Effect of aortic stiffness versus stenosis on ventriculo-arterial interaction in an experimental model of coarctation repair.

OBJECTIVES

The aim of this study was to investigate the effect of short- versus long-segment aortic stiffness and stenosis on ventriculo-arterial interaction in a porcine model of coarctation repair.

METHODS

Short-long aortic stiffness was created by transection/suture [coarctation (CoA) suture, n = 6] and stenting (stent, n = 5) of the proximal descending aorta. Short-long aortic stenosis was achieved by wrapping a prosthetic graft around the aorta to 1/3-circumference reduction, over a segment length of 1 cm (CoA suture stenosis, n = 5) and 4.5 cm (stent stenosis, n = 6). After 3 months, aortic pressure-flow haemodynamics, aortic distensibility by intravascular ultrasound and left ventricular performance by pressure-volume loops were compared to a Sham group (n = 5) at baseline and during dobutamine administration.

RESULTS

The aortic impedance increased with 30.3 (12.6%) and 41.3 (20.9%) (P < 0.001) in CoA stenosis and stent stenosis during inotropic response. Impaired haemodynamic aortic compliance was associated with lower aortic distensibility by intravascular ultrasound, specifically in long-segment stenosis. The ventriculo-arterial coupling was disturbed in both groups with stenosis, with blunted contractile response [Sham 140.3 (19.8%), CoA suture 101.3 (14.5%), CoA suture stenosis 75.0 (8.4%), stent 115.5 (12.7%), stent stenosis 55.1 (14.6%), P < 0.001] and increased myocardial stiffness during dobutamine in the long-segment aortic stenosis group [Sham -26.0 (12.9%), CoA suture -27.5 (15.9%), CoA stenosis -9.5 (8.6%), stent -23.4 (4.8%), stent stenosis 19.9 (23.1%), P < 0.001].

CONCLUSIONS

This animal study on the sequelae of coarctation repair demonstrated that aortic stiffness had little effect on aortic pressure-flow characteristics in the absence of stenosis. However, the negative chronic effect of stenosis on aortic haemodynamics-especially a longer segment-leads to the rapid impairment of ventriculo-arterial interaction, which is accentuated by inotropy. Therefore, therapeutical management needs to focus on improving aortic remodelling after coarctation repair, preferably by minimizing residual stenosis, even at the cost of inducing aortic stiffness.