Plaque regression - A new target for antiatherosclerotic therapy

Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Cleveland, Ohio
American heart journal (Impact Factor: 4.46). 04/2005; 149(3):384-7. DOI: 10.1016/j.ahj.2004.11.003
Source: PubMed
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    ABSTRACT: Inflammation and oxidative damage play direct roles in coronary artery disease. C-reactive protein (CRP) is currently the best available marker of inflammation, and statins can potentially reduce coronary inflammation. Until now, CRP testing has been somewhat controversial in the context of cardiovascular disease, as has statin treatment specifically to treat inflammation. However, three recent studies showed that early and aggressive treatment with statins reduces future cardiovascular and cerebrovascular events in patients with acute coronary syndromes; another study showed that aggressive statin treatment leads to regression of stable coronary artery disease. In all the studies, the benefit correlated with reductions in CRP.
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    ABSTRACT: Statins do not always decrease coronary heart disease mortality, which was speculated based on increased serum plant sterols observed during statin treatment. To evaluate plant sterol atherogenicity, we fed low density lipoprotein-receptor deficient (LDLr(+/-)) mice for 35 weeks with Western diets (control) alone or enriched with atorvastatin or atorvastatin plus plant sterols or stanols. Atorvastatin decreased serum cholesterol by 22% and lesion area by 57%. Adding plant sterols or stanols to atorvastatin decreased serum cholesterol by 39% and 41%. Cholesterol-standardized serum plant sterol concentrations increased by 4- to 11-fold during sterol plus atorvastatin treatment versus stanol plus atorvastatin treatment. However, lesion size decreased similarly in the sterol plus atorvastatin (-99% vs. control) and the stanol plus atorvastatin (-98%) groups, with comparable serum cholesterol levels, suggesting that increased plant sterol concentrations are not atherogenic. Our second study confirms this conclusion. Compared with lesions after a 33 week atherogenic period, lesion size further increased in controls (+97%) during 12 more weeks on the diet, whereas 12 weeks with the addition of plant sterols or stanols decreased lesion size (66% and 64%). These findings indicate that in LDLr(+/-) mice 1) increased cholesterol-standardized serum plant sterol concentrations are not atherogenic, 2) adding plant sterols/stanols to atorvastatin further inhibits lesion formation, and 3) plant sterols/stanols inhibit the progression or even induce the regression of existing lesions.
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    ABSTRACT: A number of studies using various imaging techniques have demonstrated that intensive lipid lowering with statins can halt or delay the progression of atherosclerosis and even, in some cases, lead to plaque regression. Improvements in atheroma burden with intensive statin therapy appear to be related not just to decreasing low-density lipoprotein cholesterol but also to anti-inflammatory and antiproliferative effects. Clinical trial results also suggest that achieving low-density lipoprotein cholesterol levels even lower than those currently recommended can produce improved clinical outcomes across a range of patient types. Given this body of evidence, it appears appropriate to use intensive statin therapy to treat dyslipidemic patients at high risk for coronary heart disease.
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