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AMPD1 polymorphism and response to regadenoson.

Rayan Saab1, Aline N Zouk1, Ronald Mastouri1

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

Pharmacogenomics
|November 12, 2015
PubMed
Summary
This summary is machine-generated.

Adenosine triphosphate (ATP) synthase deficiency, caused by the AMPD1 c.34C > T polymorphism, alters hemodynamic responses to regadenoson. This genetic variant is linked to greater blood pressure changes and more side effects during cardiac stress testing.

Keywords:
adenosinegeneticmyocardial perfusion imagingregadenoson

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Area of Science:

  • Cardiovascular Pharmacology
  • Human Genetics
  • Pharmacogenomics

Background:

  • Adenosine monophosphate deaminase 1 (AMPD1) deficiency, a genetic condition, arises from the c.34C > T polymorphism (rs17602729).
  • Regadenoson is a widely used pharmacologic stress agent in cardiac diagnostics.

Purpose of the Study:

  • To investigate the association between AMPD1 deficiency and variations in hemodynamic responses to regadenoson.
  • To determine if AMPD1 genetic variability influences the safety and efficacy of regadenoson stress testing.

Main Methods:

  • Genotyping for the AMPD1 c.34C > T variant was conducted in 267 patients.
  • Patients underwent regadenoson-based cardiac stress testing.

Main Results:

  • Carriers of the AMPD1 c.34C > T variant showed significantly higher relative changes in systolic blood pressure compared to wild-type individuals.
  • While heart rate changes were comparable, carriers experienced a higher incidence of side effects during regadenoson stress testing.
  • The association between the variant and increased systolic blood pressure variability was statistically significant (p=0.01).

Conclusions:

  • AMPD1 deficiency may play a role in modulating the systemic hemodynamic effects of regadenoson.
  • Genetic variations in AMPD1 could influence patient response and tolerability to regadenoson stress tests.
  • Further research is warranted to elucidate the precise mechanisms underlying these pharmacogenetic interactions.