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J M Lee and R P Choudhury (2006)

Prospects for atherosclerosis regression: HDL elevation and other emerging therapeutic technologies.

Heart.

In a process that has often been seen as progressive and irreversible, deposition and retention of lipoproteins, and the consequent inflammatory reaction, results in the accumulation of atherosclerotic plaque from an early age. Several large primary and secondary prevention trials have established the value of low density lipoprotein- cholesterol (LDL-C) reduction with statin therapy ,[1] though this probably prevents no more than 30% of all cardiovascular events and plaque regression appears to be relatively modest.[2] By contrast high density lipoprotein cholesterol (HDL-C) is well recognised as an important and independent protective factor,[3] though treatments designed to elevate HDL-C have, until now, been relatively few. Proof of principle for atherosclerosis regression is provided by the striking degree observed in response to potent interventions in experimental models. Regression is often accompanied by qualitative changes that would suggest plaque stabilization. In addition to HDL-C elevation, new appreciation of mechanisms of cellular lipid homeostasis and regulation of gene transcription has revealed novel targets for atherosclerosis treatment. This review will consider emerging approaches to plaque regression and some parallel developments in imaging technology that will improve our appreciation of response to treatment and potentially guide individual patient- tailored therapy.
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