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(Circulation. 1999;99:1922-1926.)
© 1999 American Heart Association, Inc.

Correspondence

Hypercholesterolemia, Abnormal Coronary Vasomotion, and Calcium Antagonists

David S. David, MD, FACP,

Clinical Professor of Medicine, UCLA School of Medicine, Los Angeles, Calif

To the Editor:

I was fascinated by the recent article by Kaufmann et al¹ on the reversal by calcium antagonists of the abnormal coronary vasomotion associated with hypercholesterolemia. Teleologically, this observation is quite logical, and it also explains some of the clinical observations made about coronary artery disease. Let me explain.

Studies in experimental animals have shown that the entry of cholesterol into the endothelial lining of the aorta is dependent on the concentration of cholesterol in the perfusing solution, the pulse pressure, and the number of pulses per minute.² These very early abnormalities are noted at the ultrastructural level well before there is any grossly visible modification of the vessel wall (such as the fatty streak). Because the initial injury that starts the long process of formation of the atherosclerotic plaque is very dependent on cholesterol entry into the endothelial cells, it is teleologically reasonable that the greater the level of serum cholesterol, the more the normal increase in pulse pressure with exercise should be constrained.

Also, it is now well accepted that the higher the serum cholesterol level, the greater the development of soft plaques that are more easily ruptured or fissured. Thus, it makes sense that with the higher serum cholesterol, the greater decrease in pulse pressure with exercise would in part protect against such sudden acute events in hypercholesterolemic patients.

There has been a great controversy brewing with regard to the effect of calcium channel blockers on the progression of coronary artery disease. This has especially . . . [Full Text of this Article]

Philipp A. Kaufmann, MD,

Zurich, Switzerland

Otto M. Hess, MD,

Professor of Cardiology Bern, Switzerland