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Richard J Powell

Publications and source records attributed to Richard J Powell.

At least 37 records · Page 2Linked to original sources

Management of carotid injuries in a hostile neck using endovascular grafts.

Pseudoaneurysms and iatrogenic injuries of the extracranial carotid artery are not common but represent unique operative challenges with associated high morbidity and mortality. We report two cases in which a Wallgraft was used via percutaneous femoral access to treat such injuries. In the first, a 6-cm carotid pseudoaneurysm was successfully excluded by coil embolization of the external carotid artery and stent grafting across the carotid bifurcation. In the second case, an endovascular graft was used to treat an intraoperative common carotid injury in a re-operated, radiated neck. These cases demonstrate the utility of endovascular graft treatment of emergent carotid injuries.

Aged↗

Anatomic characteristics of ruptured abdominal aortic aneurysm on conventional CT scans: Implications for rupture risk.

OBJECTIVE: The purpose of this study was to analyze anatomic characteristics of patients with ruptured abdominal aortic aneurysms (AAAs), with conventional two-dimensional computed tomography (CT), including comparison with control subjects matched for age, gender, and size. METHODS: Records were reviewed to identify all CT scans obtained at Dartmouth-Hitchcock Medical Center or referring hospitals before emergency AAA repair performed because of rupture or acute severe pain (RUP group). CT scans obtained before elective AAA repair (ELEC group) were reviewed for age and gender match with patients in the RUP group. More than 40 variables were measured on each CT scan. Aneurysm diameter matching was achieved by consecutively deleting the largest RUP scan and the smallest ELEC scan to prevent bias. RESULTS: CT scans were analyzed for 259 patients with AAAs: 122 RUP and 137 ELEC. Patients were well matched for age, gender, and other demographic variables or risk factors. Maximum AAA diameter was significantly different in comparisons of all patients (RUP, 6.5 +/- 2 cm vs ELEC, 5.6 +/- 1 cm; P <.0001), and mean diameter of ruptured AAAs was 5 mm smaller in female patients (6.1 +/- 2 cm vs 6.6 +/- 2 cm; P =.007). Two hundred patients were matched for diameter, gender, and age (100 from each group; maximum AAA diameter, 6.0 +/- 1 cm vs 6.0 +/- 1 cm). Analysis of diameter-matched AAAs indicated that most variables were statistically similar in the two groups, including infrarenal neck length (17 +/- 1 mm vs 19 +/- 1 mm; P =.3), maximum thrombus thickness (25 +/- 1 mm vs 23 +/- 1 mm, P =.4), and indices of body habitus, such as [(maximum AAA diameter)/(normal suprarenal aorta diameter)] or [(maximum AAA diameter)/(L3 transverse diameter)]. Multivariate analysis controlling for gender indicated that the most significant variables for rupture were aortic tortuosity (odds ratio [OR] 3.3, indicating greater risk with no or mild tortuosity), diameter asymmetry (OR, 3.2 for a 1-cm difference in major-minor axis), and current smoking (OR, 2.7, with the greater risk in current smokers). CONCLUSIONS: When matched for age, gender, and diameter, ruptured AAAs tend to be less tortuous, yet have greater cross-sectional diameter asymmetry. On conventional two-dimensional CT axial sections, it appears that when diameter asymmetry is associated with low aortic tortuosity, the larger diameter on axial sections more accurately reflects rupture risk, and when diameter asymmetry is associated with moderate or severe aortic tortuosity, the smaller diameter on axial sections more accurately reflects rupture risk. Current smoking is significantly associated with rupture, even when controlling for gender and AAA anatomy.

Aged↗

Mutant forms of tumour necrosis factor receptor I that occur in TNF-receptor-associated periodic syndrome retain signalling functions but show abnormal behaviour.

Tumour necrosis factor (TNF)-receptor-associated periodic syndrome (TRAPS) is a hereditary autoinflammatory disorder involving autosomal-dominant missense mutations in TNF receptor superfamily 1A (TNFRSF1A) ectodomains. To elucidate the molecular effects of TRAPS-related mutations, we transfected HEK-293 cells to produce lines stably expressing high levels of either wild-type (WT) or single mutant recombinant forms of TNFRSF1A. Mutants with single amino acid substitutions in the first cysteine-rich domain (CRD1) were produced both as full-length receptor proteins and as truncated forms lacking the cytoplasmic signalling domain (deltasig). High-level expression of either WT or mutant full-length TNFRSF1A spontaneously induced apoptosis and interleukin-8 production, indicating that the mutations in CRD1 did not abrogate signalling. Consistent with this, WT and mutant full-length TNFRSF1A formed cytoplasmic aggregates that co-localized with ubiquitin and chaperones, and with the signal transducer TRADD, but not with the inhibitor, silencer of death domain (SODD). Furthermore, as expected, WT and mutant deltasig forms of TNFRSF1A did not induce apoptosis or interleukin-8 production. However, whereas the WT full-length TNFRSF1A was expressed both in the cytoplasm and on the cell surface, the mutant receptors showed strong cytoplasmic expression but reduced cell-surface expression. The WT and mutant deltasig forms of TNFRSF1A were all expressed at the cell surface, but a proportion of the mutant receptors were also retained in the cytoplasm and co-localized with BiP. Furthermore, the mutant forms of surface-expressed deltasig TNFRSF1A were defective in binding TNF-alpha. We conclude that TRAPS-related CRD1 mutants of TNFRSF1A possess signalling properties associated with the cytoplasmic death domain, but other behavioural features of the mutant receptors are abnormal, including intracellular trafficking and TNF binding.

Antigens, CD↗

Therapeutic angiogenesis for critical limb ischemia: design of the hepatocyte growth factor therapeutic angiogenesis clinical trial.

The objective of the HGF-STAT clinical trial is to determine whether perfusion can be improved by gene transfer with a plasmid DNA containing hepatocyte growth factor (HGF) in the affected limb of patients with unreconstructable critical limb ischemia (CLI). CLI results in a high rate of limb loss and impaired quality of life. The current therapeutic strategies, including bypass surgery and percutaneous interventions, are only successful in treating a subset of patients. Therapeutic angiogenesis is an investigational method that seeks to favorably impact tissue perfusion in CLI. HGF-STAT is a double-blind, parallel-group, placebo-controlled, dose-response study in 100 patients with unreconstructable CLI. Eligible subjects will be randomized 1:1:1:1 to receive saline placebo or one of three dose/regimens of HGF plasmid DNA. The selection of outcome measures, including the primary endpoint, and changes in transcutaneous oxygen pressure (TcPO2) from baseline to 3 months will be discussed. In conclusion, this study will help to determine whether therapeutic angiogenesis with HGF is a viable option in the treatment of patients with CLI.

Adult↗

Reactivation of Epstein-Barr virus in patients with systemic lupus erythematosus.

A link between Epstein-Barr Virus (EBV) and systemic lupus erythematosus (SLE) has been suggested. However, recent advances in molecular technology now permit more detailed analysis. Sera from SLE patients were tested for antibodies to several EBV antigens and had a significantly higher prevalence of immunoglobulin G antibodies against EBV early antigens than in normal or disease controls. This suggests that recent EBV infection or virus reactivation was occurring in these patients.

Adult↗

Polymorphism at the C-reactive protein locus influences gene expression and predisposes to systemic lupus erythematosus.

Relative deficiency of pentraxin proteins is implicated in the pathogenesis of systemic lupus erythematosus. The C-reactive protein (CRP) response is defective in patients with acute flares of disease, and mice with targeted deletions of the serum amyloid P component gene (Sap) develop a lupus-like illness. In humans, the genes for CRP (CRP) and SAP (APCS) map to 1q23.2 within an interval linked with SLE. We have investigated the candidate genes CRP and APCS in two cohorts totalling 586 UK simplex SLE families. The inheritance of an intronic dinucleotide repeat and seven single nucleotide polymorphisms in the CRP and APCS genes was examined by application of family-based tests of association and linkage. Basal levels of CRP were influenced independently by two polymorphisms at the CRP locus, CRP 2 and CRP 4. Furthermore, the latter polymorphism was linked/associated with SLE and antinuclear autoantibody production. Thus, the polymorphism associated with reduced basal CRP was also associated with the development of SLE. These data support the hypothesis that defective disposal of potentially immunogenic material is a contributory factor in lupus pathogenesis. The identification of polymorphisms that determine basal CRP levels has implications in ischaemic heart disease, where CRP level is an important predictor of risk.

C-Reactive Protein↗

The mTOR/p70 S6K1 pathway regulates vascular smooth muscle cell differentiation.

Vascular smooth muscle cells (VSMC) in mature, normal blood vessels exhibit a differentiated, quiescent, contractile morphology, but injury induces a phenotypic modulation toward a proliferative, dedifferentiated, migratory phenotype with upregulated extracellular matrix protein synthesis (synthetic phenotype), which contributes to intimal hyperplasia. The mTOR (the mammalian target of rapamycin) pathway inhibitor rapamycin inhibits intimal hyperplasia in animal models and in human clinical trials. We report that rapamycin treatment induces differentiation in cultured synthetic phenotype VSMC from multiple species. VSMC treated with rapamycin assumed a contractile morphology, quantitatively reflected by a 67% decrease in cell area. Total protein and collagen synthesis were also inhibited by rapamycin. Rapamycin induced expression of the VSMC differentiation marker contractile proteins smooth muscle (SM) alpha-actin, calponin, and SM myosin heavy chain (SM-MHC), as observed by immunoblotting and immunohistochemistry. Notably, we detected a striking rapamycin induction of calponin and SM-MHC mRNA, suggesting a role for mTOR in transcriptional control of VSMC gene expression. Rapamycin also induced expression of the cyclin-dependent kinase inhibitors p21(cip) and p27(kip), consistent with cell cycle withdrawal. Rapamycin inhibits mTOR, a signaling protein that regulates protein synthesis effectors, including p70 S6K1. Overexpression of p70 S6K1 inhibited rapamycin-induced contractile protein and p21(cip) expression, suggesting that this kinase opposes VSMC differentiation. In conclusion, we report that regulation of VSMC differentiation is a novel function of the rapamycin-sensitive mTOR signaling pathway.

Animals↗

Heterogeneity among patients with tumor necrosis factor receptor-associated periodic syndrome phenotypes.

OBJECTIVE: To investigate the prevalence of tumor necrosis factor receptor-associated periodic syndrome (TRAPS) among outpatients presenting with recurrent fevers and clinical features consistent with TRAPS. METHODS: Mutational screening was performed in affected members of 18 families in which multiple members had symptoms compatible with TRAPS and in 176 consecutive subjects with sporadic (nonfamilial) "TRAPS-like" symptoms. Plasma concentrations of soluble tumor necrosis factor receptor superfamily 1A (sTNFRSF1A) were measured, and fluorescence-activated cell sorter analysis was used to measure TNFRSF1A shedding from monocytes. RESULTS: Eight novel and 3 previously reported TNFRSF1A missense mutations were identified, including an amino acid deletion (Delta D42) in a Northern Irish family and a C70S mutation in a Japanese family, both reported for the first time. Only 3 TNFRSF1A variants were found in patients with sporadic TRAPS (4 of 176 patients). Evidence for nonallelic heterogeneity in TRAPS-like conditions was found: 3 members of the "prototype familial Hibernian fever" family did not possess C33Y, present in 9 other affected members. Plasma sTNFRSF1A levels were low in TRAPS patients in whom renal amyloidosis had not developed, but also in mutation-negative symptomatic subjects in 4 families, and in 14 patients (8%) with sporadic TRAPS. Reduced shedding of TNFRSF1A from monocytes was demonstrated in vitro in patients with the T50M and T50K variants, but not in those with other variants. CONCLUSION: The presence of TNFRSF1A shedding defects and low sTNFRSF1A levels in 3 families without a TNFRSF1A mutation indicates that the genetic basis among patients with "TRAPS-like" features is heterogeneous. TNFRSF1A mutations are not commonly associated with nonfamilial recurrent fevers of unknown etiology.

Antigens, CD↗

Infliximab in the treatment of refractory posterior uveitis.

PURPOSE: To determine the efficacy and safety of infliximab in the treatment of refractory posterior uveitis. DESIGN: Noncomparative interventional case series. PARTICIPANTS: Five patients with posterior uveitis were treated: 3 had Behçet's syndrome, and 2 had idiopathic posterior uveitis. INTERVENTIONS: Patients with sight-threatening uveitis refractory to other immunosuppressive agents were treated with infliximab. MAIN OUTCOME MEASURES: Intraocular inflammation, by using binocular indirect ophthalmoscopy score, retinal vasculitis, and visual acuity. Adverse effects of infliximab were documented. RESULTS: Within 2 weeks of the first infusion of infliximab, 4 of 5 patients showed marked improvement in vitreous haze and visual acuity. By the 6-month follow-up, the same four patients had achieved remission of posterior uveitis and had successfully withdrawn all other immunosuppressive therapy. Further infusions of infliximab were required in 3 patients. One patient developed ocular and systemic tuberculosis, which responded to antituberculous treatment. CONCLUSIONS: Infliximab is effective in the treatment of sight-threatening refractory posterior uveitis. However, patients should be thoroughly screened for tuberculosis before treatment and followed up closely during and after therapy with infliximab.

Adult↗

Stent-graft treatment of a large internal carotid artery vein graft aneurysm.

Aneurysm degeneration of internal carotid artery interposition vein grafts can occur, and their repair can be complicated by repeated neck dissection and difficulty in obtaining distal artery control. We used a covered stent graft to exclude a large internal carotid artery interposition vein graft aneurysm. Retrograde flow was induced in the internal carotid artery so that an embolization protection balloon could be placed through the aneurysm. The stent graft was then placed with embolization protection. The repair was performed without complication, and the aneurysm remained successfully excluded at 6-month follow-up.

Aneurysm↗

Early results of stent-grafting to treat diffuse aortoiliac occlusive disease.

INTRODUCTION: Diffuse aortoiliac occlusive disease or isolated external iliac artery occlusion >or=10 cm long typically are treated with surgical bypass grafting because of limited durability of stent placement. We evaluated the results of stent-graft placement as an option for treatment of these diseases. METHODS: Demographic data for patients undergoing stent-grafting in one or more iliac artery segments were recorded. Technical, clinical, and hemodynamic success, and aortoiliac primary and secondary patency were analyzed with Society for Vascular Surgery/American Association for Vascular Surgery criteria. RESULTS: Thirty-four consecutive patients underwent stent-graft treatment because of rest pain (65%) or tissue loss (35%). Mean patient age was 63 years, and 38% of patients were women. Ninety-one percent of patients had hypertension, 71% had coronary artery disease, 21% had renal insufficiency (serum creatinine > 2.0 mg/dL), and 26% had diabetes; 71% were active smokers. TransAtlantic Inter-Society Consensus C or D disease was present in 85% of patients, complete common or external iliac artery occlusion was present in 41%, and external iliac artery disease requiring treatment was present in 94% of patients. Mean lesion length was 13.7 +/- 8 cm. Technical, hemodynamic, and clinical success was achieved in all patients in whom the lesion could be crossed with a wire. Ankle-brachial index increased from.30 +/-.03 to.59 +/-.04. Self-expanding stent grafts were used (Wallgraft, Boston Scientific, Boston, Mass, in 88% of patients; Viabahn, W. L. Gore, Flagstaff, Ariz, in 12% of patients). Concomitant common femoral endarterectomy was performed in 53% of patients. At 12 months, primary patency was 70% and primary assisted patency was 88%. Four stent grafts became occluded because of distal external iliac artery or proximal common femoral artery disease, which required subsequent common femoral endarterectomy and either external iliac artery stent grafting or extraanatomic bypass grafting. Eighty percent (four of five) of primary patency failures were in patients who did not undergo concomitant common femoral endarterectomy at initial stent graft placement. CONCLUSION: Early results of stent-graft placement to treat diffuse aortoiliac occlusive disease appear better than our recent experience with stenting alone. Concomitant common femoral endarterectomy or better assessment of femoral disease may improve durability.

Adult↗

Blinded comparison of preoperative duplex ultrasound scanning and contrast arteriography for planning revascularization at the level of the tibia.

PURPOSE: We examined whether preoperative duplex ultrasound scanning (DU) could replace contrast material-enhanced arteriography (CA) in selecting the recipient artery of tibial or peroneal artery bypass grafts. METHODS: In patients who underwent tibial or peroneal artery bypass grafting because of critical ischemia, images were obtained of the lower extremity arterial circulation with both DU and CA. Vascular surgeons, blinded to the operation performed, reviewed either DU or CA images for arterial visualization and patency. The tibial or peroneal artery best suited to receive the bypass graft was selected by surgeons using only data from either DU or CA images. This selection was compared with the artery actually used at bypass surgery. RESULTS: Preoperative DU and CA data for 40 lower extremities in 38 patients undergoing bypass grafting at the level of the tibia provided 110 arteries: 38 anterior tibial arteries, 32 peroneal arteries, and 40 posterior tibial arteries. Ten arteries (8 peroneal, 2 anterior tibial) were not identified with DU, and 1 artery (anterior tibial) was not identified with CA. DU enabled prediction of the artery actually used in 88% of patients (35 of 40), whereas CA enabled prediction of the artery actually used in 93% of patients (37 of 40; P =.59). Duplicate findings at DU and CA enabled selection of 85% of arteries actually used (95% confidence interval, 71%-93%). Arteries used for bypass grafting had significantly higher peak systolic velocity (35 cm/s vs 25 cm/s; P =.04), higher end-diastolic velocity (15 cm/s vs 9 cm/s; P =.005), and greater diameter (2.4 mm vs 1.7 mm; P =.003) compared with arteries not selected for bypass grafting. CONCLUSION: Findings at DU and CA typically agree when used to select tibial or peroneal arteries for bypass grafting. With DU there is occasional difficulty in identification of the peroneal artery, but selection of the actual artery used is accurate. Peak systolic velocity, end-diastolic velocity, and diameter characteristics correlate with arteriographic criteria for tibial bypass target artery selection. If DU enables adequate identification of a target artery for bypass grafting, and especially if the peroneal artery is seen, findings at CA are not likely to alter bypass execution.

Adult↗

Endovascular repair of abdominal aortic aneurysm without preoperative arteriography.

OBJECTIVE: Clinical trials of endovascular aortic aneurysm repair (EVAR) have required both preoperative aortography and computed tomography (CT). We codeveloped specialized three-dimensional (3-D) reconstruction and computer-aided measurement, planning, and simulation software (3-D CAMPS) based on CT or magnetic resonance imaging, to eliminate the need for preoperative arteriography. METHODS: EVAR with 3-D CAMPS as the sole preoperative imaging method was performed in 196 patients from 1996 to 2001, with six endograft types in three configurations. Physical examination, abdominal radiography, and CT (3D-CAMPS) were performed at 1, 6, and 12 months, then annually. RESULTS: For a subset of cases in which a comparison could be made, 3-D CAMPS was superior to angiography for prediction of endograft length and iliac access. Hospital mortality was zero, and 30-day mortality was 0.5%. In three patients immediate conversion to open repair (1.5%) was necessary because of previously unknown stent-graft mechanical limits. Incidence of endoleak was 15% at 1 month, 10% at 6 months, 6% at 12 months, and 7% at 24 months, and 92% of endoleaks were type II. Mean follow-up was 18 months. Aneurysm-related mortality was zero. Nineteen secondary procedures (all endovascular) were performed in 16 patients (8%). For all graft types, freedom from secondary procedure was 94% at 1 year and 90% at 2 years, and this was better for endografts ultimately approved by the US Food and Drug Administration (96% at 1 year, 95% at 2 years; P =.02). No known measurement-related complications occurred in the series. Results for secondary intervention and endoleak compare favorably to series with similar endograft types. CONCLUSIONS: EVAR can be performed with 3-D CAMPS as the sole preoperative imaging method to achieve outcomes comparable to the best series published for each endograft type. CT with 3-D CAMPS can effectively eliminate the need for preoperative arteriography and avert associated morbidity, expense, and exposure to contrast agent and radiation.

Aged↗

A truncated plasminogen activator inhibitor-1 protein blocks the availability of heparin-binding vascular endothelial growth factor A isoforms.

We have made deletions of the porcine plasminogen activator inhibitor-1 (PAI-1) gene to obtain recombinant truncated PAI-1 proteins to examine functions of the PAI-1 isoforms. We previously reported that one recombinant truncated protein, rPAI-1(23), induces the formation of angiostatin by cleaving plasmin. The rPAI-1(23) protein is also able to bind urokinase plasminogen activator and plasminogen and then reduce the amount of plasmin that is formed. We have now prepared three different truncated rPAI-1 proteins and demonstrate that PAI-1 conformations control the release of heparin-binding vascular endothelial growth factor (VEGF) isoforms. The rPAI-1(23) isoform can regulate the functional activity of heparan sulfate-binding VEGF-A isoforms by blocking the activation of VEGF from heparan sulfate. The rPAI-1(23) conformation induced extensive apoptosis in cultured endothelial cells and thus reduced the number of proliferating cells. The rPAI-1(23) isoform inhibited migration of VEGF-stimulated sprouting from chick aortic rings by 65%, thus displaying a role in anti-angiogenic mechanisms. This insight into anti-angiogenic functions related to PAI-1 conformational changes could provide potential intervention points in angiogenesis associated with atherosclerotic plaques and cancer.

Animals↗

Human autologous mixed lymphocyte reaction as an in vitro model for autoreactivity to apoptotic antigens.

Recent studies have indicated that cells undergoing apoptosis are the source of autoantigens which drive autoimmune responses in systemic lupus erythematosus (SLE). It has been recognized for many years that in vitro stimulation of T cells with irradiated major histocompatibility complex (MHC) class II-bearing autologous cells results in T-cell proliferation with immunological specificity and memory, namely the autologous mixed lymphocyte reaction (AMLR). The nature of the major stimulants in the AMLR is still unclear. We investigated whether apoptotic fragments from irradiated cells act as antigenic stimulators for AMLR or nucleohistone-primed T cells. T-cell proliferation in the primary AMLR was significantly suppressed by the presence of a caspase inhibitor Z-Val-Ala-Asp-CH2F (Z-VAD.fmk), indicating that apoptotic antigens released from irradiated autologous feeder cells act as stimulators of AMLR T cells. This inhibitory effect of Z-VAD was not caused by toxic effects, because the T-cell response to the mitogen phytohaemagglutinin (PHA) was not inhibited by Z-VAD. A nucleohistone preparation was shown to contain antigens that are important in the AMLR, as culture with nucleohistone (but not with thyroglobulin or hen-egg lysozyme) primed T cells to respond with secondary kinetics in a subsequent AMLR that was also suppressed by Z-VAD. Our data provide evidence that the AMLR constitutes a model for the evaluation of cellular and molecular mechanisms that may be relevant to the pathogenesis of SLE and similar autoimmune diseases.

Amino Acid Chloromethyl Ketones↗

The effect of endothelial cell overexpression of plasminogen activator inhibitor-1 on smooth muscle cell migration.

INTRODUCTION: Plasminogen activator inhibitor-1 (PAI-1), a known inhibitor of plasminogen activators, may regulate smooth muscle cell migration (SMC) through alteration in matrix metalloproteinase (MMP) activity. METHODS: To study the effect of endothelial cell (EC) PAI-1 overexpression on SMC migration, RT-PCR was used to clone the full length PAI-1 gene, which was ligated into the pCMV/myc/ER expression vector. With electroporation, bovine aortic ECs were transfected with either the PAI-1 construct or the empty vector as control. EC PAI-1 overexpression was shown with a specific PAI-1 activity assay and enzyme-linked immunosorbent assay. The effect of EC PAI-1 overexpression on SMC migration was measured with a modified Boyden-chamber assay. SMC MMP expression was measured with zymography. RESULTS: Selected clones (EC9, EC21) had a three-fold to five-fold increase in PAI-1 activity compared with untransfected EC and empty vector EC (ECC). Similarly, enzyme-linked immunosorbent assay results showed a 3.5-fold to 5.5-fold increase in PAI-1 levels in EC9 and EC21 versus ECC. Untransfected EC and ECC had similar effects on SMC migratory patterns. Migration of SMC exposed to PAI-1 overexpressing EC was inhibited by 35% to 57% compared with ECC. This inhibitory effect was reversed with addition of exogenous urokinase-type plasminogen activator (uPA). Zymography showed downregulation of MMP-2 and MMP-9 in SMCs exposed to PAI-1 overexpressing EC. CONCLUSION: PAI-1 overexpression with transfected EC inhibits SMC migration. This effect may be mediated through decreased SMC MMP activity.

Animals↗

Early results of external iliac artery stenting combined with common femoral artery endarterectomy.

PURPOSE: The endovascular approach to external iliac artery (EIA) disease extending into the common femoral artery (CFA) has been avoided because of problems with stent placement across the inguinal ligament. Surgical treatment for this disease distribution includes extensive endarterectomy or bypass procedures or both. We report our initial experience with a combined open and endovascular approach to these patients. METHODS: We performed a retrospective analysis of all patients who underwent intraoperative EIA stenting after CFA endarterectomy/patch angioplasty between 1997 and 2000. Stents were positioned to end at the proximal endarterectomy endpoint, without crossing the inguinal ligament. Technical success, hemodynamic success, and clinical success were determined according to Society of Vascular Surgery/International Society of Cardiovascular Surgery criteria. Life-table analysis was performed for patency. RESULTS: Thirty-four patients (mean age, 68 years; 23 male, 11 female) had combined endovascular and open treatment of iliofemoral occlusive disease. Indications were claudication in 41% and critical limb ischemia in 59%. Femoral reconstruction included endarterectomy with patch angioplasty in all patients. EIA stent deployment incorporated the stenotic iliac segment and the proximal endpoint of the endarterectomy in all patients. Four patients (12%) also needed common iliac angioplasty at the same time for proximal iliac disease, and 14 patients (41%) also needed distal revascularization for associated femoropopliteal or tibial disease. Technical success and hemodynamic success were achieved in 100% of patients. Clinical success was achieved in 97% of patients. The mean postoperative increase in ankle-brachial index in patients with inflow procedures only was 0.36 (range, 0.1 to 0.85). The overall complication rate was 15%. With a mean follow-up period of 13 months (range, 0.5 to 28 months), 1-year primary patency and primary-assisted patency rates were 84% and 97%, respectively. No perioperative mortality was seen. CONCLUSION: EIA stenting as an adjunct to CFA endarterectomy/patch angioplasty allows for more localized surgery than conventional bypass. This approach also allows a better interface between the stent and endarterectomy than staged preoperative stenting. Technical success and early patency rates are excellent.

Aged↗