Genetic variants are not associated with outcome in patients with coronary artery disease and left ventricular dysfunction: results of the Genetic Substudy of the Surgical Treatment for Ischemic Heart Failure (STICH) trials.


Journal Article

OBJECTIVES AND BACKGROUND: We evaluated the ability of 23 genetic variants to provide prognostic information in patients enrolled in the Genetic Substudy of the Surgical Treatment for Ischemic Heart Failure (STICH) trials. METHODS: Patients assigned to STICH Hypothesis 1 were randomized to medical therapy with or without coronary artery bypass grafting (CABG). Those assigned to STICH Hypothesis 2 were randomized to CABG or CABG with left ventricular reconstruction. RESULTS: In patients assigned to STICH Hypothesis 2 (n = 714), no genetic variant met the prespecified Bonferroni-adjusted threshold for statistical significance (p < 0.002); however, several variants met nominal prognostic significance: variants in the β2-adrenergic receptor gene (β2-AR Gln27Glu) and in the A1-adenosine receptor gene (A1-717 T/G) were associated with an increased risk of a subject dying or being hospitalized for a cardiac problem (p = 0.027 and 0.031, respectively). These relationships remained nominally significant even after multivariable adjustment for prognostic clinical variables. However, none of the 23 genetic variants influenced all-cause mortality or the combination of death or cardiovascular hospitalization in the STICH Hypothesis 1 population (n = 532) by either univariate or multivariable analysis. CONCLUSION: We were unable to identify the predictive genotypes in optimally treated patients in these two ischemic heart failure populations.

Full Text

Duke Authors

Cited Authors

  • Feldman, AM; She, L; McNamara, DM; Mann, DL; Bristow, MR; Maisel, AS; Wagner, DR; Andersson, B; Chiariello, L; Hayward, CS; Hendry, P; Parker, JD; Racine, N; Selzman, CH; Senni, M; Stepinska, J; Zembala, M; Rouleau, J; Velazquez, EJ; Lee, KL

Published Date

  • 2015

Published In

Volume / Issue

  • 130 / 2

Start / End Page

  • 69 - 81

PubMed ID

  • 25592552

Pubmed Central ID

  • 25592552

Electronic International Standard Serial Number (EISSN)

  • 1421-9751

Digital Object Identifier (DOI)

  • 10.1159/000368221


  • eng

Conference Location

  • Switzerland