Background: 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.

Patients and methods: 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 (AGTR I, c.I 166A > C), endothelin 1 (EDNI, EDNI/ex5-c.5665G > T), G protein (GNB3, c.825C > 7), and two polymorphisms each of the beta 1-adrenoreceptor (ADRBI, c.I 45G > A and c.I 165C > G), beta 2-adrenoreceptor (ADRB2, c.46A > G and c.79C > G), and endothelial NO synthase (NOS3, intron 4 I/D and NOS3, c.894G > 7) were determined by PCR amplification and fragment length analysis. Exercise capacity was determined by an upright bicycle exercise test.

Results: Only the c.46A > G polymorphism of the ADRB2 = 0.024) and the c.704T > C AGT polymorphism = 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.

Conclusions: 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 beta 2-receptor c.46A > G polymorphism. Therefore, the exercise capacity of coarctation patients does not profit from an enhanced down regulation of their beta receptors.