title: Angiotensin converting enzyme insertion/deletion polymorphism does not influence postcardiac transplantation hypertension onset or progression.
abstract: BACKGROUND
  The angiotensin converting enzyme insertion deletion polymorphism (ACE I/D) has been associated with much cardiovascular pathology, including posttransplantation hypertension. Hypertension is a significant cause of morbidity and mortality after cardiac transplantation. We investigated the influence of the ACE I/D polymorphism on posttransplantation hypertension.
  
  
  METHODS
  A total of 211 heart transplant recipients and 154 corresponding donors were genotyped for the ACE I/D polymorphism by polymerase chain reaction. ACE enzymatic activity was measured by spectrophotometric kinetic analysis. Sitting systolic and diastolic blood pressures were recorded at 3 consecutive visits, and the mean was calculated. Clinical data, including demographics and medication, were collected for all recipients. Results were analyzed by the chi-square test and analysis of variance, taking a p value of <0.05 to be significant.
  
  
  RESULTS
  A total of 41.7% of the subjects were hypertensive (diastolic blood pressure >90 mm Hg) at the time of the study, with 79.6% taking at least one antihypertensive agent. We found no difference between the number of antihypertensive agents, cyclosporin dose and level, renal function, or systolic blood pressure for the different recipient or donor genotypes. We also found no significant correlation between ACE enzymatic activity and systolic or diastolic blood pressure.
  
  
  CONCLUSIONS
  Our study of 211 recipients and 154 corresponding donors is the largest investigation of this polymorphism in a cardiac transplantation population. We found no apparent relationship between the ACE genotype (of either donor or recipient) and systemic hypertension (absolute measurements and the number or dose of antihypertensive agents used).
authors.affiliation: Transplant Centre, South Manchester University Hospitals NHS Trust, Wythenshawe Hospital, Manchester, United Kingdom.
authors.forename: J E
authors.initials: JE
authors.lastname: Fildes
authors.forename: A H
authors.initials: AH
authors.lastname: Walker
authors.forename: C G
authors.initials: CG
authors.lastname: Densem
authors.forename: A K
authors.initials: AK
authors.lastname: Deiraniya
authors.forename: I V
authors.initials: IV
authors.lastname: Hutchinson
authors.forename: C T
authors.initials: CT
authors.lastname: Leonard
authors.forename: N
authors.initials: N
authors.lastname: Yonan
mesh_terms: D000483:Alleles; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001794:Blood Pressure / Q000502:physiology; D004247:DNA / Q000032:analysis; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D005787:Gene Frequency / Q000235:genetics; D005819:Genetic Markers; D005838:Genotype; D016027:Heart Transplantation / Q000009:adverse effects*; D006801:Humans; D006973:Hypertension / Q000201:enzymology* / Q000209:etiology; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000097:blood / Q000235:genetics*; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D011379:Prognosis; D012189:Retrospective Studies; D014019:Tissue Donors
chemical_list: D000959:Antihypertensive Agents; D005819:Genetic Markers; D004247:DNA; D007703:Peptidyl-Dipeptidase A