Carotid Atherosclerosis Progression and ACAT Inhibition
- Paolo Parini, MD, PhD paolo.parini@ki.seDepartment of Laboratory Medicine;
- Mats Eriksson, MD, PhDDepartment of MedicineKarolinska InstitutetStockholm, Sweden;
- Lawrence L. Rudel, PhDDepartment of PathologyWake Forest University School of MedicineWinston-Salem, North Carolina
Since this article does not have an abstract, we have provided the first 150 words of the full text.
- KEYWORDS:
- ACAT1 PROTEIN, HUMAN
- ACYLTRANSFERASES
- ATHEROSCLEROSIS
- CAROTID ARTERY DISEASES
- CHOLESTEROL, LDL
- DISEASE PROGRESSION
- DRUG THERAPY
- EZETIMIBE
- HYDROXYMETHYLGLUTARYL-COA REDUCTASE INHIBITORS
- HYPERLIPIDEMIAS
- PACTIMIBE
- STEROL O-ACYLTRANSFERASE
To the Editor: Dr Meuwese and colleagues1 presented results of the Carotid Atherosclerosis Progression Trial Investigating Vascular ACAT Inhibition Treatment Effects (CAPTIVATE). In this study, patients who were heterozygous for familial hypercholesterolemia were randomized to receive either pactimibe (a nonspecific acyl coenzyme A:cholesterol acyltransferase [ACAT] inhibitor) or placebo, in addition to standard lipid-lowering therapy. Consistent with data from macrophage ACAT1 knockout mice, treatment with a nonspecific ACAT inhibitor may not result in apparent positive effects on atherosclerosis.2
Although the authors did not provide evidence that either ACAT-1 or ACAT-2 was inhibited by the treatment regimen in this study, they discussed the possibility that the pactimibe treatment was accessing both ACAT enzymes. It is likely that any effect on thickness of the artery wall (where ACAT-1 resides2) would be related to ACAT-1 inhibition. However, the discussion focused on ACAT-2. It was suggested that ACAT-2 might be up-regulated in …
