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Biomedical subjects

Mitchell H Goldman

Publications and source records attributed to Mitchell H Goldman.

16 recordsLinked to original sources

The importance of thrombophilia in the treatment of Paget-Schroetter syndrome.

Venous thoracic outlet syndrome (V-TOS) and associated subclavian vein thrombosis (SVT) result in significant patient morbidity and can be difficult to manage. Previous studies have suggested that both mechanical compressive factors and pathological alterations in patient coagulation may contribute to the development of SVT; however, no study has specifically evaluated the role of thrombophilia in the treatment of V-TOS and the need for long-term anticoagulation as an adjunct to surgical decompression. This retrospective study describes the clinical courses of 18 patients treated for V-TOS with and without acute SVT. In this review, 67% of patients with SVT are found to have relatively common coagulation disorders and 90% of postoperative complications were associated with some form of thrombophilia. This study suggests that thrombophilia may play an important role in the pathogenesis of V-TOS and may be a determinant of the success of surgical decompression. Clotting disorders should therefore be aggressively evaluated in this patient population and can improve therapeutic outcome.

Adult↗

Nitric oxide mediates the effect of fluvastatin on intercellular adhesion molecule-1 and platelet endothelial cell adhesion molecule-1 expression on human endothelial cells.

Leukocyte and platelet adhesion to endothelial cells, an early step in the pathogenesis of atherosclerosis, is mediated through adhesion molecules. It has been shown that statins decrease adhesion molecule expression. We examined the hypothesis that fluvastatin decreased intercellular adhesion molecule-1 (ICAM-1) and platelet endothelial cell adhesion molecule-1 (PECAM-1) expression through a nitric oxide-mediated pathway. Human iliac artery endothelial cells were exposed to fluvastatin in the presence or absence of 2 mM N-monomethyl-L-arginine (L-NMMA). Flow cytometry analysis was used to measure ICAM-1 and PECAM-1 expression. In a separate experiment, confluent cell cultures were exposed in a serum-free medium to fluvastatin 20 microM, and the supernatant was collected for nitrate/nitrite determination after 6 and 48 hr of incubation. Protein was isolated and processed for immunoblotting with monoclonal antibodies specific for endothelial nitric oxide synthase (eNOS), Ser(1177)-phosphorylated eNOS, and AMP kinase. Relative band intensity was assessed with densitometry. Results are presented as the mean +/- standard deviation (SD), and p < 0.05 was considered significant. ICAM-1 and PECAM-1 were expressed constitutively. Human iliac artery endothelial cells (HIAECS) treated with 5 microM fluvastatin did not exhibit reduced expression of PECAM-1 or ICAM-1. Incubation with 10 microM fluvastatin reduced basal expression of both ICAM-1 and PECAM-1. Fluorescence intensity (FI) for these substance was as follows: 3638 +/- 1671, p = 0.01 and PECAM-1 vs. control FI 276 +/- 52 vs. 522 +/- 78, p = 0.02. In the presence of 2 mM L-NMMA, fluvastatin failed to decrease the expression of ICAM-1 (fluvastatin 10 microM + L-NMMA: FI was 3042 +/- 1378 vs. 3638 +/- 1671 for the control p = 0.01) or PECAM-1 (fluvastatin 10 microM + L-NMMA: FI was 415 +/- 188 vs. 522 +/- 78 for the control, p = 0.1). Incubation with 20 microM fluvastatin similarly reduced ICAM-1 expression (FI was 2014 +/- 1595 vs. 3638 +/- 1671 for the control, p = 0.02) and PECAM-1 expression (FI was 196 +/- 109 vs. 522 +/- 78 for the control, p = 0.02). This reduction was prevented in the presence of 2 mM L-NMMA. L-NMMA in a concentration of 2 mM had no significant effect on adhesion molecule expression (p > 0.05 for all comparisons of the control FI versus 2 mM L-NMMA mean FI). After a 48 hr incubation with 20 microM fluvastatin there was a 219 +/- 35% increase in the cell eNOS protein content (p = 0.01) and a 170 +/- 26% increase in the cell AMPK protein content (p = 0.02). Ser(1177)-phosphorylated eNOS protein levels were increased by 41 +/- 8% (p = 0.03). The nitric oxide concentration in the medium of the HIAEC treated with 20 microM fluvastatin for 48 hr was significantly higher than that in the control (p = 0.0004), pointing to increased production during the incubation period. Fluvastatin thus decreases basal expression of ICAM-1 and PECAM-1. Competitive inhibition of eNOS with L-NMMA abolishes the effect of fluvastatin on ICAM-1 and PECAM-1 expression. The statin up-regulates eNOS and AMP kinase, one of the enzymes that activates eNOS via phosphorylation at Ser(1177). We have shown that after a 48-hr exposure to fluvastatin there is an increased amount of the phosphorylated enzyme in the endothelial cells.

Blotting, Western↗

Open versus endo: early experience with endovascular abdominal aortic aneurysm repair beyond the clinical trials.

OBJECTIVE: To analyze and compare open (OR) versus endovascular (EVAR) abdominal aortic aneurysm repair at our institution. METHODS: EVAR was attempted in 256 patients at the University of Tennessee Medical Center, Knoxville, between December 1999 and November 2002. One hundred forty patients underwent attempted EVAR, and 116 underwent OR. All patients were included on an intent-to-treat basis, and results were reviewed retrospectively. Statistical methods included the Student t test and chi-square analysis. RESULTS: Patients were age matched between the 2 groups (70.2 years versus 69.0 years; P = .936). Patients in the OR group had significantly higher American Society of Anesthesiologists classes than the EVAR group (2.96 versus 3.07; P = .006). However, there was no difference between the groups, OR versus EVAR, with respect to the presence of chronic obstructive pulmonary disease (55% versus 46%; P = .129), coronary artery disease (69% versus 66%; P = .638), diabetes mellitus (12% versus 18%; P = .167), mean left ventricular ejection fraction (51.8% versus 53.9%; P = .28), or mean preoperative creatinine level (1.2 mg/dL versus 1.1 mg/dL; P = .167). Tobacco use was more prevalent in the OR group (78.4% versus 64.2%; P = .013), and known carotid artery disease was more prevalent in the EVAR group (20.0% versus 6.9%; P = .003). The EVAR group had significantly shorter lengths of stay ( 4.2 versus 9.0 days; P = .000), intensive care unit days (0 versus 3.2; P = .000), time in the operating room (119.6 minutes versus 225.7 minutes; P = .000), and estimated blood loss (189.1 mL versus 897.9 mL; P = .000). Mean aneurysm size was larger in the OR group (5.6 cm versus 4.9 cm; P = .000). Perioperative complications occurred in 31 patients in the OR group and 5 in the EVAR group (P = .000). Two perioperative deaths occurred in the OR group and none in the EVAR group. As of this writing there has been no significant difference in all-cause mortality in the 2 groups (OR 9.6% versus EVAR 8.0%; P = .651). Seven patients in the EVAR group needed secondary interventions. Six were managed with endovascular techniques, and 1 underwent femoral-femoral bypass. CONCLUSIONS: Patients who undergo EVAR have significantly less morbidity and mortality in the perioperative period than do equally matched patients undergoing open repair. In midterm follow-up (2-5 years), mortality is no different. Morbidity conferred by the need for secondary intervention in the endovascular group is minimal.

Aged↗

Activation of 5'-AMP-activated kinase is mediated through c-Src and phosphoinositide 3-kinase activity during hypoxia-reoxygenation of bovine aortic endothelial cells. Role of peroxynitrite.

AMP-activated kinase (AMPK) is a fuel-sensing enzyme present in most mammalian tissue. In response to a decrease in the energy state of a cell AMPK is phosphorylated and activated by still poorly characterized upstream events. Exposure of bovine aortic endothelial cells (BAEC) to chemically synthesized ONOO- acutely and significantly increased phosphorylation of c-Src, PDK1, AMPK, and its downstream target, acetyl-CoA carboxylase (ACC), without affecting cellular AMP. This novel pathway for AMPK activation was confirmed by the use of pharmacological inhibitors and dominant-negative mutants. Exposure of BAEC to hypoxia-reoxygenation (H/R) caused a biphasic increase in AMPK and ACC phosphorylation, which was prevented by adenoviral overexpression of superoxide dismutase (SOD) or inhibition of nitric-oxide synthase (NOS) implicating a role of ONOO- formed during H/R. Furthermore, dominant-negative mutants of c-Src or kinase-defective PDK1 also blocked H/R-induced AMPK activation indicating that, as with addition of exogenous ONOO-, both c-Src and PI 3-kinase are upstream of AMPK. Moreover, H/R, like ONOO-, significantly increased co-immunoprecipitation of AMPK with c-Src, suggesting that ONOO- favors physical association of AMPK with upstream kinases. Taken together, our results indicate a novel pathway by which H/R via ONOO- activates AMPK in a c-Src-mediated, PI 3-kinase-dependent manner, and suggest that ONOO--induced activation of AMPK might thereby regulate metabolic enzymes, such as ACC.

3-Phosphoinositide-Dependent Protein Kinases↗

Iliac artery stenting versus surgical reconstruction for TASC (TransAtlantic Inter-Society Consensus) type B and type C iliac lesions.

OBJECTIVE: The TransAtlantic Inter-Society Consensus (TASC) document did not define the best treatment for moderately severe iliac artery lesions, ie, TASC type B and type C iliac lesions, because of insufficient solid evidence to make firm recommendations. The purpose of this study was to evaluate the influence of risk factors on outcome of iliac stenting and operative procedures used to treat TASC type B and type C lesions. METHODS: Over the 5 years from 1996 to 2001, 188 endovascular and direct aortoiliac surgical reconstruction procedures were performed in 87 women and 101 men with TASC type B and type C iliac lesions and chronic limb ischemia. The criteria prepared by the Ad Hoc Committee on Reporting Standards (Society for Vascular Surgery/International Society for Cardiovascular Surgery (SVS/ISCVS) were followed to define variables. Both univariate analysis (Kaplan-Meier method) and multivariate analysis (Cox proportional hazards model) were used to determine the association between variables, cumulative patency rate, limb salvage, and survival. RESULTS: Indications for revascularization were disabling claudication (73%), limb salvage (25%), and blue toe syndrome (2%). Patients in the surgery group (n = 52) had significantly higher primary patency rates compared with patients in the stent group (n = 136) at univariate analysis (Kaplan-Meier method, log-rank test; P =.015). Primary patency rates at 1, 3, and 5 years were 85%, 72%, and 64% after iliac stenting, and 89%, 86%, and 86% after surgical reconstruction, respectively. Univariate and multivariate Cox regression analysis enabled identification of poor runoff (ie, runoff score >5 for unilateral procedures or >2.5 for bilateral outflow procedures; relative risk, 2.5; 95% confidence interval [CI], 1.4-4.2; P =.001) as the only independent predictor of decreased primary patency in all patients. However, stratified analysis including only patients with poor runoff revealed that patients undergoing iliac stenting had significantly lower primary patency rates compared with those undergoing surgical reconstruction (Kaplan-Meier method, log-rank test; P =.05). External iliac artery disease and female gender were also identified as independent predictors of decreased primary stent patency. CONCLUSIONS: Poor infrainguinal runoff is the main risk factor for decreased primary patency after surgical reconstruction and iliac stenting to treat TASC type B and type C iliac lesions. However, primary patency is less affected by poor runoff in patients undergoing surgical procedures. The presence of poor runoff, external iliac artery disease, and female gender are independent predictors of poor outcome after iliac stenting, and therefore these risk factors should determine the need for surgical reconstruction.

Angioplasty↗

Iliac artery stenting in patients with poor distal runoff: Influence of concomitant infrainguinal arterial reconstruction.

OBJECTIVE: Inadequate infrainguinal runoff is considered an important risk factor for iliac stent failure. However, the influence of concomitant infrainguinal arterial reconstruction (CIAR) on iliac stent patency is unknown. This study evaluated the influence of CIAR on outcome of iliac angioplasty and stenting (IAS) in patients with poor distal runoff. METHODS: Over 5 years (1996 to 2001), 68 IAS procedures (78 stents) were performed in 62 patients with poor distal runoff (angiographic runoff score >or=5). The SVS/AAVS reporting standards were followed to define outcome variables and risk factors. Data were analyzed with both univariate analysis (Kaplan-Meier method [K-M]) and regression analysis (Cox proportional hazards model). RESULTS: Indications for iliac artery stenting were disabling claudication (59%) and limb salvage (41%). Of the 68 procedures, IAS with CIAR was performed in 31 patients (46%), and IAS alone was performed in 37 patients (54%). Patients undergoing IAS with CIAR were older (P =.03) and had more extensive and multifocal iliac artery occlusive disease, with more TASC (TransAtlantic Inter-Society Consensus) type C lesions (P =.03), compared with patients undergoing IAS alone. No other significant differences in risk factors were noted. Runoff scores between patients undergoing IAS with CIAR and those undergoing IAS alone were not significantly different (median runoff scores, 6 [range, 5-8] and 7 [range, 5-9], respectively; P =.77). Primary stent patency rate at 1, 3, and 5 years was 87%, 54%, and 42%, respectively, for patients undergoing IAS with CIAR, and was 76%, 66%, and 55%, respectively, for patients undergoing IAS. Univariate analysis revealed that primary stent patency rate was not significantly different between the 2 groups (K-M, log-rank test, P =.81). Primary graft patency rate for CIAR was 81%, 52%, and 46% at 1, 3, and 5 years, respectively. Performing CIAR did not affect primary iliac stent patency (relative risk, 1.1; 95% confidence interval, 0.49-2.47; P =.81). Overall, there was a trend toward improved limb salvage in patients undergoing IAS with CIAR, compared with those undergoing IAS alone (K-M, log rank test, P =.07). CONCLUSION: In patients undergoing IAS with poor distal runoff, CIAR does not improve iliac artery stent patency. Infrainguinal bypass procedures should therefore be reserved for patients who do not demonstrate clinical improvement and possibly for those with limb-threatening ischemia.

Adult↗

Histopathological study of renal transplant artery stenosis: role of rejection and cold ischaemia time in the pathogenesis of intimal hyperplasia in an arterial allograft.

INTRODUCTION: Intimal hyperplasia of renal allograft arteries is a cause of hypertension and graft loss and the predisposing factors are poorly understood. We performed a histopathological study focusing on cold ischaemia time and immunological factors and their effect on the donor artery. METHODS: Primary renal artery branches were obtained from patients undergoing transplant nephrectomy for chronic rejection. Non-transplant patients undergoing nephrectomy served as controls. Clinical information including immunosuppression and rejection episodes, cold ischaemia time and graft survival were collected from the patients' charts. Collagen, smooth muscle cells, T cells, macrophages, and neutrophils were quantified using immunohistochemistry. The intima to media ratio was also calculated using imaging software. Statistical analysis was performed using linear regression and the Mann-Whitney test with P < 0.05 significant. RESULTS: Nine transplant patients and five controls were included. All transplant patients received maximum immunosuppression according to clinical standards. The median number of acute rejection episodes was 1 (range 0-5). Cold ischaemia time was 24.3 +/- 9.6 h (mean +/- SD). Mean allograft longeviy was 87.4 +/- 72.9 months (mean +/- SD). The intima/media ratio in the transplant group was higher as compared with the control (P = 0.002). The same was true for intima collagen content (P = 0.001) and intima smooth muscle content (P = 0.036). Cold ischaemia time was 19.6 +/- 11.1 h (mean +/- SD) and did not correlate with intima/media ratio. Also the number of rejection episodes did not correlate with the intima/media ratio. CONCLUSION: Intimal hyperplasia in the allograft artery has a multifactorial aetiology. We were not able to establish an association between intimal hyperplasia and acute rejection episodes or length of cold ischaemia time. It appears that immunosuppression does not prevent the development of intimal hyperplasia.

Adult↗

Distribution of sac pressure in an experimental aneurysm model after endovascular repair: the effect of endoleak types I and II.

PURPOSE: To study in an experimental aneurysm model the differential distribution of strain/pressure (S/P) on the aneurysm wall before and after endograft exclusion and in the presence of individual type I and type II endoleaks. METHODS: Two tapered elliptical Gore-Tex patches were sutured to an anterior and posterior longitudinal arteriotomy of an 8-mm Gore-Tex tube graft, thus creating a fusiform aneurysm. Two S/P transducers were placed at the proximal sac adjacent to the proximal neck, 2 at the site of the widest sac diameter, and 2 at the sac adjacent to the distal neck. The aneurysm, which was connected to a pulsatile pump system, was excluded using a 10-mm endograft. Type I and type II endoleaks were created and tested individually. S/P measurements were obtained at systemic systolic pressures (BP) of 80, 110, and 150 mmHg. Thrombosis of the sac contents was induced by injection of thrombin and calcium in the sac. Angiography was used to verify presence or absence of flow in the sac. RESULTS: Aneurysm exclusion resulted in significant S/P reductions at all 3 BP levels versus prior to exclusion (p<0.05). Thrombus in the sac did not alter S/P in the excluded sac (p>0.05 for all 3 BP levels). In the presence of a proximal type I endoleak, S/P distribution was not uniform, and S/P at the proximal neck was close to S/P prior to exclusion (p>0.05 no graft versus type I endoleak for all 3 BP levels). This was also true in the presence of thrombus. With a type II endoleak, S/P was more evenly distributed and was not significantly elevated compared to the pressure without an endoleak (p>0.05, graft versus type II endoleak for all 3 BP levels). Thrombus had no effect on intrasac S/P with a type II endoleak. Intrasac S/P was significantly higher in the presence of a type I endoleak compared to a type II endoleak when BP=150 mmHg (p=0.008). CONCLUSIONS: Endovascular exclusion of an aneurysm results in uniform S/P reduction in the aneurysm sac. Type I endoleak, but not type II endoleak, results in significantly higher S/P in an area of the sac adjacent to the proximal neck. Thrombus does not result in significantly different S/P distribution in the aneurysm sac.

Angioplasty↗

Effects of estrogen, progesterone, and combination exposure on interleukin-1 beta-induced expression of VCAM-1, ICAM-1, PECAM, and E-selectin by human female iliac artery endothelial cells.

The cardioprotective effect of hormone replacement therapy (HRT) in healthy, postmenopausal women is well documented. Little work has been performed on the effect of HRT in peripheral arteries. Recent work suggests that HRT may adversely affect the patency of peripheral grafts. This study investigates the in vitro effects of estrogen and/or progesterone exposure on adhesion molecule expression by normal human female iliac artery endothelial cells (HIAEC). Control and interleukin-1 beta (IL-1 beta)-stimulated HIAEC monolayers were labeled with fluorescent-tagged antibodies against the adhesion molecules VCAM-1, ICAM-1, PECAM, and E-selectin. FACS analysis was used to measure antibody-labeled adhesion molecule expression. ICAM-1 and PECAM were found to be constitutively expressed. VCAM-1 and ICAM-1 expression were significantly upregulated by IL-1 beta, while E-selectin was neither constitutively expressed nor upregulated by IL-1 beta. Pretreatment with estrogen or progesterone alone decreased IL-1 beta-stimulated VCAM-1 and ICAM-1 expression, but not to statistically significant levels. Combined hormone exposure significantly decreased, in an additive fashion, the expression of VCAM-1 and ICAM-1 in stimulated cells. This study supports extension of the beneficial effects ascribed to HRT to include the peripheral arterial endothelium of healthy women.

Adult↗

Infrainguinal bypass grafting using lyophilized saphenous vein allografts for limb salvage.

Critical ischemia in patients with extensive femoropopliteal occlusive disease often ends in amputation in the absence of a suitable autologous vein for reconstruction. Cryopreserved vascular allografts have been used as an alternative conduit with poor results. Antigenicity and rejection are assumed to account for graft failure. Lyophilized vessels have demonstrated patency and structural integrity in the vascular system in our previous experimental studies. We report four patients that underwent femorodistal bypass grafting with lyophilized saphenous veins who lacked usable autologous vein for arterial reconstruction. Early graft thrombosis occurred in three patients who required major amputations. Duplex scans for graft surveillance did not reveal previous significant abnormalities. These cases demonstrate that the clinical use of lyophilized venous allografts for infrainguinal arterial reconstructions failed to yield satisfactory patency and limb salvage. Lyophilized veins therefore are not useful alternative conduits in patients with critical ischemia and no suitable autologous vein grafts.

Aged↗

Predictors for adverse outcome after iliac angioplasty and stenting for limb-threatening ischemia.

OBJECTIVE: The role of iliac artery angioplasty and stenting (IAS) for the treatment of limb-threatening ischemia is not defined. IAS has been used primarily for patients with disabling claudication. Because poorer results have been shown in patients with critical ischemia after iliac artery angioplasty, the purpose of this study was to estimate the influence of risk factors on the outcome of iliac angioplasty and stent placement in patients with limb-threatening ischemia. METHODS: During a 5-year period (from 1996 to 2001), 85 iliac angioplasty and stent placement procedures (107 stents) were performed in 31 women and 43 men with limb-threatening ischemia. Patients with claudication were specifically excluded. The criteria prepared by the Ad Hoc Committee on Reporting Standards (Society for Vascular Surgery/International Society for Cardiovascular Surgery) were followed to define the variables. The TransAtlantic InterSociety Consensus classification was used to characterize the type of iliac lesions. Both univariate (Kaplan-Meier [KM]) and multivariate analyses (Cox proportional hazards model) were used to determine the association between variables, cumulative patency, limb salvage, and survival. RESULTS: Indications for iliac angioplasty with stenting were ischemic rest pain (56%) and tissue loss (44%). Primary stenting was performed in 36 patients (42%). Stents were placed selectively after iliac angioplasty mainly for residual stenosis or pressure gradient (43%). Overall, primary stent patency rate was 90% at 1 year, 74% at 3 years, and 69% at 5 years. Primary stent patency rate was significantly reduced in women compared with men (KM, log-rank test, P <.001). Primary patency rates at 1, 3, and 5 years were 79%, 57%, and 38% for women and 92%, 88%, and 88% for men. Primary stent patency rate also was significantly reduced in patients with renal insufficiency (creatinine level, >1.6 mg/dL; KM, log-rank test, P <.001). Cox regression analysis identified female gender (relative risk, 5.1; 95% CI, 1.8 to 7.9; P =.002) and renal insufficiency (relative risk, 6.6; 95% CI, 1.6 to 14.2; P =.01) as independent predictors of decreased primary stent patency. No independent predictors for limb salvage and survival were identified. CONCLUSION: Women undergoing iliac angioplasty and stenting for limb-threatening ischemia have significantly reduced primary stent patency rates and may need additional procedures to obtain satisfactory clinical improvement and limb salvage. Patients with renal insufficiency and critical ischemia also have reduced primary stent patency rates after IAS. Limb salvage, as shown in this study, is not affected by previous iliac stent failure.

Adult↗

Endotension distribution and the role of thrombus following endovascular AAA exclusion.

PURPOSE: To determine the pattern of strain and pressure transmitted to an aortic aneurysm wall before and after endovascular exclusion and to evaluate the role of sac thrombus on the conduction of pressure and wall strain. METHODS: Three canine thoracic aortas were used to create abdominal aortic aneurysms (AAA). The segments were placed on a pulsatile pump system, and 8 strain transducers were positioned in the aneurysm sac. Baseline strain/pressure (S/P) was recorded in 1 animal, then the AAA was excluded with a stent-graft. Thrombin was injected into the sac, and strain/pressure was recorded at 7 systemic pressures (35 to 120 mmHg) over 6 hours. The thrombus was replaced with fibrin glue, and S/P was recorded over 4 hours. Additional trials using whole and 50% diluted unclotted blood were performed prior to sac thrombosis. Computed tomography and angiography were performed before and after aneurysm exclusion. RESULTS: Pressure transmitted to the aneurysm wall decreased following stent-graft placement (p<or=0.001). Strain/pressure was not distributed evenly in the sac (p<or=0.05), and varying systemic pressures did not affect this distribution. Pressures near the stent-graft were higher than those laterally (p<or=0.001) in all trials with interposed fresh thrombus and fibrin thrombus. The fibrin group had elevated baseline measurements, but correction for the elevated values did not influence the statistical significance (p<or=0.001). Blood and fibrin thrombus reduced transmitted wall pressure to a similar degree. Overall S/P in the fluid-filled nonclotted sac was significantly lower (p<or=0.001) than in the thrombus groups. CONCLUSIONS: Endovascular AAA exclusion reduced strain and pressure conducted to the aneurysm wall, and the distribution of transmitted pressure in the excluded sac without endoleak differed regardless of the sac contents. Fresh thrombus reduced transmittedS/P in all trials at all systemic pressures, as did fibrin thrombus but in a less predictable fashion.

Animals↗

Endotension in an experimental aneurysm model.

PURPOSE: The purpose of this study was to design an experimental model of endotension and to investigate whether attachment site failure without endoleak results in higher aneurysm sac pressure (ASP). METHODS: Infrarenal aortic aneurysms were created in canines with an elliptical knitted polyester patch. Pressure transducers were inserted into the aneurysm. Group I (n = 4) underwent endovascular stent graft exclusion of the aneurysm. An attachment site failure was formed in group II (n = 5) before aneurysm exclusion. ASP measurements were obtained for 3 weeks, and the ratio of mean ASP to mean systemic blood pressure (ASP/BP) was calculated. Before explant, norepinephrine was administered and ASPs were recorded at varying systemic pressures. Stent graft cuff exclusion of the attachment site failure was performed in group II. RESULTS: Intraoperative arteriography and duplex ultrasonagraphy did not reveal an endoleak in either group. ASP/BP in group I was 0.39 +/- 0.02 compared with 1.01 +/- 0.02 in group II (P <.001). Mean systemic pressure varied from 55 to 177 mm Hg after norepinephrine administration. Within this interval, ASP/BP was 0.51 +/- 0.10 in group I compared with 0.91 +/- 0.10 in group II (P <.001). ASP/BP before cuff deployment in group II was 0.98 +/- 0.08 compared with 0.46 +/- 0.04 after cuff deployment (P <.001). CONCLUSION: Systemic pressure is transmitted to the aneurysm sac through an attachment site failure, despite no endoleak, resulting in endotension. Cuff exclusion of the attachment site failure decreases ASP. ASP may help determine the need for future intervention after endovascular aneurysm repair.

Animals↗

Endoleak: the achilles heel of endovascular abdominal aortic aneurysm exclusion--a case report.

Endovascular exclusion of abdominal aortic aneurysms (EAAA) is an alternative treatment to open surgical repair in patients with suitable anatomy. The development of endoluminal vascular procedures has allowed aneurysm exclusion via remote arterial access techniques. Aneurysm exclusion by these methods revealed the phenomenon of endoleak, a unique complication characterized by an extravasation of blood into the aneurysm sac after stent-graft deployment. We present a patient treated for an endoleak following EAAA repair and review the endoleak classification system and management.

Aged↗

Endovascular exclusion of saphenous vein graft aneurysms complicating abdominal aortic aneurysm repair--a case report.

A 64-year-old man was referred for vascular evaluation before renal transplantation for ischemic nephropathy. In the past he had undergone bilateral renal artery revascularizations using saphenous vein. At the time of transplant evaluation, he was found to have bilateral aneurysms of the saphenous veins used to bypass his renal artery stenoses. He underwent successful endovascular exclusion of the aneurysms with 2 endovascular AneuRx extension cuffs. This case highlights both the versatility of endovascular treatments as well as the importance of a comprehensive vascular examination.

Aortic Aneurysm, Abdominal↗