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Platelet Glycoprotein Iib/Iiia Inhibitors in Acute Ischemic Stroke

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Platelet Glycoprotein Iib/Iiia Inhibitors in Acute Ischemic Stroke Review Article Platelet glycoprotein IIb/IIIa inhibitors in acute ischemic stroke Sudhir Kumar, G. Rajshekher, Subhashini Prabhakar Stroke Unit, Department of Neurological Sciences, Apollo Hospitals, Jubilee Hills, Hyderabad, India Acute ischemic stroke (AIS) is a common cause of morbidity plasminogen activator (rt-PA) is the only proven and mortality worldwide. Thrombolytic therapy with tissue beneficial therapy in acute ischemic stroke (AIS). plasminogen activator, the only approved treatment for Thrombolysis within 3-6 h of symptom-onset improves AIS, is received by less than 2% of patients. Moreover, clinical outcomes and reduces disability in stroke there is a slight increase in hemorrhagic complications with patients. This benefit is at the cost of an increased rate thrombolysis. Therefore, there is a need for newer therapeutic of symptomatic intracranial hemorrhage (ICH) without modalities in AIS, which could be used in window periods a significant effect on overall mortality. In general, the beyond 3-6 h after stroke onset with fewer hemorrhagic benefit of thrombolysis decreases and the risks increase [4] complications. Glycoprotein IIb/IIIa inhibitors (GPI), after their with progressing time after symptom onset. Despite initial success in patients with acute coronary syndromes, the benefits of thrombolysis, less than 2% of eligible [5] promised much in patients with AIS over the past decade or patients receive it, even at the best of stroke centers. so. However, their exact role in patients with AIS, including The reasons include lack of adequate transport facilities, the window periods and type of strokes, and the risk of high cost of tissue plasminogen activator, lack of proper symptomatic or asymptomatic hemorrhage are unclear at infrastructure including facilities for thrombolysis in the moment. The current review focuses on the literature most centers, and lack of awareness among public and [2,6] concerning the use of GPI in AIS and looks at the available doctors. Inability to reach hospital within a window evidence regarding their use. Abciximab thought to be safe period of 6 h is the most important limiting factor for [6] and effective in initial case series and early trials, has not the use of thrombolytic therapy. Therefore, there is an been shown to improve outcomes in AIS, and is associated urgent need for effective therapies in AIS beyond the 6-h with higher rates of hemorrhage. Tirofiban appears to be safe window period, which are relatively safer (lesser risk and effective in initial trials and there is a need to conduct of ICH) and more economical. Drugs that belong to the further trials to establish its role in AIS. glycoprotein IIb/IIIa inhibitors (GPI) could be useful in such a scenario. The purpose of this article is to review Key words: Abciximab, acute ischemic stroke, cerebrovascular the available evidence regarding their use in AIS. disease, platelet glycoprotein IIb/IIIa inhibitors, tirofiban Glycoprotein IIb/IIIa receptors Introduction GP IIb/IIIa receptors are found on the platelet surface numbering 50-60,000 per platelet. These are responsible Acute stroke is among the leading causes of death and for the final step of platelet aggregation leading to disability worldwide. Data regarding stroke in India thrombus formation. In addition to thrombosis, these is limited, however, the estimated prevalence is 2 per receptors are also involved in inflammation and 1000 population.[1] In a recently published review, the atherogenesis. GP IIb/IIIa receptors belong to a class of crude prevalence rate of stroke was estimated to be integrins with a specificity of binding to fibrinogen. 40 to 270 per 100,000 population, based on several community-based studies.[2] Majority of the strokes Glycoprotein IIb/IIIa inhibitors are ischemic in nature, accounting for about 75% of all strokes. This proportion of ischemic strokes is Blockage of GP IIb/IIIa receptors interferes with the relatively higher in the Asian as compared to Western final step of platelet aggregation, which could result in population.[3] Thrombolysis with recombinant tissue better outcomes in acute coronary syndromes (ACS) and Dr. Sudhir Kumar Department of Neurological Sciences, Apollo Hospitals, Jubilee Hills, Hyderabad - 500 033, India. E-mail: [email protected] Neurology India | October-December 2008 | Vol 56 | Issue 4 399 Kumar, et al.: Platelet glycoprotein IIb/IIIa inhibitors in stroke AIS. GPI can be classified into two groups:[7] strokes 1. Naturally occurring peptide inhibitors- These are MRI-guided trial of abciximab in AIS: isolated from Viper venoms and Puff adder and are Twenty-nine patients with AIS presenting within the not clinically used. Examples include Trigramin, 3-24-h window period were treated with abciximab or Barbourin and Kistrin. placebo.[11] Treated patients showed early neurological 2. Synthetic inhibitors- These are of three types: improvement (NIH stroke scale score improvement of a) Monoclonal antibodies- Abciximab, used 4.4 ± 3.2); 45% of patients had ≥ 5 point NIH stroke parenterally. scale score decrease or deficit resolution. Twenty- seven per cent of treated patients had a reduction b) Peptide- Eptifibatide, used parenterally. of lesion size as seen on diffusion-weighted MRI, a c) Non-peptide- finding uncommonly seen in untreated patients. No i. Parenteral use, e.g. tirofiban, lamifiban; treatment-related symptomatic ICH or death occurred ii. Oral use, e.g. xemlofiban, orofiban, in this study. roxifiban, lotrafiban. Abciximab-heparin combination therapy in AIS: GPIs in clinical use include Abciximab (ReoPro), In an open label study, 22 patients were treated with Tirofiban (Aggrastat) and Eptifibatide (Integrillin). abciximab at a dose of 0.2 mg/kg bolus, followed by a 12-h infusion of 0.05 µg/kg/h, in conjunction with short Clinical use of glycoprotein IIb/IIIa inhibitors course intravenous heparin, within a window of 6 h for anterior and 24 h for posterior circulation strokes.[12] Acute coronary syndromes No cases of symptomatic ICH occurred and the rate of GPIs were initially used in patients with acute asymptomatic ICH was 12.5%. Ninety-day functional coronary syndromes (ACS). It was found that aggressive outcome too appeared promising. platelet inhibition with abciximab during primary Abciximab-rt-PA combination therapy in AIS: percutaneous transluminal coronary angioplasty In a Phase I safety trial, five patients were treated with (PTCA) for acute myocardial infarction (MI) yielded the combination of half-dose rt-PA (0.45 mg/kg) and a substantial reduction in the acute (30-day) phase abciximab (0.25 mg/kg bolus followed by a 0.125 µg/ for death, reinfarction, and urgent target vessel kg/min infusion over 12 h).[13] No cases of symptomatic [8] revascularization. ICH occurred, however, one out of five experienced Subsequently, other GP IIb/IIIa inhibitors were also asymptomatic ICH. A trend of treatment efficacy was tested in patients with ACS. Additional eptifibatide also seen. therapy resulted in reduced incidence of death and In another study, 47 patients with acute vertebrobasilar nonfatal MI at 30 days in patients with acute MI or stroke were treated with abciximab and low-dose unstable angina, as compared to the routine management rt-PA (FAST).[14] The results were compared with [9] with aspirin and heparin. The success seen with the a retrospective cohort of 41 patients, treated by usage of GPIs in ACS gave the hope that they could be intraarterial rt-PA monotherapy (median dosage: 40 mg). useful in patients with AIS too; as both the conditions Additional PTA/stenting was performed in case of severe share common pathophysiologic mechanisms. residual stenosis. Overall bleeding rate was higher under the combined therapy, but the symptomatic ICH rate did Acute ischemic strokes not differ. Thrombolysis in MI (TIMI)2/3 recanalization Abciximab (ReoPro) rate was similar (FAST, 72%; rtPA, 68%), but TIMI3 Initial (Phase 1) safety study of Abciximab in AIS: rate was remarkably higher under combined therapy In a randomized, double-blind, placebo-controlled (FAST, 45%; rtPA, N=22%). Neurological outcome trial designed to evaluate the safety of abciximab in AIS appeared better under combined therapy (FAST versus and to obtain pilot efficacy data, no cases of major ICH rtPA: favorable outcome rate: 34% versus 17%) with a occurred among 54 patients that received the drug.[10] significantly lower mortality rate (FAST versus rtPA: Seven per cent of patients had asymptomatic ICH. At 38% versus 68%; P=0.006). Overall, the combination three months, there was a trend toward a higher rate therapy of abciximab and rt-PA was better than rt-PA of minimal residual disability (Barthel Index > or =95 alone in this trial. or modified Rankin scale < or =1) among abciximab Reperfusion of the reoccluded artery after patients as compared with those who received placebo. successful thrombolysis: It was concluded that abciximab was safe when Thrombolytic therapy fails in many patients with acute administered up to 24 h after stroke onset, and it might ischemic stroke. The reocclusion that occurs during or improve functional outcome. immediately after successful thrombolysis may be an important treatment target because 1) this type of Case series evaluating abciximab in acute ischemic reocclusion involves platelet-mediated thrombotic 400 Neurology India | October-December 2008 | Vol 56 | Issue 4 Kumar, et al.: Platelet glycoprotein IIb/IIIa inhibitors in stroke mechanisms; 2) the highly potent and selective (AbESTT I): inhibition of platelet aggregation can be achieved by An international randomized, double-blind, placebo- GP IIb/IIIa receptor inhibitors; and 3) early reperfusion controlled Phase 2 trial enrolled 400 patients within 6 is crucial for the prognosis of stroke patients.[15] h of onset of ischemic stroke to study the safety and In a recent study, reocclusion occurred in four of efficacy of abciximab.[18] Two hundred patients received 18 patients (22%) with initial recanalization.[15] Three abciximab at a bolus dose of 0.25 mg/kg, followed by a reocclusion patients had suboptimal (TIMI 2) flow.
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