Treatment of type II endoleaks with a novel polyurethane thrombogenic foam: induction of endoleak thrombosis and elimination of intra-aneurysmal pressure in the canine model.

OBJECTIVE: The clinical significance and treatment of retrograde collateral arterial perfusion of abdominal aortic aneurysms after endovascular repair (type II endoleak) have not been completely characterized. A canine abdominal aortic aneurysm model of type II endoleak with an implanted pressure transducer was used to evaluate the use of polyurethane foam to induce thrombosis of type II endoleaks. The effect on endoleak patency, intra-aneurysmal pressure, and thrombus histology was studied. METHODS: Prosthetic aneurysms with an intraluminal, solid-state, strain-gauge pressure transducer were created in the infrarenal aorta of 14 mongrel dogs. Aneurysm side-branch vessels were reimplanted into the prosthetic aneurysm of 10 animals by using a Carrel patch. Type II (retrograde) endoleaks were created by excluding the aneurysm from antegrade perfusion with an impermeable stent graft. Thrombosis of the type II endoleak was induced by implantation of polyurethane foam into the prosthetic aneurysm sac of four animals. Six animals with type II endoleaks were not treated. In four control animals, no collateral side branches were reimplanted, and therefore no endoleak was created. Intra-aneurysmal and systemic pressures were measured daily for 60 to 90 days after the implantation of the stent graft. Endoleak patency and flow were assessed during surgery and at the time of death by using angiographic imaging and duplex ultrasonography. Histologic analysis of the intra-aneurysmal thrombus was also performed. RESULTS: Intra-aneurysmal pressure values are indexed to systemic pressure and are represented as a percentage of the simultaneously obtained systemic pressure, which has a value of 1.0. All six animals with untreated type II endoleaks maintained patency of the endoleak and side-branch arteries throughout the study period. Compared with control aneurysms that had no endoleak, animals with patent type II endoleaks exhibited significantly higher intra-aneurysmal pressurization (systolic pressure: patent type II endoleak, 0.702 +/- 0.283; control, 0.172 +/- 0.091; P < .001; mean pressure: endoleak, 0.784 +/- 0.229; control, 0.137 +/- 0.102; P < .001; pulse pressure: endoleak, 0.406 +/- 0.248; control, 0.098 +/- 0.077; P < .001; P < .001 for comparison for all groups by analysis of variance). Treatment of the type II endoleak with polyurethane foam induced thrombosis of the endoleak and feeding side-branch arteries in all four animals with type II endoleaks. This resulted in intra-aneurysmal pressures statistically indistinguishable from the controls (systolic pressure, 0.183 +/- 0.08; mean pressure, 0.142 +/- 0.09; pulse pressure, 0.054 +/- 0.04; not significant). Angiography and histology documented persistent patency up to the time of death (mean, 64 days) for untreated type II endoleaks and confirmed thrombosis of polyurethane foam-treated endoleaks in all cases. CONCLUSIONS: Untreated type II endoleaks were associated with intra-aneurysmal pressures that were 70% to 80% of systemic pressure. Treatment with polyurethane foam resulted in a reduction of intra-aneurysmal pressure to a level that was indistinguishable from control aneurysms that had no endoleak. CLINICAL RELEVANCE: Endovascular repair of abdominal aortic aneurysms is dependent on the successful exclusion of the aneurysm from arterial circulation. Type II endoleaks originate from retrograde flow into the aneurysm sac. This study demonstrates the use of polyurethane foam to induce thrombosis in a canine model of a type II endoleak, thereby reducing intra-aneurysmal pressure to levels similar to levels in animals without endoleaks. This approach may be a strategy for future treatment of type II endoleaks.

Endoluminal recanalization in a patient with phlegmasia cerulea dolens using a multimodality approach-a case report.

Phlegmasia cerulea dolens is a limb-threatening form of deep venous thrombosis and should be treated aggressively. The authors report a patient who presented with iliocaval and femoral deep venous thrombosis and posed an additional therapeutic challenge based on a recent history of heparin-induced thrombocytopenia. Catheter-directed pharmacologic thrombolysis and balloon venoplasty were applied in treatment. The direct thrombin inhibitor argatroban was used in place of heparin for concurrent anticoagulation. This multimodality endovascular approach (chemical and mechanical interventions) was successful in relieving the venous occlusion and salvaging the limb, while maintaining appropriate treatment for heparin-induced thrombocytopenia.

Postcarotid endarterectomy pseudoaneurysm treated with combined stent graft and coil embolization--a case report.

Pseudoaneurysm formation is a rare complication following carotid endarterectomy (CEA); however, its occurrence is associated with significant risk of morbidity. The patient in this report presented 2 years following CEA with headache and lateral neck mass. The diagnosis of a 3.5 x 3.0 cm carotid artery bifurcation pseudoaneurysm was made by using magnetic resonance angiography (MRA). Endovascular exclusion of the aneurysm was accomplished with coil embolization of the external carotid artery followed by deployment of a 7 x 50 mm wall stent graft into the common carotid artery-internal carotid artery (CCA-ICA). The patient's symptoms improved and at 6-months postexclusion, duplex ultrasound demonstrated a significant reduction in pseudoaneurysm size. This case highlights the feasibility and safety of using endovascular techniques in the treatment of post-CEA pseudoaneurysm.

Multimodal percutaneous intervention for critical venous occlusive disease.

Critical deep venous thrombosis and occlusion constitutes a small percentage of patients with venous disease, who exhibit severe symptomatology. This study examined the results of multimodal percutaneous therapy for the treatment of complex critical venous thrombotic and occlusive disease. Twenty-five patients presented with critical venous thromboses or occlusions (11 with debilitating unilateral lower extremity edema causing ambulatory impairment, 2 with debilitating bilateral lower extremity edema, 3 with phlegmasia cerulea dolens, 2 with venous claudication, 2 with superior vena cava (SVS) syndrome with respiratory compromise, 4 with debilitating upper extremity edema, and 1 with renal insufficiency). Therapeutic modalities including thrombolysis, mechanical thrombectomy, percutaneous venoplasty and stent placement, temporary inferior vena cava filtration, and ultrasound guidance were used in all cases in conjunction with long-term systemic anticoagulation. The venous access site was determined by the anatomic location of the lesion and included popliteal, femoral, brachial, and lesser saphenous. Patients were followed with clinical exam and duplex surveillance. Resolution of symptoms was achieved in 18 of 25 patients (72%) and partial resolution occurred in 4 of 25 (16%). Failure of treatment identified as both lack of clinical response and evidence of continued venous thrombosis occurred 3 of 25 patients (12%). Restoration of arterial pulses and limb salvage was achieved in the three patients with phlegmasia cerulea dolens and acute limb-threatening ischemia. Both patients with SVC syndrome experienced resolution of respiratory compromise and facial edema. The mean length of follow-up was 11 +/- 2.7 months. Complications included transfusion requirement (2), hematuria (2), retroperitoneal hematoma (1), and cellulitis (1). Acute critical venous thrombotic and occlusive disease is responsive to multimodal percutaneous treatment. The relief of pain and resolution of acutely life and limb-threatening conditions in this most severely symptomatic subset of patients represents the immediate goal of treatment.

Tibial angioplasty as an alternative strategy in patients with limb-threatening ischemia.

The purpose of this study was to assess the technical feasibility and early outcome of tibial angioplasty for a subset of patients with limb-threatening ischemia who were not candidates for bypass grafting. A retrospective analysis was conducted of 19 patients (7 male, 12 female) who underwent crural angioplasty for limb-threatening ischemia using 0.018- or 0.014 inch-based systems. Contraindications to bypass were insufficient conduit in 7 patients and severe comorbid illness in 12. Concurrent treatment of inflow lesions was performed in 12 of 20 limbs via either angioplasty alone (5) or combined with stenting (12). Outcome measures were ankle-brachial indices (ABI), relief of rest pain, and healing or healed wounds. Twenty-three vessels were treated, including 14 tibial occlusions and 9 stenoses. The average length of diseased segment was 11 cm (range, 3-25 cm). Thirteen of 14 occlusions were treated with subintimal recanalization, the remainder with laser recanalization. Technical success was achieved in 22 of 23 treated vessels. Mean preoperative ABI was 0.53 and mean postoperative ABI was 0.85. Palpable pulses were present in 11 of 20 limbs (55%). There was one perioperative mortality (5.2%). Mean follow-up was 3 months. Three failures occurred requiring amputation (15.8%). The remaining 16 patients were improved with healing (8) or healed (4) wounds and relief of rest pain (4). These results indicate that technical success may be achieved with outflow lesion angioplasty in the majority of patients encountered. The durability of this method of therapy is unknown, and our length of follow-up is not sufficient to answer this question. However, an attempt at angioplasty appears justified before primary amputation and before surgical bypass in those patients at high risk for intervention.

Rupture of excluded popliteal artery aneurysm: implications for type II endoleaks--a case report.

The fate of popliteal artery aneurysms after ligation and bypass is believed to be relatively innocuous. The patient presented in this report, however, experienced spontaneous rupture of a popliteal aneurysm 11 years after ligation and bypass. Magnetic resonance angiography was used to establish the diagnosis of rupture, which was subsequently confirmed at surgery. Intraoperative arteriography demonstrated persistent collateral arterial perfusion of the excluded popliteal aneurysm sac. The collateral arterial flow originated from the superior and inferior lateral genicular arteries. The persistent arterial perfusion resulted in growth of the aneurysm from 4.2 to 7.0 cm over the 11-year period. The ruptured aneurysm was successfully treated by direct arterial exposure and suture ligation of the collateral vessels performed from within the aneurysm sac. The development of popliteal aneurysm expansion and rupture as a result of collateral arterial perfusion suggests that persistent collateral perfusion of abdominal aortic aneurysms after endovascular repair (type II endoleak) may lead to aneurysm rupture. Therefore, close observation and intervention for aneurysm expansion to prevent rupture of the excluded aneurysm are warranted.

Continuity in the treatment of carotid artery disease: results of a carotid stenting program initiated by vascular surgeons.

The treatment of carotid artery stenosis currently constitutes a major component of vascular surgical practice. Carotid angioplasty and stenting (CAS), however, is mainly performed by nonvascular surgeon interventionalists with cerebral protection devices available only through investigational protocols. This study reports the initial results of a CAS program initiated and performed by vascular surgeons using commercially available cerebral protection devices. Fifty-seven patients were enrolled in the study over a 14-month period. All patients were at high risk for conventional endarterectomy (7 resentosis, 4 irradiation, and 46 medically high-risk ASA III). Mean age was 75.7 years (range, 45-93 years). High-grade stenosis of the carotid artery was present in all cases (mean stenosis, 85%; range, 80-99%). Twenty-four percent of patients were symptomatic. Cerebral protection was performed with an occlusion balloon-wire in 32 cases and with a filter-wire device in 24; no cerebral protection was used in 1 patient with restenosis after endarterectomy. Initially in the study, atropine was administered selectively for the development of bradycardia. Currently atropine is administered routinely prior to the initial balloon angioplasty of the carotid bulb. Clopidogrel (75 mg/day) was administered for 5 days prior to CAS and for 30 days after CAS. All 57 patients underwent successful dilatation of their carotid stenoses without occlusion or dissection. Ten of 32 patients in whom balloon occlusion was used for cerebral protection exhibited transient evidence of cerebral ischemia during protection balloon occlusion. These symptoms resolved completely without permanent neurological deficit in all cases. Development of bradycardia with a heart rate <50 bpm was significantly reduced by routine administration of atropine prior to the initial dilatation within the carotid bulb (p = 0.01). Mean hospital length of stay was 1.33 days (range, 1-5 days). There were two periprocedure myocardial infarctions, two postprocedure transient ischemic attacks, and one reversible ischemic neurologic deficit. There was no 30-day mortality. There have been no instances of hemodynamically significant restenosis during a mean follow-up period of 5.4 months. From these results we have concluded that CAS can be performed effectively and safely using commercially available cerebral protection devices. A program initiated and performed exclusively by vascular surgeons is effective and should be the standard model used in the endovascular treatment of carotid artery stenosis.

Computer simulation as a component of catheter-based training.

INTRODUCTION: Computer simulation has been used in a variety of training programs, ranging from airline piloting to general surgery. In this study we evaluate the use of simulation to train novice and advanced interventionalists in catheter-based techniques. METHODS: Twenty-one physicians underwent evaluation in a simulator training program that involved placement of a carotid stent. Five participants were highly experienced in catheter-based techniques (>300 percutaneous cases), including carotid angioplasty and stenting (CAS); the remaining 16 participants were interventional novices (<5 percutaneous cases). The Procedicus VIST simulator, composed of real-time vascular imaging simulation software and a tactile interface coupled to angiographic catheters and guide wires, was used. After didactic instruction regarding CAS and use of the simulator, each participant performed a simulated CAS procedure. The participant's performance was supervised and evaluated by an expert interventionalist on the basis of 50 specific procedural steps with a maximal score of 100. Specific techniques of guide wire and catheter manipulation were subjectively assessed on a scale of 0 to 5 points based on ability. After evaluation of the initial simulated CAS procedure, each participant received a minimum of 2 hours of individualized training by the expert interventionalist, with the VIST simulator. Each participant then performed a second simulated CAS procedure, which was graded with the same scale. After completion, participants assessed the training program and its utility via survey questionnaire. RESULTS: The average simulated score for novice participants after the training program improved significantly from 17.8 +/- 15.6 to 69.8 +/- 9.8 (P < .01), time to complete simulation decreased from 44 +/- 10 minutes to 30 +/- 8 minutes (P < .01), and fluoroscopy time decreased from 31 +/- 7 minutes to 23 +/- 7 minutes ( P < .01). No statistically significant difference in score, total time, or fluoroscopy time was noted for experienced interventionalists. Improvement was noted in guide wire and catheter manipulation skills in novices. Analysis of survey data from experienced interventionalists indicated that the simulated clinical scenarios were realistic and that the simulator could be a valuable tool if clinical and tactile feedback were improved. Novices also thought the simulated training was a valuable experience, and desired further training time. CONCLUSIONS: An endovascular training program using the Procedicus VIST haptic simulator resulted in significant improvement in trainee facility with catheter-based techniques in a simulated clinical setting. Novice participants derived the greatest benefit from simulator training in a mentored program, whereas experienced interventionalists did not seem to derive significant benefit.

Characterization of retrograde collateral (type II) endoleak using a new canine model.

OBJECTIVE: The clinical significance of retrograde collateral arterial perfusion of abdominal aortic aneurysms after endovascular repair (type II endoleak) has not been completely characterized. In this study a canine model was used to analyze intra-aneurysmal pressure, thrombus histologic characteristics, endoleak patency, and radiographic appearance of type II endoleaks originating from single and multiple aneurysm side branches. METHODS: Prosthetic aneurysms with an intraluminal solid-state strain-gauge pressure transducer were created in the infrarenal aorta of 14 mongrel dogs. A single collateral side branch was reimplanted in 4 animals, multiple side branches were reimplanted in 6 animals, and no side branches were reimplanted in 4 control animals. Intra-aneurysmal and systemic pressure was measured for 60 to 90 days after creation of the type II endoleak. Endoleak patency and flow were assessed with duplex ultrasound scanning and cine-magnetic resonance angiography. Histologic analysis of the intra-aneurysmal thrombus was also performed. RESULTS: Stent-graft exclusion reduced intra-aneurysmal pressure significantly in all animals, as compared with systemic pressure (P < .001). All intra-aneurysmal pressure values are indexed to the systemic pressure, and are represented as a percentage of the simultaneously obtained systemic pressure, which has a value of 1.0. Type II endoleaks originating from multiple side branches exhibited significantly increased intra-aneurysmal systolic pressure, mean pressure, and pulse pressure, as compared with endoleaks derived from either a single side branch (systolic pressure: multiple, 0.70 +/- 0.28 vs single, 0.50 +/- 0.19; P < .001; mean pressure: multiple, 0.78 +/- 0.23 vs single, 0.59 +/- 0.22, P < .001; pulse pressure: multiple, 0.41 +/- 0.25 vs single, 0.17 +/- 0.15, P < .001) or excluded control aneurysms that had no side branches and no endoleak (systolic pressure, 0.17 +/- 0.09; mean pressure, 0.14 +/- 0.10; pulse pressure, 0.098 +/- 0.08; P < .001). Cine-magnetic resonance angiograms and duplex ultrasound scans documented persistent patency of multiple branch endoleaks up to the time of euthanasia. In contrast, single side branch endoleaks thrombosed within 3 days (P < .001). Thrombus in the aneurysm sac in close proximity to the endoleak contained intact red blood cells and limited fibrin. Thrombus distant from the endoleak demonstrated extensive fibrin deposition and degraded red blood cells. CONCLUSION: The canine model may be used to reliably measure intra-aneurysmal pressure in the presence of patent and thrombosed type II endoleaks. In this model 2 or more side branches are necessary to maintain persistent patency of type II endoleaks. These endoleaks are associated with significantly elevated intra-aneurysmal pressure, that is, 70% to 80% of systemic pressure. These results suggest that persistent type II endoleaks have clinical significance. CLINICAL RELEVANCE: Endoleaks originating from retrograde flow in the side branch vessels of the aneurysm generate significant levels of intra-aneurysmal pressure, that is, 70% to 80% of systemic pressure. At least 2 patent side branch vessels appear to be necessary to cause persistent patency of type II endoleak in the canine model. Further studies will be necessary to enable more complete characterization of retrograde endoleaks and to extend these findings to allow clinical application. However, these results suggest that persistently patent type II endoleaks are clinical significance and may require more intensive follow-up intervention.

Acute lower extremity ischemia in a 7-year-old boy: an unusual case of popliteal entrapment syndrome.

Popliteal artery entrapment syndrome is a rare cause of acute limb ischemia that most commonly is seen in young adults. The most significant complications associated with popliteal entrapment include aneurysm formation and acute thrombosis. This case presents the youngest patient ever reported with this syndrome and highlights the advantages of multimodal treatment including thrombolysis, popliteal aneurysm resection, and revascularization. Although a significant body of literature exists on popliteal entrapment syndrome in teenagers and young adults, it has not been reported previously in a patient younger than 11 years. Limb salvage was achieved in this patient with a combination of endovascular and surgical techniques.

Increased recognition of type II endoleaks using a modified intraoperative angiographic protocol: implications for intermittent endoleak and aneurysm expansion.

Retrograde arterial perfusion of the aneurysm sac (type II endoleak) may complicate endovascular abdominal aortic aneurysm (AAA) repair and may lead to AAA expansion and rupture. Aneurysm expansion may also occur in the absence of a demonstrable endoleak. Current intraoperative assessment techniques may underrepresent the incidence of type II endoleaks. This study evaluated the incidence and impact of previously unrecognized type II endoleaks using a modified intraoperative angiographic protocol. A total of 391 patients undergoing endovascular AAA repair were evaluated. In 264 patients standard completion angiograms were performed. In 127 patients a modified angiographic protocol was used to visualize collateral lumbar and inferior mesenteric arteries as well as the aneurysm sac. The modified protocol uses digital subtraction fluoroscopy continuously for 60 sec after injections of 20 mL iodinated contrast both in the pararenal aorta and within the endovascular graft. Postoperative CT scans were performed at 1, 6, and 12 months and annually thereafter. The average age was 73.3 years; 324 patients were men and 67 were women. Mean follow-up was 11.4 months (range, 1-60 months). Type II endoleaks were documented intraoperatively in a significantly increased proportion of patients in whom the modified angiographic protocol was used: modified, 53/127 = 41% vs. standard, 17/264 = 6%; p < 0.001. No significant difference in the incidence of type II endoleaks was present on CT scan at 6 or 12 months after surgery (6 months: modified, 6/72 = 8% vs. standard, 10/159 = 6%, p = NS; 12 months: modified, 2/36 = 5% vs. standard, 6/138 = 4%, p = NS). Forty-six type II endoleaks resolved spontaneously (10 in the standard cohort, 36 in the modified cohort). One patient had a 10-mm increase in AAA diameter after spontaneous thrombosis of a type II endoleak 18 months postoperatively. One patient had a type II endoleak intraoperatively and at 12 months after surgery but the endoleak was absent at 1 and 6 months. Thirteen patients from the standard protocol cohort and 1 from the modified protocol cohort developed newly visualized type II endoleaks during follow-up. These findings may imply intermittent patency of the artery supplying the type II endoleak. The overall morbidity rate was 14% and the perioperative mortality rate was 1.8%. Retrograde (type II) endoleaks originating from AAA side branches occur intraoperatively more frequently than is currently recognized. Intermittent patency and thrombosis of these vessels may also occur and may contribute to AAA expansion. The full significance of these previously unrecognized endoleaks with respect to risk of aneurysm rupture remains to be definitively determined.

Use of cine magnetic resonance angiography in quantifying aneurysm pulsatility associated with endoleak.

OBJECTIVE: Persistent aneurysm perfusion or endoleak is associated with pulsatility of abdominal aortic aneurysm (AAA) after endovascular repair. However, the resultant pulsatile change in aneurysm diameter may be difficult to quantify, and therefore its significance is unknown. In this study cine magnetic resonance angiography (MRA) was used to quantify aneurysm wall motion during the cardiac cycle and to correlate it with the presence and type of endoleak. METHODS: Cine MRA was performed in 16 patients undergoing endovascular repair of AAA. A 1.5 T magnet and post-processing with GEMS 4.0 Fiesta computerized video image analysis software were used to calculate maximum aortic diameter during systole and diastole. Changes in aortic diameter were determined from these measurements. Cine MRA was performed on aneurysms before treatment and in patients with and without endoleak after endovascular repair. Type of endoleak was confirmed at angiography in all cases. Four patients had antegrade (type I) endoleak, and eight patients had retrograde (type II) endoleak; no endoleak was present in four patients. Endovascular grafts with stent support throughout the entire length of the graft (Talent) were used in all cases (14 bifurcated grafts, 2 tube grafts). RESULTS: Cine MRA demonstrated significantly greater wall motion and resultant change in aneurysm diameter in patients with type I endoleak compared with patients without endoleak (type I, 2.14 +/- 1.28 mm vs no endoleak, 0.12 +/- 0.09 mm, P =.001). Change in aneurysm diameter in patients with type II endoleak was not significantly greater than in patients with no endoleak (type II, 0.26 +/- 0.21 mm vs no endoleak, 0.12 +/- 0.09 mm, P = NS). Untreated aneurysms demonstrated the greatest change in diameter during the cardiac cycle (3.51 +/- 0.79 mm). CONCLUSION: Cine MRA may be used to accurately quantify AAA wall motion before and after endovascular stent-graft treatment. The extent of change in diameter corresponds to the type of endoleak, with antegrade (type I) endoleak generating greater pulsatile change in diameter than retrograde-collateral (type II) endoleak or no endoleak. Cine MRA may provide a noninvasive means of assessing the success of endovascular treatment of AAA. Further studies will be necessary to confirm the utility and efficacy of cine MRA in postoperative assessment of endovascular aneurysm repair.