No abstract

Lowering serum lipid levels prevents myocardial infarctions. But are we targeting the right lipoproteins in our preventive therapy? Are we getting the maximum benefit? Triglycerides certainly deserve more attention than they have yet received. Most of the trials of lipid-lowering therapy have ignored them and this omission may explain the divergence between the fall in morbidity predicted from the epidemiological evidence and the reductions observed in the clinical trials. The evidence that the statins reduce coronary morbidity and mortality, and that this reduction is associated with a fall in LDL cholesterol, is overwhelming. But the potential value of the statins may be limited by their relative inability to increase the concentration of cardioprotective HDL. The fibrates, either alone, or in combination with a statin, retain a central role in the management of patients with mixed hyperlipidaemia who are undoubtedly at high risk of premature coronary artery disease.

SUMMARYThe availability of treatment guidelines has revolutionised our approach to detection, evaluation and treatment of dyslipidaemias in adults. Such guidelines focus on lowering low‐density lipoprotein‐cholesterol (LDL‐C), the primary risk factor for coronary heart disease, and provide physicians with specific goals to be attained by dietary and, if necessary, pharmacological therapy. However, the guidelines were published in 1993, which means that the pivotal findings from large intervention trials with statins were not included. This has led to calls for the guidelines to be amended to take into account the findings of these studies and other evolving issues such as the pathogenesis of the acute coronary event and the contribution of low HDL‐C and other lipid parameters. More importantly, the mostly epidemiological basis of the guidelines has instilled the concept that the lower the LDL‐C level after lipid‐lowering intervention the better the result in terms of prevention of coronary events. Available data now refute this assumption. Indeed, maximal therapeutic benefit is already obtained with a decrease in LDL‐C level of 20‐30%, irrespective of baseline levels or LDL‐C levels on treatment and, until now, there have been no data to suggest that decreases in LDL‐C of >30% give any additional benefit to patients in terms of improving their long‐term outcome. The concept of absolute LDL‐C treatment goals therefore needs to be revisited. A more appropriate goal of lipid‐lowering therapy with statins is to ensure LDL‐C levels are reduced by 20‐30%, with statin dosages as used in the intervention trials. Furthermore, there are insufficient data to advise that LDL‐C levels should be lowered to 2.6 mmol/l. This issue will be resolved only when the results of the appropriate intervention trials are published. (Int J Clin Pract 2000; 54(5): 307‐313)