The Journal of Thoracic and Cardiovascular Surgery, Vol 103, 146-152, Copyright © 1992 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
Improved healing of small-caliber polytetrafluoroethylene vascular prostheses by increased hydrophilicity and by enlarged fibril length. An experimental study in rats
JW Stronck, B van der Lei and CR Wildevuur
Department of Cardiopulmonary Surgery, University Hospital of Groningen, The Netherlands.
This study was undertaken to test whether increasing the hydrophilicity of
small-caliber polytetrafluoroethylene vascular prostheses by alcohol
pretreatment or increasing their fibril length might improve their healing
without affecting their patency. Polytetrafluoroethylene vascular
prostheses (length 1 cm, inside diameter 1.2 mm) (1) with a fibril length
of 30 microns (control group; n = 18), (2) pretreated with alcohol (n =
18), or (3) with a fibril length of 60 microns (n = 18) were implanted into
the abdominal aorta of rats. The prostheses were evaluated by means of
routine light and scanning electron microscopy during a 6-week period after
implantation. All prostheses were patent at harvesting. On implantation,
the control polytetrafluoroethylene vascular prostheses were only scarcely
covered with platelets. At 6 weeks they had healed in a small area adjacent
to the anastomoses only. In contrast, both the alcohol-pretreated
polytetrafluoroethylene prostheses and the polytetrafluoroethylene
prostheses with a fibril length of 60 microns were completely covered by a
thin clot layer on implantation. At 6 weeks after implantation these
prostheses had almost completely healed as a result of organization of the
thin clot layer by ingrowth of both endothelial and smooth muscle cells.
These results demonstrate that increasing hydrophilicity of
polytetrafluoroethylene vascular prostheses by alcohol pretreatment or
enlarging their fibril length improves their healing by induction of a thin
luminal clot layer. This clot layer provides a suitable matrix for ingrowth
of both endothelial and smooth muscle cells and does not lead to
thromboembolic complications.
