Key result
Adventitial mast cell densities were threefold higher in dissected versus nondissected coronary arterial sections in cases of eosinophilic coronary periarteritis.
Case Report (n=2)
Mast cells may play a key role in orchestrating inflammation in eosinophilic coronary periarteritis associated with arterial dissection.
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Mast cell infiltration may contribute to dissection in eosinophilic coronary periarteritis; hypothesis-generating case report requiring validation before any clinical inference.
A subset of coronary arterial dissections is associated with eosinophilic coronary periarteritis (ECPA); however, the pathogenesis of the process remains unclear. Mast cells normally reside in coronary arterial adventitia and are known mediators of eosinophilic inflammatory conditions such as type I hypersensitivity reactions. We report two cases in which coronary arterial dissection with ECPA was detected at autopsy. Tryptase, CD68, CD4, CD8, and CD1a immunohistochemical staining was performed to better characterize inflammation. While eosinophils represented a prominent periadventitial inflammatory cell, there were slightly more lymphocytes: CD4/CD8 ratios were within expected reference ranges. There were moderate numbers of macrophages, and few neutrophils or dendritic cells. Numbers of mast cells in dissected versus nondissected sections were compared: adventitial mast cell densities were threefold higher in dissected portions and showed a trend toward increased degranulation. These findings suggest that mast cells may play a role in orchestrating inflammation in cases of ECPA.
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Mandal et al. (2015) conducted a case report in Coronary arterial dissection with eosinophilic coronary periarteritis (ECPA) (n=2). Dissected coronary arterial sections vs. Nondissected sections was evaluated on Adventitial mast cell densities (threefold higher). Adventitial mast cell densities were threefold higher in dissected versus nondissected coronary arterial sections in cases of eosinophilic coronary periarteritis.
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