STROKE TREATMENT
Posted by on Saturday, 3rd March 2012
role of endovascular intervention in stroke treatment– By Dr. Sunil BhargavaMD, DNB, MNAMS, STA certified equivalence CCST (UK)
Endovascular therapy is a well-established treatment modality for a variety of cerebrovascular central nervous system disorders. Neuroendovascular approaches provide treatment options for conditions previously thought to be untreatable. Ongoing device developments and refinements continue to revolutionize the field. These refinements, along with a better understanding of the disease process allow minimally invasive neuroendovascular techniques to be used for treatment acute ischemic stroke and stroke prevention.
The majority of ischemic strokes are due to thromboembolic arterial occlusion
75% occurring in the ICA distribution. While mortality from middle cerebral artery strokes is low, there is a high morbidity, with only 20 – 25% of patients returning to an independent lifestyle. Posterior circulation strokes are more ominous, with significant mortality rates, up to 86.4% in one study. Over the past few years, there has been intensive investigation of intravenous thrombolytic therapy for the treatment of acute ischemic stroke. At the present time, only tissue plasminogen activator (t-PA)/Urokinase, when administered within three hours of symptom onset, has definitively been shown to be an effective therapy.
The benefits of this therapy were demonstrated in the National Institutes of Neurologic Disorders and Stroke (NINDS) sponsored trial in 1995.This trial led to the FDA approval of t-PA for stroke treatment in June 1996. At present, only a small fraction of potentially eligible stroke patients are receiving treatment. The primary reason that patients are not eligible for this treatment is the very short, three-hour time window from symptom onset in which the agent should be administered. Intra-arterial recombinant t-PA (rt-PA) is suggested to be more effective than intravenous rt-PA. In local intraarterial (IA) thrombolysis, fibrinolytic agents are infused distal to, proximal to, and directly within thrombotic occlusions of main stem cerebral arteries, using an endovascular micro catheter delivery system. The dosage used is 0.3 mg/kg, up to a maximum of 10-20 mg intra-arterially. Direct infusion of thrombolytic agent near the thrombus allows greater concentration of agent, fewer systemic effects, more rapid dissolution of large
or multiple clots and an opportunity to carry out gentle mechanical disruption of the clot with the delivery catheter and wire. IA thrombolysis also has a number of potential disadvantages, including manipulation of a catheter within cerebral vessels, potentially increasing vulnerability to hemorrhage; the requirements for systemic heparinization during catheterization to deter catheter-induced thrombosis; and delay in initiation of thrombolysis.
The procedure is labour and capital intensive, and the number of facilities skilled in IA thrombolysis is small. Intra-arterial thrombolysis may be used in the anterior circulation (carotid circulation) up to 6 hours after onset of symptoms, although better results have been shown when administered within 3 hours. It is also used up to 12 – 24 hours after onset in posterior (vertebrobasilar) circulation lesions, because of the poor prognosis without therapy.
Despite the increased rate of symptomatic hemorrhage with intra-arterial administration of rt-PA, many trials have still demonstrated improved clinical outcomes versus placebo Of particular note is the first Phase III trial of IA thrombolysis, the Prolyse in Acute Cerebral Thromboembolism II (PROACT II) trial (5). In PROACT II, patients within 6 hours of symptom onset with symptomatic M1 or M2 middle cerebral artery (MCA) occlusions were randomized to receive IA thrombolysis with systemic heparinization vs. heparinization alone. The prespecified primary outcome in PROACT II, a good or excellent score on the modified Rankin Scale of handicap, was achieved by 40% of the IA group vs. 25% of control patients (p=0.043). In addition, recanalisation rates 2 hours after initiation of infusion were markedly increased in the IA group. Intracerebral hemorrhage rates at 36 hours were increased in the IA group; however, no difference in overall mortality between the two groups was observed.
Another potential role for intra-arterial rt-PA is for postoperative stroke patients. The risk of stroke is approximately 2.9% in the immediate postoperative period. During a recent multicenter study of intra-arterial rt-PA administered during the immediate postoperative period, good results were obtained with only minimal complications. The local delivery of thrombolytic agent reduces systemic effects. Only patients who had previously undergone intracranial surgery had an unacceptably high complication rate. Further research is being conducted in the use of mechanical thrombolytic devices, as well as laser clot fragmentation. The advantages of these approaches include lack of systemic and hemorrhagic complications. Better public awareness is also needed, since fewer than 5% of eligible stroke patients actually receive thrombolytic therapy. In addition, faster diagnosis with MR diffusion and CT perfusion may help to identify patients who can benefit from thrombolysis.
Carotid artery stenting has important role in preventing stroke. It is of particularly suitable in case unfit for surgery, unfavorable anatomy, tandem lesions and relatively poor medical risk.