Exercise capacity after coarctation repair relates to the c.46A > G genomic polymorphism of the ß2-adrenoreceptor and the c.704T > C angiotensinogen polymorphism

Even after excellent repair of aortic coarctation without restenosis there are limitations in exercise capacity at long-term follow-up. This study was performed to assess the contribution of inherited genomic polymorphisms to exercise capacity in patients without restenosis.

122 patients aged 17–72 years, 46 female, 76 male, seen 2–27 years after repair of aortic coarctation with a residual brachial-ankle-gradient ≤20 mmHg were investigated. Genomic polymorphism of angiotensin converting enzyme (ACE I/D), angiotensinogen (AGT, c.704C > T), angiotensin II receptor type 1 (AGTR1, c.1166A > C), endothelin 1 (EDN1, EDN1/ex5-c.5665G > T), G protein (GNB3, c.825C > T), and two polymorphisms each of the ß1-adrenoreceptor (ADRB1, c.145G > A and c.1165C > G), ß2-adrenoreceptor (ADRB2, c.46A > G and c.79C > G), and endothelial NO synthase (NOS3, intron 4 I/D and NOS3, c.894G > T) were determined by PCR amplification and fragment length analysis. Exercise capacity was determined by an upright bicycle exercise test.

Only the c.46A > G polymorphism of the ADRB2 (p = 0.024) and the c.704T > C AGT polymorphism (p = 0.042) were positively correlated with peak workload. Patients with one or especially two polymorphic alleles showed a significant higher exercise performance compared with those patients homozygous for the wild type.

In contrast to a previous study in heart failure patients, after coarctation repair adults had a better exercise capacity with the G allele of the ß2-receptor c.46A > G polymorphism. Therefore, the exercise capacity of coarctation patients does not profit from an enhanced down regulation of their beta receptors.