Abstract
There is clearly more to the pathogenesis of coronary heart disease in all its manifestations than just fatty arteries, but if we assume the validity of the general relation of the disease to atherosclerosis where do we stand with respect to its pathogenesis and prevention? Two strikingly polar attitudes persist on this subject, with much talk from each and little listening between. These I like to call the "academic" and the "pragmatic" views.1 An attempt is made here to characterize these attitudes briefly because they now dominate cardiologic thought and affect diagnostic and therapeutic approaches, as well as cardiovascular researches . . .