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410 Part IV / Practical Issues and Future Applications
and atrial fibrillation or flutter (3). The complicating stroke morbidity of 40–60% impacts
in turn on the aggressiveness of treatment for the underlying cardiac disease and trans-
lates into a stroke-related mortality of 15–20% (4).
The risk of stroke in patients with acute coronary syndromes (ACS) not managed with
thrombolysis or glycoprotein (GP) IIb/IIIa receptor antagonists is approx 0.6–0.8%, is
largely ischemic in nature, and occurs at a median of 6.5 d. Risk factors for stroke with
ACS are similar to those in the setting of AMI and include advanced age, prior anterior
myocardial infarction, female gender, lower body weight, higher heart rate, history of prior
stroke, hypertension, diabetes mellitus, hypercholesterolemia, history of prior myocardial
infarction, and prior coronary bypass surgery. Stroke victims experience more in-hospital
complications of atrial fibrillation, hypotension, congestive heart failure, cardiogenic shock,
and coronary bypass surgery, and at 1 mo, half are dead or disabled (5–7).
Cardiac catheterization, for purposes of diagnosis or therapeutic intervention, is compli-
cated by ischemic stroke in 0.1–1.0%, and half of the cases resolve within 48 h (8). There
is a vertebrobasilar predominance, with 60–70% presenting as confusion, visual field
defects, and brainstem signs and 30–40% with carotid distribution symptoms of hemipar-
esis, hemisensory deficits, dysphasia, and retinal ischemia (9). As the confusional states
can mimic medication effects and metabolic encephalopathy, the true incidence may be
underestimated (10). The mechanism is attributed to cerebral embolism of particulate mat-
ter or air during catheter manipulation or flushing, and as the posterior circulation predom-
inance persists regardless of the method of arterial access, it is likely to be related to the
catheter position within the aorta (11).
The risk of stroke during percutaneous coronary intervention (PCI) is similar to that
of diagnostic angiography. A combined analysis of four trials (EPIC, EPILOG, CAPTURE,
and EPISTENT) assessing the risk of stroke in 8555 patients undergoing PCI with abcixi-
mab vs placebo as well as aspirin and heparin demonstrated no significant difference in the
rate of both hemorrhagic and ischemic stroke between those assigned to placebo (9/3079,
0.29%) vs any abciximab dose (22/5476, 0.40%; p = 0.46) or abciximab bolus plus infu-
sion (15/4680, 0.32%) (Table 1) (12). The numbers of patients with ischemic stroke were
small but not significantly different between the two groups (0.17% vs 0.2%) overall. The
challenge of finding the optimum combination of antithrombotic therapies is highlighted
by the interesting observation that although overall bleeding complications were greater
in abciximab-treated patients, the rate of ischemic stroke was less in those who received
the standard heparin dose vs the low-dose heparin regimen (0.09% vs 0.24%; p = 0.3).
Hemorrhagic Stroke Complicating Coronary Artery Disease and Treatment
The risk of any intracranial bleeding increases with the aggressiveness of antithrombo-
tic and antifibrinolytic therapies, particularly with higher dosages and combination thera-
pies (13). Intracranial hemorrhage following aspirin or heparin therapy for AMI is typically
caused by a delayed hemorrhagic transformation of an ischemic stroke. Risk factors for
hemorrhagic transformation of an ischemic stroke include advanced age, hypertension,
embolic mechanism, volume of cerebral infarct by neuroimaging or severity of clinical
deficit, early anticoagulant therapy of large ischemic stroke, use of bolus dosing of hepa-
rin, higher heparin dosages, and excessive prolongation of the activated partial thrombo-
plastin time (14–16).
The risk of stroke with platelet GPIIb/IIIa inhibition for PCI was not increased in patients
receiving abciximab vs placebo with aspirin and heparin in a combined analysis of 8555
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Chapter 20 / Cerebrovascular Aspects of GPIIb/IIIa Receptor Inhibitors 411
Table 1
Stroke Risk (%) with Glycoprotein IIb/IIIa Inhibitors in Cardiac Trials
a
Heparin
Abciximab Control
(n = 5476) (n = 3079) Standard Low-dose
Percutaneous interventions
(8555 patients from EPIC, CAPTURE, EPILOG, and EPISTENT)
All stroke 0.4 0.29 ( p = 0.46)
Ischemic 0.17 0.20
Hemorrhagic 0.15 0.10 0.27 0.04 (p = 0.057)
Various Control
Acute coronary syndromes
(31,402 patients from PRISM, PRISM-PLUS, PARAGON-A, PARAGON-B, PURSUIT, and
GUSTO-IV ACS)
Hemorrhagic 0.09 0.06 (p = 0.40)
Abciximab + heparin Heparin from GUSTO-V
(n = 8328) (n = 8260)
Acute MI: combination therapy with thrombolysis
All stroke 1.0 0.9 (p = 0.37)
Ischemic 0.3 0.3
Hemorrhagic 0.7 0.6
LMWH
Abciximab + heparin Heparin (n = 2040)
(n = 2017) (n = 2038) from ASSENT-3
All stroke 1.49 1.52 1.62 (p = 0.94)
Ischemic 0.35 0.54 0.59
Hemorrhagic 1.14 0.98 1.08
Abbreviations: LMWH, low-molecular-weight heparin; MI, myocardial infarction.
a
Hemorrhagic stroke includes intracranial hemorrhage, hemorrhagic conversion of ischemic stroke, and
unknown type.
patients from four trials (12). There was no significant difference in the rate of hemorrha-
gic stroke (0.15% vs 0.1%) between abciximab-treated patients vs controls. However, the
rate of hemorrhagic stroke was greater in patients who received abciximab with standard-
dose heparin at 0.27% vs low-dose, weight-adjusted heparin at 0.04% (p = 0.057), and
mortality after hemorrhagic stroke was greater in abciximab-treated patients, supporting
the recommendations for the use of low-dose, weight-adjusted heparin when patients
receive abciximab for PCI.
The risk of stroke with platelet GPIIb/IIIa inhibition for ACS was prospectively addressed
in the PURSUIT trial, which compared two doses of eptifibatide in addition to aspirin
and recommended heparin (6). There was no significant difference between eptifibatide
and control in the rate of all stroke (0.6% vs 0.8%) or hemorrhagic stroke (0.13% vs 0.11%,
including intracranial hemorrhage, hemorrhagic conversion of infarction, and uncertain
type). In a meta-analysis of GPIIb/IIIa inhibitors in ACS combining these data with data from
PRISM, PRISM-PLUS, PARAGON-A and B, and GUSTO-IV ACS, although overall
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412 Part IV / Practical Issues and Future Applications
bleeding complications were significantly more frequent, there was no significant increase
in the rate of intracranial bleeding (0.09% vs 0.06%, p = 0.40) (17).
Although the overall rate of stroke with AMI is reduced with thrombolytic therapy, the
rate of hemorrhagic stroke is significantly increased at 0.3–1.5% and includes spontaneous
intracerebral, subdural, subarachnoid, and intraventricular hemorrhage as well as hemor-
rhagic transformation of cerebral infarcts (1,18). Hemorrhagic transformation compli-
cates 30% of ischemic strokes and is severe enough to produce symptoms of neurologic
deterioration in two-thirds (2).
Intracranial hemorrhage after thrombolysis for AMI is usu-
ally caused by a solitary intracerebral hemorrhage involving the deep lobar white matter.
However, there is substantial variability in the size and nature of intracranial hemorrhages,
with multifocality, bizarre-appearing hemorrhages, and blood-fluid levels or a mottled
appearance typical of an underlying coagulopathy (18). Many are recognized during the
infusion as a subacute but rapidly progressive headache with nausea, vomiting, and focal
neurologic signs, and most occur within 24 h, but the risk of persists for days. The fear of
stroke complicating cardiac interventions emanates from the dismal outcome of patients
with intracranial hemorrhage, as 60% die and an additional 25% remain disabled (4,19).
Risk factors for intracranial hemorrhage after thrombolysis for AMI include advanced age,
hypertension, and prior neurologic disease, as well as the intensity of the coagulopathy
induced by the type, dosage, and concomitant therapies administered (20). Amyloid angio-
pathy is the most common substrate in surgical or autopsy specimens and probably explains
the important relationship between advanced age and risk of cerebral hemorrhage (21).
The reduction in the rate of cardiac complications after AMI treated with combination
therapy with thrombolytics, GPIIb/IIIa inhibitors, and heparin comes at the price of an
increase in overall bleeding complications, particularly in those over 75 yr or when strep-
tokinase is used. Small, nonpivotal trials had rates of intracranial hemorrhage similar to
that seen with thrombolysis alone (22). In GUSTO-V, the rates of all stroke (1.0% vs 0.9%,
p = 0.37), ischemic stroke (0.3% vs 0.3%), and hemorrhagic stroke (0.7% vs 0.6%) were
quite low overall and were no different with abciximab and reduced-dose reteplase over
standard-dose reteplase (23). Similarly, in ASSENT-3, the rates of all stroke were low and
not significantly different among those who received tenecteplase with abciximab and
heparin vs heparin vs enoxaparin (1.49% vs 1.52% vs 1.62%, p = 0.94) (24). Although the
events were few and <15% of patients were over 75 yr, there was a suggestion that the com-
bination of abciximab with heparin had a somewhat lower rate of ischemic stroke and
higher rate of hemorrhagic stroke (including hemorrhagic transformations and unknown
type) compared with heparins alone. The differential risk of ischemic vs hemorrhagic
stroke may warrant tailoring combination therapy to special at-risk patients with AMI and
will be particularly important as these combinations are explored for patients with acute
ischemic stroke (AIS).
TREATMENTS FOR CEREBROVASCULAR DISEASE
Risks and Benefits of Antiplatelet Therapy
for the Prevention of Recurrent Ischemic Stroke
Although aspirin remains the standard preventive therapy for patients at risk for stroke,
the effect, operating through inhibition of thromboxane A
2
, is modest and calls for improve-
ment. Despite numerous metaanalyses, there is no consensus on the optimum dose of aspi-
rin for prevention of ischemic stroke, and most physicians now use low to medium doses
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Chapter 20 / Cerebrovascular Aspects of GPIIb/IIIa Receptor Inhibitors 413
(50–325 mg/d). Establishing superior preventive efficacy has been the goal of develop-
ment of other antiplatelet agents that target platelet surface glycoproteins, ADP recep-
tors, or platelet-dependent thrombin generation in the hopes that combination therapy will
provide synergistic effects. Although the orally active platelet GPIIb/IIIa inhibitor lotrafiban
was felt to be safe and well tolerated in combination with aspirin in a preliminary trial, the
pivotal trial including patients with cerebrovascular disease was prematurely terminated
owing to an excess of adverse events (25).
The antiplatelet effect achieved by the inhibition of ADP binding to its platelet receptor
with ticlopidine and clopidogrel has been compared with that of aspirin in two trials of
stroke prevention. The Ticlopidine Aspirin Stroke Study (TASS) compared ticlopidine
(250 mg twice daily) with high-dose aspirin (650 mg twice daily) in 3069 patients with
transient ischemic attacks (TIAs) or minor stroke (26). Ticlopidine reduced the risk of
stroke by 21% over high-dose aspirin, but with small numbers of other events, the 9%
reduction in the combined endpoint of stroke, myocardial infarction, or vascular death
did not reach significance. In the Clopidigrel versus Aspirin in Patients at Risk of Ische-
mic Events (CAPRIE) study, clopidogrel (75 mg once daily) reduced the annual risk of
the combined endpoint of stroke, myocardial infarction, or vascular death by 9% (5.32%
vs 5.83%, p = 0.043) over aspirin 325 mg daily in 19,185 patients with various manifesta-
tions of vascular disease (27). As the study was designed to detect an overall relative risk
reduction of 12–13%, the 7.3% reduction in recurrent events, mostly stroke, for the stroke
subset of 6431 patients did not reach significance (7.15% vs 7.71%, p = 0.26). Hematologic
side effects include neutropenia in <2% of ticlopidine-treated patients and thrombotic
thrombocytopenic purpura (TTP) in 200–625/million ticlopidine-treated and 3.7/million
clopidogrel-treated patients (28). Only ticlopidine warrants hematologic monitoring every
2 wk for the first 3 mo to screen for neutropenia, but as 80% of TTP cases appeared within
the first few weeks of therapy, hematologic monitoring is not reliable for surveillance of
this condition. Given the similar efficacy and superior safety, clopidogrel has essentially
replaced ticlopidine as an aspirin alternative.
Combination antiplatelet therapy with aspirin and dipyridamole has been studied in
various dosing schedules in five clinical trials. The combination of aspirin (330 mg tid) and
dipyridamole (75 mg tid) reduced stroke by 38% and the combined endpoint of stroke,
myocardial infarction, or vascular death by 31% over placebo but smaller trials did not
demonstrate efficacy over high-dose aspirin alone (29–31). The Second European Stroke
Prevention Study (EPSP-2) compared the combination of low-dose aspirin (50 mg daily)
and modified-release dipyridamole (400 mg daily) with each agent alone and placebo.
The combination reduced stroke by 23.1% (p = 0.006) over low-dose aspirin alone, and
comparisons suggested a synergistic effect (32). None of the treatments reduced mortality,
and there were too few endpoints to demonstrate any effect on fatal stroke or myocardial
infarction. EPSP-2 prompted the ACCP guidelines for lower doses of aspirin, 50–325 mg
daily, for secondary stroke prevention.
Combination therapy with clopidogrel (75 mg daily) and aspirin (75 mg daily) for sec-
ondary stroke prevention is currently being studied in 7600 high-risk patients with recent
TIA or ischemic stroke, with results anticipated by 2004.
Complications of Endovascular Therapy for Cerebrovascular Disease
Endovascular treatment of cerebrovascular disease began in the 1980s with primary
angioplasty of extracranial vessels. By 1995, stents dedicated to the extracranial carotid
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414 Part IV / Practical Issues and Future Applications
artery were available and were followed shortly by numerous emboli protection devices.
Although case series report results that are comparable to those of carotid endarterectomy,
this has not been confirmed by randomized clinical trials. Between 1992 and 1997, the
Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS) trial rando-
mized 560 patients (most with symptomatic >80% carotid stenosis) to angioplasty, sur-
gery, or medical therapy if patients were not appropriate candidates for surgery (33). The
30-d rate of stroke and death was high, 9.9% for the 253 patients who underwent carotid
endarterectomy and 10% for the 251 patients who underwent angioplasty, 26% with
stenting. At 1-yr follow-up, restenosis of >70% was rare in endartectomy patients but was
present in 21% with endovascular therapy. The Schneider trial randomized 223 patients with
>60% symptomatic carotid stenosis to carotid stenting with aspirin and ticlopidine vs end-
arterectomy (34). Statistically designed as an equivalency analysis, stenting was deter-
mined not to be equivalent or better to endarterectomy based on the 12% vs 3.5% rate in
the primary endpoint of ipsilateral stroke, periprocedural death, or vascular death at 1 yr.
Currently, there are numerous uncontrolled registry-based studies investigating differ-
ent stents and emboli protection devices as well as two randomized trials. The NIH-funded
Carotid Revascularization: Endarterectomy vs Stent Trial (CREST) is randomizing patients
with symptomatic >50% extracranial carotid stenosis who are eligible for either procedure.
The Stenting and Angioplasty for Patients at High Risk for Endarterectomy (SAPPHIRE)
trial employs both a randomized trial and registry approach to patients with symptomatic
>50% and asymptomatic >80% extracranial carotid stenosis who are at high risk for treat-
ment. Antiplatelet and antithrombotic regimens vary, but many specify aspirin 325 mg
and clopidogrel 75 mg for 72 h before and 4 wk after the procedure and periprocedural hep-
arin therapy titrated to a target activated clotting time (ACT) of 200–250 s.
The safety of adding GPIIb/IIIa receptor inhibition in carotid stenting has been explored
in several case series with no bleeding complications reported in bolus and infusion regi-
mens of 10 patients receiving eptifibatide and 15 patients receiving abciximab for carotid
interventions (35,36). In the largest series, 151 patients at high risk for carotid endarter-
ectomy underwent carotid angioplasty and stenting with heparin, aspirin, and ticlopidine
or clopidogrel (37). The initial 23 patients served as historical controls for the subsequent
128 patients (134 arteries), who also received an abciximab bolus and 12 h infusion. In the
abciximab group, one patient developed a minor hemorrhagic transformation of a prior
stroke 4 d after the procedure. In the control group, 1 patient died of an intracranial hemor-
rhage, but this occurred in the setting of intraarterial thrombolysis for a procedural embolic
stroke. Although the numbers are small, no other significant bleeding complications were
reported with this approach.
Endovascular techniques now offer a therapeutic option for patients with intracranial
atherosclerosis Angioplasty, with or without stenting, of intracranial carotid, middle cere-
bral artery, or vertebrobasilar stenoses with variable antithrombotic regimens has been
described in multiple case reports and small series to be now technically feasible in >80%
but associated with periprocedural risks of 5–15%. The largest reported prospective reg-
istry of endovascular therapy of intracranial atherosclerosis included 42 patients with
symptomatic intracranial stenosis, primarily involving the internal carotid or basilar arter-
ies, and 19 patients with vertebral ostial stenosis. All received combination antiplatelet
therapy with GPIIb/IIIa inhibitors and heparin at the discretion of the investigator. They
reported a 6.6% risk of stroke at 30 d, restenosis of >50% at 6 mo, and 11.5% risk of
ipsilateral stroke at 1 yr (38). In a series of eight patients with stent-assisted angioplasty
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Chapter 20 / Cerebrovascular Aspects of GPIIb/IIIa Receptor Inhibitors 415
of symptomatic vertebrobasilar stenosis with abciximab bolus and 12 h infusion, heparin
during the procedure, aspirin and ticlopidine or clopidogrel, one patient died after a dis-
section-related subarachnoid hemorrhage, and two had other serious bleeding (39).
Hemorrhagic Stroke Complicating Therapy for Acute Ischemic Stroke
When administered within 48 h of acute AIS, 160–300 mg of aspirin significantly reduced
absolute recurrent ischemic stroke by 0.5–1.1% and early mortality by 0.5–0.6% while
increasing the risk of symptomatic hemorrhagic stroke by a nonsignificant 0.1–0.2% (Table
2) (40,41). The International Stroke Trial also evaluated combination therapy with subcu-
taneous heparin (10,000 or 25,000 U/d) with or without aspirin 300 mg/d, and placebo.
Heparin was not effective in reducing overall stroke, as the early reduction in recurrent
ischemic stroke in patients allocated to heparin compared with those without heparin (2.9%
vs 3.8%) was negated by a delayed increase in the rate of hemorrhagic stroke (1.2% vs
0.4%) (41).
Thrombolysis for AIS is complicated by an increased risk of intracranial hemorrhage
related to petechial or confluent hemorrhagic transformation of the infarct. The NINDS
trial of weight-adjusted tissue plasminogen activator (tPA) given intravenously within
3 h of symptom onset, without any concomitant antiplatelet or antithrombotic agent for
the first 24 h, is the only Food and Drug Administration-approved thrombolytic regimen
for AIS (12). Thrombolytic therapy significantly increased the rate of excellent neuro-
logic outcome at 3 mo by an absolute 11–13%, but the risk of symptomatic and fatal intra-
cranial hemorrhage was increased 10-fold from 0.6 to 6.4%, and mortality was unchanged.
However, the benefit-to-risk ratio was marginal for patients with severe stroke (NIH
Stroke Scale Score >22) or over 77 yr of age, who were at increased risk for intracranial
hemorrhage. Excessive rates of symptomatic and fatal intracranial hemorrhage in numer-
ous trials have thus far resulted in the abandonment of streptokinase, streptokinase with
aspirin, and tPA after 3 h of symptom onset but agents with greater fibrin selectivity, like
desmetoplase, are in Phase I trials (42–44).
Intraarterial thrombolysis for AIS owing to middle cerebral artery occlusion was studied
in a randomized controlled trial of 180 patients who received heparin, 2000 U bolus and
500 U/h for 4 h, with or without prourokinase within 6 h of symptom onset (46). No adjunc-
tive antithrombotic agents were then allowed until after 24 h of treatment. Thrombolytic
therapy increased the chance of a good neurologic outcome by an absolute 15%, but the
absolute risk of symptomatic intracranial hemorrhage was increased 8.3% over heparin
alone at 24 h. At 10 d, however, evidence of any intracranial bleeding was present in 50.4%
Table 2
Hemorrhagic Stroke Complicating Therapy of Acute Ischemic Stroke
Increased absolute risk (%)
Therapy Symptomatic Asymptomatic Reference
Aspirin 160–300 mg/d (IST, CAST) 0.1–0.2 40,41
Heparin 10,000–25,000 U/d (IST) 0.8 41
IV tPA (NINDS protocol) 5.8 22
IA prourokinase (PROACT-2) 8.4 45
Abciximab (AbESTT pilot) 0 13 47
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416 Part IV / Practical Issues and Future Applications
of those who received prourokinase and heparin vs 44.1% with heparin alone, and overall
mortality was unchanged.
Risk factors for intracranial hemorrhage after thrombolysis for AIS include the presence
of early infarct signs on brain computed tomography (CT), stroke severity, hyperglycemia
at time of presentation, history of diabetes, advanced age, and use of high-dose heparin (47).
Given the limited applicability of thrombolysis in AIS dictated by the narrow margin
between reperfusion benefit and hemorrhagic risk, it is hoped that GPIIb/IIIa receptor
antagonists, alone or with reduced doses of thrombolytics, can expand therapy to more
patients with AIS and beyond the 3-h window. Abciximab was demonstrated to be safe
when administered within 24 h of AIS in a small, randomized, double-blind, placebo-con-
trolled, dose-escalation trial. No patient had a major intracranial hemorrhage. Asympto-
matic parenchymal hemorrhagic transformation was noted on surveillance brain CT scans
in 7% (4/54) of abciximab-treated patients and 5% (1/20) of controls at 24–36 h. An addi-
tional six abciximab-treated patients had an asymptomatic hemorrhagic transformation
during follow-up for a total rate of 18% (48). Anecdotally, however, symptomatic parenchy-
mal hemorrhagic transformation can complicate abciximab therapy after acute ischemic
stroke (Figs. 1 and 2). Safety and perhaps efficacy data will be available in late 2002 with
the results of AbESTT, the follow-up randomized, placebo-controlled clinical trial of abci-
ximab in AIS of <6 h duration.
Asymptomatic hemorrhagic transformation was also noted in one-third of 18 patients
who received weight-adjusted intravenous tirofiban for a mean period of 46 h in the setting
of progressing ischemic stroke (48).
Abciximab has been used in several case reports as rescue therapy in the treatment of
acute ischemic stroke failing other chemical and mechanical reperfusion strategies as
well as for reocclusion after initially successful cerebral reperfusion (Figs. 3–8) (50,51).
Of a consecutive series of 49 patients evaluated for intraarterial thrombolysis, 37 patients
were treated with intraarterial tPA, and 24 of them also received eptifibatide in a reduced
regimen of 90 µg/kg bolus and 0.5–2.0 µg/kg/min infusion. The small series suggested that
the combination showed a trend toward improved reperfusion (58% vs 31% TIMI 2+3)
and could rescue resistant reocclusion without an apparent increase in the rate of sympto-
matic or asymptomatic intracranial bleeding (52).
CONCLUSIONS
The challenge of treating coronary artery disease and stroke is often one of maximizing
reperfusion while limiting hemorrhagic complications. The risk of ischemic stoke, largely
cardioembolic in nature, is lessened with those strategies that improve myocardial out-
come while bleeding complications, including hemorrhagic stroke from transformation
of ischemic stroke or primary intracranial hemorrhages, limit the aggressiveness of the
therapies. This complex interplay is illustrated in the shifting risks of stroke subtypes since
the introduction of thrombolysis for AMI.
GPIIb/IIIa receptor inhibitors in combination with aspirin and heparin and even reduced-
dose thrombolytics for coronary interventions appear to be safe, with low rates of stroke.
However, the reported rare cases of intracranial hemorrhage are similar to those seen with
a coagulopathy. At present, there are no reliable means of prospectively identifying those
patients at increased risk for intracranial hemorrhage, although amyloid angiopathy, com-
mon in the very elderly and cognitively impaired, is probably a major determinant (Fig. 9).
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Chapter 20 / Cerebrovascular Aspects of GPIIb/IIIa Receptor Inhibitors 417
Although hemorrhagic transformation of acute ischemic stroke occurs in the absence
of any antiplatelet, anthrombotic, or antifibrinolytic therapy, it is progressively enhanced
with the aggressiveness of such therapies and reduces the risk-to-benefit ratio to a critical
margin. Interventional neurologists will continue to follow in the footsteps of the interven-
tional cardiologists in considering data on stroke risk from large clinical trials of patients
with heart disease and translating them cautiously to smaller clinical trials of patients
with threatened or evolving ischemic stroke.
Fig. 1. Hemorrhagic transformation of acute ischemic stroke associated with abciximab therapy.
Fig. 2. Expansion of hemorrhagic transformation within the first 18 h.
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418 Part IV / Practical Issues and Future Applications
Figs. 3–8. Cerebral angiograms demonstrating left middle cerebral artery occlusion (Fig. 3) with par-
tial reperfusion of perforating lenticulostriate vessels (left, Fig. 4; see below) and middle cerebral
artery branches (right, Fig. 4) after intraarterial infusion of tPA; reocclusion occurred minutes later
(Fig. 5; see opposite page). Reperfusion was finally established after intraarterial abciximab (Fig. 6;
see opposite page and Fig. 7; see p. 420). Vessel patency was documented by CT angiography the fol-
lowing day (Fig. 8; see p. 420).
Fig. 4.
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Chapter 20 / Cerebrovascular Aspects of GPIIb/IIIa Receptor Inhibitors 419
Fig. 5.
Fig. 6.
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