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390 Part IV / Practical Issues and Future Applications
wall, such as adenosine diphosphate, thrombin, and collagen, contributes to the activation
and aggregation of platelets at the stented site.
All parenteral GPIIb/IIIa antagonists (abciximab and small-molecule blockers) have the
ability to suppress platelet recruitment and thereby consequent steps of the cycle. Acti-
vated platelets display on their surface CD40 ligand (CD154), which in turn stimulates
neighboring vascular cells, thus provoking the production of cytokines like IL-1, IL-6,
and MCSF and chemokines like MCP-1. MCSF induces the maturation and activation
of macrophages recruited by MCP-1 and other proinflammatory chemokines and enables
the activated macrophages to kill smooth muscle cells (SMCs), a key step in the process
of plaque destabilization. MCSF binding to its receptor on macrophages appears to func-
tion as a “final common pathway” in the induction of SMC death by activated macrophages,
as many cytokines can induce SMC killing by macrophages, but in a process that requires
the production of MCSF by cytokine-stimulated macrophages.
Such killing of SMCs by activated macrophages is a two-step process mediated through
activation of programmed cell death within SMCs (apoptosis) and requires a functional
CD11b/18 (Mac1), and the death receptor Fas (CD95) on the surface of SMCs. First,
CD11b/18 on the surface of activated macrophages establishes a firm contact with its
adhesive ligands (ICAM1) on the surface of target SMCs. Second, the Fas death pathway
of SMCs is activated by crosslinking of Fas-ligand (CD95-ligand) displayed by macro-
phages. The loss of SMCs triggers a series of reactions, which in turns disturbs the homeo-
stasis of extracellular matrix proteins, the production of metalloproteinases, growth factors
like platelet-derived growth factor (PDGF), and transforming growth factor-β (TGF-β).
The migration and proliferation of residual SMCs are then triggered, resulting in substan-
tial remodeling of the vascular wall. Abciximab, with its blocking activity toward CD11b/
18 and α
v
β
3
, can affect the vicious cycle at two additional strategic points (Fig. 3). Such
Fig. 4. Apoptotic index for combination of vascular smooth muscle cells, monocytes, and monocyte
colony-stimulating factor (mono-MCSF) and with addition of ReoPro (abciximab), eptifibatide, tiro-
fiban, or the human monoclonal antibody to CD11b/18, CD18. Both ReoPro and CD18 provide pro-
tection (reduction in vascular smooth muscle cell death) in physiologic concentrations.
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Chapter 18 / Effects Beyond the Platelet 391
a pleiotropic effect of abciximab on the vicious cycle may explain its superior impact on
survival post PCI, compared with small-molecule inhibitors of GPIIb/IIIa.
The non-GPIIb/IIIa receptor-mediated antiinflammatory, cytoprotective effects of abci-
ximab could thus confer late clinical stability.
PREDICTING LATE SURVIVAL
As stated previously, the completed pooled analysis of the EPIC, EPILOG, and EPISTENT
trials demonstrated a statistically significant 22% reduction in mortality at 3 yr following
PCI in those patients who received abciximab (vs placebo). A multivariate proportional
hazards model was developed using a step-down procedure on available baseline clinical
characteristics from patients included in this pooled analysis to identify factors associated
with increased risk of death to 3-yr follow-up. The minimum p value required for reten-
tion of individual variables in the model was 0.05. Variables found to be statistically sig-
nificantly associated with risk of death in late follow-up included age, diabetes mellitus,
history of congestive heart failure, history of prior coronary artery bypass grafting, history
of smoking (defined as current smoker or quit <1 yr), history of hypertension, history of
clinical peripheral vascular disease, creatinine, and history of prior myocardial infarction
Fig. 5. Cycle of thrombosis and inflammation induced by percutaneous coronary intervention (PCI)
and acute coronary syndrome (ACS). Spontaneous or induced (PCI) disruption of coronary plaque
triggers a cascade of molecular reactions that culminate with the recruitment of platelets, activation
of macrophages, death or smooth muscle cells (SMCs), and remodeling of the vessel wall. Parenteral
GPIIb/IIIa blockers (eptifibatide, tirofiban, HCl, and abciximab) suppress the platelet contribution
to this cycle. As a consequence of thrombosis and inflammation, cytokines and chemokines are pro-
duced [interleukin-1 (IL-1), IL-6, and monocyte chemoattractant protein-1 (MCP-1)]. Monocytes and
macrophages secrete macrophage colony stimulating factor (M-CSF), which enables macrophages to
bind SMCs, via their CD11b/18 (Mac1) receptor, and to induce apoptosis through the Fas cell death
pathway. Abciximab can impact on this cycle at the binding of macrophage Mac1 to adhesive
ligands on SMCs [such as intercellular adhesion molecule (ICAM1)] and on the migration of SMCs,
which requires the activity of the α
V
β
3
receptor. ECM, extracellular matrix; PDGF, platelet-derived
growth factor; TGFβ, transforming growth factor β.
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392 Part IV / Practical Issues and Future Applications
(Table 1). Patients were stratified into tertiles of risk using the simple arithmetic sum of
coefficients for those clinical variables found to be associated with mortality to 3-yr
follow-up. Using simple tertiles, those patients at lowest risk had a coefficient sum of
<3.5, those at moderate risk had a sum of 3.5–4.1, and those in the highest risk tertile had
sums >4.1. Mortality at 3 yr by risk tertile using this model is depicted in Fig. 6.
No survival advantage is demonstrated for abciximab in the lowest risk tertile. Patients
in the moderate risk tertile manifest a 1.1% (absolute) reduction in mortality, and those
in the highest risk tertile were observed to have a 2.7% (absolute) reduction in mortality
to 3 yr. Again, the lack of correlation between early platelet-mediated MACE ischemic
Table 1
Multivariate Regression for Variables Associated with Mortality to 3 Years
Variable analyzed Coefficient SD p value
Diabetes mellitus 0.426 0.086 <0.001
Age 0.049 0.004 <0.001
History of congestive
heart failure 0.859 0.104 <0.001
Previous coronary
artery bypass graft 0.570 0.094 <0.001
Smoker 0.460 0.094 <0.001
History of hypertension 0.246 0.085 0.002
History of peripheral
vascular disease 0.290 0.113 0.007
Previous myocardial
infarction 0.200 0.082 0.010
Creatinine 0.236 0.080 0.007
Fig. 6. Mortality to 3 yr by pharmacologic treatment strategy (intention to treat) and tertile of risk
profile using multivariate regression model.
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Chapter 18 / Effects Beyond the Platelet 393
outcomes and late survival is illustrated by the relationship between the similar primary
composite clinical endpoint for each trial (death, myocardial infarction, and urgent revas-
cularization to 30 d) by randomly allocated pharmacologic treatment regimen and risk
tertile (Fig. 7). Those patients in the lowest risk tertile who derived no survival benefit to
3 yr from abciximab administration demonstrated the greatest relative magnitude of reduc-
tion (57%) in primary endpoint events, whereas those patients in the highest risk tertile
who derived the greatest magnitude of reduction in mortality to 3-yr follow-up had the
least magnitude (44%) reduction in the same primary endpoint events at 30 d. This relation-
ship (between early MACE and late survival) again underscores the fact that late survival
benefit was not accurately reflected in the magnitude of early primary endpoint reduction.
CONCLUSIONS
Although this class of new therapeutic agents has been simplistically defined by a com-
mon affinity for the platelet GPIIb/IIIa receptor, important differences exist between
members of this class with respect to pharmacokinetic and pharmacodynamic profiles,
specific binding sites on the GPIIb/IIIa receptor, and differential receptor affinities (40).
The affinity of abciximab for the α
v
β
3
and CD11b/18 receptors coupled with the phenome-
non of pharmacodynamic gradual redistribution may contribute to a profound and sustained
antiinflammatory effect of this agent. Late myocardial cell death (apoptosis) engendered
by the inflammatory response that follows PCI and that appears to be mediated by MCSF
and macrophages may be prevented by the specific affinity of abciximab for the CD11b/
18 receptor. These non-GPIIb/IIIa receptor activities of abciximab are distinct from its
platelet-inhibitory effects and yet probably contribute to specific and preferential plaque
stabilization and enhanced late survival following administration of this agent.
Fig. 7. Composite clinical primary endpoint (death, myocardial infarction, or requirement for urgent
coronary revascularization) by pharmacologic treatment regimen (intention to treat) and tertile of
risk profile. Patients in the lowest risk tertile manifest the greatest relative reduction in early (30-d)
primary endpoint events despite absence of a survival advantage in favor of abciximab, as noted pre-
viously (Fig. 5).
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394 Part IV / Practical Issues and Future Applications
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Chapter 19 / Cerebrovascular Interventions 397
397
From: Contemporary Cardiology: Platelet Glycoprotein IIb/IIIa
Inhibitors in Cardiovascular Disease, 2nd Edition
Edited by: A. M. Lincoff © Humana Press Inc., Totowa, NJ
19 Cerebrovascular Interventions
CONTENTS
INTRODUCTION
CAROTID STENTING
ADJUNCTIVE THERAPY: ASPIRIN AND THIENOPYRIDINES
ADJUNCTIVE THERAPY: GPIIb/IIIa INHIBITORS
EMBOLI PROTECTION DEVICES
CONCLUSIONS
REFERENCES
Leslie Cho, MD and Jay S. Yadav, MD
INTRODUCTION
Carotid angioplasty was first proposed by Mathias in 1997 (1), and in 1980 both Kerber
et al. (2) and Mullan et al. (3) published case reports of successful carotid angioplasty
during carotid endarterectomy. A percutaneous carotid intervention offers several advan-
tages to surgery. It eliminates the potential risk of general anesthesia and surgical compli-
cations of endarterectomy, such as neck hematoma, infection, cervical strain, and cranial
nerve damage. Also, high-risk patients such as those with previous ipsilateral carotid end-
arterectomy, previous radiation therapy to the neck or previous neck surgery, contralateral
carotid occlusion, lesions above the mandible or below the clavicle, or neurologic instabil-
ity, with coexistent coronary or pulmonary disease may be treated (4). Although percuta-
neous transcatheter techniques have been widely accepted in other vascular areas, they
have met with tempered enthusiasm in the carotid arteries owing to the fear of cerebral
embolism. However, the recent rapid growth of new technologic advances has aroused
greater interest in the endovascular procedures.
CAROTID STENTING (TABLE 1)
In 1987, Theron et al. (5) published the first small series of internal carotid angioplas-
ties. With the advent of the stent, multiple reports of carotid stenting have been published
(Table 1).
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398 Part IV / Practical Issues and Future Applications
Table 1
Carotid Stent Studies
Stroke
30-d stroke 30-d MI 30-d death Follow-up after 30 d Emboli
Study Lesion Success (%) (%) (%) (mo) (%) protection
Diethrich et al. (7) 117 116 8.3 0.0 0.9 7.6 2 (no.) None
Henry et al. (9) 174 173 2.9 0.0 0.0 12.7 0.0 None
Laborde (26) 87 87 5.3 0.0 1.1 8.7 1.1 None
Wholey et al. (10) 114 108 3.5 0.9 1.9 6 0.0 None
Shawl (25) 96 96 3.1 0.0 0.0 8 0.0 None
Yadav et al. (6) 126 126 6.3 0.0 0.8 6 0.0 None
Global Exp (10) 3129 3091 3.9 2.0 6 0.7 None
Roubin et al. (11) 604 592 5.8 1.3 36 0.6 None
CAVATAS (12) 251 213 8.0 2 36 None
Henry et al. (21) 270 1.5 0.0 6 PercuSurge
Tubler et al. (22) 58 58 5.2 0.0 PercuSurge
Reimer et al. (24) 88 86 1.2 2.3 0.0 Filter
CAFÉ-USA (27) 212 207 2.4 1.4 Distal balloon
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Chapter 19 / Cerebrovascular Interventions 399
Yadav et al. (6) published their initial experience of carotid stenting in 107 consecutive
patients. There was a 100% procedural success rate. Periprocedural complications included
one stent thrombosis, six minor strokes, and one major stroke. The incidence of combined
endpoint of all strokes and death was 7.9%, with 1.6% ipsilateral major stroke and death.
Of 107 patients, 76% underwent repeat angiography or ultrasound evaluation at 6 mo fol-
lowing stenting. There was 4.9% asymptomatic restenosis. At 6 mo, there were no addi-
tional strokes or deaths from cerebrovascular disease. These initial carotid stents were
performed in a high-risk cohort and represent the early learning curve years for percu-
taneous carotid intervention.
Diethrich et al. (7) have also reported their experience in 110 patients with severe caro-
tid stenosis. They reported a 99% procedural success rate with 6.4% stroke (two major and
five minor), 4.5% transient ischemic attack (TIA), and two asymptomatic stent occlusion
in the first 30 d. During 7.6-mo follow-up, no additional neurologic events were reported.
Wholey et al. (8) reported on their carotid stenting experience in 114 lesions in 108 con-
secutive patients with severe stenosis. The total stroke or death rate at 30 d was 5.3%. There
were no neurologic sequelae, cranial nerve palsies, or cases of stent or vessel thrombosis
at follow-up. However, there was one case of restenosis owing to stent compression. In
addition, Henry et al. (9) have published their experience of 174 carotid stenting proce-
dures. Unlike other studies, a small portion of the patients in this study had a cerebral emboli
protection device. There was a 99.4% procedural success rate with a 4.6% (eight patients)
periprocedural neurologic complication rate. Of these, three were TIAs, two were minor
strokes, and three were major strokes. Two major complications were seen in the patients
with emboli protection devices. Over a 1-yr follow-up, there was a 2.3% restenosis rate
with no ipsilateral neurologic complications.
Wholey et al. (10) published the global experience of carotid stent placement. They
surveyed 36 centers that performed 5210 procedures in 2757 patients. Even though com-
parative analysis of these centers is made difficult by the different patient populations,
lesion characteristics, endovascular techniques, and follow-up data, this review under-
scores the safety of carotid stenting in the hands of experienced operators. They reported
a 98.4% procedural success rate, with technical success defined as <30% residual steno-
sis covering a region longer than the original lesion without any alteration of intracranial
arterial anatomy. Various different stents were used depending on the availability and oper-
ator preferences. In most of these patients, no emboli protection device was used. There were
2.8% reported TIAs. Minor strokes were defined as new neurologic events that resulted
in functional impairment that either completely resolved within 7 d or caused an increase
in the National Institutes of Health (NIH) stroke scale of <4. Minor stroke rate was 2.7%.
A major stroke was defined as a new neurologic deficit that persisted after 7 d and increased
the NIH stroke scale by 4 or more. Major stroke rates were 1.5%, and procedure-related
mortality at 3 d was 0.96%. There was a restenosis rate of 2.3% and a stent deformation rate
of 2.5%.
Recently, Roubin et al. (11) reported a 5-yr prospective analysis of immediate and late
clinical outcomes in carotid artery stenting in patients with symptomatic and asymptoma-
tic carotid artery stenosis. In 528 consecutive patients undergoing percutaneous carotid
intervention, they reported a procedural success rate of 98%, with a 0.6% fatal stroke rate
and a 1% nonstroke death rate at 30 d (11). In this study, 83% patients were ineligible for
carotid endarterectomy according to the NASCET trial. The major stroke rate was 1% and
the minor stroke rate was 4.8%. The overall 3-d stroke and death rate was 7.4%. After
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