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A potential pharmacogenomic strategy for anticoagulant treatment in non‐ST elevation acute coronary syndromes: the role of interleukin‐1 receptor antagonist genotype

Summary.  Objectives: Our aim was to determine a pharmacogenomic approach to heparin use in non‐ST elevation acute coronary syndromes, specifically the impact of interleukin (IL)‐1 receptor antagonist polymorphisms upon von Willebrand factor (vWF) responses to unfractionated heparin (UFH) and low molecular weight heparin (LMWH). Background: In acute coronary syndromes (ACS), identification of specific biological or genetic targets to direct pharmacological treatment remains a challenge. vWF has been shown to predict future cardiovascular risk and the response to anticoagulant treatments during non‐ST elevation ACS. IL‐1 receptor antagonist (IL‐1RN) polymorphisms predict the change in vWF between 24 and 48 h (Δ vWF) during non‐ST elevation ACS. Methods: We genotyped at the IL‐1 locus, 67 patients with non‐ST elevation ACS who received either LMWH or UFH, and measured vWF levels at 24 and 48 h. Results: LMWH was superior to UFH in reducing the rise in vWF between 24 and 48 h in the cohort as a whole. However, when patients were stratified by IL‐1RN genotype, LMWH was superior to UFH in reducing Δ vWF only in allele *2 carriers (0.51 iU mL−1 vs. 1.37, P < 0.01), but not in non‐carriers (− 0.03 iU mL−1 vs. 0.15, P = NS). Conclusion: IL‐1RN genotype may be a useful marker to identify patients that benefit from LMWH in non‐ST elevation ACS.