TY - JOUR
T1 - Impact of the β-1 adrenergic receptor polymorphism on tolerability and efficacy of bisoprolol therapy in korean heart failure patients
T2 - Association between β adrenergic receptor polymorphism and bisoprolol therapy in heart failure (ABBA) study
AU - Lee, Hae Young
AU - Chung, Wook Jin
AU - Jeon, Hui Kyung
AU - Seo, Hong Seog
AU - Choi, Dong Ju
AU - Jeon, Eun Seok
AU - Kim, Jae Joong
AU - Shin, Joon Han
AU - Kang, Seok Min
AU - Lim, Sung Cil
AU - Baek, Sang Hong
N1 - Publisher Copyright:
© 2016 The Korean Association of Internal Medicine.
PY - 2016/3
Y1 - 2016/3
N2 - Background/Aims: We evaluated the association between coding region variants of adrenergic receptor genes and therapeutic effect in patients with congestive heart failure (CHF). Methods: One hundred patients with stable CHF (left ventricular ejection fraction [LVEF] < 45%) were enrolled. Enrolled patients started 1.25 mg bisoprolol treatment once daily, then up-titrated to the maximally tolerable dose, at which they were treated for 1 year. Results: Genotypic analysis was carried out, but the results were blinded to the investigators throughout the study period. At position 389 of the β-1 adrenergic receptor gene (ADRB1), the observed minor Gly allele frequency (Gly389Arg + Gly389Gly) was 0.21, and no deviation from Hardy-Weinberg equilibrium was observed in the genotypic distribution of Arg389Gly (p = 0.75). Heart rate was reduced from 80.8 ± 14.3 to 70.0 ± 15.0 beats per minute (p < 0.0001). There was no significant difference in final heart rate across genotypes. However, the Arg389Arg genotype group required significantly more bisoprolol compared to the Gly389X (Gly389Arg + Gly389Gly) group (5.26 ± 2.62 mg vs. 3.96 ± 2.05 mg, p = 0.022). There were no significant differences in LVEF changes or remodeling between two groups. Also, changes in exercise capacity and brain natriuretic peptide level were not significant. However, interestingly, there was a two-fold higher rate of readmission (21.2% vs. 10.0%, p = 0.162) and one CHF-related death in the Arg389Arg group. Conclusions: The ADRB1 Gly389X genotype showed greater response to bisoprolol than the Arg389Arg genotype, suggesting the potential of individually tailoring β-blocker therapy according to genotype.
AB - Background/Aims: We evaluated the association between coding region variants of adrenergic receptor genes and therapeutic effect in patients with congestive heart failure (CHF). Methods: One hundred patients with stable CHF (left ventricular ejection fraction [LVEF] < 45%) were enrolled. Enrolled patients started 1.25 mg bisoprolol treatment once daily, then up-titrated to the maximally tolerable dose, at which they were treated for 1 year. Results: Genotypic analysis was carried out, but the results were blinded to the investigators throughout the study period. At position 389 of the β-1 adrenergic receptor gene (ADRB1), the observed minor Gly allele frequency (Gly389Arg + Gly389Gly) was 0.21, and no deviation from Hardy-Weinberg equilibrium was observed in the genotypic distribution of Arg389Gly (p = 0.75). Heart rate was reduced from 80.8 ± 14.3 to 70.0 ± 15.0 beats per minute (p < 0.0001). There was no significant difference in final heart rate across genotypes. However, the Arg389Arg genotype group required significantly more bisoprolol compared to the Gly389X (Gly389Arg + Gly389Gly) group (5.26 ± 2.62 mg vs. 3.96 ± 2.05 mg, p = 0.022). There were no significant differences in LVEF changes or remodeling between two groups. Also, changes in exercise capacity and brain natriuretic peptide level were not significant. However, interestingly, there was a two-fold higher rate of readmission (21.2% vs. 10.0%, p = 0.162) and one CHF-related death in the Arg389Arg group. Conclusions: The ADRB1 Gly389X genotype showed greater response to bisoprolol than the Arg389Arg genotype, suggesting the potential of individually tailoring β-blocker therapy according to genotype.
UR - http://www.scopus.com/inward/record.url?scp=84959007985&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84959007985&partnerID=8YFLogxK
U2 - 10.3904/kjim.2015.043
DO - 10.3904/kjim.2015.043
M3 - Article
C2 - 26879662
AN - SCOPUS:84959007985
VL - 31
SP - 277
EP - 287
JO - Korean Journal of Internal Medicine
JF - Korean Journal of Internal Medicine
SN - 1226-3303
IS - 2
ER -