The Effects of Atorvastatin on Vulnerable Plaques in Untreated Dyslipidemic Patients.
Condition: Hyperlipidemia
MeSH terms: Hyperlipidemias
Study type: Interventional

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.
    

Intervention name(s): Atorvastatin
Intervention type(s): Drug
Intervention description(s): Atorvastatin, 40 mg/day for 12 weeks
Other intervention name(s): Atorvastatin (Lipitor, 40mg)
Intervention MeSH terms: Atorvastatin
Intervention model: Single Group Assignment
Masking: None (Open Label)
Primary purpose: Treatment
Keywords: statin, inflammation, FDG, positron emission tomography