Impact of angiotensin-converting enzyme gene polymorphism on neurohormonal responses to high- versus low-dose enalapril in advanced heart failure

Am Heart J. 2004 Nov;148(5):889-94. doi: 10.1016/j.ahj.2004.05.020.

Abstract

Background: The impact of angiotensin-converting enzyme (ACE) gene polymorphism on neurohormonal dose response to ACE inhibitor therapy is unclear.

Methods: ACE Insertion (I) or Deletion (D) genotype was determined in 74 patients with chronic heart failure who were randomly assigned to receive either high-dose or low-dose enalapril over a period of 6 months. Monthly pre-enalapril and post-enalapril neurohormone levels (serum ACE activity (sACE), plasma angiotensin II (A-II), plasma renin activity (PRA), and serum aldosterone (ALDO) were compared between genotype subgroups and between patients who received high- or low-dose enalapril within each genotype subgroup.

Results: At baseline, predose/postdose sACE and postdose PRA were significantly higher in the DD genotype. At 6-month follow-up, postdose sACE was reduced in a dose-dependent fashion in all three genotypes (P < .05). However, predose and postdose ALDO and A-II levels did not differ between each genotype subgroup at baseline or by enalapril dose within each genotype subgroup. ALDO escape and A-II reactivation were not affected by ACE genotype or enalapril dosage.

Conclusions: Predose sACE were consistently higher in the DD genotype when compared with ID or II subgroups. Despite a dose-dependent suppression of sACE, there were no observed statistically significant differences in ALDO and A-II suppression or escape with escalating doses of enalapril within each subgroup.

Publication types

  • Clinical Trial
  • Randomized Controlled Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aldosterone / blood
  • Angiotensin II / blood
  • Angiotensin-Converting Enzyme Inhibitors / administration & dosage*
  • Dose-Response Relationship, Drug
  • Double-Blind Method
  • Enalapril / administration & dosage*
  • Female
  • Genotype
  • Heart Failure / blood
  • Heart Failure / drug therapy
  • Heart Failure / genetics*
  • Humans
  • Male
  • Middle Aged
  • Neurotransmitter Agents / blood*
  • Peptidyl-Dipeptidase A / blood
  • Peptidyl-Dipeptidase A / genetics*
  • Polymorphism, Genetic*
  • Renin / blood

Substances

  • Angiotensin-Converting Enzyme Inhibitors
  • Neurotransmitter Agents
  • Angiotensin II
  • Aldosterone
  • Enalapril
  • Peptidyl-Dipeptidase A
  • Renin