Does compliance mismatch alone cause neointimal hyperplasia?

Abstract

To define the relationship between compliance mismatch and the development of neointimal hyperplasia, one 3 cm segment of common iliac artery was externally banded in seven dogs, thereby fixing the arterial diameter at end diastole. To quantify compliance, end-diastole diameter and its change with pulse pressure were measured by induction angiometry. This technique uses intravascular soft trifilar wire probes introduced through distally placed polytetrafluoroethylene sidearms. Compliance was checked in the banded and contralateral undissected unbanded control iliac arteries at 3 and 6 months, at which times the vessels were fixed by perfusion, excised, and examined histologically. Sustained (6-month) compliance mismatch was successfully induced within the banded segments (p < 0.0001), and no compliance mismatch was seen in the control segments (p = 0.357). The intima of all banded vessels was virtually indistinguishable from that in controls grossly and histologically. Mild focal intimal thickening, <3 cell layers thick involving <5% of the vessel circumference, was typically seen in both banded and control vessels (range 6.57 ± 6.80 μm to 38.86 ± 57.16 μm). In marked contrast, at the sites of the polytetrafluoroethylene-to-femoral artery anastomosis, near-occlusive neointimal hyperplasia (1714 ± 415.47 μm) was seen in all animals. Residual lumen area in the banded and control vessels was only minimally abnormal (range 98.65% ± 2.18% to 99.96% ± 0.08%). These data indicate that compliance mismatch alone is an insufficient stimulus for the development of neointimal hyperplasia in the canine model.