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ObjectivePercutaneous transluminal angioplasty (PTA) has had an expanding role as primary therapy for vein graft stenosis with variable results. The aim of this study is to identify patient and graft characteristics predictive of failure after PTA of infrainguinal vein grafts.MethodsRetrospective review from Jan 2004 to Mar 2007 of patients undergoing angioplasty for failing grafts. Demographics, comorbidities, procedural data, and follow-up information were recorded. PTA failure was defined as first significant event including restenosis by duplex scan (>3.5 × velocity ratio), occlusion, redo-PTA, surgical revision, or amputation. Descriptive, logistic regression and life-table analyses were performed.ResultsEighty-seven grafts in 79 patients underwent PTA. Mean age was 70 years (median 70; range, 39-89 years), 71% were male and 52% were symptomatic (40% with limb-threat). Mean follow-up was 17 months (median 17.4; range, 0.03-39.8 months). Freedom from PTA failure was 58% (standard error [SE] 0.0574) at 12 months. Predictors of PTA failure by multivariate analysis were: time from bypass 2 cm (HR 2.7; 95% CI 1.33-5.83; P = .007) and multiple stenoses (HR 2.5; 95% CI 1.29-5.1; P = .007). PTA patency for grafts with favorable lesions (single, less than 2 cm lesions in grafts older than 3 months) was 71% vs 35% for unfavorable lesions at 12 months. Limb-salvage was 95% and 90% and overall survival was 92% and 81% at 12 and 24 months, respectively.ConclusionPTA of failing infrainguinal vein grafts is a reasonable primary therapy for favorable lesions. Early graft stenosis, long, and multiple stenoses are markers for procedural failure and are better served with surgical revision.

OBJECTIVES The purposes of this study were to analyze coronary specimens from patients with diabetes mellitus (DM) and to compare them with specimens from patients without DM. BACKGROUND Diabetes mellitus is associated with an increased incidence of restenosis after percutaneous transluminal coronary angioplasty (PTCA). Increased hypercellular smooth muscle cell proliferation with exaggerated intimal hyperplasia formation may be responsible for this predisposition. METHODS Eighteen coronary atherectomy specimens with restenosis after PTCA from patients with DM were compared with 18 coronary atherectomy specimens with restenosis after PTCA from patients without DM. Total and segmental areas were quantified on trichrome-stained tissue of hypercellular tissue, collagen-rich sclerotic tissue, atheroma and thrombus. Demographic and angiographic data were similar in both groups. RESULTS The percentage of total plaque area composed of hypercellular tissue was lower in restenotic specimens from patients with DM than in restenotic specimens from patients without DM (19 ± 6% vs. 44 ± 5%; p = 0.003). The percentage of collagen-rich sclerotic tissue area was larger in restenotic specimens from patients with DM than in restenotic specimens from patients without DM (77 ± 9% vs. 53 ± 4%; p = 0.004). The percentages of atheroma and thrombus were similar in both groups. CONCLUSIONS Intimal hypercellular tissue content is reduced in restenotic tissue from patients with DM. Collagen-rich sclerotic content is increased in restenotic lesions from patients with DM. These results suggest an accelerated fibrotic rather than a proliferative response in diabetic lesions from patients with restenosis after PTCA.

Objectives The healing response to vascular injury is characterized by neointimal thickening. Proliferation and phenotypic transformation of vascular smooth muscle cells (SMCs) have been implicated in this process. We sought to investigate the role of survivin, a dual regulator of cell proliferation and apoptosis, in lesion formation after diverse forms of vascular injury. Methods Rabbits underwent either carotid interposition vein grafting (n = 17) or bilateral femoral balloon injury (BI; n=29); some in the BI group were placed on a high-cholesterol diet. A subset of BI arteries were treated with local adenoviral gene delivery of a survivin dominant negative-mutant (AdT34A) versus vector or saline controls. Survivin expression in vessels was analyzed by quantitative reverse transcriptase polymerase chain reaction (RT-PCR) and by immunohistochemistry (IHC), which also included markers of SMC differentiation. Specimens of human tissue including failed lower extremity bypass grafts and carotid plaque were also examined. Results RT-PCR and IHC demonstrated increased survivin expression in all experimental models, colocalizing at early times with proliferating and α-actin-expressing cells but was largely absent in mature, contractile SMCs. Delivery of AdT34A after BI attenuated neointimal hyperplasia. Conclusion These studies provide strong evidence supporting a role for survivin in the cellular response to vascular injury. Clinical relevance The regulation of cell proliferation, death, and phenotype after vascular interventions remains incompletely understood. We investigated the role of the inhibitor of apoptosis protein survivin in diverse models of vascular injury. The results suggest that survivin is an important modulator of the generalized vascular injury response and may represent a relevant target for therapies targeting intimal hyperplasia.