I want to express my thanks to Dr Sidney Smith, President of the American Heart Association, for selecting me to present the 1995 Conner Memorial Lecture. I want also to express my admiration for and gratitude to this remarkable organization, the American Heart Association, and its wonderful staff, with whom I have worked for more than 30 years. I have missed very few AHA meetings since 1959 when the American Society for Study of Arteriosclerosis became the American Heart Association Council on Arteriosclerosis. I− indeed all of us− owe a great debt to the AHA for its tireless efforts over the years to support medical research and improve medical care.

I start with the assumption that we can all agree that hypercholesterolemia− particularly hyperbetalipoproteinemia− is an important causative factor in atherogenesis and that correction of it can strikingly reduce the risk of coronary heart disease (CHD). Yet it was not so long ago that this argument had to be vigorously defended. It was only in 1983 that the National Institutes of Health (NIH) officially endorsed the position that hypercholesterolemia must be treated. That decision followed closely on the completion of the landmark Lipid Research Clinic Intervention Trial, initiated by Dr Donald S. Fredrickson and Dr Robert I. Levy and shepherded to completion by Dr Basil Rifkind. 1 The following year I had the privilege of chairing the NIH Consensus Conference on Lowering Blood Cholesterol, 2 which concluded unanimously that there was an unarguable cause-and-effect relationship and that lowering blood cholesterol should be an important national goal. The following year the National Heart, Lung, and Blood Institute (NHLBI) organized and spearheaded the National Cholesterol Education Program (NCEP). Actually this year marks the 10th anniversary of the NCEP, and I think we can again all agree that it has accomplished a great deal under the able directorship of Dr James I. Cleeman and his staff. 3 The introduction of the HMG CoA reductase inhibitors and the astonishing successes with them in recent clinical trials 4 5 has removed any lingering doubts about the efficacy of cholesterol lowering as a means not only of reducing morbidity and mortality from CHD, but also, in some studies, significantly reducing all-cause mortality. And yet, deaths from CHD continue to outnumber deaths from any other single cause in the United States. We still have a long way to go. We will undoubtedly see further decreases in CHD morbidity and mortality when we get better at treating hypercholesterolemia. But will the epidemic of coronary artery disease be wiped out by even the most intensive efforts to lower blood cholesterol levels? I doubt it.