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(Circulation. 2003;107:1237.)
© 2003 American Heart Association, Inc.

Editorial

Allograft Arteriosclerosis and Immune-Driven Angiogenesis

Peter Libby, MD; David Xiao-Ming Zhao, MD

From the Leducq Center of Cardiovascular Research, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass (P.L.); and Division of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tenn (D.X.-M.Z.).

Correspondence to Peter Libby, MD, Brigham and Women’s Hospital, 221 Longwood Ave, Eugene Braunwald Research Center 307, Boston, MA 02115. E-mail plibby@rics.bwh.harvard.edu

Key Words: Editorials • angiogenesis • arteriosclerosis • transplantation • inflammation

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

During most of the last century, the concept of atherosclerosis as a cholesterol storage disease prevailed.¹ By the mid-1980s, it had become clear that in addition to lipid-engorged macrophage foam cells, cells of the adaptive immune response, particularly T lymphocytes, localized in atheromatous lesions.² These observations raised the possibility that immune and inflammatory processes might participate in atherogenesis. However, it remained unclear whether the immune response in atherosclerosis simply followed cholesterol-inflicted damage or could possibly play a more primary role in arterial disease.

See p 1308

As can happen when the experimentalist maintains clinical contact, observation of the patient afforded a perspective on this puzzle. The adoption of cardiac transplantation created a new disease: accelerated coronary arteriosclerosis.³ Even in recipients with nonischemic cardiomyopathy and normal lipids, an aggressive form of intimal disease could narrow epicardial and intramyocardial coronary branches and all too often threaten graft survival. We have preferred the term arteriosclerosis (hardening of the arteries) to atherosclerosis (gruel in the arteries) because the allograft coronary artery lesions often lack a lipid-rich core typical of atheroma.

This iatrogenic disease provided a strong indication that immune activation could induce explosive intimal disease even in the absence of a strong lipid stimulus. Most cases of atherosclerosis depend at least in part on dyslipidemia. At one end of the spectrum, a child whose only risk factor is elevated low-density lipoprotein (LDL) due to homozygous familial hypercholesterolemia can develop severe atherosclerosis in the first decade of life (Figure).⁴ However, allograft coronary disease . . . [Full Text of this Article]

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