Abstract
Atherosclerosis is a disease of the walls of the aorta and the large arteries. Although there is evidence that this disease begins early in life, clinical symptoms of atherosclerosis do not usually occur until over half of the lumen becomes occluded by plaque, typically in the fifth and sixth decades1. Most epidemiological and genetic observations of atherosclerotic disease have used clinical disease manifestations as the end points. Coronary heart disease (CHD), because it is a significant contributor to morbidity and mortality in many countries and is the leading cause of death in North America and most countries of central and western Europe, has received the greatest attention2. The study of familial clustering of CHD as a risk factor for the disease gained its popularity, not due to the simple fact that aggregation of CHD indeed occurs in families, but, in the way this clustering has been interpreted. MacMahon3 has stated: ‘Every disease of which I can conceive and, for that matter, every human trait — has been shown to occur more frequently in the siblings of affected individuals than in the population at large, or can, on theoretical grounds, be expected to show this feature if sufficient and appropriate data were collected.’ The burgeoning interest in familial aggregation of CHD relates, first, to whether findings support the view that this aggregation may well be explained solely by genetic factors, or also by environmental factors which are communicated rather than inherited.
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© 1994 Springer Science+Business Media Dordrecht
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Friedlander, Y. (1994). Familial Clustering of Coronary Heart Disease: A Review of its Significance and Role as a Risk Factor for the Disease. In: Goldbourt, U., de Faire, U., Berg, K. (eds) Genetic factors in coronary heart disease. Developments in Cardiovascular Medicine, vol 156. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-1130-0_3
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DOI: https://doi.org/10.1007/978-94-011-1130-0_3
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