Clinico-pathologic, immunohistochemical, and TUNEL study in early cardiac allograft failure

Citation
A. Panizo-santos et al., Clinico-pathologic, immunohistochemical, and TUNEL study in early cardiac allograft failure, CARDIO PATH, 9(3), 2000, pp. 153-159
Citations number
28
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CARDIOVASCULAR PATHOLOGY
ISSN journal
10548807 → ACNP
Volume
9
Issue
3
Year of publication
2000
Pages
153 - 159
Database
ISI
SICI code
1054-8807(200005/06)9:3<153:CIATSI>2.0.ZU;2-8
Abstract
Early cardiac allograft failure (ECAF) was defined as acute allograft failu re in the early transplant period. The aim of this study is to elucidate th e clinicopathological and immunohistochemical characteristics and the role of apoptosis in ECAF in nine patients. We reviewed preoperative clinical da ta and morphological data at the time of autopsy or retransplantation. We a lso performed TUNEL assay and immunohistochemistry to study fibronectin and tubulin P-II. The average recipient and donor age was 48 +/- 10.3 and 28 /- 7.11 respectively. Seven patients died at a mean time of 26 hours. The r emaining two patients underwent retransplantation and are alive. The mean c old ischemic time was 124.1 +/- 44.5 minutes. No patient had a panel reacti ve antibody >15% and lymphocytic crossmatch was positive in one case. All c ases had grade 2-3 of coagulative necrosis, which correlated positively wit h fibonectin accumulation in myocyte cytoplasm, and cytoplasmic tubulin los s (p < 0.05). TUNEL technique showed in all cases some degree of DNA strand breaks in cardiomyocytes. Endothelium DNA strand breaks were seen in seven cases. Patients transplanted because of idiopathic dilated cardiomyopathy had a significantly higher degree of DNA strand breaks in cardiomyocytes an d endothelial cells (p = 0.03 and p = 0.02) than those transplanted because of ischemic cardiomyopathy. These results indicate that ECAF may be caused by ischemic reperfusion damage to the donor heart assessed by myocyte coag ulative necrosis, fibronectin accumulation in myocytes, tubulin loss, and D NA strand breaks of cardiomyocytes and endothelium. The use of a combinatio n of these techniques might be appropriate in the diagnosis of ECAF in endo myocardial biopsies when it is suspected clinically. Cardiovasc Pathol 2000 ;9:153-159 (C) 2000 by Elsevier Science Inc.