Working…
ClinicalTrials.gov
ClinicalTrials.gov Menu
Trial record 1 of 1 for:    NCT00172419
Previous Study | Return to List | Next Study

The Effects of Atorvastatin on Vulnerable Plaques in Untreated Dyslipidemic Patients.

The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details.
 
ClinicalTrials.gov Identifier: NCT00172419
Recruitment Status : Completed
First Posted : September 15, 2005
Last Update Posted : January 5, 2009
Sponsor:
Collaborators:
National Science Council, Taiwan
Pfizer
Information provided by:
National Taiwan University Hospital

Tracking Information
First Submitted Date  ICMJE September 12, 2005
First Posted Date  ICMJE September 15, 2005
Last Update Posted Date January 5, 2009
Study Start Date  ICMJE March 2007
Actual Primary Completion Date December 2008   (Final data collection date for primary outcome measure)
Current Primary Outcome Measures  ICMJE
 (submitted: January 2, 2009)
Plaque location and activity at baseline, and compare with the follow-up scans site by site. [ Time Frame: 12 w ]
Original Primary Outcome Measures  ICMJE
 (submitted: September 12, 2005)
Plaque location and activity at baseline, and compare with the follow-up scans site by site.
Change History
Current Secondary Outcome Measures  ICMJE
 (submitted: January 2, 2009)
  • Lipid profile [ Time Frame: 12 w ]
  • Biomarkers [ Time Frame: 12 w ]
Original Secondary Outcome Measures  ICMJE
 (submitted: September 12, 2005)
  • 1. Lipid profile
  • 2. hs-CRP
Current Other Pre-specified Outcome Measures Not Provided
Original Other Pre-specified Outcome Measures Not Provided
 
Descriptive Information
Brief Title  ICMJE The Effects of Atorvastatin on Vulnerable Plaques in Untreated Dyslipidemic Patients.
Official Title  ICMJE Statin-Induced Vulnerable Plaque Regression After Atorvastatin Treatment: Serial Evaluation by 18F-Fluorodeoxyglucose Positron Emission Tomography Study
Brief Summary Inflammation is important in the both pathogenesis and outcome of atherosclerosis. Plaques containing numerous inflammatory cells, particular macrophages, have a high risk of rupture.We hypothesize that statin-induced plaque regression could be monitored clinically by use of FDG PET/CT approach, and can be detected noninvasively earlier than previously reported.
Detailed Description

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, including conventional X-ray contrast angiography, catheter capable of detecting temperature heterogeneity, infrared light or pH heterogeneity, ultrasonography (including intravascular ultrasound), high-resolution computed tomography and MRI. However, most of them are based on morphologic characteristics of atheroma. Moreover, although statin-induced lipid lowering and clinical benefits may occur in a matter of weeks, stain-mediated plaque volume regression has been measured in terms of years after the initiation of statin therapy. These discrepancies highlight the need for greater insight into the mechanisms and time course of statin-induced plaque regression.

As we know, inflammation may play a significant role in the pathogenesis and progression of atherosclerosis and subsequent vulnerable plaque rupture. Recently, 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET), by use of 18FDG taken up by surrounding macrophages and smooth muscle cells, has been reported to detect atherosclerotic lesions by bio-pathologic functions. More and more evidence showed that FDG uptake is a marker of hypermetabolic state of atheromatous plaques, which is related to dense cellular infiltrate, and contributes to the identification of a subgroup of patients at high risk of complications. Recently, a combined PET/CT is emerged as a promising modality and is now beginning to be used more routinely in clinical situation, providing better localization and detecting calcification at the same time. Therefore, the use of FDG PET/CT might be a more sensitive and quantification method to monitor the inflammatory activity of vulnerable plaque after aggressive statin treatment. It could also provide the mechanism of early beneficial effects of statin treatment.

Our subject is to investigate prospectively the statin effects of lipid lowering and anti-inflammatory on human atherosclerotic lesions. We hypothesize that statin-induced plaque regression could be monitored clinically by use of FDG PET/CT approach, and can be detected noninvasively earlier than previously reported, and providing information of early statin efficacy caused by stabilization of vulnerable plaque without affecting the lumen size.

Study Type  ICMJE Interventional
Study Phase  ICMJE Not Applicable
Study Design  ICMJE Allocation: N/A
Intervention Model: Single Group Assignment
Masking: None (Open Label)
Primary Purpose: Treatment
Condition  ICMJE Hyperlipidemia
Intervention  ICMJE Drug: Atorvastatin
Atorvastatin, 40 mg/day for 12 weeks
Other Name: Atorvastatin (Lipitor, 40mg)
Study Arms  ICMJE Experimental: Atorvastatin
Intervention: Drug: Atorvastatin
Publications * Chang YY, Wu YW, Lee JK, Lin YM, Lin YT, Kao HL, Hung CS, Lin HJ, Lin YH. Effects of 12 weeks of atorvastatin therapy on myocardial fibrosis and circulating fibrosis biomarkers in statin-naïve patients with hypertension with atherosclerosis. J Investig Med. 2016 Oct;64(7):1194-9. doi: 10.1136/jim-2016-000092. Epub 2016 Jul 18.

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Recruitment Information
Recruitment Status  ICMJE Completed
Actual Enrollment  ICMJE
 (submitted: January 2, 2009)
43
Original Enrollment  ICMJE
 (submitted: September 12, 2005)
60
Actual Study Completion Date  ICMJE December 2008
Actual Primary Completion Date December 2008   (Final data collection date for primary outcome measure)
Eligibility Criteria  ICMJE Inclusion Criteria: Untreated dyslipidemic (LDL cholesterol >110 mg/dl) subjects with documented atherosclerosis in at least 1 vascular territory: at least moderate (≧4.0mm) aortic atherosclerosis by transesophageal echocardiography or CT/MRI, angiographically documented with coronary artery stenosis (≧50% luminal stenosis), ultrasonographically documented significant extracranial arterial stenosis (≧50%), history of ischemic stroke and transient ischemic attack (TIA), or documented peripheral vascular disease. Exclusion Criteria: Acute illness,infection, inflammation or major systemic diseases, T-Bil >3 mg/dl, or Creatinine >3 mg/dl.
Sex/Gender  ICMJE
Sexes Eligible for Study: All
Ages  ICMJE 30 Years to 80 Years   (Adult, Older Adult)
Accepts Healthy Volunteers  ICMJE No
Contacts  ICMJE Contact information is only displayed when the study is recruiting subjects
Listed Location Countries  ICMJE Taiwan
Removed Location Countries  
 
Administrative Information
NCT Number  ICMJE NCT00172419
Other Study ID Numbers  ICMJE 931204
Has Data Monitoring Committee No
U.S. FDA-regulated Product Not Provided
IPD Sharing Statement  ICMJE Not Provided
Responsible Party Wei-Shiung Yang, National Taiwan University Hospital
Study Sponsor  ICMJE National Taiwan University Hospital
Collaborators  ICMJE
  • National Science Council, Taiwan
  • Pfizer
Investigators  ICMJE
Principal Investigator: Wei-Shiung Yang, MD, phD Department of Internal Medicine, National Taiwan University Hospital
PRS Account National Taiwan University Hospital
Verification Date December 2008

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