Abstract
For some time now the concept of the multifactorial genesis of atherosclerosis has been well accepted. Originally, it was based on the results of large epidemiological studies, which showed a powerful correlation between certain habits of life or metabolic or pathophysiological states, on the one hand, and the probability of contracting an atherosclerotic disease, on the other. The parameters of prognostic value were called risk factors. The 18-year follow-up of the Framingham study confirmed, among other factors; that serum cholesterol is a risk factor in the development of cardiovascular disease. In addition, different risk factors, when present at the same time, potentiate each other to an enormous risk. The coronary risk increases overproportionately with the blood cholesterol level, growing to a life-threatening danger in patients with familial homozygous hypercholesterolemia. An evaluation of the data of the Pooling Project by means of the Framingham HDL-risk-multipliers shows the incidence of fatal or nonfatal myocardial infarction to decrease in men at any concentration of total cholesterol by a factor of 2.5 as HDL-cholesterol increases from less than 40 mg dl-1 to more than 50 mg dl-1. For this reason the atherogenic index LDL-cholesterol/HDL-cholesterol beats the concentration of total cholesterol in estimating the coronary risk. Hyperlipoproteinemia is not only correlated with coronary vascular disease, but also with peripheral arterial acclusion disease (PAOD). In a group of patients with symptomatic PAOD, hyperlipoproteinemia was found in 76% of the patients, which was twice as much as in subjects without PAOD.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Altomonte L, Mingrone G, Negrini A, De Cunto F, Greco AV (1981) Studio a doppio cieco sull’at-tivita terapeutica di un nuovo farmaco ipolipemizzante: L’etofibrato. Clin Ther 96:31–38
Betz E, Hämmerle H (1986) Effect of etofibrate and its metabolites on atheromas of rabbits and on smooth muscle cell cultures. Drug Res 36:92–98
Diehm C (1984) Carbohydrate-metabolism and fat-metabolism in normal persons and patients with peripheral arterial occlusive disease — the consequences of strenuous exercise. VASA J Vasc Dis (Suppl 13):1–61
Ernst E (1986) Hämorheologie und zerebrale Insuffizienz. Therapiewoche 36:2514–2526
Heinrich D, Thilo-Körner DGS, Roka L (1983) Die Bedeutung des Gefäßendothels für die Regulation der Fibrinolyse. Drug Res 33:1375–1378
Hess H, Mietaschik A, Deichsel G (1985) Drug-induced inhibition of platelet function delays progression of peripheral occlusive arterial disease. Lancet 1:415–419
Longenecker GL (1985) The platelets. Physiology and pharmacology. Academic Press, London New York Orlando
Lowe GDO, Drummond MM, Lorimer AR, Hutton I, Forbes CD, Prentice CRM, Barbenel JC (1980) Relation between extent of coronary artery disease and blood viscosity. Br Med J 673:674
Pfeiffer M, Tilsner V (1978) Der Einfluß von Etofibrat auf die Plasmaviskosität bei Hyperlipoprote-inämien. Med Klin 73:60–62
Schatton W, Holm E (1986) Etofibrat bei schweren diätrefraktären Fällen von Hyperlipoprotein-ämie. Fortschr Med 13:281–282
Spöttl F, Forschauer J (1976) Influence of etofibrate on plasma fibrinogen and plasminogen concentrations in patients with different forms of primary hyperlipoproteinemia. Atherosclerosis 25:293–301
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1987 Springer-Verlag Berlin Heidelberg
About this paper
Cite this paper
Seifert, T., Schatton, W. (1987). Effects of Etofibrate on Risk Factors of Atherosclerosis. In: Paoletti, R., Kritchevsky, D., Holmes, W.L. (eds) Drugs Affecting Lipid Metabolism. Proceedings in Life Sciences. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-71702-4_72
Download citation
DOI: https://doi.org/10.1007/978-3-642-71702-4_72
Publisher Name: Springer, Berlin, Heidelberg
Print ISBN: 978-3-642-71704-8
Online ISBN: 978-3-642-71702-4
eBook Packages: Springer Book Archive