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