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Review
. 2006 Feb;22 Suppl B(Suppl B):81B-84B.
doi: 10.1016/s0828-282x(06)70991-6.

Morphological characteristics of coronary atherosclerosis in diabetes mellitus

Renu Virmani  1 , Allen P Burke, Frank Kolodgie
Affiliations
Review

Morphological characteristics of coronary atherosclerosis in diabetes mellitus

Renu Virmani et al. Can J Cardiol. 2006 Feb.

Abstract
in English, French

The incidence of diabetes is increasing in the general population because of increasing obesity, and is likely to result in a higher incidence of coronary artery disease. It was recently reported that diabetics (types I and II) dying suddenly from coronary artery disease have greater macrophage and T lymphocyte infiltration in atherosclerotic plaques, as well as larger necrotic cores compared with nondiabetics. The inflammatory cell infiltrates showed human leukocyte antigen-DR expression, which was greater in diabetics. The receptors for advanced glycosylation end-products expression, demonstrated by immunohistochemistry, was greater in diabetics than in nondiabetics in macrophages, smooth muscle cells and endothelial cells, and was associated with apoptosis of macrophages and smooth muscle cells, but not of endothelial cells. There is also a higher incidence of healed plaque ruptures and healed myocardial infarct in type II diabetics. Plaque burden is higher in diabetics than in nondiabetics; however, distal plaque burden was only significantly different in type II diabetics compared with nondiabetics. There was greater positive remodelling in diabetic coronary arteries than in nondiabetic ones, which correlated with the per cent necrotic core. Further studies are needed to better understand the mechanisms that govern greater inflammation and plaque burden in diabetics.

L’incidence du diabète est en hausse dans la population générale à cause de l’augmentation des cas d’obésité, et elle risque fort d’entraîner à sa suite une forte incidence de la maladie coronarienne. On a récemment signalé que comparativement aux non-diabétiques, les diabétiques (de type I et de type II) décédés subitement de coronaropathie présentaient une infiltration plus importante des macrophages et des lymphocytes T dans leurs plaques d’athérome et des noyaux nécrotiques plus volumineux. Les infiltrats cellulaires inflammatoires ont révélé une expression plus marquée de l’antigène HLA-DR chez les diabétiques que chez les non-diabétiques. Les récepteurs de l’expression des produits terminaux de la glycosylation avancée observés en immunohistochimie étaient plus présents dans les macrophages, les cellules des muscles lisses et les cellules endothéliales des diabétiques que des non-diabétiques et étaient associés à l’apoptose des macrophages et des cellules des muscles lisses, mais non des cellules endothéliales. On note en outre une incidence plus forte de plaques rompues cicatrisées et d’infarctus du myocarde cicatrisés chez les diabétiques de type II. Le rôle de la plaque est plus important chez les diabétiques que chez les non-diabétiques. Par contre, la différence ne s’est révélée significative qu’entre les diabétiques de type II et les non-diabétiques. On a noté un remodelage positif plus marqué au niveau des coronaires des diabétiques, phénomène qui était en corrélation avec le pourcentage de noyaux nécrotiques. Il faudra poursuivre la recherche pour mieux comprendre les mécanismes qui sont à l’origine de l’inflammation plus marquée et du rôle plus prépondérant de la plaque chez les diabétiques.

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Figures

Figure 1)
Figure 1)
Top Coronary lesions (fibroatheromas) illustrating the extent of inflammatory infiltrate (macrophages [MACs] and T cells [CD45RO]) and human leukocyte antigen-DR (HLA-DR) expression in patients with type I and II diabetes mellitus (DM) and nondiabetics. Bottom Bar graph showing a semiquantitative comparison of the extent of macrophage and T cell infiltration, and HLA-DR expression in coronary arteries from diabetics and nondiabetics. Plaque T cell infiltration was maximal in type I diabetics, while HLA-DR expression is significantly higher in type I and II diabetics
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