Vulnerable Plaque

Guha Krishnaswamy; David S. Chi; Jim Kelley

doi:10.7326/0003-4819-131-5-199909070-00015

Letters |7 September 1999

Vulnerable Plaque

Guha Krishnaswamy, MD; David S. Chi, PhD; Jim Kelley, PhD

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TO THE EDITOR:

Kullo and colleagues have presented an excellent review of the cellular and molecular aspects of a vulnerable plaque (1). Their Table 1 mentions the cellular composition of rupture-prone plaques and lists macrophages, T cells, and mast cells. However, although their discussion involves the role of macrophages, T cells, and smooth-muscle cells, little attention was paid to the potential role of mast cells in plaque instability or rupture.

Kaartinen and colleagues (2) demonstrated very clearly that mast cells localize to areas of erosion or rupture sites of atheromas, and these cells expressed tumor necrosis factor-α. Mast cells have also been shown to aid in the formation of foam cells by assisting smooth-muscle uptake of low-density lipoprotein remnants (3). More recently, Johnson and coworkers (4) investigated the role of mast-cell proteases in activating matrix-degrading metalloproteinases (MMPs) in human carotid endarterectomy specimens. By stimulating mast cells to degranulate in vitro by adding the compound 48/80 to atherectomy samples, these investigators showed increased MMP activity, a process inhibited by the tryptase inhibitor antipain and the chymase inhibitor chymostatin (4). Using dual immunocytochemistry, these investigators also showed co-localization of MMP-1 and MMP-3 with mast cells in the shoulder region of plaques, where the maximal numbers of degranulated mast cells also occurred.

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1999 American College of Physicians

Letters |7 September 1999

Vulnerable Plaque

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Letters |7 September 1999

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