Lipids and vascular restenosis.

Coronary artery restenosis after angioplasty continues to affect about 30% of patients undergoing this procedure despite extensive efforts to reduce its incidence.3 Recurrent carotid artery stenosis after endarterectomy occurs in about 20% of these arteries, but functional impairment necessitating surgery develops in only a fraction of the cases.4,5 Whereas angioplasty and carotid endarterectomy produce different types of damage to the vessel wall, the reparative response to both kinds of insults is thought to involve an initial proliferation of smooth muscle cells within the intima and, in the case of angioplasty, within gaps in the old atherosclerotic plaques.6'7 This is followed later by deposition of collagen and in some cases lipids within the intima. In most cases, this intimal proliferative response is selflimited, but in a minority of instances the proliferation is more exuberant, resulting in a localized stenosis at that site. Because of the morphological resemblance of these restenoses to early atheromas and because hyperlipidemia is known to stimulate the development of intimal hyperplasia in rabbits,8 it has long been suspected that elevated plasma lipid levels may be involved in vascular restenoses associated with excessive intimal smooth muscle proliferation. The case control study of Colyvas et a12 in this issue of Circulation presents strong evidence that those patients undergoing carotid endarterectomy who develop restenosis of sufficient severity to require reoperative endarterectomy exhibit widespread abnormalities of serum lipids. Elevations of total cholesterol, total triglycerides, and apolipoprotein (apo) B were observed in the 20 patients with restenosis as compared with controls, whereas high density lipoprotein cholesterol (HDL-C) was reduced in patients with restenosis. Multivariant analysis indicated that low density lipoprotein (LDL) apo B and HDL-C were independent predictors of