Cholesterol lowering and the vessel wall: new insights and future perspectives.
The basis for most acute coronary events is either rupture or fissuring of unstable atherosclerotic plaques with subsequent thrombosis leading to coronary artery occlusion. The development of atherosclerotic plaques takes several decades, but the mechanical features determining its stability and the risk of rupture can change very rapidly depending on a number of internal factors. Unstable plaques have a large lipid core, a thin overlying fibrous cap and an abundance of inflammatory cells. The most important factor determining the plaque stability is the plasma level of atherogenic LDL particles. Increased levels of these particles cause endothelial dysfunction with impaired vasodilatation capacity and prevalence of vasoconstriction, maintain inflammatory infiltration of the plaque, impair the strength of the fibrous cap and facilitate aggregation and coagulation. Effective lowering of plasma cholesterol by pharmacological and non-pharmacological means can revert most of these processes and increase the plaque's mechanical stability within several hours to days. Lipid lowering therapy can therefore decrease the risk of acute coronary events within a very short space of time. Thus a radical decrease in lipid levels, along with modification of other risk factors, may become the cornerstone for treatment of acute coronary syndromes, in addition to being an effective treatment in primary and secondary prevention of coronary heart disease (CHD).
Stulc
T
T
Third Department of Internal Medicine, First Faculty of Medicine, Charles University, Prague, Czech Republic. tstulc@LF1.cuni.cz
Ceska
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R
D000924:Anticholesteremic Agents / Q000627:therapeutic use; D001161:Arteriosclerosis / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control; D002784:Cholesterol / Q000097:blood*; D003327:Coronary Disease / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control; D003331:Coronary Vessels / Q000473:pathology* / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000503:physiopathology; D006801:Humans; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D008077:Lipoproteins, LDL / Q000097:blood
D000924:Anticholesteremic Agents; D000960:Hypolipidemic Agents; D008077:Lipoproteins, LDL; D002784:Cholesterol