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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:1950.)
© 2002 American Heart Association, Inc.

Editorials

Oxidized LDL Autoantibodies, Endothelial Dysfunction, and Transplant-Associated Arteriosclerosis

R. Wayne Alexander

From the Department of Medicine, Emory University School of Medicine, Atlanta, Ga.

Correspondence to R. Wayne Alexander, MD, PhD, Department of Medicine, Emory University School of Medicine, EUH H-153, 1364 Clifton Rd NE, Atlanta, Georgia 30322. E-mail ralexan@emory.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

One of the major limitations of cardiac transplantation is the development of transplant coronary arteriopathy or transplant-associated arteriosclerosis that can be associated with progressive coronary artery occlusion.¹ The condition is thought to be immune-mediated and may be related to the expression by the endothelium of the transplanted coronary artery of HLA-DR, which is recognized as foreign by CD4⁺ T-lymphocytes.² The resulting interaction is associated with a chronic, localized inflammatory response.

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One manifestation of transplant-associated arteriosclerosis is reflected in abnormality of the vasodilator function of the endothelium (endothelial dysfunction).³ Endothelium-dependent vasodilation is mediated by several factors generated by endothelial cells, most prominently NO.^4,5 One of the important mechanisms by which endothelial vasodilator function becomes impaired is by the excessive production of reactive oxygen species (ROS) and especially oxygen free radicals (O₂^-).⁴ At appropriate stoichiometry, O₂^- reacts with NO to degrade it, causing the loss of its dilator effect on vascular smooth muscle. This chemistry is particularly relevant to the article in this issue of Arteriosclerosis, Thrombosis, and Vascular Biology by Fang and colleagues⁶ in which they show that in heart transplant patients the extent of acetylcholine-induced, endothelial-dependent coronary artery dilation at one year is inversely related to the blood levels of autoantibodies to oxidized low density lipoprotein (OxLDL). In contrast, there was no correlation between endothelial dysfunction in these patients and levels of either circulating OxLDL or LDL.

Oxidized LDL has been thought to play an important role in the pathogenesis of atherosclerosis since the original observations . . . [Full Text of this Article]