title: Angiotensin converting enzyme gene polymorphism and myocardial infarction a large association and linkage study.
abstract: The DD genotype of the angiotensin converting enzyme (ACE) polymorphism has been associated with myocardial infarction (MI). However, sample sizes of many case-control studies showing positive association were small and data were inconsistent. Furthermore, no family-based study is available. In a case-control study frequencies of the ACE genotypes were compared in 1319 unrelated patients with previous MI before 60 years of age (616 from the MONICA Augsburg region and 703 from rehabilitation centers in south Germany) and in 2381 population controls from the MONICA Augsburg study region). Furthermore, linkage and association of the ACE I/D polymorphism with MI were tested in 246 informative families using the sib-transmission/disequilibrium test (S-TDT).Overall, no excess of the D allele was found in MI patients (frequency 0.53 versus 0.57 in the general population; P=0.2). The ACE DD genotype was even slightly less frequent in groups with MI compared to the general population controls (0.26 versus 0.33 in women and 0.28 versus 0.33 in men). Similar results were also obtained in 247 men with low cardiovascular risk. In the family-based study, the frequency of the D allele was not different in siblings with or without previous MI (0.53 versus 0.50, respectively; S-TDT P=0.15) indicating no linkage or association of the D allele with MI. In a case-control study of MI patients and controls from the general population as well as a family study neither association nor linkage of the ACE D allele with MI was detected despite sample sizes that were among the largest samples studied so far.
authors.affiliation: Klinik and Poliklinik für Innere Medizin II, University of Regensburg, 93042 Regensburg, Germany. stephan.holmer@klinik.uni-regensburg.de
authors.forename: Stephan R
authors.initials: SR
authors.lastname: Holmer
authors.forename: Heike
authors.initials: H
authors.lastname: Bickeböller
authors.forename: Christian
authors.initials: C
authors.lastname: Hengstenberg
authors.forename: Friederike
authors.initials: F
authors.lastname: Rohlmann
authors.forename: Susanne
authors.initials: S
authors.lastname: Engel
authors.forename: Hannelore
authors.initials: H
authors.lastname: Löwel
authors.forename: Björn
authors.initials: B
authors.lastname: Mayer
authors.forename: Jeannette
authors.initials: J
authors.lastname: Erdmann
authors.forename: Christian
authors.initials: C
authors.lastname: Baier
authors.forename: Gernot
authors.initials: G
authors.lastname: Klein
authors.forename: Günter A J
authors.initials: GA
authors.lastname: Riegger
authors.forename: Heribert
authors.initials: H
authors.lastname: Schunkert
mesh_terms: D016022:Case-Control Studies; D005260:Female; D008040:Genetic Linkage; D005838:Genotype; D005858:Germany / Q000453:epidemiology; D006801:Humans; D008297:Male; D009203:Myocardial Infarction / Q000201:enzymology* / Q000453:epidemiology; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D015995:Prevalence; D012307:Risk Factors
chemical_list: D007703:Peptidyl-Dipeptidase A