Faculty Bibliography

OBJECTIVE: Carotid artery stenting (CAS) for treatment of carotid stenosis has not received wide acceptance because of the availability of carotid endarterectomy (CEA) with its excellent results and because of the risk of embolic stroke associated with CAS. The feasibility and efficacy of cerebral protection devices that may prevent such embolic complications have yet to be shown. We report our initial results with CAS performed with cerebral protection. METHODS: For a period of 28 months, 31 patients with carotid artery stenosis, most of whom were considered at high risk for CEA (87%), underwent treatment with CAS in conjunction with either the PercuSurge GuardWire (n = 19; Medtronic, Minneapolis, Minn), the Cordis Angioguard filter (n = 7; Cordis, Warren, NJ), or the ArteriA Parodi Anti-embolization catheter (n = 4; ArteriA, San Francisco, Calif) with US Food and Drug Administration-approved investigational device exemptions. Factors that made CEA high risk included restenosis after CEA (n = 6), hostile neck (n = 6), high or low lesions (n = 4), and severe comorbid medical conditions (n = 11). Preoperative neurologic symptoms were present in 58%, and the mean stenosis was 85% +/- 12%. Data were prospectively recorded and analyzed on an intent-to-treat basis. Neurologic evaluation was performed before and after CAS by a protocol neurologist. RESULTS: CAS was performed with local anesthesia with the Wallstent (n = 23; Boston Scientific Corp, Natick, Mass) or the PRECISE carotid stent (n = 7; Cordis) in conjunction with one of the protection devices in an operating room with a mobile C-arm. Each patient received dual antiplatelet therapy before surgery. The overall technical success rate was 97% (30/31). In one patient, the lesion could not be crossed with a guidewire because of a severely stenosed and tortuous lesion. This patient was not a candidate for CEA and was treated conservatively. In the remaining 30 cases, CAS had a good angiographic result (residual stenosis, <10%). All patients tolerated the protection device well, and no intraprocedural neurologic complications occurred. Macroscopic embolic particles were recovered from each case. One patient (3%) with a severely tortuous vessel had a major stroke immediately after CAS, and no deaths occurred. The combined 30 day stroke/death rate was 3%. During a mean follow-up period of 17 months, one subacute occlusion of the stent occurred but did not result in a stroke. Three other patients had duplex scan-proven in-stent restenosis, and two underwent treatment with repeat percutaneous transluminal angioplasty with a good result. No patient had a stroke during the follow-up period. CONCLUSION: CAS with cerebral protection devices can be performed safely with a high technical success rate. Although many patients who underwent treatment with CAS were at high risk, the neurologic complication rate was low and CAS appears to be an acceptable treatment option for select patients at high risk for CEA. Tight lesions and tortuous anatomy may make the use of distal protection devices difficult. Further study is warranted

OBJECTIVE: An accepted fact is that abdominal aortic aneurysms (AAAs) larger than 5.5 cm should undergo elective repair. However, subsets of these patients have serious comorbid conditions, which greatly increase operative risk. This study evaluated the outcomes of periods of protracted nonoperative observational management with selective delayed surgery in patients at high risk with large infrarenal and pararenal AAAs. METHODS: Among 226 patients with AAAs more than 5.5 cm, we selected 72 with AAAs from 5.6 to 12.0 cm (mean, 7.0 cm) for periods of nonoperative management because of their prohibitive surgical risks. Comorbid factors included a low ejection fraction of 15% to 34% (mean, 22%) in 18 patients, 1 second forced expiratory volume less than 50% (mean, 38%) in 25, prior laparotomy in 10, and morbid obesity in 22. Follow-up examination was complete in the 72 patients for the 6 to 76 months (mean, 23 months) that they underwent nonoperative treatment. Fifty-three patients ultimately underwent operation because of AAA enlargement or onset of symptoms after 6 to 72 months (mean, 19 months) of nonoperative treatment. RESULTS: Of the 72 selected patients, 54 (75%) are living and 18 (25%) are dead. Seven patients who underwent only nonoperative treatment presently survive after 28 to 76 months (mean, 48 months). Of the 18 deaths, AAA rupture occurred in only three patients (4%) who were observed for 12, 31, and 72 months before rupture. Nine other deaths (13%) occurred after 6 to 72 months from comorbidities unrelated to the AAA. Six of the 53 patients who underwent delayed operation died within 30 days of operation (11% mortality rate). The mortality rate for the 154 good-risk patients with an AAA who underwent prompt open or endovascular repair was 2.2%. CONCLUSION: These data indicate that some patients with large AAAs and serious comorbidities are acceptably managed for long periods (6 to 76 months) with nonoperative means. Substantial delays of 12 to 76 months resulted in an AAA rupture rate of only 4%, and 13% of these patients (nine of 72) died of comorbidities unrelated to AAA rupture or surgery. Mortality rate in this group of patients, when operated, was 11% (six of 53). These findings support the selective use of nonoperative management in some patients with large AAAs and serious comorbidities

BACKGROUND: Ruptured abdominal aortoiliac aneurysms (RAAAs) carry a high mortality when treated by open surgical repair. Since 1994, we have employed endovascular approaches to treat this entity. METHODS: Patients with presumed RAAAs were treated with restricted fluid resuscitation (hypotensive hemostasis), rapid transport to the operating room, placement of a transbrachial or transfemoral guidewire under local anesthesia, and urgent arteriography. In patients with suitable anatomy, endovascular graft repair was performed. If the anatomy was unsuitable, standard open repair was performed. If the patient had circulatory collapse, proximal balloon control was employed. RESULTS: Of 31 patients managed in this fashion, 25 underwent endovascular graft repair. Six required open repair. Total operative mortality was 9.7% (3 patients). Only 10 patients required proximal balloon aortic control. CONCLUSIONS: Endovascular techniques (proximal balloon control and endografts) may improve treatment outcomes for RAAAs. Restricted resuscitation (hypotensive hemostasis) can be effective in the RAAA setting

OBJECTIVE: Endoleaks and endotension are critically important complications of some endovascular aortic aneurysm repairs (EVARs). For the resolution of controversial issues and the determination of areas of uncertainty relating to these complications, a conference of 27 interested leaders was held on November 20, 2000. METHODS: These 27 participants (21 vascular surgeons, five interventional radiologists, one cardiologist) had previously answered 40 key questions on endoleaks and endotension. At the conference, these 40 questions and participant answers were discussed and in some cases modified to determine points of agreement (consensus), near consensus (prevailing opinion), or disagreement. RESULTS: Conference discussion added two modified questions for a total of 42 key questions for the participants. Interestingly, consensus was reached on the answers to 24 of 42 or 57% of the questions, and near consensus was reached on 14 of 42 or 33% of the questions. Only with the answers to four of 42 or 10% of the questions was there persistent controversy or disagreement. CONCLUSION: The current endoleak classification system with some important modifications is adequate. Types I and II endoleak occur after 0 to 10% and 10% to 25% of EVARs, respectively. Many (30% to 100%) type II endoleaks will seal and have no detrimental effect, which never or rarely occurs with type I endoleaks. Not all endoleaks can be visualized with any technique, and increased pressure (endotension) can be transmitted through clot. Aneurysm pulsatility after EVAR correlates poorly with endoleaks and endotension. An enlarging aneurysm after EVAR mandates surgical or interventional treatment. These and other conclusions will help to resolve controversy and aid in the management of these vexing complications and should also point the way to future research in this field