Intimate association of eosinophils to collagen bundles in eosinophilic myocarditis and ranitidine-induced hypersensitivity myocarditis.
BACKGROUND
Eosinophilic myocarditis is an inflammatory condition of the heart in which the infiltrate is composed predominately of eosinophils.


METHODS
We identified three cases of eosinophilic myocarditis in which the infiltrating eosinophils showed a remarkable intimate association with bundles of collagen. Two of the hearts examined were explants from heart transplant recipients with hypersensitivity myocarditis at the time of transplant and the third was from an autopsied patient with Churg-Strauss syndrome. These hearts were examined using light and electron microscopy. The cellular infiltrate in all three cases was characterized using immunoperoxidase stains with a panel including antibodies against myeloperoxidase, common leukocyte antigen (CD45), B lymphocytes (CD20), T lymphocytes (CD3), active-memory T lymphocytes (CD45RO), inactive T lymphocytes (CD45RA), and macrophages (CD68).


RESULTS
Ultrastructural examination in all three cases confirmed the apposition of eosinophils to both large bundles of collagen and smaller aggregates of collagen fibrils. The eosinophils and the bundles of collagen stained strongly for myeloperoxidase, suggesting at least partial degranulation of the eosinophils. A KP-1 stain (CD68) revealed macrophages admixed with the eosinophils adjacent to the collagen bundles, and stains for CD45RA (naive lymphocytes) and CD45RO (memory T cells) showed an interstitial infiltrate of predominantly CD45RO-positive cells. Clinically, the cardiac decompensation of one of the transplant patients was most likely due to ranitidine-induced hypersensitivity myocarditis.


CONCLUSIONS
These results suggest that some cases of eosinophilic myocarditis may be caused by the expression of novel antigens bound to collagen bundles. In one of the patients awaiting cardiac transplant, cardiac decompensation was temporally associated with ranitidine therapy, an agent not previously implicated as a cause of hypersensitivity myocarditis.
Kendell
K R
KR
Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, Maryland, USA.
Day
J D
JD
Hruban
R H
RH
Olson
J L
JL
Rosenblum
W D
WD
Kasper
E K
EK
Baughman
K L
KL
Hutchins
G M
GM
D000328:Adult; D000897:Anti-Ulcer Agents / Q000009:adverse effects*; D015703:Antigens, CD / Q000032:analysis; D003094:Collagen / Q000276:immunology* / Q000648:ultrastructure; D004802:Eosinophilia / Q000473:pathology*; D004804:Eosinophils / Q000473:pathology*; D005260:Female; D006801:Humans; D006967:Hypersensitivity; D008297:Male; D008875:Middle Aged; D009205:Myocarditis / Q000139:chemically induced / Q000276:immunology* / Q000473:pathology; D009206:Myocardium / Q000473:pathology; D011899:Ranitidine / Q000009:adverse effects*
D000897:Anti-Ulcer Agents; D015703:Antigens, CD; D011899:Ranitidine; D003094:Collagen