ABSTRACT
Despite the remarkable therapeutic progress made during the last 20 years, coronary heart disease (CHD) remains one o f the major causes o f morbidity and mortality in Europe and North America. Myocardial infarction (MI) constitutes a paradigm o f multifactorial disease with complex physiopathology. Its frequency increases with age, varies considerably among populations, and is influenced by a large number o f environmental and hereditary factors. The contribution o f genetic factors to CHD is important, but appears to be stronger on premature than on late-onset forms o f the disease. However, the Swedish Twin Registry study has shown that the impact o f these factors remains fairly important in patients aged 56 to 75 (1), especially in terms of population-attributable risk since most Mis occur in that age range. Con versely, the contribution o f genetic factors to MI occurring after 75 is negligi ble. The evolution o f atherosclerosis, which appears to be a necessary condition for the development o f CHD, depends largely on the effect of environmental factors-in particular, diet with a high content o f saturated fats and cholesterol-and o f genetic factors affecting lipid metabolism. The devel opment o f atherosclerosis occurs over several decades, but rupture o f the atheroma plaque may considerably accelerate its evolution and eventually lead to acute occlusion o f a coronary artery and MI or sudden death. Thrombosis and vasoconstriction contribute synergistically to the acute complications of
atheroma (2). Interestingly, these processes, as the response o f the vessel wall to injury, which appears to be a major determinant o f atheroma (3), are beneficial under normal circumstances; indeed, in the presence o f a lesion, they normally both contribute to the prompt termination o f the hemorrhage and to the reparation o f the injured area.
