Saturday 21 July 2012

Interventional approach : management of Ischaemic Stroke

oleh : Fritz Sumantri Usman Sr ( Neurologist - Interventional Neurologist )


Abstract

Stroke gave a big number as cause of the death and a leading cause of severe and disability in any kind part of the world. Ischaemic stroke showed a rise and a fall number due to vascular disease. From Interventionalist approach, we gave comprehensives therapy for Ischaemic stroke by Revascularization by thrombolysis therapy in acute phase and intracranial or intracarotid stenting to prevent secondary stroke.

Keywords: Ischaemic stroke ¨C revascularization ¨C intracarotid and intracranial stenting

Abstrak


Hingga saat ini , stroke masih merupakan salah satu penyebab kematian dan kecacatan terbesar di berbagai belahan dunia . Angka kejadian stroke iskemik sendiri amat bervariasi , namun pada dasarnya memiliki pola untuk mengikuti angka kejadian penyakit penyakit yang mengenai pembuluh darah . Para interventionalist mencoba untuk menyumbangkan gagasan mengenai penatalaksanaan stroke iskemik secara menyeluruh dengan cara revascularisasi , dengan metode thrombolisis pada fase akut stroke iskemik ; dan dengan melakukan stenting pada pembuluh darah karotis dan pembuluh darah di dalam otak .

Kata kunci : Stroke iskemik ; revascularisasi ¨C stenting pembuluh darah karotis dan
                    intrakranial

Introduction

            Stroke is the third most common cause of the death and a leading cause of severe and disability in both developed and developing countries. The burden of stroke is becoming greater as the population ages, and making its prevention is a must priority.1   A several modalities could become a factors for stroke induced, modifiable or unmodifiable, and family history (A sibling history of stroke increased the likelihood of a more severe stroke).2
            Unlike Hemorrhagic stroke, Ischaemic stroke showed a rise and a fall, mirroring the vascular heart disease pandemic. These different secular trends indicate that the risk factors for the two type of factors could be differ.1 In Japan, even though concentration of blood cholesterol rose up to 1980s, rise of Ischaemic has fallen dramatically.3
So many trial and study continuous to explore and recognized a lot of multifactor caused stroke, especially Ischaemic stroke, so many drug i.e. antiplatelet or anticoagulant found , to prevent recurrent or first time attack. The newest one named Ximelagatran (contain active agent melagatrant), anticoagulant (direct thrombin inhibitor) that has been investigated extensively as a replacement for warfarin, that would overcome the problematic dietarydrug interaction, and monitoring issues associated with warfarin therapy,4 but the question about how to manage ischaemic stroke in acute phase and how to prevent its, still being the most debate and curious topics for discuss.
In interventionalist approach, there are two main aspects that we have to think to give a comprehensive serve in ischaemic stroke management, revascular assessment by thrombolytic drugs and secondary preventing stroke by intracranial or intracarotid stenting.


I. Revascular Assessment
            In acute phase of Ischaemic stroke, the most important action is revascularization by thrombolytic therapy in some condition. We have to give a marked in ¡°condition¡± word because there are still many criterias (which despite patient into exclusion and inclusion candidates) for consider before we give the patient a thrombolytic therapy.5
 Two parameters which become important criteria of this action are recanalization of occlusion artery and global reperfusion from a distal part.6 The aim of that action is to prevent spread of ischaemic area and reduce the risk of hemorrhagic transformation.7    
For revascular assessment we use a lot of variant of thrombolytics, even though FDA proved rtPA as a major thrombolytic8, unless for elderly stroke patients ( up 80 years old ) and another conditions else,9 so many specimen become profitable to use as a single therapy or combined.8,9
So, when didi we have to give trombolytic therapy? Although the traditional use of intravenous (IV) thrombolytics is restricted to within 3 hours of Ischaemic stroke onset, the use of intraarterial (IA) therapy is proving to be more flexible, with the ultimate time window yet to be determined, above that methods, local/selective intra arterial thrombolytic who gave by an interventionists, become the best way to reduce risk of hemorrhage.10
A combination between thrombolytics therapy which was given by intravenous and intraarterial gave a better functional outcome compare than placebo in a several studies. The next question is: is it safe to give intra arterial thrombolysis after intravenous thrombolysis?, the answer is appear safe if persisting occlusion and /or lack of clinical improvement appears.11
 Intraarterial urokinase (10,000 ¨C 20,000 iu/minutes) and  abciximab intravenous (0.25 mg/kgBW as a bolus, then continue with 0.125 microgram/kgBW/minutes) have a better outcome compare than urokinase only.12  RtPA (IV) and pro urokinase (IA) give a better outcome and reduce the mortality if compare with placebo even it is not statistically significant.13 Tirofiban (IV), dose 0.4 microgram/kgBW/minutes  give as a bolus for 3 minutes follows by tirofiban 0.1 micrograms/kgBW/minutes combined with heparin 2500-3000 IU for 30 ¨C 80 minutes  (IV) then Urokinase 300 thousand ¨C 600 thousand IU could give a very good outcome and promising, even more trials are still needed, with  sample and randomized trials.14 A combination of mechanical clot retrieval and adjunctive thrombolytic therapies in 111 patients participating in the multi MERCI trial resulted in successful recanalization in 69% of vessel versus 54% with the retriever alone. The Preliminary result of the IMS II trial indicated that the MicroLysus ultrasound device (EKOS corp) may improve recanalization rates compared with the standard microcathether techniques. Multimodal therapy combining IV or IA abciximab and intracranial angioplasty has been reported to achieve high recanalization rates, and preliminary experience with intracranial stenting in acute stroke suggest that this may be an attractive adjunct to IA thrombolytic. A retrospective review of 168 patients treated with a combination of IA thrombolytic and mechanical interventions reported recanalization in 63% and improvement in NIHSS of at least 4 points in 21% of patients at 24 hour follow up.10 
            For the Basilar Artery occlusion, which invariably leads to death or long-term disability if not recanalyzed, intraarterial or intravenous thrombolytics, could reach a good outcome. Lindsberg in a systematic analysis comparing intraarterial and intravenous thrombolysis of Therapy of Basilar Artery Occlusion shows recanalization occurs in more than half patients treated with Intraarterial or intravenous thrombolytics (65% and 53%), and an equal survival rates (45%-50%). Without recanalization, the likelihood of good outcome was close to nil (2%).14

II. Secondary prevent of stroke by intracranial and carotid stenting
            In patients who have symptomatic intracranial Atherosclerosis or stenosis  and who have suboptimal results of medical management using antiplatelet agent or anticoagulant to prevent stroke develop, use of intracranial or carotid stenting can make this disease less debilitating by improving cerebral perfusion, by reducing the risk of thrombosis / embolic event  or by both action .8
            Over the past years, the results of 4 large extra cranial carotid angioplasty (CAS) investigations have been reported. The industry supported ARCHeR and BEACH registries of non randomized, symptomatic and asymptomatic patients at high risk for carotid endarterectomy found 30 day stroke or death rates of 6,9% and 5,8% respectively, and ARCHeR reported a 1 year composite outcome including myocardial infarction of 9,6%.10
            Cerebrovascular embolization and hemodynamic changes after CAS continue to be investigated. Changes on diffusion-weighted MR images are seen less often with the use of embolic protection devices, but can still be seen in up to 42% patients in the distribution of the stented artery.10, 12
            Preprocedural use of statins in CAS patients may lower the 30-day risk of stroke, myocardial infarction or death. And patients undergoing CAS are pre-treated with antiplatelet agents and the procedure itself is performed under local anesthesia via the femoral artery. The patient is systemically heparins and the carotid artery catheterized. Some centers use clopidogrel and aspirin maintain for three months.10, 13
            Perforator strokes after intracranial angioplasty and stenting were found in 3% of patients, with pre existing stroke adjacent to the stenotic segment with greatest risk of symptom exacerbation. A new, self expanding intracranial stent for Atherosclerosis treatment (Wingspan, Boston Scientific) has shown initial promise in small number of patients.10
            The vertebral artery stenting become interesting in case of the vertebral artery origin. Because it is difficult to access surgically, and recognized surgical risk, include the development of a Horner¡¯s, lymphatic injury, thrombosis, and laryngeal nerve injury; so endovascular treatment plays its role as for CAS. The immediate goal is to obtain < 50% residual stenosis, no deficit and resolution of symptoms. Technical success is high and estimated at 94%-98%. Procedure related complications are rare at 0-6% and include stroke and arterial dissection.14, 15

Conclusion

            There are two problems which become important for acute ischaemic stroke. Revascularization and prevent for stroke or second stroke. Interventional neuro-radiology offers a very good pathway in that case; offers thrombolysis therapy and intracranial and carotid artery stenting. The update of that management still and keep studying to find more improvement and reach a better goal for acute Ischaemic stroke management.

References
1.      Shah E et al. Serum cholesterol,haemorhagic stroke, ischaemic stroke, and myocardial infarction : Korean  national health system prospective cohort study. BMJ 2006 ; 333 : 22
2.      Meschia JF et al. Family history of stroke and severity of neurologic deficit after stroke Neurology  2006;67:1396-1402
3.      Kubo M. et al. Trends in the incidens, mortality and survival rate of cardiovascular disease in a Japanesse community. The Hisayama Study. Stroke 2003 ; 34 : 2349-54
4.      Akins PT et al. Secondary stroke prevention with Ximelagatran versus Warfarin in patients with atrial fibrillation. Pooled analysis of SPORTIF III and V clinical trials.      Stroke 2007 (published Jan 7 , 2007) doi:10.1161/01.STR.0000258004.64840.0b
5.      Cloft HJ,Joseph GJ,Dion JE. Risk of cerebral angiography in patients with subarachnoid  hemorrhage, cerebral aneurysm, and arteriovenous Malformation. Stroke 1999;30:317-320
6.  Khatri P et al. Reperfusion versus rekanalisation. Stroke 2005 ; 36: 240
7.  Furlan AJ. Interventional therapy in acute stroke. AAN 2003 in CD ROM format
8.  Liu AY. Update in interventional neuroradiology. The Permanent Journal 2006; 10:1
9. Engelter ST,Bonati LH,Lyrer PA. Intravenous thrombolysis in stroke patients of ¡Ý 80    versus <80 years of age, a systematic review across cohort studies. Age and Ageing 2006;35(6):572-580
10. Pelz D et al . Advance in interventional neuroradiology 2006 . Stroke 2007 (published online Jan 2007) doi: 10.1161/01.STR.0000254713.97631.d3
11. Shaltoni HM et al. Is intra-arterial thrombolysis safe after full-dose intravenous recombinant tissue plasminogen activator for acute ischemic stroke? Stroke 2007;38:80
12. Lee DH. Local intra arterial urokinase thrombolysis of acute ischaemic stroke with or without intravenous abciximab: a pilot study. Journal of Vascular and Interventional Radiology 2002;13:769-774
13. Flaherty ML, et al. Combined IV and intra-arterial thrombolysis for acute ischemic stroke. Neurology 2005;64:386-388
14. Mangiafico S, et al. Tirofiban intravenous and urokinase intraarterial in management stroke by  trombolisis. Stroke 2006;36:2154
15. Lindsberg PJ,Mattle HP. Therapy of basilar artery occlusion . Stroke 2006; 37:922.



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