Donor ACE gene polymorphism: a genetic risk factor for accelerated coronary sclerosis following cardiac transplantation

被引:21
作者
Cunningham, DA
Crisp, SJ
Barbir, M
Lazem, F
Dunn, MJ
Yacoub, MH [1 ]
机构
[1] Harefield Hosp, Dept Cardiothorac Surg, Natl Heart & Lung Inst, Heart Sci Ctr, Harefield UB9 6JH, Middx, England
[2] Univ London Imperial Coll Sci Technol & Med, Div Cardiothorac Surg, Natl Heart & Lung Inst, London, England
关键词
angiotensin; genes; arteriosclerosis; transplantation;
D O I
10.1053/euhj.1997.0587
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Aims To investigate the role of angiotensin converting enzyme (ACE) (IID) gene polymorphism in the development of coronary sclerosis after cardiac transplantation. Methods and results Eighty cardiac transplant recipients (44 transplant associated coronary artery disease; 36 nontransplant associated coronary artery disease) and their donors were genotyped by polymerase chain reaction. The allele frequencies of the recipients in the transplant associated coronary artery disease and non-transplant associated coronary artery disease groups (I=0.47 and 0.48, D=0.53 and 0.52, respectively) did not differ significantly between the groups. However, there was a negative association between the frequency of the I allele in the donor and the development of transplant associated coronary artery disease. The D allele in the donor population of the nontransplant associated coronary artery disease group had a significantly (P<0.01) lower frequency (0.35) than either the transplant associated coronary artery disease group (0.53) or that of the general population (0.57). Other factors analysed were recipient family history, cholesterol levels, age, sex and body mass index, donor age and acute rejection, of which the significant (P<0.05) factors were acute rejection and sex of the recipient. Conclusion These results suggest that the ACE genotype of the donor organ may be an additional risk factor for the development of coronary artery disease following cardiac transplantation and that tissue rather than circulating ACE could be implicated in the pathogenesis of this disease.
引用
收藏
页码:319 / 325
页数:7
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