The mortality rate of chronic systolic HF patients carrying no α(2c)-adrenoceptor Del322-325 alleles was significantly higher (almost 2.5-fold) than that of HF patients carrying ≥1 allele.
The alpha(2C) Del322-325 polymorphism exclusively or in combination with the beta(1)Arg389 allele is not associated with an increased risk of adverse events in HF.
A four-amino acid deletion was identified within the alpha 2C-adrenergic receptor (alpha 2C Del322-325) that, when homozygous, increases the risk of heart failure in African-Americans nearly six-fold.
Genotypes and haplotypes of ADRB1, ADRB2, and ADRA2C did not significantly affect survival in metoprolol-treated or carvedilol-treated HF patients in this study.
The purpose of this study was to investigate possible synergistic effects of polymorphisms of these two intronless genes (ADRB1 and ADRA2C, respectively) on the risk of death/transplant in heart failure patients.
We tested whether the ADRA2C insertion/deletion polymorphism was associated with beta-blocker response in heart failure, either alone or in combination with the ADRB1Arg389Gly polymorphism.
Patients with a deletion of 4 consecutive amino acids in the gene encoding for the alpha(2C)-adrenergic receptor (alpha(2C)Del322-325) have an increased prevalence of clinical heart failure, worse clinical status, and a lower left ventricular ejection fraction compared with patients without this deletion.