(Radiology. 2001;218:733-738.)
© RSNA, 2001
Vascular and Interventional Radiology |
Initial Angiographic Appearance of Intracranial Vascular Occlusions in Acute Stroke as a Predictor of Outcome of Thrombolysis: Initial Experience1
Jay J. Pillai, MD,
Charles F. Lanzieri, MD,
Salvador B. Trinidad, MD,
Robert W. Tarr, MD,
Jeffrey L. Sunshine, MD, PhD and
Jonathan S. Lewin, MD
1 From the Case Western Reserve University School of Medicine, University Hospitals of Cleveland, Ohio. From the 1999 RSNA scientific assembly. Received December 9, 1999; revision requested January 18, 2000; revision received July 10; accepted July 25. Address correspondence to J.J.P., Department of Radiology, Division of Neuroradiology, Medical College of Georgia, 1120 15th St, Augusta, GA 30912 (e-mail: jpillai@mail.mcg.edu).
 |
ABSTRACT
|
|---|
PURPOSE: To determine whether the initial angiographic morphology and location of intracranial arterial occlusions in acute stroke are reliable predictors of success of thrombolysis.
MATERIALS AND METHODS: Thirty-three intracranial occlusions were studied in 32 patients who underwent intraarterial thrombolysis with urokinase within 6 hours from clinical onset of stroke symptoms. The initial angiographic appearance of each occlusion was categorized as cutoff, tapered, meniscus, tram-track, or tandem. Following thrombolysis, outcomes were classified as complete, partial, or no recanalization.
RESULTS: Complete recanalization was accomplished in 17 of the 33 lesions, partial recanalization in nine, and no effect in seven. Tram-track (n = 3) and tapered (n = 7) lesions demonstrated the highest rates of at least partial recanalization (100% and 86%, respectively), whereas cutoff lesions (n = 13) demonstrated the lowest rate (69%). Intracranial hemorrhage was associated with higher doses of urokinase. Complete recanalization success rates were 60% for M1 lesions (n = 10), 43% for M2 or A2 lesions (n = 14), and 33% for M3 lesions (n = 3). Vertebrobasilar lesion (n = 5) success rates for complete and at least partial recanalization were 80% and 100%, respectively.
CONCLUSION: Relationships were found to exist between the success rate of recanalization and initial angiographic lesion location and morphology, which represent important trends; however, further studies with a larger sample size are needed.
Index terms: Brain, infarction, 173.781, 174.781, 175.781 • Cerebral blood vessels, stenosis or obstruction, 173.7214, 174.7214, 175.7214 • Thrombolysis, 173.1265, 174.1265, 175.1265
|
INTRODUCTION
|
|---|
Although several large-scale, multicenter, placebo-controlled trials (1–5) have been conducted to date to examine the efficacy and safety of thrombolysis for the treatment of acute stroke, only two (the PROACT [Prolyse in Acute Cerebral Thromboembolism] I and II trials [6,7]) have specifically evaluated the use of intraarterial thrombolysis. In addition, very few studies have explored the possible relationships between intracranial arterial occlusive lesion location or angiographic morphology and therapeutic outcomes following thrombolysis (8–13). Given the nonnegligible incidence of symptomatic hemorrhagic transformation within the first 24 hours following administration of thrombolytic agents (15.4% in the PROACT I trial [7]; 10% in the PROACT II trial [6]; 8.8% in the Second European-Australasian Acute Stroke Study [5]; 19.4% in the original European Cooperative Acute Stroke Study [3]; 7.0% in the ATLANTIS [Alteplase Thrombolysis for Acute Non-interventional Therapy in Ischemic Stroke] trial [4]), judicious use of these agents is crucial. Intrinsic safety and efficacy advantages of intraarterial delivery of these agents over intravenous delivery include the need for lower total doses and greater local intraarterial concentration at the site of thrombus (12). Nevertheless, any criteria that may be established to guide the interventional neuroradiologist in decision making regarding feasibility of treatment of intracranial arterial occlusive lesions with intraarterial delivery of thrombolytic agents would obviously be valuable.
Our objective in pursuing the following study was to determine whether the initial diagnostic angiographic appearance of intracranial arterial occlusive lesions is in any way predictive of angiographic success following thrombolysis. Specifically, we were interested in examining how lesion morphology and location affect thrombolysis success rates.
|
MATERIALS AND METHODS
|
|---|
A retrospective analysis of a total of 33 cases of separately treated intracranial arterial occlusions in 32 patients who were admitted to our university hospital from January 1994 to October 1998 and for whom complete radiologic (angiographic) records were available was performed. These patients all presented within 6 hours of onset of clinical signs and symptoms of stroke and were evaluated through our Brain Attack Pathway protocol. This protocol includes rapid initial evaluation by a neurologist and/or neurosurgeon and nonenhanced brain computed tomographic (CT) scanning. Diffusion and perfusion echo-planar magnetic resonance imaging was also initiated as a screening method during the last 2 years of data collection. Intraarterial thrombolysis was considered in those cases in which the therapy could be initiated before 6 hours had elapsed from the onset of ischemia (12).
Inclusion criteria for patient selection included a National Institutes of Health Stroke Scale (NIHSS) score of 4, age older than 18 years and younger than 80 years, and absence of clinical improvement to the time of evaluation (12). Presence of intracranial hemorrhage, mass effect, or early signs of infarction (hypoattenuation and loss of gray matter–white matter differentiation) on the nonenhanced CT scan were absolute exclusion criteria (12), whereas questionable clinical diagnosis of stroke, high risk of hemorrhage (recent surgery, cardiopulmonary resuscitation, or trauma in the previous 14 days; genitourinary or gastrointestinal bleeding during the last 21 days; pregnancy or delivery within the last 7 days; lumbar puncture within the last 7 days; prothrombin time >15 seconds or platelet count <100 x109/L), or diastolic blood pressure greater than 120 mm Hg despite nitroprusside therapy were relative exclusion criteria (12). However, no patients were excluded from our experience thus far, based on the relative exclusion criteria.
The Brain Attack Pathway protocol was approved by the institutional review board at our university hospital (12). All patients gave written informed consent prior to cerebral angiography and thrombolysis (12).
Cerebral angiography was performed via a femoral approach, and a variety of microcatheter–base catheter combinations were used to deliver the thrombolytic agent and attempt mechanical disruption of the thrombus remnants following thrombolytic drug infusion (12). The initial dose of intraarterial urokinase used was 250,000 U. Additional 125,000–250,000-U increments of urokinase were administered until satisfactory recanalization had occurred. The doses were administered in 50,000-U aliquots in 20 mL of saline over 5 minutes by means of hand-controlled injection. Injections were made into or immediately proximal to the occlusion. The total dose of urokinase was limited to under 2,000,000 U, and rarely did patients receive greater than 1,250,000 U. Each dose listed in our report represents the cumulative administered dose for a particular patient that was needed to reach our study’s endpoint, which was the reestablishment of flow. However, additional incremental doses were frequently given beyond this point in an attempt to achieve the maximal clinical benefit, that is, the best possible degree of recanalization. When no further improvement in degree of recanalization was achieved with additional incremental doses, the thrombolysis was then terminated. All the patients who demonstrated no recanalization received the maximal dose of urokinase (2,000,000 U).
All patients received heparin for anticoagulation following thrombolysis (1,000 U/h without bolus) unless the postthrombolysis CT scan demonstrated evidence of intracranial hemorrhage. The outcome measures used included neurologic assessment 24 hours and 5 days following arrival: Improvement consisted of at least a four-point improvement on the NIHSS at 24 hours, and symptomatic intracranial hemorrhage was defined as a four-point or greater worsening on the NIHSS, accompanied by hemorrhage on CT scans obtained at 24 hours (12).
All the initial cerebral angiograms were reviewed jointly in our retrospective analysis by three board-certified radiologists, including the director of our neuroradiology division (C.F.L.) and two neuroradiology fellows (J.J.P., S.B.T.). The final morphologic designations for both initial and postthrombolysis images were based on consensus among the three observers. The initial intracranial arterial occlusive lesions were classified as cutoff, meniscus, tapered, tram-track, or tandem lesions. The descriptions of these morphologies are included in Figure 1. Conventional angiographic image examples of these various morphologies before thrombolysis are depicted in Figure 2. The single view that best (unequivocally) demonstrated the lesion morphology was used for determination of the classification. The postthrombolysis images were classified as complete recanalization, partial recanalization, or no change. The postthrombolysis images considered illustrated the morphology of the occluded segment at the end of the procedure. All of the analysis was based on changes noted in the initial lesion; in rare cases where thrombus fragment migration may have resulted in new distal smaller vessel occlusion, these additional occlusions were not considered. In cases where there may have been more than one initial lesion, only the lesion that was treated was considered.
View larger version (21K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 1. Schematic depiction of the five different types of morphologies used to classify intracranial arterial occlusive lesions: meniscus, tram-track, tapered, tandem, and cutoff. For each morphology, the portion of the vessel with normal blood flow and luminal caliber is depicted as black, whereas areas devoid of flow are depicted as white. The only exception is the tram-track model, in which the portion of the vessel lumen depicted as black distal to the thrombus represents markedly attenuated flow. The tandem morphology consists of proximal partially obstructive and distal occlusive lesions resulting from two serial intraluminal thrombi; the proximal lesion is depicted as a tram-track lesion and the distal lesion is depicted as a gray intraluminal region surrounding a central white focus. The central white focus represents intraluminal thrombus, and the peripheral gray region represents possible areas of intraluminal flow depending on whether the distal lesion is cutoff, meniscoid, tram-track, or tapered.
|
|
View larger version (179K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 2a. Conventional angiographic images display examples of each of the different morphologic categories. An arrow indicates the occlusive lesion. (a) Posteroanterior projection from a selective right internal carotid artery injection demonstrates a meniscoid occlusion of the carotid terminus. (b) Posteroanterior projection from a superselective microcatheter injection into the basilar artery via a right vertebral base catheter demonstrates a tram-track occlusive lesion involving the distal basilar artery. (c) Left anterior oblique projection from a selective left vertebral artery injection demonstrates a tapered occlusive lesion involving the proximal basilar artery just distal to the vertebrobasilar junction. (d) Left anterior oblique projection from a superselective microcatheter injection into the left middle cerebral artery via an indwelling base catheter within the left internal carotid artery demonstrates a tandem occlusive lesion in the M3 segment of the middle cerebral artery. (e) Posteroanterior projection from a selective left internal carotid artery injection demonstrates a cutoff occlusive lesion in the M1 segment of the left middle cerebral artery.
|
|
View larger version (166K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 2b. Conventional angiographic images display examples of each of the different morphologic categories. An arrow indicates the occlusive lesion. (a) Posteroanterior projection from a selective right internal carotid artery injection demonstrates a meniscoid occlusion of the carotid terminus. (b) Posteroanterior projection from a superselective microcatheter injection into the basilar artery via a right vertebral base catheter demonstrates a tram-track occlusive lesion involving the distal basilar artery. (c) Left anterior oblique projection from a selective left vertebral artery injection demonstrates a tapered occlusive lesion involving the proximal basilar artery just distal to the vertebrobasilar junction. (d) Left anterior oblique projection from a superselective microcatheter injection into the left middle cerebral artery via an indwelling base catheter within the left internal carotid artery demonstrates a tandem occlusive lesion in the M3 segment of the middle cerebral artery. (e) Posteroanterior projection from a selective left internal carotid artery injection demonstrates a cutoff occlusive lesion in the M1 segment of the left middle cerebral artery.
|
|
View larger version (172K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 2c. Conventional angiographic images display examples of each of the different morphologic categories. An arrow indicates the occlusive lesion. (a) Posteroanterior projection from a selective right internal carotid artery injection demonstrates a meniscoid occlusion of the carotid terminus. (b) Posteroanterior projection from a superselective microcatheter injection into the basilar artery via a right vertebral base catheter demonstrates a tram-track occlusive lesion involving the distal basilar artery. (c) Left anterior oblique projection from a selective left vertebral artery injection demonstrates a tapered occlusive lesion involving the proximal basilar artery just distal to the vertebrobasilar junction. (d) Left anterior oblique projection from a superselective microcatheter injection into the left middle cerebral artery via an indwelling base catheter within the left internal carotid artery demonstrates a tandem occlusive lesion in the M3 segment of the middle cerebral artery. (e) Posteroanterior projection from a selective left internal carotid artery injection demonstrates a cutoff occlusive lesion in the M1 segment of the left middle cerebral artery.
|
|
View larger version (165K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 2d. Conventional angiographic images display examples of each of the different morphologic categories. An arrow indicates the occlusive lesion. (a) Posteroanterior projection from a selective right internal carotid artery injection demonstrates a meniscoid occlusion of the carotid terminus. (b) Posteroanterior projection from a superselective microcatheter injection into the basilar artery via a right vertebral base catheter demonstrates a tram-track occlusive lesion involving the distal basilar artery. (c) Left anterior oblique projection from a selective left vertebral artery injection demonstrates a tapered occlusive lesion involving the proximal basilar artery just distal to the vertebrobasilar junction. (d) Left anterior oblique projection from a superselective microcatheter injection into the left middle cerebral artery via an indwelling base catheter within the left internal carotid artery demonstrates a tandem occlusive lesion in the M3 segment of the middle cerebral artery. (e) Posteroanterior projection from a selective left internal carotid artery injection demonstrates a cutoff occlusive lesion in the M1 segment of the left middle cerebral artery.
|
|
View larger version (166K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 2e. Conventional angiographic images display examples of each of the different morphologic categories. An arrow indicates the occlusive lesion. (a) Posteroanterior projection from a selective right internal carotid artery injection demonstrates a meniscoid occlusion of the carotid terminus. (b) Posteroanterior projection from a superselective microcatheter injection into the basilar artery via a right vertebral base catheter demonstrates a tram-track occlusive lesion involving the distal basilar artery. (c) Left anterior oblique projection from a selective left vertebral artery injection demonstrates a tapered occlusive lesion involving the proximal basilar artery just distal to the vertebrobasilar junction. (d) Left anterior oblique projection from a superselective microcatheter injection into the left middle cerebral artery via an indwelling base catheter within the left internal carotid artery demonstrates a tandem occlusive lesion in the M3 segment of the middle cerebral artery. (e) Posteroanterior projection from a selective left internal carotid artery injection demonstrates a cutoff occlusive lesion in the M1 segment of the left middle cerebral artery.
|
|
Intracranial hemorrhage was recorded when it was evident on nonenhanced brain CT scans obtained 24 hours after admission or earlier, if the patient’s symptoms warranted such a study.
Analysis of the effect of each explanatory variable (presence or absence of hemorrhage, initial angiographic appearance, anatomic location of occlusive lesion, and dose of urokinase) on the response variable (postthrombolysis appearance) was performed individually by conducting 
2 tests of association. Specifically, the standard 2 test and the Mantel-Haenszel 2 test were used (Sethuraman S, personal communication, 1999). For purposes of this statistical analysis, the explanatory variable hemorrhage was considered to have two levels (absent or present), while initial angiographic appearance had five levels (cutoff, meniscoid, tandem, tapered, or tram-track), anatomic location of the lesion had two levels (anterior or posterior circulation), and dose of urokinase was considered to be a continuous variable. Postthrombolysis appearance was considered to have two levels (recanalization to any degree or no recanalization). Because of the very small numbers involved within each subcategory, location of the lesion was not further subdivided into M1, M2 or A2, and M3, and postthrombolysis appearance was not further subdivided into partial or complete recanalization. With such small sample sizes and so many variables involved in an analysis such as this, the statistical power would naturally be expected to be low, and thus the effects considered would not be expected to achieve statistical significance. Therefore, the identification of any clinically important trends was the true aim of this analysis.
|
RESULTS
|
|---|
When the cases were stratified according to final angiographic appearance following thrombolysis, they were placed into one of three categories: complete recanalization, partial recanalization, or no recanalization. Seventeen of the 33 lesions demonstrated complete recanalization, whereas nine demonstrated partial recanalization, and seven demonstrated no change following thrombolysis. Cutoff and tram-track lesions required greater doses to achieve any degree of recanalization (mean, 783,333 U for each ± 432,471 and 375,278 [SD], respectively) than that for lesions in other morphologic categories (575,000 U ± 111,803 for meniscoid lesions; 733,333 U ± 275,379 for tandem lesions; 737,500 U ± 478,474 for tapered lesions). Furthermore, cutoff lesions demonstrated the lowest success rate (69% [nine of 13]) for at least partial recanalization of all the categories (as compared with 100% [three of three] for tram-track lesions, 75% [three of four] for tandem lesions, 83% [five of six] for meniscoid lesions, and 86% [six of seven] for tapered lesions. Thus, tram-track and tapered lesions demonstrated the highest success rates of at least partial success in recanalization (Fig 3), and tram-track lesions demonstrated the highest rate of complete recanalization (67% [two of three]). Intracranial hemorrhage was associated with higher doses of urokinase; 100% (nine of nine) of such cases (nine of the 33) were noted in patients receiving 750,000 U or more of urokinase (mean ± SD, 1,000,000 U ± 375,000).
View larger version (74K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 3. Graph shows success rates in percentages for achieving complete or at least partial recanalization based on intracranial intraarterial lesion morphology. Note that the light gray bars designate the rates for achievement of at least partial recanalization (reestablishment of distal flow without return to normal vessel caliber), whereas the darker gray bars represent rates of complete recanalization (ie, return to both normal flow and vascular caliber distal to the initially occlusive lesion). n = 3 for tram-track lesions; n = 4 for tandem lesions; n = 6 for meniscoid lesions; n = 7 for tapered lesions; and n = 13 for cutoff lesions.
|
|
In the anterior circulation, the success rates for achieving complete recanalization were 60% (six of 10) for M1 lesions, 43% (six of 14) for M2 or A2 lesions, and 33% (one of three) for M3 lesions (Fig 4). M3 lesions also required by far the highest mean urokinase doses for complete recanalization (1,750,000 U; n = 1).
View larger version (64K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 4. Graph shows success rates in percentages for achieving complete recanalization based on intraarterial occlusive lesion location. n = 5 for vertebrobasilar lesions (VB); n = 10 for M1 (segment of the middle cerebral artery) lesions; n = 14 for M2/A2 (M2 segment of the middle cerebral artery or A2 segment of the anterior cerebral artery) lesions; and n = 3 for M3 (segment of the middle cerebral artery) lesions.
|
|
Posterior circulation lesions had much higher success rates for complete and at least partial recanalization (80% [four of five] and 100% [five of five], respectively) than did anterior circulation lesions (Fig 4) but required higher mean doses of urokinase (930,000 U ± 390,000).
The results of our statistical analysis of the relationships between lesion location and morphology and postthrombolysis outcome were not statistically significant (P = .209 and .344, respectively) but did demonstrate statistical trends.
|
DISCUSSION
|
|---|
Although numerous published studies have been conducted to date regarding the efficacy of intracranial thrombolysis with a number of different agents such as urokinase, alteplase or recombinant tissue plasminogen activator (rt-PA), and streptokinase, only a few have explored the relationship between anatomic location of vascular occlusion and outcomes (8–12). Furthermore, almost all of these studies have focused on clinical measures of outcome following thrombolysis rather than purely angiographic measures. In addition, to the best of our knowledge, no other studies to date have specifically examined the relationship between initial angiographic morphology of vessel occlusions and the success rates of intraarterial intracranial thrombolysis. Although both the recent PROACT I and II trials (6,7), as well as the recent study by Jahan et al (14), included broad categorization of intracranial vascular lesions according to the Thrombolysis in Acute Myocardial Infarction, or TIMI, classification, this approach relied more on perfusion criteria than on actual lesion morphology. According to this classification, occlusions were designated as grade 0, lesions allowing contrast material penetration with minimal perfusion were designated as grade I, lesions displaying partial recanalization following thrombolysis were classified as grade II, and those displaying complete recanalization were classified as grade III (6,7).
Furthermore, investigators in the two other previous large placebo-controlled multicenter trials that demonstrated the benefits of thrombolytic drugs in the treatment of stroke (the European Cooperative Acute Stroke Study [3] and the National Institute of Neurological Disorders and Stroke [NINDS] rt-PA Stroke Study [1]) evaluated intravenous thrombolysis rather than intraarterial thrombolysis (1–3). Furthermore, the follow-up randomized double-blind placebo-controlled multicenter study, the Second European-Australasian Acute Stroke Study (5), in which intravenous alteplase was evaluated, failed to demonstrate any statistically significant benefit of thrombolysis. The ATLANTIS study (4) further demonstrated no benefit of intravenous rt-PA beyond 3 hours following symptom onset. Earlier studies, such as the Multicentre Acute Stroke Trial—Europe, the Australia Streptokinase trial, and the Multicentre Acute Stroke Trial—Italy, had evaluated intravenous streptokinase with a single dose (1.5 x 106 IU) applied to all patients; these trials were all terminated prematurely due to high complication rates, especially with intracranial hemorrhage (13). In fact, concerns regarding the risk-to-benefit ratio of intracranial thrombolysis have been raised in many reports in the literature (11,15–22), and the only multicenter randomized study that unequivocally demonstrated significant benefit of intravenous thrombolysis was the NINDS rt-PA study, and this study demonstrated benefit only during the first 3 hours following symptom onset (1). The recent multicenter prospective Standard Treatment with Alteplase to Reverse Stroke Study (23) not only confirmed efficacy of rt-PA during the initial 3-hour time window but also provided evidence of its safety (the symptomatic intracranial hemorrhage rate during the first 3 days was only 3.3%, as compared with 6.4% in the NINDS trial).
Recently, many reports in the literature have specifically described intraarterial delivery of thrombolytic agents (6–12,16,17, 21,22,24–34). However, the only multicenter double-blind randomized placebo-controlled trial data published to date regarding intraarterial thrombolysis are from the PROACT I and II studies (6,7) and involve the use of recombinant prourokinase within the first 6 hours of stroke symptom onset. Although investigators in these studies evaluated efficacy of intraarterial thrombolysis both in the context of angiographic recanalization and clinical outcomes, they did not specifically address initial angiographic appearance as a predictor of thrombolysis outcome.
Our results indicate that a relationship exists between the success rate of recanalization and the initial angiographic lesion location and morphology. Our data support the findings reported in several other studies (9,11,12). Distal lesions (M3) required greater doses and demonstrated lower success rates for complete recanalization than did more proximal intracranial lesions (success rates of M3 lesions < M2 or A2 lesions < M1 lesions) just beyond the circle of Willis; in addition, the thrombolysis success rates of posterior circulation lesions (vertebrobasilar lesions) surpassed those of all anterior circulation lesions. In addition, on the basis of success rates of achieving at least partial recanalization, tram-track lesions were most amenable to thrombolysis, and cutoff lesions were the least responsive to thrombolysis.
However, the association between lesion location and thrombolysis outcome was more impressive than the one between lesion morphology and outcome. Because of the small sample sizes involved, however, neither of these relationships achieved statistical significance.
In addition, a relationship between thrombolytic dose and intracranial hemorrhage incidence was demonstrated; such hemorrhage was associated only with high doses of urokinase. In 100% of patients with postthrombolysis intracranial hemorrhage, the dose administered reached or exceeded 750,000 U. No clear relationship between initial angiographic appearance or degree of recanalization and hemorrhage rates was noted, however.
Our results suggest that the relationships between lesion location or morphology and success of recanalization with urokinase represent important trends that, given larger sample sizes, may achieve statistical significance (P < .05). Future investigation with multicenter clinical trials similar to PROACT I and II will enable us to better address these issues. In addition, future studies involving animal models are necessary to explore the pathophysiology of these occlusive lesions and understand their anatomic substrates. The clinical relevance of these results lies in the recognition that unnecessary morbidity and mortality associated with intraarterial thrombolysis may be avoided if reliable criteria for excluding lesions that are not amenable to such therapy by virtue of their initial angiographic appearance can be established.
Another limitation of our current study includes the choice of thrombolytic agent. All of our data involve thrombolysis performed with urokinase, which is no longer commercially available in the United States. It will be necessary to determine whether similar results will be obtained with other thrombolytic agents, especially since other drugs such as rt-PA are now in widespread use for intracranial thrombolysis. To our knowledge, no published study to date has examined these issues in the context of any thrombolytic drug; therefore, no meta-analysis can be performed at this time for this purpose. Efforts to address this issue need to be made in the near future as well.
A final limitation of our present study is the fact that the contribution of mechanical thrombus disruption by placement of the microcatheter proximal to or within the occlusive arterial lesion to the entire process of thrombolysis has not been considered, since to our knowledge no effective way of quantitatively measuring this contribution exists.
Thus, future studies are needed to build on the foundation established by the current analysis to enable interventional neuroradiologists in the future to make informed decisions that will minimize risks and maximize effectiveness of intracranial intraarterial thrombolysis.
|
FOOTNOTES
|
|---|
Abbreviations: ATLANTIS = Alteplase Thrombolysis for Acute Noninterventional Therapy in Ischemic Stroke,
NIHSS = National Institutes of Health Stroke Scale,
NINDS = National Institute of Neurological Disorders and Stroke,
PROACT = Prolyse in Acute Cerebral Thromboembolism,
rt-PA = recombinant tissue plasminogen activator
Author contributions: Guarantors of integrity of entire study, J.J.P., C.F.L.; study concepts, J.L.S., R.W.T., C.F.L., J.S.L., J.J.P.; study design, J.J.P., C.F.L., R.W.T., J.L.S.; definition of intellectual content, all authors; literature research, J.J.P., J.S.L.; clinical studies, R.W.T., J.L.S., C.F.L.; data acquisition, R.W.T., J.L.S., C.F.L., J.S.L.; data analysis, J.J.P., S.B.T., C.F.L.; statistical analysis, J.J.P., S.B.T.; manuscript preparation, J.J.P., C.F.L., J.S.L.; manuscript editing, all authors; manuscript review, J.J.P., C.F.L., manuscript final version approval, all authors.
|
REFERENCES
|
|---|
-
National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med 1995; 333:1581-1587.[Abstract/Free Full Text]
-
Willig V, Steiner T, Hacke W. Thrombolytic therapy in ischemic infarct. Wien Klin Wochenschr 1997; 109:795-803.[Medline]
-
Hacke W, Kaste M, Fieschi C, et al. Intravenous thrombolysis with recombinant tissue plasminogen activator for acute hemispheric stroke: the European Cooperative Acute Stroke Study. JAMA 1995; 274:1017-1025.[Abstract]
-
Clark WM, Wissman S, Albers GW, et al. Recombinant tissue-type plasminogen activator (alteplase) for ischemic stroke 3 to 5 hours after symptom onset: the ATLANTIS Study—a randomized controlled trial. JAMA 1999; 282:2019-2026.[Abstract/Free Full Text]
-
Hacke W, Kaste M, Fieschi C, et al. Randomised double-blind placebo-controlled trial of thrombolytic therapy with intravenous alteplase in acute ischaemic stroke (ECASS II): Second European-Australasian Acute Stroke Study investigators. Lancet 1998; 352:1245-1251.[Medline]
-
Furlan A, Higashida R, Wechsler L, et al. The PROACT II study: a randomized controlled trial. JAMA 1999; 282:2003-2011.[Abstract/Free Full Text]
-
del Zoppo GJ, Higashida RT, Furlan AJ, et al. PROACT: a phase II randomized trial of recombinant pro-urokinase by direct arterial delivery in acute middle cerebral artery stroke. Stroke 1998; 29:4-11.[Abstract/Free Full Text]
-
Pillai JJ, Trinidad SB, Lanzieri CF, Sunshine JL, Tarr RW, Lewin JS. Initial angiographic appearance of intracranial vascular occlusions in acute stroke as a predictor of outcome of thrombolysis (abstr). Radiology 1999; 213(P):393-394.
-
Kucinski T, Grzyska U, Groden C, Heesen C, Koch C, Zeumer H. Intracranial arterial occlusion site predicts outcome in carotid artery stroke (abstr). Radiology 1999; 213(P):394.
-
Cronqvist M, Pierot L, Boulin A, Cognard C, Castaings L, Moret J. Local intraarterial fibrinolysis of thromboemboli occurring during endovascular treatment of intracerebral aneurysm: a comparison of anatomic results and clinical outcome. AJNR Am J Neuroradiol 1998; 19:157-165.[Abstract]
-
Cross DT, 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.[Abstract]
-
Suarez JI, Sunshine JL, Tarr RW, et al. Predictors of clinical improvement, angiographic recanalization, and intracranial hemorrhage after intra-arterial thrombolysis for acute ischemic stroke. Stroke 1999; 30:2094-2100.[Abstract/Free Full Text]
-
Del Zoppo GJ. Thrombolytic therapy in the treatment of stroke. Drugs 1997; 54(suppl 3):90-98.
-
Jahan R, Duckwiler GR, Kidwell CS, et al. Intraarterial thrombolysis for treatment of acute stroke: experience in 26 patients with long-term follow-up. AJNR Am J Neuroradiol 1999; 20:1291-1299.[Abstract/Free Full Text]
-
Wardlaw JM, Warlow CP, Counsell C. Systematic review of evidence on thrombolytic therapy for acute ischaemic stroke. Lancet 1997; 350:607-614.[Medline]
-
Cross DT, 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.[Abstract]
-
Schumacher M, Kraft S, Siekmann R. Is local intra-arterial fibrinolysis contraindicated in elderly patients with cerebral artery occlusion?. Neuroradiology 1998; 40:822-826.[Medline]
-
Warlow C, Wardlaw J. The drug trials that have influenced our clinical practice in acute ischaemic stroke. Thromb Haemost 1997; 78:558-561.[Medline]
-
Simoons ML. Risk-benefit of thrombolysis. Cardiol Clin 1995; 13:339-345.[Medline]
-
Samama MM, Acar J. Thrombolytic therapy: future issues. Thromb Haemost 1995; 74:106-110.[Medline]
-
Barnwell SL, Clark WM, Nguyen TT, O’Neill OR, Wynn ML, Coull BM. Safety and efficacy of delayed intraarterial urokinase therapy with mechanical clot disruption for thromboembolic stroke. AJNR Am J Neuroradiol 1994; 15:1817-1822.[Abstract]
-
Gress D. Intraarterial thrombolysis for cerebral infarction: to treat or not to treat, and how?. AJNR Am J Neuroradiol 1999; 20:1194-1196.[Free Full Text]
-
Albers GW, Bates VE, Clark WM, Bell R, Verro P, Hamilton SA. Intravenous tissue-type plasminogen activator for treatment of acute stroke: the standard treatment with alteplase to reverse stroke (STARS) study. JAMA 2000; 283:1145-1150.[Abstract/Free Full Text]
-
Barr JD, Mathis JM, Wildenhain SL, Wechsler L, Jungreis CA, Horton JA. Acute stroke intervention with intraarterial urokinase infusion. J Vasc Interv Radiol 1994; 5:705-713.[Medline]
-
Burnette WC, Nesbit GM, Barnwell SL. Intra-arterial thrombolysis for acute stroke. Neuroimaging Clin N Am 1999; 9:491-508.[Medline]
-
Gonner F, Remonda L, Mattle H, et al. Local intra-arterial thrombolysis in acute ischemic stroke. Stroke 1998; 29:1894-1900.[Abstract/Free Full Text]
-
Ueda T, Hatakeyama T, Kohno K, Kumon Y, Sakaki S. Endovascular treatment for acute thrombotic occlusion of the middle cerebral artery: local intra-arterial thrombolysis combined with percutaneous transluminal angioplasty. Neuroradiology 1997; 39:99-104.[Medline]
-
Schumacher M, Yin L, Klisch J, Hetzel A. Local intra-arterial fibrinolysis without arterial occlusion?. Neuroradiology 1999; 41:530-536.[Medline]
-
Hoffman AI, Lambiase RE, Haas RA, Rogg JM, Murphy TP. Acute vertebrobasilar occlusion: treatment with high-dose intraarterial urokinase. AJR Am J Roentgenol 1998; 172:709-712.[Abstract/Free Full Text]
-
Jungreis CA, Wechsler LR, Horton JA. Intracranial thrombolysis via a catheter embedded in the clot. Stroke 1989; 20:1578-1580.[Abstract/Free Full Text]
-
Tarr R, Taylor CL, Selman WR, Lewin JS, Landis D. Good clinical outcome in a patient with a large CT scan hypodensity treated with intra-arterial urokinase after an embolic stroke. Neurology 1996; 47:1076-1078.[Abstract/Free Full Text]
-
Edwards MT, Murphy MM, Geraghty JJ, Wulf JA, Konzen JP. Intra-arterial cerebral thrombolysis for acute ischemic stroke in a community hospital. AJNR Am J Neuroradiol 1999; 20:1682-1687.[Abstract/Free Full Text]
-
Gruber A, Nasel C, Lang W, Kitzmuller E, Bavinzski G, Czech T. Intra-arterial thrombolysis for the treatment of perioperative childhood cardioembolic stroke. Neurology 2000; 54:1684-1686.[Abstract/Free Full Text]
-
Yang Y, Li Q, Miyashita H, Howlett W, Siddiqui M, Shuaib A. Usefulness of postischemic thrombolysis with or without neuroprotection in a focal embolic model of cerebral ischemia. J Neurosurg 2000; 92:841-847.[Medline]
This article has been cited by other articles:
|
|
|
|
 
T.G. Jovin, R. Gupta, M.B. Horowitz, S.Z. Grahovac, C.A. Jungreis, L. Wechsler, J.M. Gebel, and H. Yonas
Pretreatment Ipsilateral Regional Cortical Blood Flow Influences Vessel Recanalization in Intra-Arterial Thrombolysis for MCA Occlusion
AJNR Am. J. Neuroradiol.,
January 1, 2007;
28(1):
164 - 167.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G.A. Christoforidis, Y. Mohammad, B. Avutu, A. Tejada, and A.P. Slivka
Arteriographic Demonstration of Slow Antegrade Opacification Distal to a Cerebrovascular Thromboembolic Occlusion Site As a Favorable Indicator for Intra-Arterial Thrombolysis
AJNR Am. J. Neuroradiol.,
August 1, 2006;
27(7):
1528 - 1531.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. A. Christoforidis, Y. Mohammad, D. Kehagias, B. Avutu, and A. P. Slivka
Angiographic Assessment of Pial Collaterals as a Prognostic Indicator Following Intra-arterial Thrombolysis for Acute Ischemic Stroke
AJNR Am. J. Neuroradiol.,
August 1, 2005;
26(7):
1789 - 1797.
[Abstract]
[Full Text]
[PDF]
|
|
|
TOP
ABSTRACT
INTRODUCTION
