[Pharmacogenetic study of the response to flecainide and propafenone in patients with atrial fibrillation]

Rev Esp Cardiol. 2005 Jun;58(6):745-8.
[Article in Spanish]

Abstract

We analyzed cytochrome P450 2D6 polymorphism by determining phenotype as the metabolic ratio between dextromethorphan and its main metabolite, dextrorphan. We studied 18 men and 22 women in whom mean age was 54.6+/-11.9 years. In 9 patients metabolic ratio was determined before antiarrhythmic treatment and again during treatment, with a mean increase of 0.13+/-0.15 (P=.03). We found 19 poor metabolizers and 21 extensive metabolizers. Adverse effects were more frequent in poor metabolizers (21.1%) than in extensive metabolizers (4.8%; P=.12). Antiarrhythmic treatment was effective in 27 patients (67.5%), with no difference between poor and extensive metabolizers.

Publication types

  • Comparative Study
  • English Abstract

MeSH terms

  • Adult
  • Aged
  • Anti-Arrhythmia Agents / adverse effects
  • Anti-Arrhythmia Agents / therapeutic use*
  • Atrial Fibrillation / drug therapy*
  • Cytochrome P-450 CYP2D6 / genetics*
  • Cytochrome P-450 CYP2D6 / metabolism*
  • Female
  • Flecainide / adverse effects
  • Flecainide / metabolism
  • Flecainide / therapeutic use*
  • Follow-Up Studies
  • Humans
  • Male
  • Middle Aged
  • Multivariate Analysis
  • Pharmacogenetics
  • Polymorphism, Genetic
  • Propafenone / adverse effects
  • Propafenone / metabolism
  • Propafenone / therapeutic use*
  • Retrospective Studies
  • Time Factors
  • Treatment Outcome

Substances

  • Anti-Arrhythmia Agents
  • Propafenone
  • Cytochrome P-450 CYP2D6
  • Flecainide