Why the study?
Adrenergic activity via beta-1 adrenoceptors plays a central role in HCM, but the impact of ADRB-1 gene polymorphisms on clinical aspects and beta-blocker response required investigation.
Does ADRB-1 gene polymorphism impact the structural and clinical response to beta-blocker therapy in patients with hypertrophic cardiomyopathy?
Cohort (n=147)
No
Does ADRB-1 gene polymorphism impact the structural and clinical response to beta-blocker therapy in patients with hypertrophic cardiomyopathy?
ADRB-1 Ser49Gly polymorphism identifies HCM patients who are more likely to have a robust reduction in ventricular ectopy and NT-proBNP in response to beta-blocker therapy.
Answers are grounded in this paper and cite their sources.
Suggests ADRB-1 genotyping may eventually help predict antiarrhythmic response to beta-block.
BACKGROUND: Hypertrophic cardiomyopathy (HCM) is a genetically inherited cardiac disorder with diverse clinical presentations. Adrenergic activity, primarily mediated through beta-adrenoceptors, plays a central role in the clinical course of HCM. Adrenergic stimulation increases cardiac contractility and heart rate through beta-1 adrenoceptor activation. Beta-blocker drugs are recommended as the primary treatment for symptomatic HCM patients to mitigate these effects. METHODS: This prospective study aimed to investigate the impact of common ADRB-1 gene polymorphisms, specifically serine-glycine at position 49 and arginine-glycine at position 389, on the clinical and structural aspects of HCM. Additionally, the study explored the association between these genetic variations and the response to beta-blocker therapy in HCM patients. RESULTS: A cohort of 147 HCM patients was enrolled, and comprehensive assessments were performed. The findings revealed that the Ser49Gly polymorphism significantly influenced ventricular ectopic beats, with beta-blocker therapy effectively reducing them in Ser49 homozygous patients. Moreover, natriuretic peptide levels decreased, particularly in Ser49 homozygotes, indicating improved cardiac function. Left ventricular outflow obstruction, a hallmark of HCM, was also reduced following beta-blocker treatment in all patient groups. In contrast, the Arg389Gly polymorphism did not significantly impact baseline parameters or beta-blocker response. CONCLUSION: These results emphasize the role of the Ser49Gly polymorphism in the ADRB-1 gene in shaping the clinical course and response to beta-blocker therapy in HCM patients. This insight may enable a more personalized approach to managing HCM by considering genetic factors in treatment decisions. Further research with larger populations and longer follow-up periods is needed to confirm and expand upon these findings.
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Damla Raimoglou (2024) conducted a cohort in Hypertrophic cardiomyopathy (HCM) (n=147). Metoprolol (beta-blocker therapy) vs. Baseline (pre-treatment) across ADRB-1 polymorphism groups was evaluated on Reduction in daily premature ventricular contractions (VES count) following therapy in Ser49 homozygotes (p=<0.001).
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