Abstract

It is now possible to modify dramatically risk factors that contribute to atherogenesis as well as morbidity and mortality. This has raised a number of crucial questions, such as how early should risk factor modification be started both before and after clinical presentation of atherosclerosis, and how low should risk factor targets be to obtain the best event reduction. Recent and ongoing clinical studies are starting to provide answers to these questions. Risk factors are known to interact to affect cardiovascular outcome, and recent data in high-risk populations have shown the importance of targeting blood pressure and low-density lipoprotein cholesterol, with increased benefit from lowering levels to below the targets that are currently accepted. In addition to more active treatment of high-risk groups, attention should be directed at the impact of risk factors on atherogenesis and eventual clinical complications in the pre-clinical population. This ‘investment’ component of risk factor modification is largely ignored in current risk reduction strategies. In the individual at average risk, optimal life prolongation without clinical events may require initiation of therapy in middle age (40–45 years) rather than waiting for high absolute risk in older patients. In order to optimize coronary event reduction, a rational approach to risk factor modification must be introduced, which evaluates overall lifetime risks. The best results are obtained by both treatment of high-risk individuals and early treatment of pre-clinical patients in order to modify the evolution of atherosclerosis to clinical disease.

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