[Calcium antagonists and development of the atheromatous plaque].

Transmembrane movements of calcium are implicated at different stages od the process of formation of the human atheromatous plaque. Calcium antagonist drugs have been shown, in several experimental models and in preliminary clinical trials, to slow the progression of atheromatous lesions. These pharmacodynamic effects could represent one of the mechanisms of the eventual long-term benefits of this pharmacological class. There are many techniques of assessing the atheromatous plaque in vivo but none of them represent a "criterion of substitution" establishing the confirmation of a therapeutic effect of a calcium antagonist drug or any other pharmacological class of drugs. The techniques applicable on a large scale are mainly ultrasonic evaluation of the non-coronary carotid and femoral arteries, providing information on the dimensions of the plaque rather than on its structure. The risk of progression of atheromatous plaques depends more on its structure, its histological and chemical composition, than on its dimensions, at least with regards to coronary lesions. In addition, the influence of treatment of atheromatous plaques of large arteries is not always representative of its effect on coronary lesions which are smaller and are submitted to very different conditions of perfusion. Only long-term studies of morbidity and mortality on large populations may demonstrate a beneficial effect on the progression of coronary artery disease itself. Techniques of evaluation of the atheromatous plaques have a role to play in ancilliary trials, satellites of these large scale studies of morbidity and mortality, but cannot be accepted as criteria of substitution.