[Arterial dysfunction after treatment of coarctation of the aorta]

The long term follow-up after successful coarctation repair has a late cardiovascular morbidity, includes systemic hypertension at rest or/and after exercise. The pathophysiology mechanisms responsible have not been well determined. We studied 70 normotensive subjects at rest (age, 14 +/- 5 y; pressure, 116 +/- 13/56 +/- 9 mmHg), who had an isolated coarctation with a good repair defined by the absence of gradient between upper and lower right limb (0.-26 mmHg). After exercise testing we defined two groups: Coa HT: Hypertension at exercise equal or over 200 mmHg, n = 20 (228 +/- 23 mmHg) and Coa HT: Normotensive at exercise = 10 (163 +/- 24 mmHg). These subjects were mached sex-age and blood pressure to 70 controls (age, 13 +/- 3 y; pressure, 115 +/- 10/56 +/- 6 mmHg). Using a high-resolution echographic technique, we assessed the systolic, diastolic diameter and the intima media thickness (IMT) of the common carotid artery (CCA) to define mechanical indexes: Cross sectional compliance (CSC), distensibility (CSD) and incremental elastic modulus (Einc) in each group. CCA pressure waveform and the local pulse pressure were determined in 32 subjects to define augmentation index (AI). The changes of the brachial artery diameter in response to reactive hyperaemia (flow mediated dilation: FDM) and to glyceryltrinitrate (GTNMD) were measured. The IMT was significantly increased in the Coa group (by 8%, p < 0.001) and higher in the Coa HT group compared with the Coa NT group (0.57 +/- 0.04 mm vs 0.54 +/- 0.05 mm, p < 0.05). The CSD was lower and the Einc was higher in both groups. The carotid pulse pressure amplitude was significantly higher in the Coa HT Group (41 +/- 14 vs 33 +/- 7 mmHg; p < 0.05). The AI was higher in both Coa repair groups. Both flow-mediated dilation (FMD) and GTN-mediated dilation (GTNMD) of the brachial artery were lower in the Coa group (respectively 5 +/- 3 vs 7 +/- 3%; p < 0.01; 16 +/- 8 vs 23 +/- 9%; p < 0.01). GTNMD was inversely correlated with maximum systolic blood pressure on exercise (r = 0.31, p = 0.03). The IMT of the CCA was related to the local pulse pressure in both groups of coarctation repair. The combination of distensibility decrease in the proximal arterial bed with an impairment of distal artery reactivity would account for the elevation of exercise blood pressure in subjects who had coarctation repair. The increase of local pulse pressure influences the carotid wall hypertrophy.