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The role of dyslipidaemia in coronary heart disease

Consultant Chemical Pathologist, St Thoma's Hospital, Lambeth Palace Road, London, SE1 7EH, UK, Anthony.Wierzbicki{at}kcl.ac.uk

The role of cholesterol in cardiovascular disease (CVD) and especially coronary heart disease (CHD) is well established. Epidemiological studies show consistent relationships between total cholesterol, low-density lipoprotein cholesterol (LDL-C) and CHD risk. These same studies show a strong inverse relationship for levels of high-density lipoprotein cholesterol (HDL-C) and CHD risk and a possible relationship for triglycerides.

The metabolic syndrome is a common syndrome affecting 20—25% of the population whose features include abdominal obesity, low-HDL-C, elevated triglycerides, hypertension, hyperglycaemia, hyperinsulinaemia, elevated inflammatory markers, renal dysfunction and microalbuminuria. In the UKPDS study in type 2 diabetes that compared the effects of improved glycaemic and blood pressure control, though some benefit was seen on cardiovascular end points with tighter control, the critical factors predisposing to later macrovascular disease were LDL-C and HDL-C.

There is extensive trial evidence for the benefits of statins in secondary and primary prevention. All guidelines state these are first-line agents for the treatment of cardiovascular risk. Statins have undoubted benefits in the treatment of patients with type 2 diabetes. Statins are also effective in reducing CVD in patients with metabolic syndrome. However, the focus on the benefits of statin therapy has limited discussion of their limitations. In all statin trials to date they reduce CVD events by 25—30% with the largest reduction in the GREACE study being 50%. Only high-dose statin therapy prevents progression of atherosclerosis. Thus, a single minded concentration on LDL-C may underestimate the benefits of a more integrated approach to the management of hyperlipidaemia.

Key Words: coronary heart disease • cholesterol • HDL-cholesterol • diabetes • risk.

The British Journal of Diabetes & Vascular Disease, Vol. 5, No. 1 suppl, S2-S6 (2005)
DOI: 10.1177/14746514050050010201


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