AMPD1 polymorphism and response to regadenoson

Rayan Saab, Aline N. Zouk, Ronald Mastouri, Todd C. Skaar, Santosh Philips, Rolf P. Kreutz

Research output: Contribution to journalArticle

2 Scopus citations

Abstract

Aims: AMPD1 c.34C > T (rs17602729) polymorphism results in AMPD1 deficiency. We examined the association of AMPD1 deficiency and variability of hemodynamic response to regadenoson. Subjects & methods: Genotyping for c.34C>T was performed in 267 patients undergoing regadenoson cardiac stress testing. Results: Carriers of c.34C >T variant exhibited higher relative changes in systolic blood pressure (SBP) compared with wild-type subjects ([%] SBP change to peak: 12 ± 25 vs 5 ± 13%; p = 0.01) ([%] SBP change to nadir:-3 ± 15 vs-7 ± 11%; p = 0.04). Change in heart rate was similar between groups, but side effects were more common in carriers of the variant (+LR = 4.2; p = 0.04). Conclusion: AMPD1 deficiency may be involved in the modulation of regadenoson's systemic effects.

Original languageEnglish (US)
Pages (from-to)1807-1815
Number of pages9
JournalPharmacogenomics
Volume16
Issue number16
DOIs
StatePublished - Nov 2015

    Fingerprint

Keywords

  • adenosine
  • genetic
  • myocardial perfusion imaging
  • regadenoson

ASJC Scopus subject areas

  • Molecular Medicine
  • Genetics
  • Pharmacology

Cite this