The European Society of Cardiology
Non-high-density lipoprotein cholesterol as a risk factor: addressing risk associated with apolipoprotein B-containing lipoproteins
a Hôpital de la Pitiè, Paris, France
b Institute of Pathological Biochemistry, Glasgow, UK
* M. John Chapman, PhD, DSc, Pavillon Benjamin Delassert, INSERM Unite 321, Hôpital de la Pitiè, 83 Boulevard de l’hôpital, Paris Cedex 13 75651, France. Tel: +33-142177878; fax: +33-145828198
chapman{at}infobiogen.fr
Abstract
There is increasing interest in the use of non-high-density lipoprotein (non-HDL-C) cholesterol as a marker of coronary heart disease risk. Non-HDL-C provides a measure of all apolipoprotein B-containing lipoproteins, including very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), LDL (including small, dense LDL) and lipoprotein(a), all of which have the potential to deliver cholesterol into the arterial wall. This measure thus reflects atherogenic risk not captured by low-density lipoprotein cholesterol (LDL-C) measurement alone, particularly in the context of elevated triglycerides – a setting in which there are increased concentrations of VLDL and atherogenic VLDL remnants. In patients requiring lipid-lowering therapy, non-HDL-C is currently recommended for use as a secondary outcome measure, after LDL-C, in patients with elevated triglycerides. Statins are the most effective agents for reducing levels of atherogenic lipoproteins. Consistent with its distinct pharmacologic properties compared with earlier members of the statin class, rosuvastatin reduces LDL-C significantly more than other statins and produces marked attenuation in atherogenic lipid profiles at a low dose across a wide range of dyslipidaemic phenotypes and patient subpopulations. A recent randomised, double-blind, crossover trial assessed the effects of rosuvastatin 40 mg in hypercholesterolaemic patients with normal triglyceride levels (type IIa dyslipidaemia) or elevated triglyceride levels (type IIb dyslipidaemia). In hypertriglyceridaemic patients, rosuvastatin reduced VLDL1 by 46%, VLDL2 by 42%, IDL by 54%, LDL by 58% and small, dense LDL by 69%. In normotriglyceridaemic patients, who have lower VLDL and remnant concentrations, rosuvastatin reduced VLDL1 by 18%, VLDL2 by 26%, IDL by 57%, LDL by 52% and small, dense LDL by 44%. Rosuvastatin thus has the ability to correct substantially the atherogenic lipoprotein profile across a wide range of phenotypes even when elevated concentrations of atherogenic lipoproteins are present as VLDL.
Key Words: Non-high-density lipoprotein cholesterol • Coronary heart disease • Low-density lipoprotein • Hypercholesterolaemia • Atherogenic risk • Statins
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