabetic drugs.

Exclusion Criteria:

  1. Insulin use
  2. Patients who receive any PPARγ agonist in recent one year.
  3. Women of child-bearing potential are excluded (i.e. menopausal women or post-hysterectomy women are included in this study) due to radiation exposure in this study.
  4. Significant concomitant disease such as active infection, malignancy, hepatic or renal dysfunction at the time of enrollment (i.e. T-Bil > 3 mg/dl,ALT > 2.5 times the upper limit of normal range and Creatinine > 3 mg/dl in our hospital).
Both
50 Years to 80 Years
No
Contact information is only displayed when the study is recruiting subjects
Taiwan
 
NCT00166803
931110
Not Provided
Pan-Chyr Yang, National Taiwan University Hospital
National Taiwan University Hospital
National Science Council, Taiwan
Principal Investigator: Wei-Shiung Yang, MD, phD National Taiwan University Hospital
National Taiwan University Hospital
December 2008

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP