Published online before print October 30, 2001, 10.1148/radiol.2213010444
(Radiology. 2001;221:795-801.)
© RSNA, 2001
Treatment of Acute Basilar Artery Thrombosis with a Combination of Systemic Alteplase and Tirofiban, a Nonpeptide Platelet Glycoprotein IIb/IIIa Inhibitor: Report of Four Cases1
Ulrich Junghans, MD,
Rüdiger J. Seitz, MD,
Hans J. Wittsack, PhD,
Albrecht Aulich, MD and
Mario Siebler, MD
1 From the Department of Neurology (U.J., R.J.S., M.S.) and Institute of Diagnostic Radiology (H.J.W., A.A.), University Hospital Düsseldorf, Moorenstrasse 5, D-40225 Düsseldorf, Germany. Received February 12, 2001; revision requested March 28; revision received May 14; accepted June 5. Supported by the Deutsche Forschungsgemeinschaft (SFB 194, A13) and BMBF (Kompetenznetzwerk Schlaganfall, B5). Address correspondence to M.S. (e-mail: siebler@uni-duesseldorf.de).
 |
ABSTRACT
|
|---|
In four patients with acute basilar artery thrombosis, complete arterial recanalization and good neurologic outcome were achieved with a treatment combining alteplase with tirofiban. In no cases were cerebral or extracerebral hemorrhagic complications observed. Combined fibrinolytic agents and glycoprotein IIb/IIIa inhibitors may have high potential in the treatment of acute cerebrovascular thrombosis.
Index terms: Arteries, basilar, 1753.751 • Arteries, stenosis or obstruction, 1753.721, 1753.751 • Thrombolysis
|
INTRODUCTION
|
|---|
Thrombosis of the basilar artery has a very poor prognosis. If affected patients are untreated, fatality rates of up to 90% have been reported, depending on the site and extent of the thrombus (1). Clinically suspected acute basilar artery thrombosis is currently confirmed with intraarterial angiography and treated with local application of a thrombolytic agent; the goal is complete basilar artery recanalization (2–4). Nevertheless, due to reocclusion or fatal bleeding complications, death is still a probable outcome for these patients (5–7). Moreover, intraarterial fibrinolysis requires skilled procedural neuroradiologists and technical facilities that are available 24 hours a day. Therefore, it is often necessary to transfer these critically ill patients to highly specialized centers, thereby extending the time needed to initiate effective treatment. Fast, noninvasive tools like magnetic resonance (MR) imaging (8) and ultrasonography (US) (9) have essentially improved physicians’ ability to accurately diagnose vessel occlusion in acute stroke. MR imaging has also been shown to reliably monitor the efficiency of systemic thrombolysis with the recombinant tissue plasminogen activator alteplase (10), to our knowledge the only drug approved by the U.S. Food and Drug Administration for treatment of acute stroke (11).
Treatment of acute ischemic stroke and myocardial infarction with thrombolytic agents inevitably leads to concomitant activation of the coagulatory system (12,13). This activation contributes to incomplete or delayed reperfusion, microcirculatory disturbances (the "no-reflow" phenomenon), or even repeated vessel occlusion (14,15). In accordance with experimental results (16), recent clinical data demonstrate that in acute myocardial infarction, thrombolytic and glycoprotein IIb/IIIa inhibitor agents have a synergistic effect in achieving fast and complete arterial reperfusion (17,18). This increase in vessel patency has not been associated with an increase in severe bleeding or intracerebral hemorrhage.
In a patient with basilar reocclusion during intraarterial fibrinolysis with alteplase, we intravenously administered tirofiban, a highly selective, nonpeptide platelet glycoprotein IIb/IIIa receptor antagonist (19), and observed prompt recanalization accompanied by a good neurologic recovery. Herein we report our findings with this patient and three others with proven basilar artery thrombosis who were simultaneously treated with a combination of alteplase and the platelet aggregation inhibitor tirofiban. Both drugs were administered intravenously.
|
Case Reports
|
|---|
The study was approved by our local ethics committee. All patients or their relatives gave written informed consent prior to treatment.
Case 1
A previously healthy 75-year-old man suddenly developed vertigo, dizziness, and nausea and subsequently lost consciousness. At admission he had a severe brainstem syndrome, with coma, right-sided hemiplegia, divergent bulbi, and upbeat nystagmus. Immediate time-of-flight MR angiography (Magnetom Vision 2000; Siemens, Erlangen, Germany) failed to depict flow signal intensity in the basilar artery. Correspondingly, at perfusion-weighted MR imaging, severely impaired perfusion was noted in the thalamus, brainstem, and cerebellum. At this point, diffusion-weighted MR images of the brain were normal. Acute basilar artery thrombosis was suspected.
The patient received a 10-mg intravenous bolus dose of alteplase (Boehringer Ingelheim, Ingelheim, Germany) as well as intravenously administered heparin (Liquemin; Roche, Switzerland) (in a 5,000 U bolus followed by infusion of 1,000 U/h) targeted to an activated partial thromboplastin time of 50–70 seconds. Subsequent intraarterial angiography revealed an occluding midbasilar clot (Fig 1), and local application of alteplase (mixed as 1 mg per milliliter saline) was initiated about 2
hours after symptom onset. Only short periods of partial recanalization could be achieved during the procedure. After intraarterial application of a total dose of 40 mg of alteplase, the final superselective angiogram revealed a complete reocclusion of the basilar artery (Fig 1).
View larger version (127K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 1a. Case 1. Intraarterial digital subtraction angiogram obtained in the anteroposterior (A, B) and lateral (C, D) projections prior to (A, C) and at the end of (B, D) local alteplase treatment. An occluding midbasilar clot (arrows) was observed about 130 minutes after symptom onset. Basilar artery occlusion persisted, despite concomitant systemic heparin treatment after local application of a total of 40 mg of alteplase over a period of 150 minutes (B, D). This finding was accompanied by the patient’s progressive neurologic decline (see text).
|
|
View larger version (127K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 1b. Case 1. Intraarterial digital subtraction angiogram obtained in the anteroposterior (A, B) and lateral (C, D) projections prior to (A, C) and at the end of (B, D) local alteplase treatment. An occluding midbasilar clot (arrows) was observed about 130 minutes after symptom onset. Basilar artery occlusion persisted, despite concomitant systemic heparin treatment after local application of a total of 40 mg of alteplase over a period of 150 minutes (B, D). This finding was accompanied by the patient’s progressive neurologic decline (see text).
|
|
View larger version (123K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 1c. Case 1. Intraarterial digital subtraction angiogram obtained in the anteroposterior (A, B) and lateral (C, D) projections prior to (A, C) and at the end of (B, D) local alteplase treatment. An occluding midbasilar clot (arrows) was observed about 130 minutes after symptom onset. Basilar artery occlusion persisted, despite concomitant systemic heparin treatment after local application of a total of 40 mg of alteplase over a period of 150 minutes (B, D). This finding was accompanied by the patient’s progressive neurologic decline (see text).
|
|
View larger version (136K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 1d. Case 1. Intraarterial digital subtraction angiogram obtained in the anteroposterior (A, B) and lateral (C, D) projections prior to (A, C) and at the end of (B, D) local alteplase treatment. An occluding midbasilar clot (arrows) was observed about 130 minutes after symptom onset. Basilar artery occlusion persisted, despite concomitant systemic heparin treatment after local application of a total of 40 mg of alteplase over a period of 150 minutes (B, D). This finding was accompanied by the patient’s progressive neurologic decline (see text).
|
|
The patient’s condition deteriorated further, and he developed severe difficulty in breathing and in regulating blood pressure. A postprocedural noncontrast computed tomographic (CT) scan of the brain obtained with a Magnetom Plus Vision 2000 scanner (Siemens, Erlangen, Germany) excluded cerebral hemorrhage, and the patient was transferred to the intensive care unit. Here, tirofiban (Aggrastat; MSD, Haar, Germany) was given intravenously, starting with a bolus of 0.4 µg/kg/min for 30 minutes followed by a continuous infusion of 0.1 µg/kg/min (in accordance with the PRISM-PLUS protocol) (20). Tirofiban treatment was initiated 5 hours after symptom onset and 45 minutes after intraarterial fibrinolysis was terminated. Within the next hour the patient recovered dramatically and regained consciousness; he had no paresis (Table).
Insonation of the basilar artery with transcranial Doppler US (EME; Pioneer, Überlingen, Germany) revealed a normal flow signal, suggesting that complete recanalization had been achieved. Intraarterial angiography on the following day showed complete recanalization of the basilar artery and unimpeded perfusion of the distal vasculature (Fig 2). After 24 hours, tirofiban was stopped. Clinically, the patient had nearly fully recovered; he showed only a mild, nondisabling, right-sided hemiataxia. The follow-up CT scan revealed ischemic changes in the cerebellum but showed no evidence of cerebral hemorrhage (Fig 3).
View larger version (159K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 2a. Case 1. Intraarterial digital subtraction angiograms in the anteroposterior (A) and lateral (B) projections. Note complete reperfusion of the basilar artery (arrows) with no residual stenosis after tirofiban treatment for 24 hours. This finding confirmed the information obtained with transcranial Doppler US 30 minutes after the start of tirofiban treatment. These observations were accompanied by the patient’s prompt neurologic recovery.
|
|
View larger version (147K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 2b. Case 1. Intraarterial digital subtraction angiograms in the anteroposterior (A) and lateral (B) projections. Note complete reperfusion of the basilar artery (arrows) with no residual stenosis after tirofiban treatment for 24 hours. This finding confirmed the information obtained with transcranial Doppler US 30 minutes after the start of tirofiban treatment. These observations were accompanied by the patient’s prompt neurologic recovery.
|
|
View larger version (98K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 3. Case 1. A, Initial transverse T2-weighted MR image (repetition time msec/echo time msec, 7,040/115) of the brainstem shows an absent flow void in the basilar artery 90 minutes after symptom onset, but no obvious ischemic lesion. B, Follow-up CT scan shows right-sided ischemic changes (arrows) in the cerebellum.
|
|
Case 2
A previously healthy 59-year-old woman was admitted 3 hours after sudden onset of unconsciousness. At examination she was in a state of coma and responded to painful stimuli with only reflex motor movements, but she moved both arms and legs equally. Her muscle reflexes were low, and she had bilateral Babinski signs. Both pupils were equally wide and unresponsive to light. Her gaze had a left skew with an accompanying vertical and horizontal palsy. Respiration, blood pressure, and blood glucose levels were normal, and the results of drug screening were negative. Immediate MR angiography revealed an extinction of flow signal in the distal part of the basilar artery and in both P1 segments of the posterior cerebral artery. T2-weighted MR imaging of the brain was normal. A "top of the basilar" syndrome was diagnosed, and the patient was treated with an intravenously administered bolus dose of 20 mg of alteplase followed by heparin (1,000 U/h) and body weight–adjusted tirofiban (see case 1).
Within 5 hours after initiation of treatment, the patient recovered completely (Table). Tirofiban treatment was continued for 24 hours. Subsequently, a previously asymptomatic underlying sticky platelet syndrome type II was confirmed by platelet aggregometry (21), and the patient began taking aspirin. On follow-up MR images, complete recanalization of the basilar artery and both P1 segments without hemorrhage or ischemic lesion was observed.
Case 3
A 59-year-old man with known coronary artery disease was admitted to the hospital 30 minutes after sudden onset of a severe right-sided hemiparesis with dysarthria and progressive loss of consciousness. His left pupil was dilated and unresponsive to light. On the previous day he had undergone electrical conversion of an atrial flutter to normal sinus rhythm. He had not received anticoagulants periprocedurally, but transesophageal echocardiography performed just before electrotherapy was started revealed no evidence of atrial thrombus formation. At MR angiography, flow signals in the right vertebral artery and in the basilar artery were absent. Transcranial Doppler US of the basilar artery revealed absent diastolic flow and a short systolic peak, findings suggestive of occlusive basilar thrombosis.
After the possibility of cerebral hemorrhage was excluded at CT, the patient was treated simultaneously with alteplase (as a 10-mg bolus followed by 40 mg within 1 hour), body weight-adjusted tirofiban (see case 1), and heparin (in a 5,000 IU bolus followed by infusion of 25,000 IU over 24 hours). All three drugs were administered intravenously 100 minutes after symptom onset.
Within 1 hour after initiation of treatment, the patient regained consciousness and his hemiparesis resolved completely. He had only a combined vertical and horizontal gaze palsy with a left skew and vertical diplopia. The left pupil was still dilated and unresponsive to light. At this time, transcranial Doppler US of the basilar artery showed a pulsatile signal with normal acceleration and positive end-diastolic flow. Twelve hours later, diffusion-weighted and T2-weighted MR imaging revealed acute left-sided ischemic lesions in the hypothalamus and midbrain. MR angiography showed a circumscribed flow extinction at the most distal segment of the basilar artery.
Tirofiban administration was continued for a total of 84 hours. In addition to the previously observed lesions, bilateral occipital ischemic lesions in the posterior cerebral artery territories were noted on follow-up MR images. However, no hemorrhagic transformation was observed. Both MR angiography and intraarterial angiography showed complete flow restoration of the basilar artery. Although the patient’s horizontal gaze palsy resolved completely, a right-sided complete hemianopia persisted (Table).
Case 4
A 60-year-old man with previously unrecognized atrial fibrillation suddenly developed a left-sided hemiparesis and severe dysarthria. At admission, about 110 minutes later, progressive neurologic deterioration was noted. The patient was alert but hemiplegic on the left side, anarthric, and had a complex oculomotoric dysfunction that included spontaneous horizontal nystagmus to the right, a left-sided oculomotor nerve palsy, and a fixed right eye. Immediate diffusion-weighted MR imaging (Fig 4) revealed a marked delay in the arrival of the bolus of contrast material in the cerebellum and brainstem and a corresponding right-sided pontine lesion. The T2-weighted MR images appeared normal. At MR angiography, only the proximal portion of the basilar artery showed very faint flow signal intensity. Both posterior cerebral arteries were fed by their respective internal carotid arteries. About 150 minutes after symptom onset, intravenous treatment with combined thrombolytic and glycoprotein IIb/IIIa inhibitory agents was initiated. The treatment included a 20-mg bolus of alteplase, a dose of tirofiban adjusted for body weight, and a dose of heparin adjusted to a targeted activated partial thromboplastin time (see case 1). Within 1 hour the patient had fully recovered. Follow-up MR imaging (Fig 5) showed complete recanalization of the basilar artery, and perfusion-weighted imaging revealed hemodynamic normalization. On diffusion-weighted and T2-weighted fluid-attenuated inversion recovery MR images, small, clinically asymptomatic ischemic lesions in both cerebellar hemispheres were detected, but the pontine lesion that had been revealed on initial diffusion-weighted images had completely resolved. There was no evidence of cerebral hemorrhage, even on T2*-weighted MR images.
View larger version (147K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 4. Case 4. Three-dimensional time-of-flight MR angiogram (35/7.2) (A), perfusion-weighted time-to-peak map (2,000/60) (B), and diffusion-weighted (5,200/103) (C) and T2-weighted (2,000/60) (D) MR images obtained 120 minutes after symptom onset and just before start of treatment. Note the only very faintly enhanced basilar artery with circumscribed flow signal extinctions (arrow in A), a severe perfusion deficit in the brainstem (arrows in B; numbers indicate time in seconds between first MR image and image obtained when gadolinium chelate concentration was at its maximum), and a corresponding right-sided brainstem lesion (arrow in C) visible on diffusion-weighted images but not on T2-weighted images (D).
|
|
View larger version (162K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 5. Case 4. Three-dimensional time-of-flight MR angiogram (35/7.2) (A) and perfusion-weighted time-to-peak map (2,000/60) (B), diffusion-weighted (5,200/103) (C), and T2-weighted (2,000/60)(D) MR images obtained 1 day after combined systemic treatment with a 20 mg alteplase bolus and tirofiban. Note complete basilar artery reperfusion (arrow in A), normal perfusion imaging (B; numbers indicate time in seconds between first MR image and image obtained when gadolinium chelate concentration was at its maximum), and resolution of the right-sided brainstem lesion at diffusion-weighted imaging (C). Compared with those shown on the initial images (Fig 4, B and C), the postischemic lesions (arrows in C and D) are remarkably small on follow-up images, indicating fast achievement of sufficient reperfusion.
|
|
|
Discussion
|
|---|
We believe, to the best of our knowledge, that this is the first case series describing the combined thrombolytic and nonpeptide platelet glycoprotein IIb/IIIa inhibitor treatment of acute basilar artery thrombosis. Fassbender et al (13) demonstrated a pronounced response of markers of procoagulant activity in stroke patients treated with alteplase, indicating that thrombolytic therapy for ischemic stroke strongly activates the coagulation cascade and results in thrombin formation. It is believed that heparin binding sites are masked on thrombin bound to fibrin or its soluble fragments. This may explain the observed failure of heparin to prevent reocclusion (22). Moreover, because thrombin is the most potent platelet activator (23), alteplase treatment may lead not only to increased fibrin deposition but also to incorporation of platelets into the growing thrombus. Regardless of the event that stimulates the aggregation of platelets, the glycoprotein IIb/IIIa receptor (a member of the integrin family) has a key role in the process. Activated glycoprotein IIb/IIIa receptor binds fibrinogen molecules, which form bridges between adjacent platelets and thus facilitate platelet aggregation and accumulation (24). Therefore, formation of a platelet-rich, alteplase-resistant thrombus seems to be the most probable cause of the recanalization failure observed in case 1 and accounts best, on pathophysiologic grounds, for the reperfusion achieved with tirofiban treatment in that case. Our observations are supported by the fact that administration of abciximab, a chimeric monoclonal antibody that inhibits the platelet glycoprotein IIb/IIIa receptor, prevented reocclusion in a young woman after incomplete resolution of basilar artery obstruction following intraarterial thrombolysis with urokinase (25). Thus, even in the event of recurrent vessel occlusion during thrombolysis, complete reperfusion may be facilitated by treatment with a highly selective platelet glycoprotein IIb/IIIa inhibitor.
For cases of basilar artery thrombosis, intraarterial angiography and local application of fibrinolytic agents are presently considered the optimal management (4,26). However, this complex approach can be performed at only a few highly specialized centers. Furthermore, the procedure is sometimes time consuming, resulting in a delayed initiation of thrombolysis. Although intravenous thrombolysis has previously been used to treat vertebrobasilar artery stroke (27,28), only scarce information exists regarding its feasibility in treating patients with proven basilar artery thrombosis (29,30), and, to our knowledge, no studies have yet evaluated dosage regimens in either situation. In the treatment of acute myocardial infarction, the combination of partial doses of alteplase and abciximab (both given intravenously) achieved rates of reperfusion that could be classified according to the flow grading system used in the Thrombolysis in Myocardial Infarction (TIMI) trial as "TIMI III". The reperfusion rates obtained with alteplase and abciximab were similar to those obtained with primary angioplasty and were superior to those obtained with a regimen of front-loaded alteplase alone (18). In line with what had been determined to be effective dosages in the TIMI 14 trial (18), we administered 20 mg of alteplase as a single bolus in two patients (case 2 and case 4), and as a bolus of 10 mg followed by infusion of 40 mg over 60 minutes in one patient (case 3). To our knowledge, the chimeric Fab fragment abciximab is the only glycoprotein IIb/IIIa inhibitor previously reported to have been used in cases of basilar artery disease (25,31,32). In contrast to abciximab, which has a half-life of about 2 days, the terminal elimination half-life of tirofiban is very short (about 2 hours), with median bleeding times returning to near-normal levels within about 3 hours (33). Once administered, tirofiban is thus a potentially controllable agent. In addition, tirofiban has no known antigenetic potency, a feature that could allow several consecutive treatments without the risk of incurring allergic reactions. Peter et al (34) demonstrated in vitro that glycoprotein IIb/IIIa inhibitors of all three known structural classes may possess an intrinsic glycoprotein IIb/IIIa receptor activating property, as measured by induction of fibrinogen binding and increased platelet activation. Because at low antagonist concentrations this intrinsic activating property is strongest relative to the blocking effect, a situation that could result in a proaggregatory state, we treated all patients with a body weight–adjusted dosage regimen of tirofiban adopted from the PRISM-PLUS trial (20). In dose-finding studies, this dosage regimen inhibited ex vivo adenosine diphosphate-induced platelet aggregation by 86% (19).
In the patients described in cases 2-4, combined intravenous treatment with partial alteplase doses and tirofiban led to complete basilar artery reperfusion and survival with a good neurologic outcome (defined as a Rankin Scale score 
2; see Table). All but one patient (case 2) had ischemic lesions in the posterior circulation at follow-up CT or MR imaging. On pretreatment diffusion-weighted MR images, one patient (case 4) had a right-sided brainstem lesion corresponding to left-sided hemiplegia present at admission. Follow-up diffusion-weighted MR imaging 1 day after combined treatment revealed complete resolution of the lesion. There was no evidence of a residual lesion on T2-weighted MR images. No symptomatic or asymptomatic cerebral or extracerebral hemorrhagic complications were observed in any of our four patients. None of the patients developed thrombocytopenia, a well-known possible side effect of glycoprotein IIb/IIIa inhibitors (35).
We conclude that, analogous to recent advances in the management of acute myocardial infarction (18,36), combining the systemic administration of fibrinolytic agents at reduced dosages with potent platelet glycoprotein IIb/IIIa inhibitory drugs may have high potential in the treatment of acute cerebral vessel thrombosis. Clinical trials are needed to further evaluate these pilot observations.
|
ACKNOWLEDGMENTS
|
|---|
We gratefully acknowledge the excellent technical assistance of E. Rädisch and thank MSD of Haar, Germany, for providing study medication.
|
FOOTNOTES
|
|---|
Abbreviation: TIMI = Thrombolysis in Myocardial Infarction
Author contributions: Guarantors of integrity of entire study, U.J., M.S.; study concepts and design, U.J., R.J.S., M.S.; literature research, U.J.; clinical studies, U.J., R.J.S., M.S.; data acquisition, U.J., H.J.W., A.A., M.S.; data analysis/interpretation, all authors; manuscript preparation, U.J.; manuscript definition of intellectual content and editing, U.J., R.J.S., M.S.; manuscript revision/review and final version approval, all authors.
|
REFERENCES
|
|---|
-
Archer CR, Horenstein S. Basilar artery occlusion: clinical and radiological correlation. Stroke 1977; 8:383-390.
-
Zeumer H, Hacke W, Ringelstein EB. Local intraarterial thrombolysis in vertebrobasilar thromboembolic disease. AJNR Am J Neuroradiol 1983; 4:401-404.
-
Hacke W, Zeumer H, Ferbert A, Bruckmann H, del Zoppo GJ. Intra-arterial thrombolytic therapy improves outcome in patients with acute vertebrobasilar occlusive disease. Stroke 1988; 19:1216-1222.
-
Zeumer H, Freitag HJ, Grzyska U, Neunzig HP. Local intraarterial fibrinolysis in acute vertebrobasilar occlusion: technical developments and recent results. Neuroradiology 1989; 31:336-340.
-
Brandt T, von Kummer R, Muller-Kuppers M, Hacke W. Thrombolytic therapy of acute basilar artery occlusion: variables affecting recanalization and outcome. Stroke 1996; 27:875-881.
-
Cross DT, 3rd, Moran CJ, Akins PT, Angtuaco EE, Diringer MN. Relationship between clot location and outcome after basilar artery thrombolysis. AJNR Am J Neuroradiol 1997; 18:1221-1228.
-
Cross DT, 3rd, Moran CJ, Akins PT, Angtuaco EE, Derdeyn CP, Diringer MN. Collateral circulation and outcome after basilar artery thrombolysis. AJNR Am J Neuroradiol 1998; 19:1557-1563.
-
Tong DC, Albers GW. Diffusion and perfusion magnetic resonance imaging for the evaluation of acute stroke: potential use in guiding thrombolytic therapy. Curr Opin Neurol 2000; 13:45-50.
-
Babikian VL, Feldmann E, Wechsler LR, et al. Transcranial Doppler ultrasonography: year 2000 update. J Neuroimaging 2000; 10:101-115.
-
Schellinger PD, Jansen O, Fiebach JB, et al. Monitoring intravenous recombinant tissue plasminogen activator thrombolysis for acute ischemic stroke with diffusion and perfusion MRI. Stroke 2000; 31:1318-1328.
-
Brott T, Bogousslavsky J. Treatment of acute ischemic stroke. N Engl J Med 2000; 343:710-722.
-
Scharfstein JS, Abendschein DR, Eisenberg PR, et al. Usefulness of fibrinogenolytic and procoagulant markers during thrombolytic therapy in predicting clinical outcomes in acute myocardial infarction. TIMI-5 Investigators. Thrombolysis in Myocardial Infarction. Am J Cardiol 1996; 78:503-510.
-
Fassbender K, Dempfle CE, Mielke O, et al. Changes in coagulation and fibrinolysis markers in acute ischemic stroke treated with recombinant tissue plasminogen activator. Stroke 1999; 30:2101-2104.
-
Lincoff AM, Topol EJ. Illusion of reperfusion: does anyone achieve optimal reperfusion during acute myocardial infarction?. Circulation 1993; 88:1361-1374.
-
Busch E, Kruger K, Allegrini PR, et al. Reperfusion after thrombolytic therapy of embolic stroke in the rat: magnetic resonance and biochemical imaging. J Cereb Blood Flow Metab 1998; 18:407-418.
-
Gold HK, Coller BS, Yasuda T, et al. Rapid and sustained coronary artery recanalization with combined bolus injection of recombinant tissue-type plasminogen activator and monoclonal antiplatelet GPIIb/IIIa antibody in a canine preparation. Circulation 1988; 77:670-677.
-
Ohman EM, Kleiman NS, Gacioch G, et al. Combined accelerated tissue-plasminogen activator and platelet glycoprotein IIb/IIIa integrin receptor blockade with Integrilin in acute myocardial infarction: results of a randomized, placebo-controlled, dose-ranging trial. IMPACT-AMI Investigators. Circulation 1997; 95:846-854.
-
Antman EM, Giugliano RP, Gibson CM, et al. Abciximab facilitates the rate and extent of thrombolysis: results of the thrombolysis in myocardial infarction (TIMI) 14 trial. The TIMI 14 Investigators. Circulation 1999; 99:2720-2732.
-
McClellan KJ, Goa KL. Tirofiban: a review of its use in acute coronary syndromes. Drugs 1998; 56:1067-1080.
-
Platelet Receptor Inhibition in Ischemic Syndrome Management in Patients Limited by Unstable Signs and Symptoms (PRISM-PLUS) Study Investigators. Inhibition of the platelet glycoprotein IIb/IIIa receptor with tirofiban in unstable angina and non-Q-wave myocardial infarction. N Engl J Med 1998; 338:1488-1497[Erratum: N Engl J Med 1998; 339:415.].
-
Mammen EF. Sticky platelet syndrome. Semin Thromb Hemost 1999; 25:361-365.
-
Weitz JI, Leslie B, Hudoba M. Thrombin binds to soluble fibrin degradation products where it is protected from inhibition by heparin-antithrombin but susceptible to inactivation by antithrombin-independent inhibitors. Circulation 1998; 97:544-552.
-
Siess W. Molecular mechanisms of platelet activation. Physiol Rev 1989; 69:58-178.
-
Lefkovits J, Plow EF, Topol EJ. Platelet glycoprotein IIb/IIIa receptors in cardiovascular medicine. N Engl J Med 1995; 332:1553-1559.
-
Kuker W, Friese S, Vogel W, Schmidt F, Weller M. Incomplete resolution of basilar artery occlusion after intra-arterial thrombolysis: abciximab and heparin prevent early rethrombosis. Cerebrovasc Dis 2000; 10:484-486.
-
Wijdicks EF, Nichols DA, Thielen KR, et al. Intra-arterial thrombolysis in acute basilar artery thromboembolism: the initial Mayo Clinic experience. Mayo Clin Proc 1997; 72:1005-1013.
-
Huemer M, Niederwieser V, Ladurner G. Thrombolytic treatment for acute occlusion of the basilar artery. J Neurol Neurosurg Psychiatry 1995; 58:227-228.
-
Grond M, Rudolf J, Schmulling S, Stenzel C, Neveling M, Heiss WD. Early intravenous thrombolysis with recombinant tissue-type plasminogen activator in vertebrobasilar ischemic stroke. Arch Neurol 1998; 55:466-469.
-
Henze T, Boeer A, Tebbe U, Romatowski J. Lysis of basilar artery occlusion with tissue plasminogen activator (letter). Lancet 1987; 2:1391.
-
Wildemann B, Hutschenreuter M, Krieger D, Hacke W, von Kummer R. Infusion of recombinant tissue plasminogen activator for treatment of basilar artery occlusion (letter). Stroke 1990; 21:1513-1514.
-
Lempert TE, Malek AM, Halbach VV, Phatouros CC, Dowd CF, Higashida RT. Rescue treatment of acute parent vessel thrombosis with glycoprotein IIb/IIIa inhibitor during GDC coil embolization (letter). Stroke 1999; 30:693-695.
-
Wallace RC, Furlan AJ, Moliterno DJ, Stevens GH, Masaryk TJ, Perl J, 2nd. Basilar artery rethrombosis: successful treatment with platelet glycoprotein IIB/IIIA receptor inhibitor. AJNR Am J Neuroradiol 1997; 18:1257-1260.
-
Kereiakes DJ, Kleiman NS, Ambrose J, et al. Randomized, double-blind, placebo-controlled dose-ranging study of tirofiban (MK-383) platelet IIb/IIIa blockade in high risk patients undergoing coronary angioplasty. J Am Coll Cardiol 1996; 27:536-542.
-
Peter K, Schwarz M, Ylanne J, et al. Induction of fibrinogen binding and platelet aggregation as a potential intrinsic property of various glycoprotein IIb/IIIa (alphaIIbbeta3) inhibitors. Blood 1998; 92:3240-3249.
-
Dasgupta H, Blankenship JC, Wood GC, Frey CM, Demko SL, Menapace FJ. Thrombocytopenia complicating treatment with intravenous glycoprotein IIb/IIIa receptor inhibitors: a pooled analysis. Am Heart J 2000; 140:206-211.
-
Kennedy JW, Stadius ML. Combined thrombolytic and platelet glycoprotein IIb/IIIa inhibitor therapy for acute myocardial infarction: will pharmacological therapy ever equal primary angioplasty? (editorial). Circulation 1999; 99:2714-2716.
This article has been cited by other articles:
|
|
|
|
 
T. Pfefferkorn, T. E. Mayer, C. Opherk, N. Peters, A. Straube, H.-W. Pfister, M. Holtmannspotter, S. Muller-Schunk, M. Wiesmann, and M. Dichgans
Staged Escalation Therapy in Acute Basilar Artery Occlusion: Intravenous Thrombolysis and On-Demand Consecutive Endovascular Mechanical Thrombectomy: Preliminary Experience in 16 Patients
Stroke,
May 1, 2008;
39(5):
1496 - 1500.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. E. Mayer, G. F. Hamann, G. Schulte-Altedorneburg, and H. Bruckmann
Treatment of Vertebrobasilar Occlusion by Using a Coronary Waterjet Thrombectomy Device: A Pilot Study
AJNR Am. J. Neuroradiol.,
June 1, 2005;
26(6):
1389 - 1394.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. Eckert, C. Koch, G. Thomalla, T. Kucinski, U. Grzyska, J. Roether, K. Alfke, O. Jansen, and H. Zeumer
Aggressive Therapy With Intravenous Abciximab and Intra-Arterial rtPA and Additional PTA/Stenting Improves Clinical Outcome in Acute Vertebrobasilar Occlusion: Combined Local Fibrinolysis and Intravenous Abciximab in Acute Vertebrobasilar Stroke Treatment (FAST): Results of a Multicenter Study
Stroke,
June 1, 2005;
36(6):
1160 - 1165.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M Arnold, K Nedeltchev, G Schroth, R W Baumgartner, L Remonda, T J Loher, F Stepper, M Sturzenegger, B Schuknecht, and H P Mattle
Clinical and radiological predictors of recanalisation and outcome of 40 patients with acute basilar artery occlusion treated with intra-arterial thrombolysis
J. Neurol. Neurosurg. Psychiatry,
June 1, 2004;
75(6):
857 - 862.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Straub, U. Junghans, V. Jovanovic, H. J. Wittsack, R. J. Seitz, and M. Siebler
Systemic Thrombolysis With Recombinant Tissue Plasminogen Activator and Tirofiban in Acute Middle Cerebral Artery Occlusion
Stroke,
March 1, 2004;
35(3):
705 - 709.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. J. Seitz, M. Hamzavi, U. Junghans, P. A. Ringleb, C. Schranz, and M. Siebler
Thrombolysis With Recombinant Tissue Plasminogen Activator and Tirofiban in Stroke: Preliminary Observations
Stroke,
August 1, 2003;
34(8):
1932 - 1935.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. T. Higashida and A. J. Furlan
Trial Design and Reporting Standards for Intra-Arterial Cerebral Thrombolysis for Acute Ischemic Stroke
Stroke,
August 1, 2003;
34
(8):
e109 - e137.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Hahnel, P. D. Schellinger, A. Gutschalk, K. Geletneky, M. Hartmann, M. Knauth, and K. Sartor
Local Intra-arterial Fibrinolysis of Thromboemboli Occurring During Neuroendovascular Procedures With Recombinant Tissue Plasminogen Activator
Stroke,
July 1, 2003;
34(7):
1723 - 1728.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. E. Mayer, G. F. Hamann, and H. J. Brueckmann
Treatment of Basilar Artery Embolism With a Mechanical Extraction Device: Necessity of Flow Reversal
Stroke,
September 1, 2002;
33(9):
2232 - 2235.
[Abstract]
[Full Text]
[PDF]
|
|
|
TOP
ABSTRACT
INTRODUCTION
