Ignite Creation Date:
2024-05-05 @ 11:56 AM
Last Modification Date:
2024-10-26 @ 9:16 AM
Study NCT ID:
NCT00172419
Status:
COMPLETED
Last Update Posted:
2009-01-05
First Post:
2005-09-12
Brief Title:
The Effects of Atorvastatin on Vulnerable Plaques in Untreated Dyslipidemic Patients
Sponsor:
National Taiwan University Hospital
Organization:
National Taiwan University Hospital
Study Overview
Official Title:
Statin-Induced Vulnerable Plaque Regression After Atorvastatin Treatment Serial Evaluation by 18F-Fluorodeoxyglucose Positron Emission Tomography Study
Status:
COMPLETED
Status Verified Date:
2008-12
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
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 ruptureWe hypothesize that statin-induced plaque regression could be monitored clinically by use of FDG PETCT 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 PETCT 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 PETCT 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 PETCT 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
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 PETCT 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 PETCT 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 PETCT 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 Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None