Abciximab Is a Safe Rescue Therapy in Thromboembolic Events Complicating Cerebral Aneurysm Coil Embolization
Single Center Experience in 42 Cases and Review of the Literature
Background and Purpose— The purpose of this study was to estimate the safety and efficacy of abciximab treatment in combination with prophylactic heparin, acetylsalicylic acid (ASA), and clopidogrel application in cases of thrombus formation complicating endovascular coil embolization in cerebral aneurysms.
Methods— Thromboembolic incidents during endovascular management of 515 consecutive cerebral aneurysms were observed in 48 cases (9.3%). Eight incidents were observed during embolization of incidental aneurysms (8/174; 4.6%, 95% CI: 2.0 to 8.9%). All patients underwent anticoagulation with heparin and platelet-inhibition with ASA during treatment procedure. In addition, clopidogrel orally was applied 3 days preoperatively in patients with incidental aneurysms. In case of thrombus formation, glycoprotein IIb-IIIa inhibitor abciximab was given in 42 cases. No coagulation-effective rescue treatment was conducted in 5 cases. One patient was treated with r-tPA. End points were infarction on follow-up cranial CT and the rate of intracranial hemorrhages.
Results— No infarcts on follow-up CT were observed after treatment with abciximab in 29/42 patients (69.0%, 95% CI: 52.9 to 82.4%). No coagulant rescue therapy was applied in 5 patients because of a small nonocclusive thrombus or good collateral blood supply, showing consecutive infarction on follow-up CT in 3 cases as did the 1 patient treated with r-tPA. No periprocedural bleedings or rebleedings were observed in any case.
Conclusion— Abciximab was safe as rescue treatment in cases of thrombus formation during endovascular aneurysm coiling. In our study the use of Abciximab, in combination with prophylactic anticoagulation and antiaggregation, does not lead to additional intracranial hemorrhages or any extracranial bleeding complications.
- intracranial aneurysm
- aneurysm coiling
- GP IIb-IIIa antagonist
Endovascular occlusion of intracranial aneurysms with detachable coils has an overall estimated procedure related permanent complication rate of 3.7 to 6.8%.1,2 Procedure related thromboembolic events with partially or completely persisting neurological deficits are reported in 2.4% to 5.2% of the patients.3–5 With the use of diffusion-weighted imaging the rate of silent thromboembolic events can be up to 61%.6 Clotting at the thrombogenic interventional material is considered an important source of such thromboembolism during endovascular embolization of cerebral aneurysms.
For the time being, only scarce data originate from small case series, and the discussion about the appropriate rescue management of this complication remains controversial. The use of intravenous (IV) heparin,7,8 intraarterial (IA) fibrinolytic agents,9,10 and IV or IA glycoprotein (GP) IIb-IIIa Inhibitors8,11–22 have been described previously for treatment of this complication. However, because of the small number of cases reported for each approach, no definite conclusion can be drawn regarding the appropriate rescue management.
Intraprocedural systemic administration of heparin, acetyl salicylic acid (ASA), or glycoprotein (GP) IIb-IIIa inhibitors are increasingly used in several centers to reduce the risk and to prevent thromboembolism before, during, and after endovascular aneurysm treatment.1,8,23–25
Experience with abciximab (both IA and IV) to manage thromboembolism in the setting of endovascular aneurysm treatment is limited. To our knowledge 3 case reports and 7 case series with a total of 90 patients have been published (Table 5). In 4 further reports with a total of 32 patients the use of eptifibate, tirofiban, and abciximab in combination with additional rescue treatment (fibrinolytics or mechanical clot disruption) was reported (Table 6).
The use of GP IIb-IIIa inhibitors as treatment in combination with platelet inhibition has been described by Mounayer et al in 9 cases (abciximab IA), by Aviv et al in 5 cases (abciximab IV), and by Bruening et al in 11 cases (tirofiban IV).16,19,20
This article describes our experience with abciximab in the management of acute thromboembolic events during endovascular treatment of cerebral aneurysms in combination with heparin and ASA (ruptured aneurysms) or heparin with ASA and clopidogrel (incidental aneurysms).
Whereas previous reports focused on the immediate recanalization rate, our end points were rates of infarction on follow-up cranial CT and the rate and severity of intracranial hemorrhages. Moreover, we present figure on safety and efficacy of abciximab in a pooled analysis of our data together with the data available from review of the literature.
Materials and Methods
Between January 2003 and January 2008, endovascular aneurysm embolization was performed in 477 consecutive patients with 515 cerebral aneurysms in our institution. Thromboembolic incidents during endovascular management were observed in 48 procedures.
Treatment of thromboembolism was performed as follows: abciximab IV (n=39); abciximab IA (n=3); r-tPA IA (n=1); no anticoagulative therapy (n=5).
All endovascular coil embolization in our patients were done with bare platinum coils. We use those provided by Boston Scientific and Micrus Inc in equal shares.
One balloon-assisted coiling and 5 stent-assisted procedures were performed in those patients treated with abciximab. One stent procedure was done in the “none-treatment-group.” All Stents used in our patients were Neuroform stents provided by Boston Scientific.
Preventive Anticoagulation Therapy
To minimize thromboembolic complications all flush solutions including the guiding-catheters and microcatheters were heparinized. Heparin was applied intravenously in ruptured and unruptured aneurysms before placement of the guiding catheter (activated clotting time 250 to 300 seconds).
During GDC treatment 250 to 500 mg acetyl salicylic acid (ASA; Aspisol) was additionally administered intravenously after deployment of the first coil, both in ruptured and unruptured aneurysms. In unruptured aneurysms 75 mg clopidogrel PO (Plavix, Sanofi Pharma Bristol-Myers Squibb SNC) and low-molecular-weight heparin (Clexane, Aventis Pharma) was applied from 3 days before treatment according to our anticoagulation schedule as previously published.23
One patient with artificial heart valves who was treated with abciximab received neither heparin nor ASA because of an INR of 2.9.
Definition of Clotting, Vasospasm, and Infarction
A thromboembolic event was angiographically defined as any event with complete or partial occlusion of arteries at the site of the aneurysm, distally to the vascular territory where the endovascular procedure was performed or in any other vascular territory. We use the term “proximal thrombus” when it arises at the coil/parent artery interface and “distal thrombus” when its location is distally to the aneurysm but within the same vascular territory.
An adapted TIMI scale was used to measure immediate angiographic occlusion grade (Table 1).
Mechanical narrowing or complete occlusion of the vessel lumen at the interface between the coil/parent vessel by the coils itself or in combination with vasospasm of any source was not detected.
Infarction or intracranial hemorrhage were evaluated and defined in pre- and postprocedural cranial CT. All postprocedural CT scans were performed within the first day after embolization (12 to 24 hours after the procedure). Complete infarction was defined as involvement of the whole dependent vascular territory of the occluded artery. Partial infarction was defined as infarction of parts of the dependent vascular territory of the occluded artery.
Treatment of Thromboembolism
Therapy for coil surface thrombus or distal embolus was administered at the operator’s discretion. Abciximab (ReoPro, Lilly) was applied IV or IA with a standard bolus of 0.25 mg/Kg of body weight. Infusion of r-tPA (Actilyse, Boehringer) was started by bolus injection of 10 mg and then continued with an infusion rate of 30 mg/h. Infusion was stopped once arterial flow had been reestablished or at a maximum dose of 0.9 mg/kg. No rescue treatment has been carried out in 5 cases of small nonocclusive thrombus (TIMI 3), nonocclusive thrombus (TIMI 2) with good collateral blood supply, or occlusive thrombus (TIMI 0 and 1) with excellent collateral blood supply.
Demographic and Clinical Data
Patients with subarachnoid hemorrhage (SAH) were categorized according to the scale of Hunt and Hess (H&H). For classification of patient outcome we used the Glasgow outcome scale (GOS) with the following categories: 1, dead; 2, vegetative state; 3, severe disability; 4, moderate disability, but able to live independently; 5, good recovery, able to return to work. Demographic, clinical, morphological, and treatment data of all patients with thromboembolic events are displayed in Tables 2 and 3⇓.
We analyzed our prospective aneurysm database from January 2003. All patients who had acute cerebral thromboembolic events during aneurysm coiling were identified, and their pre- and postprocedural cranial CT and digital subtraction angiographic (DSA) images were reviewed. Two experienced neuroradiologists (J.F., U.G.) reviewed the DSA images, documented all occluded arteries, and assigned a TIMI occlusion grade. CT images were rated for all patients where thromboembolic events had been detected by a single reviewer (T.R., blinded for the application of abciximab). In a second step, the territory of the infarct on CT was compared to the vessel occlusion site on DSA (T.R.). The clinical evaluation of our patients, including the discharge examination, was done by independent neurologist or neurosurgeons.
Endovascular coil embolization with Guglielmi detachable coils (GDC) was performed in 477 patients harboring 515 aneurysms (358 women, 119 men). The mean age was 50.9 (10 to 90 years). Thromboembolic incidents during endovascular management of ruptured aneurysms were observed in 40/341 (11.7%, 95% CI: 8.5 to 15.5%) of cases; 8/174 (4.6%, 95% CI: 2.0 to 8.9%) incidents were seen during therapy of incidental aneurysms.
Proximal thrombus formation at the coil/parent vessel interface was detected in 25 cases, 22 of which received abciximab as treatment, 1 patient received r-tPA, and no treatment has been conducted in two of this cases.
Distal thromboembolism was present in the remaining 23 cases, of which 20 were treated with abciximab and 3 received no treatment. Details are displayed in Table 2. The distribution of pretreatment TIMI grades according to the particular therapy is displayed in Table 4.
Complete recanalization at procedural termination was detected in 6/42 (14.3%, 95% CI: 5.4 to 28.5%) cases after treatment with abciximab. Partial recanalization at procedural termination was detected in 25/42 (59.5%, 95% CI: 43.3 to 74.4%). No effect of treatment was detected in the remaining cases.
Infarction Related to Thrombus
No infarction on follow-up CT was detected in 29/42 (69.0%, 95% CI: 52.9 to 82.4%) patients after abciximab treatment and in 2/5 (40.0%, 95% CI: 5.3 to 85.3%) of the patients without treatment.
In patients with initial complete or near complete vessel occlusion (TIMI 0 and 1), an infarct on follow-up CT after treatment with abciximab was evident in 13/42 (31%), and in cases of partial or normal vessel filling (TIMI 2 and 3) no infarct on follow-up CT was detected after abciximab rescue treatment (Table 4).
In the 8 patients with incidental aneurysms (prophylactic antiaggregation with clopidogrel and aspirin), complete infarction was detected in 1 (treated with r-tPA) and partial infarction in 2 (treated with abciximab) cases. No infarction on follow-up CT was detected in the remaining 5 (treated with Abciximab) cases. The distribution of infarction in relation to the initial clinical status is displayed in Table 3.
Bleeding Related to Rescue Therapy
We observed neither intracerebral bleeding complications nor immediate extra cerebral bleeding complications. No extra cerebral bleeding complications (eg, retroperitoneal hematoma, bleeding at the puncture site and nasal or oral bleeding related to intubation) attributable to abciximab rescue treatment have been detected during hospital stay.
Good outcome (GOS 4 and 5) was observed in 31/42 (73.8%, 95% CI, 58.0 to 86.1%) of patients treated with abciximab and in 3/5 (60%, 95% CI: 14.7 to 94.7%) of patients without treatment; GOS in the patient treated with r-tPA was 2.
The mortality rate was 3/42 (7.1%, 95% CI: 1.5 to 19.5%) among patients treated with Abciximab. Initial clinical presentation in those patients was H&H 4 (n=1) and 5 (n=2). Among all other cases the mortality rate was 0.0%.
In the presented series thromboembolic incidents during endovascular management of cerebral aneurysms were detected in 48/515 (9.3%; 95% CI: 7.0 to 12.2%) of cases. The rate of infarction was 31% after therapy with abciximab. The low infarct rate on CT, in total 13/515 (2.5%; 95% CI:1.4 to 4.3%), resulting in a thromboembolism related clinical morbidity of at most 2.5% compares favorably with previous studies.1,2 In our study no fatal bleeding occurred after abciximab therapy.
In 5 cases no treatment was applied because of a small nonocclusive thrombus (TIMI 3), nonocclusive thrombus (TIMI 2) with good collateral blood supply, or occlusive thrombus (TIMI 0 and 1) with excellent collateral blood supply. The particular hemodynamic situation in these 5 patients was considered to be favorable, and balancing this favorable hemodynamic situation with a possible bleeding risk led to the decision against a treatment. In 4 cases additional with a similar favorable hemodynamic setting, the decision was made contrariwise and abciximab has been applied despite this assumed favorable hemodynamic situation (Table 4). An infarct in the corresponding vascular territory on follow-up CT was evident in 3/5 of the patients without treatment. No infarct on follow-up CT has been observed in the 4 patients (TIMI 2 in all 4 cases) treated with abciximab. Based on this data treatment with abciximab might be beneficial even if the particular hemodynamic situation is considered still favorable.
Ischemic complications can be subdivided into thrombosis of the parent artery of the aneurysm and an embolism into any artery. Thromboembolism during endovascular embolization of cerebral aneurysms may result from acute clotting originating from arterial catheters, contrast agents, implanted devices such as coils and stents, and mobilization of thrombus from within the aneurysm which may lead to distal embolism.26,27 Thromboembolic complications are most commonly recognized as distal emboli and less common as filling defect at the coil/parent artery interface.5,12,17,28 This is not in line with our observations. We detected proximal thrombus formation at the coil/parent vessel interface in 25 cases and distal thromboembolism in 23 cases. Our findings are supported by data from Aviv et al, who observed an increased rate (69%) of local thrombosis at the coil/parent vessel interface.19
Intraprocedural thrombosis of the parent artery primarily develops probably at the interface of coils because of platelet aggregation. The response of flowing arterial blood to an intravascular foreign body is incompletely understood. In this setting platelets represent the predominant component of arterial thrombi and correspondingly it follows that platelet inhibition represent the cornerstone of antithrombotic therapy in endovascular coil embolization.26,27
The dose and safety profiles of GP IIb-IIIa inhibitors have been investigated in the prevention and treatment of thromboembolic and ischemic complications in coronary interventions.29,30 Based on the EPIC study, the most commonly used regimen consists of an intravenous 0.25 mg/kg bolus injection and then a continuous infusion for 12 hours.31 If solely the bolus is given, bleeding times recover to near normal values by 12 hours. Inhibition of platelet function is sustained throughout the duration of infusion, and this profound effect persists for 4 to 6 hours after termination of the intravenous infusion.13,27
The only approved therapy to date for acute occlusion of cerebral vessels is the intravenous infusion of r-tPA. Intraarterial thrombolysis with fibrinolytic agents has been used widely but their benefit is hampered by the risk of subsequent intracranial hemorrhage, especially in the setting of acutely ruptured aneurysms. The local treatment of thromboembolic events may have disastrous consequences.9,32,33 In ISAT, all 5 patients who had received fibrinolytic therapy with r-tPA to treat a thromboembolic complication after endovascular treatment rebled, and all of these patients died.33 Cronqvist et al used urokinase IA to treat periprocedural thromboembolism during coil treatment and reported devastating intracerebral hemorrhages in 3 of 6 patients with ruptured aneurysms.10
Two large trials have investigated intravenous abciximab in stroke patients.34,35 The larger “Phase-III AbESTT-II trial aimed to randomize patients within 5.5 hours of stroke onset. The trial was terminated prematurely because of an excess of symptomatic or fatal intracranial hemorrhage at 5 days (0.5%-placebo versus 5.5% Abciximab). We hypothesize that the absence of hemorrhage in our series may result from the very early application time point after detected vessel occlusion.
The safety and effectiveness of abciximab (Without additional fibrinolytic therapy or mechanical clot disruption) in the treatment of acute cerebral thromboembolic complications during coil embolization of cerebral aneurysms has been addressed to date in 90 cases (Table 5). After pooling our results (complete/partial recanalization in terms of restored vessel patency on angiogram) with the data given in the literature the overall successful recanalization rate can be estimated at 114/132 (86.4%, 95% CI:79.3 to 91.7%). These results seem to compare favorably with studies that reported complete recanalization in 52.6% of vessels treated with urokinase10 and in 44% of vessels treated with IA r-tPA,9 respectively. The later of which reported that all 9 patients treated with r-tPA suffered cerebral ischemic infarctions but no intracerebral hemorrhage.
Clinical relevance of a particular infarct is hard to assign in SAH patients as effects from vasospastic infarcts, from preexistent intracerebral hemorrhages and from hydrocephalus may obscure its true impact on the clinical outcome. Consequently, solely the evaluation of unruptured aneurysms provides valid clinical data. We used in our study the surrogate end point “infarct on follow-up CT.”
When again pooling our results (infarction on follow-up CT) with the available data in the literature (4 studies with a total of 34 cases11,16,17,19) the success rate of abciximab treatment can be estimated to be 56/76 (73.7%, 95% CI: 62.3 to 83.1%), yet comparing similar or possible favorable to fibrinolytic treatment.
Although abciximab has been shown to be effective in treating acute thrombus formation during coronary angioplasty and neurointerventions,8,11–14 significant concern exists regarding the potential hemorrhagic complications that can occur with this medication, especially in the treatment of ischemic stroke.35 However, this concern is not substantiated by investigations where abciximab has been used for carotid36 or vertebrobasilar stroke.37,38 Furthermore, Akkerhuis et al analyzed the risk of hemorrhagic stroke associated with IV abciximab by combining 4 randomized trials with a total of 8555 patients undergoing coronary intervention. The risk of hemorrhagic stroke was 0.15% in patients treated with abciximab and 0.10% in those treated with placebo.39
We used abciximab as treatment in 42 patients and observed no subsequent bleeding complications. This is in line with several reports using GP IIb-IIIa inhibitors for treatment in thromboembolic events complicating endovascular coil embolization (Tables 5 and 6⇓). However, Park and colleagues reported on postprocedural rebleeding after abciximab therapy in 3/16 endovascular-treated ruptured aneurysms. One of those cases showed marked thrombocytopenia, and the remaining 2 displayed a >25% reduction in platelet count.22 Although the possibility of a heparin-induced thrombocytopenia could not be ruled out completely, the bleeding risk after Abciximab therapy should not be overlooked. When summarizing the available data in regard of treatment during coil embolization using GP IIb-IIIa inhibitors, bleeding complications were reported in 7/147 (4.8%, 95% CI: 1.9 to 9.6%). Reasons for those bleedings are not necessarily attributable to GP IIb-IIIa inhibitors, because in 3 of the reported cases a small dissection was created during mechanical clot disruption with additional administration of r-tPA in 2 of those.21 In a fourth patient a rebleeding occurred after perforation with coils after abciximab administration.19 As mentioned above, in the remaining 3 cases the possibility of a heparin-induced thrombocytopenia with consecutive bleeding could not be ruled out completely.22 In the entire literature (147 cases according to our search), 3 cases have been reported where a hemorrhage during aneurysm treatment can be attributed (without additional thrombolytic agents or mechanical manipulation) to the administration of GP IIb-IIIa inhibitors. Based on this data, the true GP IIb-IIIa inhibitor related hemorrhage rate should be 2.0% (95% CI: 0.4 to 5.8%).
The interpretation of our data should be done with care because there are limitations in some points. First of all, it is a nonrandomized study with all its inherent drawbacks. The second limitation is the absence of a large control group without treatment. Therefore we do not claim our results to be definite. A third problem is the difficulty to differentiate thromboembolic infarcts from infarcts attributable to cerebral vasospasm, even though follow-up CT scans were performed within 12 to 24 hours after intervention. Vasospasm was already diagnosed angiographically in 6 cases during coil embolization but none of which showed direct vessel obstruction at the coil/parent vessel interface. Although infarction and site of thromboembolism corresponded perfectly, in these 6 cases the possibility of vasospasm induced infarction could not be ruled out completely and the true rate of thromboembolism related infarcts might be overestimated.
Infarct rate on CT is a crude surrogate marker but was feasible in all patients. However, MRI with its superior sensitivity for detection of acute ischemic lesions would have been an inappropriate burden to many SAH patients in poor clinical condition. Although infarction and site of thromboembolism corresponded perfectly, in these 6 cases the possibility of vasospasm induced infarction could not be ruled out completely and the true rate of thromboembolism related infarcts might be overestimated. Because of the limitations of this study, the safety and efficacy of GP IIb-IIIa inhibitors requires additional investigation.
The application of abciximab as rescue treatment was confirmed to be a safe option in case of thrombus formation complicating endovascular coil embolization. In particular, the application of abciximab in combination with prophylactic anticoagulation and antiaggregation did not lead to additional intracranial hemorrhages or extracranial bleeding complications. Based on our data combined with data from the literature, the GP IIb-IIIa inhibitor related hemorrhage rate is estimated to be 2.0% (95% CI: 0.4 to 5.8%).
- Received October 2, 2008.
- Revision received October 24, 2008.
- Accepted November 7, 2008.
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