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The endotoxin-lipoprotein hypothesis

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Creators Name:Rauchhaus, M. and Coats, A.J.S. and Anker, S.D.
Journal Title:Lancet
Journal Abbreviation:Lancet
Volume:356
Number:9233
Page Range:930-933
Date:9 September 2000
Keywords:Anticholesteremic Agents, Cholesterol, Congestive Heart Failure, Endotoxins, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Hypercholesterolemia, Lipopolysaccharides, Protective Agents, Protein Binding, Simvastatin, Animals
Abstract:The advent of 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins) has revolutionised the treatment of hypercholesterolaemia. Statin treatment, by lowering the atherogenic lipoprotein profile, reduces morbidity and mortality in patients with cardiovascular disease. Treatment with simvastatin causes a reduction of events of new-onset heart failure, but this may be attributable to properties other than its lipid-lowering effects. There is some evidence that lower serum cholesterol concentrations (as a surrogate for the totality of lipoproteins) relate to impaired survival in patients with chronic heart failure (CHF). Inflammation is a feature in patients with CHF and increased lipopolysaccharide may contribute substantially. We postulate that higher concentrations of total cholesterol are beneficial in these patients. This is potentially attributable to the property of lipoproteins to bind lipopolysaccharide, thereby preventing its detrimental effects. We hypothesise there is an optimum lipoprotein concentration below which lipid reduction would, on balance, be detrimental. We also propose that, in patients with CHF, a non-lipid-lowering statin (with anciilary properties such as immune modulatory and anti-inflammatory actions) could be as effective or even more beneficial than a lipid-lowering statin.
ISSN:0140-6736
Publisher:Lancet (U.K.)
Item Type:Article

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