Circulation, Vol 90, 1669-1678, Copyright © 1994 by American Heart Association
M Kaartinen, A Penttila and PT Kovanen
BACKGROUND: Rupture in the shoulder region of a coronary atheroma is
considered to be a sequel to local extracellular matrix degradation in this
highly vulnerable site. Such degradation could be triggered by mast cells,
which are filled with neutral proteases and are present in coronary
atheromas. However, the distribution and phenotype of mast cells within
coronary atheromas have not been studied. METHODS AND RESULTS: Specimens of
normal and atherosclerotic human coronary intima from 32 autopsy cases with
ages ranging from 13 to 67 years were stained with monoclonal antibodies
against the two major proteases of mast cells, tryptase and chymase. Of the
tryptase-containing mast cells, a variable proportion (average, 40%; range,
0% to 100%) also contained chymase. In the normal coronary intimas, mast
cells amounted to 0.1% of all nucleated cells. In the fatty streaks, this
proportion was higher by 9-fold, and in the cap, core, and shoulder regions
of atheromas by 5-, 5-, and 10-fold, respectively. Electron and light
microscopic studies of mast cells in the shoulder region of atheromas
revealed degranulation of mast cells, a sign of their activation, and
moreover, that the proportion of activated mast cells was much higher (85%)
in this region than in the normal intima (18%). CONCLUSIONS: The far higher
proportion (50-fold) of activated mast cells in the shoulder region of
atheromas supports the hypothesis that mast cells, a cell type capable of
triggering matrix degradation, actively participate in the destabilization
and ensuing rupture of coronary atheromas and thus may trigger an acute
coronary event.
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Accumulation of activated mast cells in the shoulder region of human coronary atheroma, the predilection site of atheromatous rupture
Wihuri Research Institute, Helsinki, Finland.
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