AMPD1 polymorphism and response to regadenoson-Reference-Cited by-同舟云学术

AMPD1 polymorphism and response to regadenoson

Published:2015-11 Issue:16 Volume:16 Page:1807-1815
ISSN:1462-2416
Container-title:Pharmacogenomics
language:en
Short-container-title:Pharmacogenomics

Author:

Saab Rayan¹,Zouk Aline N¹,Mastouri Ronald¹,Skaar Todd C²,Philips Santosh²,Kreutz Rolf P¹²

Affiliation:

1. Department of Medicine, Krannert Institute of Cardiology, Indiana University School of Medicine, 1800 N. Capitol Ave, MPC2, ME-400, Indianapolis, IN 46202, USA

2. Department of Medicine, Division of Clinical Pharmacology, Indiana University School of Medicine, Clinical Pharmacology Research Institute (R2), Room 402, 950 West Walnut Street, Indianapolis, IN 46202, USA

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.

Publisher

Future Medicine Ltd

Subject

Pharmacology,Genetics,Molecular Medicine

Link

https://www.futuremedicine.com/doi/pdf/10.2217/pgs.15.116

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