Can we reverse or retard an obstructive coronary lesion by risk factor intervention?
There is general agreement that an association exists between certain risk factors and the occurrence of arteriosclerotic heart disease. Numerous intervention trials have been aimed at reducing these risks in the hope that if applied they will provide primary prevention or a secondary treatment which may retard or reverse obstructive lesions. However, recent reports cast doubt on possible benefits of such interventions except possibly in the case of treatment of florid lipid problems or abstinence from tobacco.1–3 New critiques point out that previous clinical trials alleged to reverse the obstructive process suffer from poor design, lack of randomization, inadequate numbers, and have other serious methodologic shortcomings.3
In 1972 a Blue Ribbon Task Force of the National Heart and Lung Institute evaluated the currently available information on arteriosclerosis and formulated recommendations for long-range programs.4 It implied that we do not understand the basic mechanisms or pathogenesis underlying development of the arteriosclerotic lesions, nor how various risk factors bring about development of clinical disease. It particularly noted that single risk factor interventions have failed, but it was hoped that because hypertension, tobacco, and diet particularly stood out statistically as being associated with higher risk, control of all three at one time stood a better chance of affecting the arteriosclerotic process.
In considering the effect of lower lipids, it appears that (1) dietary trials have failed to prove that low lipid diets, as a general health measure, can prevent arteriosclerotic heart disease in man; (2) although countless studies have proved the effectiveness . . .