title: Increase and redistribution of cardiac mast cells in auricular thrombosis. Possible role of kit ligand.
abstract: BACKGROUND
  The atrial appendage is a predilection site for thrombus formation. Mast cells (MC) are a rich source of mediators that may be involved in the regulation of thrombus formation. We examined number, distribution, and phenotype of MC in thrombosed versus unaffected auricles to elucidate their possible role in auricular thrombosis (AUTHR).
  
  
  RESULTS
  Sections of atrial appendages (AUTHR, n = 14; controls (CO), n = 13) were analyzed for MC by Giemsa, toluidine blue, and berberine sulfate stains and by immunohistochemistry. Cardiac MC expressed CD antigens corresponding to the classic MC phenotype as well as tryptase, chymase, and heparin. Thrombosis was associated with a twofold increase in the number of MC in the total appendage (CO, 3.1 +/- 1.0 versus AUTHR, 6.4 +/- 1.1 MC/mm2, P < .01). Moreover, in AUTHR, a redistribution of MC to the upper endocardium was observed (AUTHR, 5.3 +/- 1.4 versus CO, 0.07 +/- 0.15 MC/mm2, P < .01). Mast cell growth factor (MGF) was expressed in the endothelium and subendothelial space of thrombosed appendages but not in the normal endocardium. Overexpression of MGF was accompanied by a weak or absent expression of the MGF receptor c-kit on redistributed MC in AUTHR. Patients with unilateral atrial appendage thrombosis did not exhibit a MC increase or redistribution in the unaffected contralateral appendage. No augmentation of other inflammatory cells was observed. Stimulation of isolated cardiac MC with MGF resulted in mediator release.
  
  
  CONCLUSIONS
  This study provides evidence that AUTHR is associated with MC increase and redistribution and MGF overexpression. The role of redistributed MC and their mediators in the pathophysiology of atrial thrombosis requires further investigation.
authors.affiliation: Department of Internal Medicine I, University of Vienna, Austria.
authors.forename: H C
authors.initials: HC
authors.lastname: Bankl
authors.forename: T
authors.initials: T
authors.lastname: Radaszkiewicz
authors.forename: G W
authors.initials: GW
authors.lastname: Klappacher
authors.forename: D
authors.initials: D
authors.lastname: Glogar
authors.forename: W R
authors.initials: WR
authors.lastname: Sperr
authors.forename: K
authors.initials: K
authors.lastname: Grossschmidt
authors.forename: H
authors.initials: H
authors.lastname: Bankl
authors.forename: K
authors.initials: K
authors.lastname: Lechner
authors.forename: P
authors.initials: P
authors.lastname: Valent
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002452:Cell Count; D005260:Female; D006325:Heart Atria / Q000737:chemistry / Q000473:pathology; D016298:Hematopoietic Cell Growth Factors / Q000032:analysis / Q000502:physiology; D006636:Histamine Release; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008407:Mast Cells / Q000166:cytology* / Q000378:metabolism; D008875:Middle Aged; D009206:Myocardium / Q000737:chemistry; D010641:Phenotype; D016028:Receptors, Leukocyte-Adhesion / Q000032:analysis; D013194:Staining and Labeling; D019089:Stem Cell Factor; D013927:Thrombosis / Q000473:pathology*
chemical_list: D016298:Hematopoietic Cell Growth Factors; D016028:Receptors, Leukocyte-Adhesion; D019089:Stem Cell Factor