Polymorphisms of the Beta Adrenergic Receptor Predict Left Ventricular Remodeling Following Acute Myocardial Infarction
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Prior studies demonstrate an association between specific beta-adrenergic receptor (β-AR) polymorphisms and clinical outcomes in patients with chronic heart failure and following acute coronary syndromes. The underlying mechanism may be due to differences in left ventricular remodeling. This study was undertaken to explore the relationship between LV remodeling after myocardial infarction and polymorphisms in the cardiac β1-AR and β2-AR genes.
After first ST-segment elevation myocardial infarction (STEMI), 122 patients on chronic β1 receptor antagonist therapy underwent baseline and 6-month LV volume evaluation. We assessed the relationships between changes in LV volumes and the polymorphisms in β1-AR, β1-Arg389Gly and β1-Ser49Gly, and in β2-AR, β2-Gly16Arg and β2-Gln27Glu.
We found that patients homozygous for the β2-Glu27 variant were 5.2 times more likely to be in the group with the highest end systolic volume (ESV) progression (OR 5.2, 95%CI 1.4–19.0). They were also more likely to have the largest progression of end diastolic volume (EDV) and decrease in LV ejection fraction (LVEF). For those with baseline LV dysfunction, being homozygous for Arg at amino acid position 389 in β1-AR was associated with decreases in ESV (−46 mL, CI −3.1, -88) and EDV (−40 mL, CI −1.1, −79) and an increase in LVEF (11%, CI 0.3, 22).
We found that polymorphisms of the β1-AR and β2-AR genes are associated with differential LV remodeling in patients treated with a β1 receptor antagonist following STEMI.