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.
journal_name
Pharmacogenomicsjournal_title
Pharmacogenomicsauthors
Saab R,Zouk AN,Mastouri R,Skaar TC,Philips S,Kreutz RPdoi
10.2217/pgs.15.116subject
Has Abstractpub_date
2015-11-01 00:00:00pages
1807-15issue
16eissn
1462-2416issn
1744-8042journal_volume
16pub_type
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