Current training and practice of endovascular surgery: a survey.

Endovascular surgery (EVS) has become of great interest to the vascular community. However, little data exist about the current status of training and utilization of EVS, thus prompting this survey. During a national vascular meeting, all participants (n = 132) filled out a 2-page questionnaire. Respondents (mean age 39 years, 87% male) were 68 vascular surgeons in practice (52%), and 64 fellows (48%), representing a significant fraction of trainees in North America. Practice location included university hospital (39%), private hospital/clinic (52%), and government hospital (8%). According to respondents, in their respective communities, most of the EVS was performed by radiologists (66%), followed by vascular surgeons (19%), cardiologists (13%), and vascular medicine physicians (2%). A majority of respondents (75%) currently perform EVS; surgeons in practice < 3 years had the highest rate (90%). Utilization rates among the nine interventions surveyed ranged from angiography (72%) and angioplasty (65%) to intravascular ultrasound (IVUS) (21%) and atherectomy (12%). Procedure totals showed that approximately 20% of fellows performed > 100 angiograms and 10% performed > 25 endovascular grafts/year, whereas nonfellows performed few of the latter. Most of the EVS (72%) was performed in the operating room with portable imaging equipment and EVS accounted for 14% of all vascular procedures. Most respondents (86%) believed that EVS would become a major component of vascular surgery and comprise 30% of their future practice. Seventy-six percent thought their training was insufficient and 85% said they would devote 3 months or less for further endovascular training. In conclusion, a vast majority of vascular trainees and surgeons are performing EVS, however, individual caseloads vary greatly. The belief that endovascular surgery will play an increasing role in vascular surgery practice is strong and interest in further training of short duration is widespread. Broader-based data collection and longitudinal studies on this issue are warranted.

Endoleaks following endovascular repair of abdominal aortic aneurysm: the predictive value of preoperative anatomic factors--a review of 100 cases.

OBJECTIVE: The failure to maintain a secure exclusion of aortic aneurysms with intraluminally placed grafts has been termed endoleak. We performed a retrospective review of our first 100 transluminally repaired abdominal aortic aneurysms (AAAs) in an effort to identify preoperative factors that could predict which patients would have endoleaks. METHODS: Between February 1993 and September 1998, 100 infrarenal aneurysms were treated with tube (39), bifurcated (45), and aortoiliac grafts (16). Endoleaks (early and late) developed in 34 patients. Preoperative computed tomography scans and angiograms for all patients were individually inspected by a single reviewer. Aortic characteristics analyzed included number of patent lumbar arteries, presence of a patent inferior mesenteric artery (IMA), calcification and thrombus at proximal and distal attachment sites, proximal aortic angulation, and graft-vessel size discrepancy at proximal and distal attachment sites. The prevalence of the preoperative factors was compared among patients with and without endoleaks. RESULTS: Endoleaks developed in 44% of tube, 33% of bifurcated, and 47% of aortoiliac grafts (P =.51). Correlation between total number of patent lumbar arteries, presence of a patent IMA, and endoleaks was not significant (P =.44,.95). Calcification at either proximal or distal attachment site did not increase the risk of endoleaks (P =.50,.62). The presence of thrombus at the attachment site (proximally or distally) also failed to increase endoleak rates (P =.12,.78). Degree of proximal aortic angulation did not differ between groups (P =.39). Size discrepancies between graft and aorta or iliac vessels at proximal or distal sites did not significantly differ (P >.54, >.13). Subgroup analysis of endoleaks with different tube types also failed to demonstrate significant differences among the three graft types (P >.05). CONCLUSION: Endoleaks develop in a significant number of endovascularly repaired AAAs. We were unable to demonstrate a statistically significant association with anatomic characteristics thought to predispose to the development of endoleaks. We find no predictive value associated with these anatomic factors.

Presentation of infantile aortic coarctation in an adult.

Rarely, the initial presentation of aortic coarctation, a congenital anomaly, occurs in adults. Surgical repair is indicated for symptomatic patients. We report the case of a 68-year-old woman who underwent successful surgical repair of the infantile (preductal) type of aortic coarctation with use of an interposition graft.

Dexamethasone and enalapril suppress intimal hyperplasia individually but have no synergistic effect.

Vascular injury is associated with complex interactions that lead to development of intimal hyperplasia (IH). We have demonstrated previously that the corticosteroid dexamethasone and the ACE-inhibitor enalapril are effective in suppressing the development of IH. We hypothesize that due to distinctly different pharmacologic mechanisms of action, a synergistic effect would be expected if these agents were given in combination. Forty New Zealand White rabbits underwent balloon catheter denudation of the carotid artery. Animals were divided into four equal treatment groups and received daily intramuscular injections: Group 1, saline; Group 2, enalapril 0.07 mg/kg, Group 3, dexamethasone 0.125 mg/kg; and Group 4, enalapril 0.07 mg/kg plus dexamethasone 0.125 mg/kg. Vessels were harvested at 12 weeks and intimal hyperplasia was measured as a ratio of the absolute area of IH to the normalized area enclosed by the internal elastic lamina (IH/IEL). Mean values for IH/IEL are expressed as a percent (SD): Group 1, 32.31 (14.9); Group 2, 9.47 (2.11); Group 3, 5.40 (4.14); and Group 4, 8.49 (4.27). All treatment groups demonstrated significant suppression of IH compared to the control group (p < 0.01); dexamethasone was more effective than enalapril (p = 0.01). There was no statistical difference in IH suppression between respective agents and the combination group (p > 0.10). Coadministration of dexamethasone and enalapril provides no advantage over single-agent therapy in suppressing the development of IH, suggesting that maximal suppression is obtained with single-agent treatment or that these agents affect IH through a common pathway.

Aspirin increases tissue oedema after skeletal muscle ischaemia and reperfusion.

PURPOSE: Skeletal muscle ischaemia reperfusion syndrome affects patients following lower limb revascularisation. Aspirin has the potential to attenuate these effects. METHODS: Using an established model of hind limb tourniquet ischaemia, the effects of oral and intravenous aspirin administration were observed after 6 h of ischaemia and 18 h reperfusion. Samples were obtained and analysed for muscle viability and oedema, and lung neutrophil infiltration. RESULTS: Aspirin, when compared to placebo and controls, significantly increased muscle interstitial oedema when given orally and intravenously. It had no effect on tissue viability or lung neutrophil infiltration. CONCLUSION: Aspirin increases tissue oedema after ischaemia and reperfusion but has no effect on tissue viability. Although its mechanism of action has not been clarified, aspirin may influence the no-reflow component of ischaemia-reperfusion syndrome.

Cigarette smoking increases the development of initial hyperplasia after vascular injury.

PURPOSE: Our purpose was to determine whether exposure to cigarette smoke increases the development of intimal hyperplasia (IH) after vascular injury. METHODS: Sixteen adult male Sprague-Dawley rats underwent standardized balloon catheter injury of the left common carotid artery. For 4 weeks before and 4 weeks after injury, animals in the experimental group (n=8) were exposed to cigarette smoke with an automated vacuum pump device. Animals in the control group (n=8) were restrained in the smoking device for an identical amount of time and underwent arterial injury at 4 vivo, prepared as histologic cross sections, and stained for elastin. IH was measured by planimetry and is reported both as the absolute area of IH and as the ratio (IH/IEL) of the absolute area of IH to the normalized area enclosed by the internal elastic lamina (expressed as a percent). RESULTS: The absolute area of IH was 2.09 +/- 0.34 for the experimental group compared with 0.94 +/- 0.25 for the control group; mean IH/IEL was 43% +/- 7.1% for the experimental group versus 17.7% +/- 4.7% for the control group (p < 0.05, two tailed unpaired t test. CONCLUSIONS: Inhalation of cigarette smoke increases the development of intimal hyperplasia in a rat model of a balloon catheter arterial injury.

The effect of vitamin E and doxycycline on the development of intimal hyperplasia.

The goal of this study is to evaluate the influence of vitamin E (alpha-tocopherol) and doxycycline on the development of intimal hyperplasia in the injured rabbit carotid artery. Three groups of New Zealand white rabbits (10 rabbits each) underwent standardized balloon catheter injury of the carotid artery. One group received 300-400 U/kg of vitamin E orally each day for 4 weeks; another group received 10 mg/kg of doxycycline orally twice daily for 4 weeks and the final group remained as a control group. No statistically significant differences in the degree of intimal hyperplasia development were noted between either treatment group and controls (P > 0.60 for vitamin E, P > 0.40 for doxycycline). We conclude that neither vitamin E nor doxycycline appear to be of benefit in reducing intimal hyperplasia in the injured rabbit carotid artery.

Laparoscopic aortofemoral bypass. Initial experience in an animal model.

OBJECTIVE: The study objective was to evaluate the feasibility of laparoscopic aortofemoral bypass in a porcine model. SUMMARY BACKGROUND DATA: Laparoscopic techniques have been applied to numerous general and thoracic surgical procedures. Their application to vascular surgery has been virtually nonexistent. Open surgery for aortoiliac occlusive disease is accompanied by significant morbidity rates, and minimally invasive procedures have the disadvantage of reduced patency rates. Laparoscopic aortofemoral replacement has the theoretical advantage of long-term patency with reduced postoperative complications. METHODS: Between January and September 1993, laparoscopic surgery was performed on 16 pigs: 6 underwent transperitoneal laparoscopic aortic dissection and vessel control alone; 7 underwent complete transperitoneal laparoscopic aortofemoral bypass; and 3 underwent a retroperitoneal approach. The aortic anastomosis was performed using a combination of sutures and titanium clips in an end-to-side fashion in five pigs, and a custom-made nonsutured graft was secured with use of an end-to-end method in five pigs. Femoral anastomoses were performed with the standard open technique. RESULTS: Technical success was achieved in all 10 animals and with no major complications. Mean blood loss was 20 ml (range, 5-50 ml), and mean operative time was 2.45 hours (range, 2-4 hrs). On aortic-clamp release, 2 of the end-to-side anastomoses required additional sutures to stop bleeding between oversized staples, and 2 of the end-to-end anastomoses required additional ties to reinforce loose ties. All 10 grafts and anastomoses were patent and free of leaks after completion of the procedure. CONCLUSIONS: Laparoscopic aortofemoral bypass is technically feasible in a porcine model. Further experimental work with new instrumentation and technical refinement will make laparoscopic surgery feasible for the treatment of vascular disease in humans.

Pharmacologic suppression of intimal hyperplasia: a dose-response suppression by enalapril.

Intimal hyperplasia is an exaggerated proliferative response to arterial intimal injury. A successful means of limiting this hyperplastic response would significantly improve patency rates of vascular reconstruction. Angiotensin-converting enzyme (ACE) inhibitors decrease the proliferation and synthetic function of vascular smooth muscle cells in vitro, which have been implicated in the production of intimal hyperplasia. We performed a dose-response study of enalapril to assess the level at which maximal suppression of intimal hyperplasia occurs. Seventy male Sprague-Dawley rats weighing 250-300 grams underwent standardized carotid artery balloon catheter endothelial denudation to induce intimal hyperplasia. Six groups of ten animals each were treated with daily intramuscular injections of one of the following doses of enalapril (mg/kg): 0.025, 0.050, 0.075, 0.100, 0.125, and 0.150. A control group (n = 10) was treated with saline. Injections were started two days before injury and continued for 4 weeks, at which time the injured arteries were pressure-fixed in vivo and harvested. EVG-stained histologic cross-sections were measured by planimetry to determine the amount of intimal hyperplasia, which was calculated as the percentage of the arterial lumen replaced by the lesion. Enalapril suppresses the development of intimal hyperplasia in a dose-responsive manner in this model. No further suppression is achieved above a dose of 0.125 mg/kg.

Computerized angiographic analysis of the outcome of peripheral thrombolysis.

BACKGROUND: Catheter-directed peripheral thrombolysis is used increasingly for the management of acute limb ischemia. The comparison of different agents and techniques has proven difficult because of the variations in patient presentation, vessel involvement, and treatment methods. METHODS: A computerized database in which angiographic information is stored on computerized arterial maps has been designed to record details of thrombolysis. RESULTS: A total of 201 patients who presented with rest pain were recorded on the database, and their angiograms were analyzed. There were 123 native-vessel and 78 graft occlusions. Immediate success of lysis and 30-day outcome were not dependent on the site of the occlusion. If an underlying stenosis was revealed, limb salvage rates were significantly greater than when none was found (82% versus 58%, P < 0.01). The presence of at least 1 run-off vessel increased limb salvage rates by 30% (P < 0.001). If more than 5 arterial segments were occluded on the prelysis angiogram, limb salvage was worse than if there were fewer than 5 (57% versus 85%, P < 0.0001). For grafts, less than 5 segments of occlusion led to limb salvage rates of 90%, and more than 5 segments of occlusion led to rates of 72% (P = 0.07). CONCLUSIONS: This simple and user-friendly system of computerized angiographic analysis will enable detailed examination of thrombolytic practice and assist in the prediction of success.

Cigarette smoking accelerates carotid artery intimal hyperplasia in a dose-dependent manner.

BACKGROUND AND PURPOSE: Intimal hyperplasia is the single most important cause of early restenosis after carotid endarterectomy. Cigarette smoking is an independent risk factor associated with peripheral vascular disease and cerebrovascular accidents. We undertook a dose-response experiment to determine the effect of cigarette smoke on development of intimal hyperplasia in a rat carotid artery intimal injury model. METHODS: Seventy-two rats were divided into six equal groups and underwent standardized balloon injury to the carotid artery. Each group received 0 (controls), 1, 2, 3, 6, or 8 cigarettes per day for 4 weeks. Resultant intimal hyperplasia was expressed as a percentage of original lumen replaced by intimal hyperplasia. RESULTS: Percent intimal hyperplasia development (+/- SD) was as follows: controls (0 cigarettes per day), 17.7 +/- 13.2; 1 cigarette per day, 22.8 +/- 15.0; 2 cigarettes per day, 20.0 +/- 14.7; 3 cigarettes per day, 19.2 +/- 12.1; 6 cigarettes per day, 43.5 +/- 15.5; and 8 cigarettes per day, 36.7 +/- 9.8. Six and 8 cigarettes per day significantly increased the development of intimal hyperplasia after intimal injury (P < .01). CONCLUSIONS: High-dose cigarette smoke accelerates development of intimal hyperplasia and may pose a significant risk factor in developing carotid restenosis.