Arterial dysfunction after coarctation repair

The long term follow-up after successful coarctation repair has a late card iovascular morbidity, includes systemic hypertension at rest or/and after e xercise. The pathophysiology mechanisms responsible have not been well dete rmined. 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 de fined by the absence of gradient between upper and lower right limb (0-26 m mHg). 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: Normot ensive at exercise= 10 (163 +/- 24 mmHg). These subjects were mached sex-ag e and blood pressure to 70 controls (age, 13 +/-3 y: pressure, 115 +/- 10/5 6 +/-6 mmHg). Using a high-resolution echographic technique, we assessed the systolic, di astolic 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 grou p. CCA pressure waveform and the local pulse pressure were determined in 32 subjects to define augmentation index (AI). The changes of the brachial ar tery diameter in response to reactive hyperaemia (flow mediated dilation: F DM) and to glyceryltrinitrate (GTNMD) were measured. The IMT was significantly increased in the Coa group (by 8%, p<0.001) and h igher in the Coa HT group compared with the Coa NT group (0.57<plus/minus>0 .04 mm vs 0.54 +/-0.05 mm, p<0.05). The CSD was lower and the Einc was high er in both groups. The carotid pulse pressure amplitude was significantly h igher in the Coa HT Group (41<plus/minus>14 vs 33 +/-7 mmHg; p<0.05). The A I was higher in both Coa repair groups. Both flow-mediated dilation (FMD) a nd GTN-mediated dilation (GTNMD) of the brachial artery were lower in the C oa group (respectively 5<plus/minus>3 vs 7 +/-3%; p<0.01; 16<plus/minus>8 v s 23 +/-9%; p<0.01). GTNMD was inversely correlated with maximum systolic b lood 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 combi nation of distensibility decrease in the proximal arterial bed with an impa irment of distal artery reactivity would account for the elevation of exerc ise blood pressure in subjects who had coarctation repair. The increase of local pulse pressure influences the carotid wall hyper-trophy.