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. Identifier: NCT00172419
Recruitment Status : Completed
First Posted : September 15, 2005
Last Update Posted : January 5, 2009
National Science Council, Taiwan
Information provided by:
National Taiwan University Hospital

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.

Condition or disease Intervention/treatment Phase
Hyperlipidemia Drug: Atorvastatin Not Applicable

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 : Interventional  (Clinical Trial)
Actual Enrollment : 43 participants
Intervention Model: Single Group Assignment
Masking: None (Open Label)
Primary Purpose: Treatment
Official Title: Statin-Induced Vulnerable Plaque Regression After Atorvastatin Treatment: Serial Evaluation by 18F-Fluorodeoxyglucose Positron Emission Tomography Study
Study Start Date : March 2007
Actual Primary Completion Date : December 2008
Actual Study Completion Date : December 2008

Resource links provided by the National Library of Medicine

Arm Intervention/treatment
Experimental: Atorvastatin Drug: Atorvastatin
Atorvastatin, 40 mg/day for 12 weeks
Other Name: Atorvastatin (Lipitor, 40mg)

Primary Outcome Measures :
  1. Plaque location and activity at baseline, and compare with the follow-up scans site by site. [ Time Frame: 12 w ]

Secondary Outcome Measures :
  1. Lipid profile [ Time Frame: 12 w ]
  2. Biomarkers [ Time Frame: 12 w ]

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Ages Eligible for Study:   30 Years to 80 Years   (Adult, Older Adult)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   No
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.

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To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.

Please refer to this study by its identifier (NCT number): NCT00172419

National Taiwan University Hospital
Taipei, Taiwan, 10012
Sponsors and Collaborators
National Taiwan University Hospital
National Science Council, Taiwan
Principal Investigator: Wei-Shiung Yang, MD, phD Department of Internal Medicine, National Taiwan University Hospital

Publications automatically indexed to this study by Identifier (NCT Number):
Responsible Party: Wei-Shiung Yang, National Taiwan University Hospital Identifier: NCT00172419     History of Changes
Other Study ID Numbers: 931204
First Posted: September 15, 2005    Key Record Dates
Last Update Posted: January 5, 2009
Last Verified: December 2008

Keywords provided by National Taiwan University Hospital:
statin, inflammation, FDG, positron emission tomography

Additional relevant MeSH terms:
Lipid Metabolism Disorders
Metabolic Diseases
Atorvastatin Calcium
Anticholesteremic Agents
Hypolipidemic Agents
Molecular Mechanisms of Pharmacological Action
Lipid Regulating Agents
Hydroxymethylglutaryl-CoA Reductase Inhibitors
Enzyme Inhibitors