Phil Purdy

Wingspan in-stent restenosis and thrombosis: Incidence, clinical presentation, and management

OBJECTIVE: Wingspan (Boston Scientific, Fremont, CA) is a self-expanding stent designed specifically for the treatment of symptomatic intracranial atheromatous disease. The current series reports the observed incidence of in-stent restenosis (ISR) and thrombosis on angiographic follow-up. METHODS: A prospective, intent-to-treat registry of patients in whom the Wingspan stent system was used to treat symptomatic intracranial atheromatous disease was maintained at five participating institutions. Clinical and angiographic follow-up results were recorded. ISR was defined as stenosis greater than 50% within or immediately adjacent (within 5 mm) to the implanted stents and absolute luminal loss greater than 20%. RESULTS: To date, follow-up imaging (average duration, 5.9 mo; range, 1.5-15.5 mo) is available for 84 lesions treated with the Wingspan stent (78 patients). Follow-up examinations consisted of 65 conventional angiograms, 17 computed tomographic angiograms, and two magnetic resonance angiograms. Of these lesions with follow-up, ISR was documented in 25 and complete thrombosis in four. Two of the 4 patients with stent thrombosis had lengthy lesions requiring more than one stent to bridge the diseased segment. ISR was more frequent (odds ratio, 4.7; 95% confidence intervals, 1.4-15.5) within the anterior circulation (42%) than the posterior circulation (13%). Of the 29 patients with ISR or thrombosis, eight were symptomatic (four with stroke, four with transient ischemic attack) and 15 were retreated. Of the retreatments, four were complicated by clinically silent in-stent dissections, two of which required the placement of a second stent. One was complicated by a postprocedural reperfusion hemorrhage. CONCLUSION: The ISR rate with the Wingspan stent is higher in our series than previously reported, occurring in 29.7% of patients. ISR was more frequent within the anterior circulation than the posterior circulation. Although typically asymptomatic (76% of patients in our series), ISR can cause neurological symptoms and may require target vessel revascularization.OBJECTIVEWingspan (Boston Scientific, Fremont, CA) is a self-expanding stent designed specifically for the treatment of symptomatic intracranial atheromatous disease. The current series reports the observed incidence of in-stent restenosis (ISR) and thrombosis on angiographic follow-up. METHODSA prospective, intent-to-treat registry of patients in whom the Wingspan stent system was used to treat symptomatic intracranial atheromatous disease was maintained at five participating institutions. Clinical and angiographic follow-up results were recorded. ISR was defined as stenosis greater than 50% within or immediately adjacent (within 5 mm) to the implanted stents and absolute luminal loss greater than 20%. RESULTSTo date, follow-up imaging (average duration, 5.9 mo; range, 1.5–15.5 mo) is available for 84 lesions treated with the Wingspan stent (78 patients). Follow-up examinations consisted of 65 conventional angiograms, 17 computed tomographic angiograms, and two magnetic resonance angiograms. Of these lesions with follow-up, ISR was documented in 25 and complete thrombosis in four. Two of the 4 patients with stent thrombosis had lengthy lesions requiring more than one stent to bridge the diseased segment. ISR was more frequent (odds ratio, 4.7; 95% confidence intervals, 1.4–15.5) within the anterior circulation (42%) than the posterior circulation (13%). Of the 29 patients with ISR or thrombosis, eight were symptomatic (four with stroke, four with transient ischemic attack) and 15 were retreated. Of the retreatments, four were complicated by clinically silent in-stent dissections, two of which required the placement of a second stent. One was complicated by a postprocedural reperfusion hemorrhage. CONCLUSIONThe ISR rate with the Wingspan stent is higher in our series than previously reported, occurring in 29.7% of patients. ISR was more frequent within the anterior circulation than the posterior circulation. Although typically asymptomatic (76% of patients in our series), ISR can cause neurological symptoms and may require target vessel revascularization.

Endovascular Treatment of Paraclinoid Aneurysms: Experience with 73 Patients

OBJECTIVEAneurysms arising from the internal carotid artery in close relation to the clinoid process have been called paraclinoid aneurysms. The surgical management of these aneurysms poses technical challenges, and such patients are frequently referred for endovascular treatment. We reviewed our experience with endovascular coil embolization of paraclinoid aneurysms to evaluate the safety and efficacy of this treatment modality. METHODSFrom December 1993 to May 2002, 70 patients underwent endovascular procedures with detachable coils for 73 paraclinoid aneurysms (8 ruptured, 65 unruptured) at the University of Pittsburgh Medical Center and the University of Texas Southwestern Medical Center. A retrospective review of the medical records, outpatient charts, and operative reports was performed. Angiographic outcome was determined at the end of each procedure and by review of follow-up angiograms. Clinical assessments and outcomes are reported according to the Glasgow Outcome Scale (GOS). RESULTSImmediate angiographic outcomes for 73 paraclinoid aneurysms demonstrated complete occlusion in 53 (72.6%), near-complete occlusion in 6 (8.2%), and partial occlusion in 14 (19.2%). Nine aneurysms required more than one coiling session to complete treatment; 8 of these aneurysms required two sessions and 1 required four, for a total of 84 endovascular procedures. Follow-up angiograms could be obtained in 49 patients with 52 paraclinoid aneurysms. During the follow-up period, 6 aneurysms demonstrating partial occlusion and 3 demonstrating near-complete occlusion showed spontaneous progression of thrombosis to complete occlusion. Twelve aneurysms initially demonstrating complete occlusion (5 aneurysms), near-complete occlusion (3 aneurysms), or partial occlusion (4 aneurysms) showed coil compaction requiring retreatment. Of these 12 aneurysms that demonstrated coil compaction, 3 were treated with surgery and 9 with coil repacking. The final angiographic outcomes, determined on the last available follow-up angiograms of 49 aneurysms, excluding 3 surgically clipped aneurysms, showed complete occlusion in 43 (87.8%), near-complete occlusion in 3 (6.1%), and partial occlusion in 3 (6.1%). The angiographic follow-up period ranged from 4 to 54 months (mean, 13.9 mo). Morbidity and mortality rates related to 84 endovascular procedures were 8.3 and 0%, respectively. There were no recurrent or new subarachnoid hemorrhages in 63 patients in whom clinical follow-up could be performed during a mean clinical follow-up period of 14.4 months. The final clinical outcomes demonstrated a GOS score of 5 (good recovery) in 56 patients (88.9%), a GOS score of 4 (moderate disability) in 2 (3.2%), and a GOS score of 3 (severe disability) in 1 (1.6%). Four patients (6.3%) died of unrelated causes. The average period of hospitalization was 17.8 days in patients with acutely ruptured aneurysms and 3.5 days in patients with unruptured or retreated aneurysms. CONCLUSIONThe results of this study indicate that endovascular treatment is a safe and effective therapeutic alternative in ruptured and unruptured paraclinoid aneurysms. The endovascular treatment may also confer a positive impact in terms of the length of hospital stay.

Intracranial arteriovenous malformation: relationships between clinical and radiographic factors and ipsilateral steal severity

Intracranial arteriovenous malformations (AVMs) are high flow shunts that may jeopardize the perfusion of adjacent tissue. Clinical and radiographic data from 62 patients were analyzed to determine their relationship to the severity of steal measured by single photon emission computed tomography (SPECT). The ipsilateral steal index [ISteal(i)] was determined by dividing regional cerebral blood flow (rCBF) values within hand-drawn regions of hypoperfusion in the ipsilateral hemisphere by total brain flow, which was calculated as the average rCBF of each hemisphere. Of the patients, 40% were less than 30 years of age, 45% were 30 to 50 years old, and 15% were over 50. Forty-eight per cent presented with hemorrhage and 34% presented with progressive deficits. There was angiographic steal in 37%, and postoperative hyperemic complications developed in 21%. All patients had ipsilateral regions of hypoperfusion. The ISteal(i) was less than 0.7 in 23 (37%), 0.7 to 0.8 in 20 (32%), and greater than 0.8 in 19 (31%). The ISteal(i) was significantly less severe in the patients over 50; 78% of these patients had an ISteal(i) of greater than 0.8 (P less than 0.01). A history of hemorrhage was associated with less severe steal than that in patients who had not bled (P = 0.088). Patients presenting with a history of progressive deficits had increased severity of steal compared with those without progressive deficits (P less than 0.05). A trend toward decreased severity of steal was noted in patients with unfavorable outcomes.(ABSTRACT TRUNCATED AT 250 WORDS)

Intracranial arteriovenous malformation: Relationship between clinical factors and surgical complications

Serious morbidity and hyperemic states continue to complicate the treatment of certain intracranial arteriovenous malformations (AVMs). Clinical and radiographic characteristics of 62 patients treated over 3 years were analyzed to determine if hyperemic complications (HCs) (defined as unusual perioperative edema or hemorrhage) and outcome could be predicted. Twenty-five (40%) of the patients were less than 30 years old, 28 (45%) were between 30 and 50, and 9 (15%) were more than 50. A history of hemorrhage was found in 48%, and 34% presented with progressive deficits. Thirteen (21%) developed evidence of HCs; 51 (82%) ultimately had a good outcome, 4 (6%) had a poor outcome, and 7 (11%) died. The incidence of HCs was higher in patients whose AVMs recruited perforating vessels (53%) than those without (7%) (P less than 0.001). The presence of preoperative angiographic steal carried a 35% risk of HCs whereas its absence carried a 13% risk (P less than 0.05). The sum of the diameters of the feeding vessels was also predictive (P less than 0.05). Outcome was clearly age-related: good outcome was achieved in 92% of the patients less than 30 years old, 86% of those 30 to 50, and 44% of patients older than 50 (P less than 0.05). Left hemispheric AVMs showed less morbidity than right (P less than 0.05) as did those without perforating vessel recruitment (P less than 0.07). HCs had a dramatic impact on outcome with 92% of patients without HCs having good outcome and 46% of those with HCs recovering well (P less than 0.001).

Postpartum cerebral angiopathy. Is there a role for sympathomimetic drugs

Background Postpartum cerebral angiopathy is associated with the use of ergot alkaloids. The exact mechanism is unclear but may be related to their sympathomimetic properties, as evidenced in patients already on other ergot derivatives who deteriorated only after taking additional sympathomimetic drugs. We postulate that sympathomimetic agents, independent of ergot alkaloids, may produce the same complication. Case Description A postpartum patient, initially presenting with headaches, subsequently manifested rapid neurological deterioration after ingesting isometheptene, a sympathomimetic drug. She was not on any ergot derivative but presented similar clinical and radiological manifestations. She experienced increased headache severity, visual disturbance, and seizures associated with multiple segmental cerebral vasoconstriction on angiography and increased T2 -weighted signal in the occipital areas on magnetic resonance imaging. Conclusions This case is additional evidence that sympathomimetic actions of some drugs, such as ergot derivatives and isometheptene, may lead to postpartum cerebral angiopathy. Documentation of medication used by postpartum women suffering similar complications is needed to verify these findings.

Microfibrillar collagen model of canine cerebral infarction

A new canine model of focal cerebral ischemia has been developed employing intravascular delivery of microfibrillar collagen via femoral catheterization. In 13 dogs, dose-effect studies showed neurologic deficits (ranging from mild hemiparesis to death) related to the dose of microfibrillar collagen delivered. In another 10 dogs, 0.5 ml of 60 mg/ml microfibrillar collagen was injected into the common carotid artery; neurologic assessment over 48 hours revealed a survivable stroke syndrome in seven dogs, death at 40 hours in one dog and at less than 12 hours in another, and no clinical effect in one dog. The eight surviving dogs were sacrificed at 48 hours; nine of the 10 dogs had middle cerebral artery distribution infarcts (two grossly hemorrhagic and five grossly nonhemorrhagic) on histologic examination. Angiography in three dogs demonstrated no significant major vascular occlusion. All seven dogs with survivable strokes demonstrated a dense hemiparesis at 24 hours that improved to ambulatory status at 48 hours. The use of microfibrillar collagen to produce middle cerebral artery strokes in dogs provides a new opportunity to study cerebral ischemia without surgery involving the cervical or cranial vasculature. Dogs have larger brains than other common animal models and thus are more amenable to study with imaging modalities. A model with a measurable but survivable insult provides an opportunity for short- and long-term clinical follow-up and for the investigation of therapeutic interventions.

Interdisciplinary evaluation of cerebral hemodynamics in the treatment of arteriovenous fistulae associated with giant varices

The techniques for the treatment of intracranial arteriovenous fistulae include angiographic balloon occlusion of the fistula as well as direct surgical attack. Regardless of the method, the occurrence of severe hyperemia caused by a lack of autoregulation after obliteration of the fistula remains a significant concern. We report the use of single photon emission computed tomography and transcranial Doppler studies to assess the occurrence of hyperemia during trial balloon occlusion of such fistulae in two patients. Single photon emission computed tomography and transcranial Doppler studies confirmed the lack of hyperemia during the test occlusion, allowing consideration of treatment plans involving acute fistula occlusion without the difficulty imposed by gradual occlusion and permitting a more accurate evaluation of risk. The purpose of this report is to illustrate how clinical evaluation of intracranial hemodynamics can contribute significantly to treatment decisions.

Elevated Transcranial Doppler Ultrasound Velocities Following Therapeutic Arterial Dilation

BACKGROUND Elevated transcranial Doppler (TCD) velocities seen after cerebral angioplasty are commonly interpreted as evidence of residual or recurrent stenosis but may conceivably arise from hyperemia and require different clinical management. SUMMARY OF REPORT Four cases of abnormally elevated mean TCD velocities obtained after therapeutic arterial dilation with either balloon angioplasty or intra-arterial administration of papaverine are described. In each case, cerebral angiography revealed a dilated vessel, suggesting that hyperemia and impaired autoregulation were the causes of the high velocities. CONCLUSIONS These examples suggest that high TCD velocities after vessel dilation may be produced by unpredictable amounts of vessel narrowing and flow alteration. Although a normalizing TCD velocity after angioplasty suggests effective vessel dilation, high velocities may be due partly to hyperemia and cannot be interpreted as arising solely from recurrent stenosis.

Reversible middle cerebral artery embolization in dogs without intracranial surgery.

Using dogs, we developed an intravascular model for reversible middle cerebral artery occlusion that does not involve intracranial surgery or enucleation. Using silicone plastic plugs with a suture embedded within them, we embolized the middle cerebral artery in 19 dogs via the cervical carotid artery. The free end of the suture remained accessible in the neck, and after variable dwell times traction was placed on the suture and the plug was withdrawn. Placement of the plug in the middle cerebral artery produced ischemia in the basal ganglia. The degree and distribution of cortical ischemia were variable as evidence by the pathologically documented scattered nature of infarcts that resulted when the plug was left permanently in the middle cerebral artery and when it was removed after 1 or 2 hours. Angiography demonstrated occlusion of the middle cerebral artery with the plug in place as well as reperfusion when the plug was withdrawn. This modification of a previously described model of middle cerebral artery occlusion provides an opportunity to study structural, physiologic, and biochemical events occurring in acutely hypoperfused cerebral tissue as well as critical changes leading to irreversible injury without the disadvantages of surgical manipulation required by all previous models of reversible cerebral ischemia.

Intraarterial thrombolysis for thromboemboli associated with endovascular aneurysm coiling. Report of five cases.

With the rapidly developing applications of GDC endovascular aneurysm embolization, the recognition and treatment of potential intra-procedural complications is crucial to reducing the morbidity and mortality of this procedure. Thromboembolic complications occur with an incidence of 2–11% with endovascular aneurysm coiling. We describe five cases in which the intraarterial use of thrombolytics was applied to disrupt a fresh clot and recanalize the occluded vessels with variable angiographic and clinical success. Five cases are presented in which thromboembolic complications occurred during or shortly after GDC endovascular aneurysm occlusion. The complication was recognized while depositing coils in two cases, on post-embolization angiogram in one, and a few hours following embolization in two cases in which a new neurologic deficit developed in the ICU. In those cases recognized while the microcatheter was near the aneurysm site, immediate thrombolysis was performed at the site of occlusion. The patients who developed a new neurologic deficit were returned to the endovascular suite and the site of occlusion was noted to be distal to the coiled aneurysm. Clot disruption was performed with the microcatheter before delivering intraarterial thrombolytics. Thromboembolic complications of GDC aneurysm embolization are fortunately rare and can be managed with delivery of thrombolytic therapy at the site of occlusion. Intraarterial thrombolysis of fresh clot caused by GDC aneurysm occlusion can successfully open the occluded vessels but not without serious risk of hemorrhage.