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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:1389.)
© 2001 American Heart Association, Inc.

Editorials

Contrasting Outcomes of Atheroma Evolution

Intimal Accumulation Versus Medial Destruction

Jean-Baptiste Michel

From Institut Federatif de Recherche "Circulation Paris VII" and INSERM Unit 460, Cardiovascular Remodeling, CHU X. Bichat, Paris, France.

Correspondence to J.B. Michel, MD, PhD, Unit 460 INSERM, CHU X. Bichat, 16, rue Henri Huchard, BP 416, 75018 Paris, France. E-mail u460@bichat.inserm.fr

Although not all forms of aneurysm, which may vary in location, are of atherosclerotic origin, atheroma is probably the main cause of acquired abdominal aneurysms in humans. In 1992, Reed et al¹ described the similarity of risk factors for occlusive and aneurysmal diseases in a cohort of 8000 men and concluded that atheroma was a causal pathway to aneurysm development. This common initial pathway has been recently confirmed through a postmortem morphological approach in humans.² The usual occlusive forms of atheroma involve intimal accumulation of material including lipids, matrix proteins, and cells, whereas the medial layer remains largely uninjured, consisting of smooth muscle cells (SMCs) and insoluble extracellular matrix. In contrast, aneurysm development involves proteolytic injury to the medial layer, including the degradation of elastin and collagen, SMC rarefaction, and compensatory fibrosis of the adventitia. Therefore, the question raised is this: What are the biological determinants that preferentially switch the outcome of atheroma from intimal accumulation of biological materials to medial destruction? The involvement of protease and antiprotease systems in the evolution of atheroma is now well documented both in aneurysm formation³ and in plaque rupture (see Libby⁴ for a review). These systems involve matrix metalloproteinases (MMPs), which are able to degrade the insoluble extracellular matrix, their activation and inhibition by tissue inhibitors (TIMPs),⁵ and the plasminogen activators and their inhibitors (PAIs).⁶

See p 1440

In the current issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Silence and coworkers⁷ have explored this interesting question of the switch from intimal accumulation . . . [Full Text of this Article]

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