The Effects of Atorvastatin on Vulnerable Plaques in Untreated Dyslipidemic Patients.
|Study Design:||Intervention Model: Single Group Assignment
Masking: Open Label
Primary Purpose: Treatment
|Official Title:||Statin-Induced Vulnerable Plaque Regression After Atorvastatin Treatment: Serial Evaluation by 18F-Fluorodeoxyglucose Positron Emission Tomography Study|
- Plaque location and activity at baseline, and compare with the follow-up scans site by site. [ Time Frame: 12 w ]
- Lipid profile [ Time Frame: 12 w ]
- Biomarkers [ Time Frame: 12 w ]
|Study Start Date:||March 2007|
|Study Completion Date:||December 2008|
|Primary Completion Date:||December 2008 (Final data collection date for primary outcome measure)|
Atorvastatin, 40 mg/day for 12 weeks
Other Name: Atorvastatin (Lipitor, 40mg)
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.
Please refer to this study by its ClinicalTrials.gov identifier: NCT00172419
|National Taiwan University Hospital|
|Taipei, Taiwan, 10012|
|Principal Investigator:||Wei-Shiung Yang, MD, phD||Department of Internal Medicine, National Taiwan University Hospital|