Complex and simple hybrid procedures enable multilevel revascularizations in high-risk patients with comparable patency and limb salvage. Femoral endarterectomy plays a central role, especially in complex hybrid repairs. An increase in perioperative morbidity and mortality was observed in the hybrid group, likely due to attempting revascularization in higher risk patients.

Management of early, deep groin wound infections with debridement, antibiotics, and VAC treatment is safe and enables graft preservation in the majority of patients with minimal morbidity, no perioperative limb loss, or mortality.

We have recently shown that nicotine and its metabolite cotinine are mitogenic for smooth muscle cells in vitro. In the present study, we examined the effect of nicotine and cotinine on the production of growth factors and the expression of matrix metalloproteinases in smooth muscle cells. Methods: Smooth muscle cells were harvested from human arteries and grown in culture. Subconfluent cultures were incubated for 24 hours in M199 containing 0.1% fetal bovine serum with or without nicotine or cotinine at concentrations ranging from 10-9 m o l / L to 10 -6 mol/L. The supernatants and cell lysates were assayed by enzyme-linked immnnosorbent assay for basic fibroblast growth factor (bFGF), tumor necrosis factor alpha (TNF-~), platelet-derived growth factor AB (PDGF-AB), and transforming growth factor beta (TGF-~). Matrix metalloproteinase expression was determined in subcontinent cultures incubated in albumin with or without nicotine or cotinine at 10 -8 m o l / L and 10 -7 m o l / L for 6, 12, 18, 24 and 36 hours. Northern blot analyses were performed with human cDNA probes for collagenase-1, stromelysin-1, gelatinase A, gelatinase B, and triose phosphate isomerase. Blots were quantified by phosphor-imaging techniques. Results: Both nicotine and cotinine stimulated the production and secretion of bFGF in a dose-dependent manner. PDGF, TNF-eg and TGF-~ secretions were not significantly affected by nicotine or cotinine. Collagenase was up-regulated by nicotine at 18 and 24 hours (4.5-fold to 5.8-fold) and by cotinine at 18 hours (from 5.0-fold to 29-fold). Stromelysin-1 was up-regulated by nicotine and cotinine at 12 and I8 hours (1.5-fold to 7.0-fold). Gelatinase A generally peaked at 12 hours and was up-regulated by both agents (2.0-fold to 6.5-fold). Conclusion: Nicotine and cotinine enhanced the production of bFGF, a major mitogen for smooth muscle cells, and up-regulated the expression of several matrix metalloproteinases that are critical in cell migration. These data demonstrate mechanisms by which smoking may contribute to the development of intimal hyperplasia, atherosclerosis, and aneurysms.

The formation of neointimal thickenings in the rat carotid artery after balloon injury was studied by a combination of electron-microscopic and stereological methods. All smooth muscle cells in the normal media had a contractile phenotype, the cytoplasm being dominated by myofilaments. Seven days after endothelial denudation, the smooth muscle cells in the innermost part of the media had assumed a synthetic phenotype by loss of myofilaments and formation of a large endoplasmic reticulum and Golgi complex. These cells moved through fine openings in the internal elastic lamina and gave rise to a growing neointima by proliferation and secretion of extracellular matrix components. Fourteen days after the operation, the neointima had almost reached its final size, and mitoses were no longer noted. Nevertheless, the cells maintained a synthetic phenotype with prominent secretory organelles, although myofilaments had started to become more abundant again. They were surrounded by an extracellular matrix made up of collagen fibrils and coalescing patches of elastin. Thirty-five days after the operation, an endothelial cell layer had reformed and covered most of the luminal vessel surface. In parallel, the smooth muscle cells in the neointima had returned to a contractile phenotype with a cytoplasm dominated by myofilaments. These findings provide a morphological basis for further analysis of the cellular and molecular interactions involved in the formation of neointimal thickenings after endothelial injury, and for the search for agents interfering with this process.

Amputation despite PETAS is the most common means of limb loss in patients undergoing endovascular revascularization for limb salvage. It is likely the result of aggressive attempts at limb salvage and usually occurs