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- Rayan Saab, Aline N Zouk, Ronald Mastouri, Todd C Skaar, Santosh Philips, and Rolf P Kreutz.
- Department of Medicine, Krannert Institute of Cardiology, Indiana University School of Medicine, 1800 N. Capitol Ave, MPC2, ME-400, Indianapolis, IN 46202, USA.
- Pharmacogenomics. 2015 Nov 1; 16 (16): 1807-15.
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 & MethodsGenotyping for c.34C>T was performed in 267 patients undergoing regadenoson cardiac stress testing.ResultsCarriers 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).ConclusionAMPD1 deficiency may be involved in the modulation of regadenoson's systemic effects.
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