title: 9p21.3 risk locus is associated with first-ever myocardial infarction in an Austrian cohort.
abstract: OBJECTIVE
  Atherosclerosis often presents as a complex systemic disease that is strongly influenced by lifestyle factors, but also by the genetic background. The sequence variant rs1333049 affects the expression of ANRIL, a noncoding RNA transcript playing a key role in the regulation of inflammatory processes. We thus aimed to replicate the predictive value of genetic information on this variant regarding the development of cardiovascular events in an Austrian high-risk cohort.
  
  
  METHODS
  Nine hundred and eighty-eight patients from an angiologic outpatient ward at a large University hospital were genotyped by means of the 5'-nuclease assay. Relative risk ratios were assessed for carriers of different alleles. Statistical independence of genetic information was evaluated in multivariable analysis including known risk markers.
  
  
  RESULTS
  In patients carrying the [G]-allele, metabolic parameters (serum low-density lipoprotein, total cholesterol) significantly decreased during the initial 6 months of the observation period (P < 0.01). Likewise, homozygous [C]-allele carriers were at a higher risk of suffering myocardial infarction (relative risk = 2.681, 95% confidence interval 1.418-5.070). In contrast, we found no interaction between rs1333049 genotype and progression of carotid atherosclerosis or stroke.
  
  
  CONCLUSIONS
  These results are in line with the previous findings, suggesting that genetic information on the rs1333049 variant might be a useful predictor of adverse cardiac events. Thus, we could successfully replicate the predictive value of the 9p21 risk allele in an Austrian cohort.
authors.affiliation: aDepartment of Laboratory Medicine, Medical University of Vienna, Waehringer Guertel 18-20 bGruppenpraxis Labors.at, Praterstrasse 22 cInnere Medizin Doebling, Billrothstrasse 49a, Vienna, Austria.
authors.forename: Helmuth
authors.initials: H
authors.lastname: Haslacher
authors.forename: Thomas
authors.initials: T
authors.lastname: Perkmann
authors.forename: Franz
authors.initials: F
authors.lastname: Ratzinger
authors.forename: Gabriele
authors.initials: G
authors.lastname: Grimm
authors.forename: Markus
authors.initials: M
authors.lastname: Exner
authors.forename: Alexandra
authors.initials: A
authors.lastname: Keller
authors.forename: Klaus
authors.initials: K
authors.lastname: Schmetterer
authors.forename: Clemens
authors.initials: C
authors.lastname: Priemer
authors.forename: Georg
authors.initials: G
authors.lastname: Endler
authors.forename: Oswald
authors.initials: O
authors.lastname: Wagner
authors.forename: Martin
authors.initials: M
authors.lastname: Schillinger
mesh_terms: D000368:Aged; D000483:Alleles; D050197:Atherosclerosis / Q000235:genetics*; D001317:Austria; D002340:Carotid Artery Diseases / Q000235:genetics*; D015331:Cohort Studies; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D006579:Heterozygote; D006720:Homozygote; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000235:genetics*; D020641:Polymorphism, Single Nucleotide; D062085:RNA, Long Noncoding / Q000235:genetics*; D012307:Risk Factors
chemical_list: C561518:CDKN2B antisense RNA, human; D062085:RNA, Long Noncoding