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(Stroke. 2005;36:2286.)
© 2005 American Heart Association, Inc.
Research Reports |
From the Departments of Neurology (A.A.-C., D.W.K., A.J.F., J.S.Y.) and Cardiovascular Medicine (C.T.B., J.S.Y.), The Cleveland Clinic Foundation, Cleveland, Ohio.
Correspondence to Jay S. Yadav, MD, Department of Cardiovascular Medicine, F25, The Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195. E-mail yadavj{at}ccf.org
| Abstract |
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Methods Patients who did not recanalize with thrombolysis were treated with GPIIb/IIIa antagonists, angioplasty, or an embolectomy device. Treatment was individualized based on vascular anatomy, stroke mechanism, patient status, and symptom duration.
Results Twelve patients were treated within 3.8±2.2 hours. The mean National Institutes of Health Stroke Scale (NIHSS) score was 19.4±4.1. Six patients had carotid terminus occlusion, whereas 5 had middle cerebral artery and 1 had basilar artery occlusion. The average doses of intraarterial tPA and reteplase were 17.1±8.6 mg and 2±0.6 units, respectively. All patients received either an intravenous or intraarterial abciximab bolus (mean 11.8±5.8mg) and heparin (mean 3278±1716U). Eleven were treated with angioplasty and 4 had mechanical embolectomy or stenting. Complete (8) or partial (3) recanalization was achieved in 11 cases. There was only one (8.3%) symptomatic hemorrhage. Patients had a favorable outcome at discharge (mean NIHSS 8.9±8.7) and 6 (50%) had an NIHSS
4 at discharge.
Conclusions Multimodal rescue therapy was effective at recanalizing occluded cerebral vessels that failed thrombolysis without an excess risk of ICH.
Key Words: acute angioplasty endovascular therapy platelet aggregation inhibitors stroke thrombolysis
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| Methods |
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| Results |
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Eleven patients were treated with angioplasty (Table 2). Five patients received aspirin and clopidogrel. Two patients were treated with stents for a severe underlying stenosis of the internal carotid artery origin. Additionally, a snare was used in 3 patients and a rheolytic thrombectomy device was used to treat one patient.
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Technical success was achieved in 11 (91.7%) patients with complete (TIMI III) recanalization in 8 (66.7%) and partial (TIMI II) recanalization in 3 (25%) (Table 2). Ten (83.3%) patients had neurologic improvement before discharge (>4-point decrease of NIHSS), whereas 7 (58%) had a >50% improvement. The mean discharge NIHSS of the 10 patients discharged to home or rehabilitation was 6.7±7.3; 6 of these patients were discharged directly to home with minimal or no residual deficits.
There were 2 complications: one symptomatic (>4-point deterioration on NIHSS) subarachnoid hemorrhage and one asymptomatic (no change in NIHSS) petechial hemorrhage. Two patients died of their strokes.
| Discussion |
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We were able to achieve recanalization in nearly all patients, despite the fact that nearly half of our patients had internal carotid occlusions, which are the most difficult occlusions to recanalize. This recanalization had a clinical benefit because 10 of 12 patients had significant clinical improvement and half were discharged to home either normal or nearly normal neurologically. For comparison, IA thrombolysis in the PROACT-II trial resulted in TIMI 3 flow in only 19% of patients, although carotid terminus occlusions were not included.1 Importantly, there was a low rate of symptomatic ICH in our patients despite combining thrombolytics, GPIIb/IIIa antagonists, high doses of heparin, and angioplasty. In PROACT-II, symptomatic ICH occurred in 10% of patients receiving thrombolytic therapy.1 Abciximab may be less prone to cause ICH as compared with standard thrombolytics.4,7 Other contributing factors to the low ICH rate may have been the adjustment of pharmacologic drug doses, particularly rtPA, and the type of mechanical intervention based on the presence of known factors that increase the risk of ICH and the likely pathophysiology of the stroke.8
Limitations of this study are the small number of patients, the lack of randomized controls, and the nonstandardized treatment approach; the latter is both a weakness and a strength because we feel that a regimented and standardized approach limits the therapeutic options.
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| Acknowledgments |
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Received March 21, 2005; accepted June 16, 2005.
| References |
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2. Doggrell SA. Alteplase: descendancy in myocardial infarction, ascendancy in stroke. Exp Opin Investig Drugs. 2001; 10: 20132029.[CrossRef]
3. Larrue V, von Kummer RR, Muller A, Bluhmki E. Risk factors for severe hemorrhagic transformation in ischemic stroke patients treated with recombinant tissue plasminogen activator: a secondary analysis of the European-Australasian Acute Stroke Study (ECASS II). Stroke. 2001; 32: 438441.
4. Lee DH, Jo KD, Kim HG, Choi SJ, Jung SM, Ryu DS, Park MS. Local intraarterial urokinase thrombolysis of acute ischemic stroke with or without intravenous abciximab: a pilot study. J Vasc Interv Radiol. 2002; 13: 769774.[Medline] [Order article via Infotrieve]
5. Nakano S, Iseda T, Yoneyama T, Kawano H, Wakisaka S. Direct percutaneous transluminal angioplasty for acute middle cerebral artery trunk occlusion: an alternative option to intra-arterial thrombolysis. Stroke. 2002; 33: 28722876.
6. Chopko BW, Kerber C, Wong W, Grorgy B. Transcatheter snare removal of acute middle cerebral artery thromboembolism: technical case report. Neurosurgery. 2000; 46: 15291531.[CrossRef][Medline] [Order article via Infotrieve]
7. Emergency administration of abciximab for treatment of patients with acute ischemic stroke: results of a randomized phase 2 trial. The Abciximab in Ischemic Stroke Investigators. Stroke. 2005; 36: 880890.
8. Levy DE, Brott TG, Haley EC Jr, Marler JR, Sheppard GL, Barsan W, Broderick JP. Factors related to intracranial hematoma formation in patients receiving tissue-type plasminogen activator for acute ischemic stroke. Stroke. 1994; 25: 291297.[Abstract]
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