Saab, RayanZouk, Aline N.Mastouri, RonaldSkaar, Todd C.Philips, SantoshKreutz, Rolf P.2016-09-022016-09-022015-11Saab, R., Zouk, A. N., Mastouri, R., Skaar, T. C., Philips, S., & Kreutz, R. P. (2015). AMPD1 polymorphism and response to regadenoson. Pharmacogenomics, 16(16), 1807–1815. http://doi.org/10.2217/pgs.15.1161744-8042https://hdl.handle.net/1805/10839AIMS: 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.en-USPublisher Policyadenosinegeneticmyocardial perfusion imagingregadenosonArticle