Parameters of arterial function and structure in adult patients after coarctation repair.

Regardless of a successful operation, patients with coarctation of aorta (CoAo) are exposed to the risk of hypertension and a propensity to vascular and end-organ damage. The aim of this study is to evaluate the influence of residual aorta stenosis as well as the age at the operation on the parameters of arterial function and structure in patients after CoAo repair. Eighty-five patients after CoAo repair (53 males; mean age: 34.6 ± 10.3 years, mean age at the repair: 10.9 ± 8.2 years) were enrolled in the study. The control group consisted of 30 healthy subjects (18 males; mean age: 33.6 ± 8.2 years). Indices of systemic arterial remodeling [flow-mediated dilatation (FMD), nitroglycerine-mediated vasodilatation (NMD), carotid intima-media thickness (IMT), pulse wave velocity (PWV)] were analyzed in all study patients. In normotensive patients after CoAo repair (47/55%), a significantly increased PWV was observed in comparison to the control group (6.8 ± 1.2 vs. 5.4 ± 0.9 m/s; p = 0.003), with no difference in IMT values (0.53 ± 0.1 vs. 0.51 ± 0.1 mm; p = 0.06). Mean FMD (4.8 ± 2.8 vs. 8.5 ± 2.3%; p = 0.00003) and NMD (11.3 ± 4.6 vs. 19.8 ± 7.2%; p = 0.00001) were lower than in the controls. In patients with a residual aorta stenosis (46/54%), defined as an arm-leg pressure gradient ≥ 20 mmHg, no differences were found within the scope of both systolic and diastolic blood pressure and of all of the examined vascular parameters. No significant correlations were revealed between the vascular parameters and the gradient across descending aorta as well as the age at the operation. Residual stenosis in the descending aorta does not affect the arterial vasodilatation nor stiffness in patients after CoAo repair. An early surgery does not influence the remodeling of the vessels, which supports the thesis that CoAo is a generalized vascular disease and that even an early operation cannot prevent the progressive and vascular changes and end-organ damage.