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Ser49Gly of beta1-adrenergic receptor is associated with effective beta-blocker dose in dilated cardiomyopathy.

Journal article
Authors Yvonne Magnusson
Malin Levin
Robert Eggertsen
Ernst Nyström
Reza Mobini
Maria Schaufelberger
Bert Andersson
Published in Clinical pharmacology and therapeutics
Volume 78
Issue 3
Pages 221-31
ISSN 0009-9236
Publication year 2005
Published at Wallenberg Laboratory
Cardiovascular Institute
Institute of Community Medicine, Dept of Primary Health Care
Institute of Internal Medicine, Dept of Medicine
Pages 221-31
Language en
Keywords Adrenergic beta-Antagonists, administration & dosage, therapeutic use, Aged, Amino Acid Substitution, Cardiomyopathy, Dilated, drug therapy, genetics, mortality, Codon, Cohort Studies, DNA, genetics, Dose-Response Relationship, Drug, Female, Genotype, Glycine, Humans, Male, Middle Aged, Polymorphism, Genetic, Prospective Studies, Receptors, Adrenergic, beta-1, drug effects, genetics, Serine, Survival Rate, Treatment Outcome
Subject categories Medical and Health Sciences


OBJECTIVE: Our objective was to evaluate the influence of polymorphisms at codons 49 and 389 of the beta1-adrenergic receptor (beta1-AR) on the response to beta-blockers and outcome in patients with dilated cardiomyopathy. METHODS: We genotyped both codons of the beta1-AR in 375 patients with dilated cardiomyopathy and 492 control subjects. RESULTS: Neither of the polymorphisms was associated with susceptibility for dilated cardiomyopathy. In a retrospective analysis of patients receiving beta-blockers, there was a significant association between long-term survival rate and codon 49 (P = .014) but not codon 389 (P = .08). Despite a similar mean heart rate (69 beats/min), patients with the Ser49 genotype tended to have higher doses of beta-blockade compared with Gly49 carriers (P = .065). In patients receiving a low dose of beta-blockade (< or = 50% of targeted full dose), the 5-year mortality rate was lower among Gly49 carriers than Ser49 patients (risk ratio [RR], 0.24; 95% confidence interval [CI], 0.07-0.80; P = .020). In patients receiving high doses of beta-blockers, there was no significant difference in outcome between genotypes (P = .20), which was attributable to a better outcome for Ser49 patients treated with a high dose of beta-blockade as compared with a low dose. Gly49 carriers had a similar survival rate with different doses of beta-blockers. With low-dose beta-blockers, both codon 49 (RR, 0.26; 95% CI, 0.08-0.89; P = .029) and codon 389 (RR, 2.42; 95% CI, 1.04-5.63, P = .039) were related to 5-year mortality rate. CONCLUSION: In patients with heart failure, the influence of codon 49 on the outcome and effect of beta-blockers appeared to be more pronounced than that of codon 389. The more common Ser49Ser genotype responded less beneficially to beta-blockade and would motivate genotyping to promote higher doses for the best outcome effect.

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