Eosinophilic Coronary Periarteritis with Arterial Dissection: The Mast Cell Hypothesis
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Published on: August 18, 2016
Rakesh Mandal1, Erin G Brooks1, Robert F Corliss1
1Department of Pathology and Laboratory Medicine, University of Wisconsin Hospital and Clinics, 1111 Highland Avenue, Madison, WI, 53705.
Insights
Mast cells may contribute to eosinophilic coronary periarteritis (ECPA) and arterial dissection. Increased mast cell density and degranulation were observed in dissected coronary arteries, suggesting a role in ECPA pathogenesis.
Area of Science:
- Cardiovascular Pathology
- Immunohistochemistry
- Mast Cell Biology
Background:
- Eosinophilic coronary periarteritis (ECPA) is linked to coronary arterial dissections, but its cause is unknown.
- Mast cells are immune cells in coronary arteries, involved in allergic reactions.
Observation:
- Two autopsy cases of coronary arterial dissection with ECPA were analyzed.
- Immunohistochemistry was used to examine inflammatory cells, including mast cells, lymphocytes, and macrophages.
Findings:
- Eosinophils were prominent, but lymphocytes were slightly more numerous.
- Adventitial mast cell density was threefold higher in dissected arterial segments.
- Mast cells showed increased degranulation in dissected areas.
Implications:
- Mast cells may play a significant role in the inflammation associated with ECPA.
- These findings suggest mast cells as potential therapeutic targets for ECPA.
- Further research is needed to elucidate the precise mechanisms of mast cell involvement in ECPA.
Abstract:
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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