title: Angiotensin-converting enzyme DD genotype is associated with worse perinatal cardiorespiratory adaptation in preterm infants.
abstract: OBJECTIVE
  The angiotensin-converting enzyme (ACE) deletion (D) variant is associated with greater ACE activity and perhaps with deleterious cardiorespiratory pathophysiological responses. We determined whether the early health status of the preterm infant was adversely influenced by homozygosity for the D allele (DD genotype) compared with ID or II genotype. Study design Angiotensin-converting enzyme genotype was determined in a cohort of 148 preterm infants born in Bristol, United Kingdom (median gestational age, 31 weeks; range, 28-32). Intensive care data were prospectively obtained. Primary analysis was by Mann-Whitney U and chi(2) tests.
  
  
  RESULTS
  Higher oxygen, circulatory support requirements, and base deficit in the first 12 hours after birth were found in infants with DD genotype (minimum inspired oxygen concentration in first 12 hours, median [interquartile range], DD 0.26 [0.21-0.40], ID/II 0.21 [0.21-0.30], P=.028; blood pressure support in first 12 hours, DD 12 [30%], ID/II 15 [14%], P=.039; worse base deficit in first 12 hours, DD 4.8 [7.7 to 0], ID/II 0 [5.3 to 0], P=.020).
  
  
  CONCLUSIONS
  Angiotensin-converting enzyme polymorphism has a role in the development of preterm cardiorespiratory disease. The DD genotype, encoding higher angiotensin-converting enzyme activity, may adversely influence the early health status of preterm infants.
authors.affiliation: Division of Child Health, University of Bristol, United Kingdom. david.harding@bristol.ac.uk
authors.forename: David
authors.initials: D
authors.lastname: Harding
authors.forename: Sukhbir
authors.initials: S
authors.lastname: Dhamrait
authors.forename: Neil
authors.initials: N
authors.lastname: Marlow
authors.forename: Andrew
authors.initials: A
authors.lastname: Whitelaw
authors.forename: Sanjay
authors.initials: S
authors.lastname: Gupta
authors.forename: Steve
authors.initials: S
authors.lastname: Humphries
authors.forename: Hugh
authors.initials: H
authors.lastname: Montgomery
mesh_terms: D002318:Cardiovascular Diseases / Q000235:genetics* / Q000503:physiopathology; D015331:Cohort Studies; D005260:Female; D017353:Gene Deletion; D006304:Health Status; D006720:Homozygote; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature; D007235:Infant, Premature, Diseases / Q000235:genetics* / Q000503:physiopathology; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D012084:Renin-Angiotensin System / Q000502:physiology; D012140:Respiratory Tract Diseases / Q000235:genetics* / Q000503:physiopathology
chemical_list: D007703:Peptidyl-Dipeptidase A