THE INFLUENCE OF LESION LENGTH ON INTIMAL HYPERPLASIA AFTER FOGARTY BALLOON INJURY IN THE RABBIT CAROTID-ARTERY - ROLE OF ENDOTHELIUM

After balloon angioplasty, retarded endothelial cell recoverage of the injured segment may lead to enhanced intimal hyperplasia. We tested t he hypothesis that long lesions result in more intimal hyperplasia tha n short lesions due to a prolonged time to complete endothelial cell r ecoverage. A 2-french Fogarty balloon was used to create 2.5- and 5-cm -long lesions in the rabbit carotid artery. After termination, the inj ured arteries (n = 9 for all groups) were serially processed for histo chemistry. Endothelial cell coverage was assessed with an antibody to CD31 and cell proliferation with a monoclonal antibody to Ki-67 nuclea r antigen. The intimal hyperplasia cross-sectional area was measured m orphometrically. All data are mean +/- SEM. At 21 days, endothelial ce ll recoverage was almost complete in the 2.5-cm lesions. In the 5-cm l esions, endothelial cell recoverage was 66 +/- 6% in the middle segmen ts (p = 0.04, 2.5 vs. 5 cm) and 100% at the cranial and caudal ends of the lesion. At 42 days, endothelial cell coverage had increased to 81 +/- 7% in the middle segments of the 5-cm lesions. The intimal hyperp lasia area was similar in the 2.5- and the 5-cm lesions both at 21 day s (0.19 +/- 0.02 and 0.20 +/- 0.01 mm(2), respectively) and 42 days (0 .27 +/- 0.02 and 0.26 +/- 0.03 mm(2), respectively). The increase in i ntimal hyperplasia from 21 to 42 days was significant for both lesion lengths (p = 0.004). At 21 days, intimal proliferation was similar for the 2.5- and 5-cm lesions. After 42 days postinjury, intimal prolifer ation had decreased (p < 0.001) equally for both lesion lengths. Earli er recoverage by endothelium in the 2.5-cm lesions did not inhibit int imal hyperplasia compared to the 5-cm lesions which were still incompl etely reendothelialized. We conclude that in the rabbit, rapid endothe lial cell recoverage of Fogarty balloon-injured arteries may not limit intimal hyperplasia in the center of the lesion. It is conceivable th at the inability of regenerated endothelium to inhibit intimal hyperpl asia is due to its initially dedifferentiated and possibly dysfunction al phenotype.