Literature DB >> 26554440

AMPD1 polymorphism and response to regadenoson.

Rayan Saab1, Aline N Zouk1, Ronald Mastouri1, Todd C Skaar2, Santosh Philips2, Rolf P Kreutz1,2.   

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.

Entities:  

Keywords:  adenosine; genetic; myocardial perfusion imaging; regadenoson

Mesh：

Substances：

Year:  2015        PMID： 26554440      PMCID： PMC4826562          DOI： 10.2217/pgs.15.116

Source DB:  PubMed          Journal:  Pharmacogenomics        ISSN： 1462-2416            Impact factor:   2.533


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