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The Second Joint Task Force of European Societies on Coronary Prevention (EAS-European Atherosclerosis Society, ESC-European Society of Cardiology, ESH-European Society of Hypertension) have established recommendations for the prevention of coronary heart disease in cooperation with the representatives of the International Society of Behavioral Medicine, the European Society of General Medicine/Family Medicine, and the European Heart-Network. These recommendations of the year 1998 are commented by Austrian cardiologists and lipidologists and supplemented with recent clinical findings.

Cardiovascular diseases are the major cause of death in European and many other countries. During the last years, our understanding of the risk factors and the possibilities of an effective prevention of coronary heart disease (CHD) has substantially increased. Since patients with established CHD are at a very high risk for a further coronary event, secondary prevention plays a predominant role. Above all, the effectiveness of secondary prevention by lowering LDL cholesterol by statins has been impressively demonstrated by a number of controlled clinical trials. Various international task forces have published recommendations with regard to the cholesterol level indicating intervention and goals of treatment. With the currently available statins these goals can be reached in most cases. Diet is an integral part of overall management. It is important to target also for the intervention of the other risk factors (smoking, physical inactivity, hypertension, diabetes and overweight).

The discovery of leptin, the product of the obese (ob)-gene, has broadened the horizons of research on energy balance. This hormone, produced and secreted by adipose tissue and some placental cells, finds its way to the hypothalamus, where it binds to the leptin receptors and signals satiety through the neuroendocrine axis. The fact that adipose tissue is not merely a storage depot, but also an important endocrine tissue, has revived the interest in the "lipostatic" theory of body fat regulation and has initiated many research efforts in the field of obesity, anorexia nervosa, bulimia, reproduction and haematology.

PHYSIOLOGY: Lipoproteins (LP) are generally classified according to their density. Triglycerides are mainly transported in chylomicrons and very low density LP (VLDL), cholesterol is mainly transported in low density LP (LDL) and high density LP (HDL). The metabolism of LP is controlled by their apolipoproteins, by specific receptors, enzymes, and transfer proteins. Triglycerides and cholesterol from the diet are transported in chylomicrons. The triglycerides are rapidly hydrolyzed by LP-lipase to yield chylomicron remnants. The released free fatty acids are used either for storage in adipose tissue or for oxidation in other tissues. Dietary cholesterol is transported in the chylomicron remnants to the liver. Cholesterol and triglyceride are also synthesized in the liver and then secreted into the blood in the form of VLDL. VLDL triglycerides are metabolized by LP-lipase to intermediate density LP (IDL), which are either taken up by the liver or further catabolized to LDL. LDL are bound and taken up by specific receptors (LDL receptors) in the liver and many other tissues. By this pathway, cholesterol is transported from the liver to peripheral tissues. LDL can be modified by oxidation and then taken up by macrophages in the arterial intima resulting in the formation of foam cells, an important step in atherogenesis. HDL play an important role in reverse cholesterol transport (transport of cholesterol back to the liver, the only site of cholesterol excretion).Various mutations in the LP-lipase gene or in the apo C-II gene result in LP-lipase deficiency. Homozygous carriers of the mutated gene show defective metabolism of chylomicrons and VLDL with extreme hypertriglyceridemia, eruptive xanthomas, hepatosplenomegaly and recurrent bouts of acute pancreatitis. Many mutations in the LDL receptor gene have been described as the primary cause of familial hypercholesterolemia due to LDL receptor deficiency. LDL receptor deficiency results in the accumulation of LDL in the plasma and deposition of LDL cholesterol in tendons and skin (xanthomas) and arteries (atheromas). In homozygotes, coronary heart disease begins in childhood. Familial defective apo B-100 is caused by a mutation in codon 3500 of the apo B gene. LDL with the mutated apo B is not recognized by the LDL receptor and LDL accumulates in the blood. Mutant forms of apo E (apo E-2 and others) are not bound to the LDL(B,E)-receptor resulting in accumulation of chylomicrons and VLDL remnants (beta-VLDL) and IDL. For the manifestation of type III hyperlipemia, additional genetic, hormonal or environmental factors are involved. Cholesterol deposition in macrophages of the arterial intima and skin gives rise to atherosclerosis of coronary and peripheral arteries and xanthomas. The pathogenesis of familial combined hyperlipemia, the most frequent form of primary hyperlipemias, is multifactorial and has not been clarified in detail.