Intravascular ultrasound evidence for stabilization of compensatory enlargement of the femoropopliteal segment after endograft placement

Citation
T. Hagenaars et al., Intravascular ultrasound evidence for stabilization of compensatory enlargement of the femoropopliteal segment after endograft placement, J ENDOVAS T, 8(3), 2001, pp. 308-314
Citations number
13
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
JOURNAL OF ENDOVASCULAR THERAPY
ISSN journal
15266028 → ACNP
Volume
8
Issue
3
Year of publication
2001
Pages
308 - 314
Database
ISI
SICI code
1526-6028(200106)8:3<308:IUEFSO>2.0.ZU;2-9
Abstract
Purpose: To document whether the vasodilatory response seen at the anastomo tic segment 6 months after placement of a balloon-expandable endograft in t he femoropopliteal segment progresses between 6 and 24 months. Methods: Twelve patients (9 men; median age 65 years, range 47-75) treated with an investigational polytetrafluoroethylene (PTFE) endograft for obstru ctive disease of the femoropopliteal segment were studied with intravascula r ultrasound (IVUS) immediately after placement and at 6 months (first foll ow-up period) and 24 months (second follow-up period). Matched IVUS cross s ections derived from the endograft and the anastomotic segment were analyze d for changes in lumen (LA), vessel (VA), and plaque areas (PLA). Results: Five patients had complete IVUS surveillance at both the first (me an 8 months, range 7-9) and second (mean 25 months, range 23-26) follow-up periods; 1 patient was lost to follow-up during the second interval, and an other 6 were excluded owing to graft occlusion (n = 4) or no IVUS surveilla nce available (n = 2) during the second follow-up period. Matched IVUS cros s sections derived from the endograft showed no significant change in LA du ring both follow-up periods (-8% and +1%, respectively). There was no evide nce for intimal hyperplasia or endograft recoil. During both follow-up peri ods, IVUS cross sections derived from the anastomotic segment revealed sign ificant increases in LA (+37% and +8%, respectively) and VA (+26% and +6%, respectively) (both p < 0.05). The change in PLA during both follow-up peri ods was not significant (+13% and +3%, respectively). Conclusions: The PTFE endograft seems to inhibit both intimal hyperplasia a nd constrictive remodeling. The short-term (6-month) vascular dilatory resp onse seen at the anastomotic segment tends to stabilize at 2 years. Therefo re, this endovascular anastomosis acts as an "ideal" end-to-end anastomosis .