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Lowering low-density lipoprotein (LDL) cholesterol levels has been proven to reduce the incidence of cardiovascular and cerebrovascular events and mortality. So far recommendations have not provided information as to a meaningful duration of cholesterol-lowering therapy and were largely guided by economic constraints and limited therapeutic options. In light of the decline in the price of statins, the essential therapeutic agent and the increased efficacy of therapeutic options, treatment can nowadays be geared to target values that can be expected to have an optimal effect even in old age. The most favorable level of LDL-cholesterol for primary prevention is around and below 100 mg/dl, provided continuous adherence to these low levels from adolescence onwards. With later onset of cholesterol reduction the existence of initial atheromatous deposits must be expected. Therefore, with age and the manifestation of other risk factors the optimal treatment targets increasingly converge to those for which experience has been gained from secondary prevention. Both measurements of the effect of cholesterol lowering on the volume of atheromatous plaques and of the incidence of vascular events indicate a target for LDL-cholesterol well below 70 mg/dl and in the range 50-60 mg/dl. At the onset of cholesterol lowering in advanced age, a smaller effect has to be expected but due to the increasing incidence rate of vascular events a higher number of events may be avoided; thus, the efficiency does not necessarily decrease; however, long-term studies indicate that earlier cholesterol lowering provides an advantage for more than a decade, in terms of preventing vascular disease, which tends to increase. Therefore, optimal cardiovascular prevention involves moderate measures to maintain the LDL-cholesterol below 100 mg/dl lifelong from childhood on.

In all patients with coronary heart disease a fasting lipid profile (total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides) should be obtained. Hyperlipidemias can then be classified as hypercholesterolemia (LDL cholesterol elevated), mixed hyperlipidemia (LDL cholesterol elevated, triglycerides elevated) and hypertriglyceridemia (triglycerides elevated). Primary goal of lipid intervention is a LDL cholesterol < 100 mg/dl, secondary goals are HDL cholesterol > 35 mg/dl and triglycerides < 200 mg/dl. These goals can be reached by dietary intervention alone (reduction in fat and modification of fat intake) or in combination with lipid lowering drugs. Monotherapy with HMG-CoA reductase inhibitors or combined therapy with bile acid sequestrants will allow a reduction in LDL cholesterol by more than 50%; in predominant hypertriglyceridemia fibrates or nicotinic acid will lower triglycerides and elevate HDL cholesterol.

Coronary artery disease has still a grave prognosis. More than half the patients die within 24 hours, mostly before reaching a hospital. A minority survives the first year. Only more intense prevention will change this. Primary prevention in a narrow sense refers to the prevention of the development of early lesions in the youth and as such is a responsibility of the education towards a healthy lifestyle. In our population a majority of middle-aged is likely to have developed arteriosclerosis, so that we deal only with clinically defined primary prevention even though they are asymptomatic. The outstanding effects of lipid therapy in patients at risk for coronary heart disease will primarily result from avoiding the development of instable plaques. Reduction of LDL-cholesterol and increase of HDL-cholesterol is most effective in patients with proven coronary artery disease. Evidently the majority of coronary events can be prevented by idealizing the lipid parameters. In contrast, the chronic coronary syndrome is the domain of the interventional cardiology. Lipid therapy will lead only gradually to a reduction of significant coronary stenoses. However, there is the still insufficiently investigated potential of improving the endothelial dysfunction by correcting the lipid metabolism to reduce angina.