Profiles in Peripheral Arterial Disease
Christopher J. White
Stephen R. Ramee
STROKE INTERVENTION
Early reperfusion therapy for acute stroke, similar to that for acute myocardial infarction, offers the best opportunity to reduce the significant morbidity and mortality. Treatment options include intravenous (IV) thrombolysis therapy and/or catheter-based therapy (CBT). Catheter-based therapies include local, intra-arterial administration of thrombolytic agents, mechanical thrombectomy, and percutaneous transluminal angioplasty (PTA) and stent techniques.
Fewer than 2% of acute stroke patients receive any form of reperfusion therapy, and sadly, little is being done to remedy this problem.1 Acute ischemic stroke is a leading cause of death and disability that will affect three-quarters of a million Americans this year.2,3 The therapeutic goal of acute stroke therapy, as with acute myocardial infarction (AMI) therapy, is early reperfusion to minimize end-organ damage. Frustratingly, even among the select centers participating in the Get With The Guidelines-Stroke (GWTG-Stroke) registry, fewer than one-third meet the goal of “door to needle time” of ≤60 minutes.4
While the national quality mandate for a 90 minute doorto-balloon time (D2B) has revolutionized AMI care,5 there are few hospitals offering “on-demand” catheter-based stroke therapy. Despite the fact that many acute stroke patients present too late (>3 to 4.5 hours) or are poor candidates for IV thrombolysis, many remain eligible for catheter-based reperfusion therapy.6, 7, 8
The nationwide shortage of interventional neuroradiologists is a significant barrier to providing on-demand stroke reperfusion treatment.9 One solution would be to expand the pool of stroke interventionalists by recruiting carotid artery stent (CAS)-capable physicians, that is, cardiologists, radiologists, vascular surgeons, and neurosurgeons, to join stroke teams.8,10,11 CAS-capable interventionalists, neurointerventionalists, and neurologists should be working together to build stroke teams.7,8,10, 11, 12
Ten years ago, the National Institute of Neurological Disorders and Stroke (NINDS) rt-PA Study Group’s randomized trial compared intravenous thrombolysis to placebo therapy in patients presenting within 3 hours of stroke onset and demonstrated a statistically significant but clinically modest benefit for this relatively small subset of acute stroke patients.13 The NINDS trial found no difference between the two groups’ neurological outcomes at 24 hours, but there was a tenfold higher (6.4% rt-PA versus 0.6% placebo, P < 0.001) risk of intracranial bleeding with lysis in the rt-PA group. At the 3-month follow-up, a higher percentage of lytic patients (34% lytic versus 21% placebo, P < 0.05) had achieved full recovery. Unfortunately, there was no difference in mortality between the groups. Ten years after the pivotal trial and despite the fact that IV thrombolysis is the only approved therapy for acute ischemic stroke, no more than 2% of ischemic stroke patients actually receive this treatment.1,14
Catheter-based therapy for stroke, like intravenous thrombolysis, is not without risks. Intracranial hemorrhage (symptomatic and asymptomatic) rates of 10% to 35% have been reported.15, 16, 17 Unfortunately, most clinical trials enroll relatively small numbers of patients, providing a small data set upon which to base clinical decision-making. The lack of large clinical trials of acute ischemic stroke treated with CBT makes it difficult to establish guidelines for the “optimal” therapy for stroke.
CASE STUDIES
CASE 46.1
A 79-year-old male was electively admitted with recurrent ventricular tachycardia for an electrophysiologically guided ablation procedure. He had past medical history of nonischemic cardiomyopathy with ejection fraction of 40%, chronic atrial fibrillation, and hypertension. His medications included amiodarone, lisinopril, metoprolol, and warfarin; warfarin had been discontinued 4 days prior to admission.
The day following his ablation procedure, he developed sudden onset of a left middle cerebral artery (MCA) stroke, manifested by right-sided weakness and aphasia. An emergency computerized tomographic (CT) scan of the brain was negative for hemorrhage. His physical examination revealed dense right hemiplegia and expressive aphasia with a score of 14 on the National Institutes of Health Stroke Scale18 (NIHSS; severe impairment).
Within 40 minutes of symptom onset, he was brought to the catheterization laboratory where selective cervical-cerebral angiography was performed from a femoral artery access site. Cerebral angiography demonstrated a large filling defect, consistent with an embolus, in the M2 segment of the left MCA with diminished distal flow (Figure 46.1). The Merci® Retrieval System (Concentric Medical, Mountain View, CA) shown in Figure 46.2 was advanced to engage the embolus (Figure 46.3). The embolus was successfully retrieved, and final angiography revealed a widely patent vessel (Figure 46.4).
The patient immediately began to recover movement of his right arm and leg while on the catheterization table. By the following morning, his speech had normalized. At the time of discharge, 3 days later, his NIHSS score was 3 (minor impairment) with mild weakness of the right arm and leg.
 Figure 46.1 Filling defect in left MCA (arrow) consistent with an embolus. |
CASE 46.2
A 56-year-old woman presented to an outside hospital’s emergency department 1 hour following sudden onset of right-sided weakness and inability to speak. Six months earlier she had undergone successful mechanical mitral valve replacement. Her chronic anticoagulation with warfarin had been discontinued 5 days prior to presentation owing to uterine bleeding.
Her examination was consistent with an acute left MCA stroke. An emergency CT scan showed no intracerebral hemorrhage, and intravenous thrombolysis with 75 mg of tissue plasminogen activator (Alteplase, Genentech, South San Francisco, CA) was initiated. One hour after receiving intravenous thrombolysis she had failed to improve. She was transferred to Ochsner 220 minutes after symptom onset and 150 minutes after receiving full-dose intravenous thrombolysis. She had persistent right hemiplegia, expressive aphasia, and an NIHSS score of 17 (severe impairment).
Emergency cervical-cerebral angiography from the right femoral artery access site revealed occlusion of the superior branch of the MCA at the M1 bifurcation and a subtotal occlusion of the inferior branch (Figure 46.5). A 6F coronary JR-4 guiding catheter (Cordis, Miami Lakes, FL) was placed in the internal carotid artery, and a 0.014 inch coronary angioplasty guidewire (Choice PT, Boston Scientific Corp, Waterville, MA) was advanced across the occluded superior branch of M1. Next, a Merci® delivery microcatheter was advanced distal to the occlusion, and a contrast injection confirmed that the microcatheter was in the vascular lumen (Figure 46.6). Contrast injections through the proximal guiding catheter confirmed that the microcatheter and guidewire passage had disrupted the thrombus and restored antegrade flow in this branch of the MCA. Next, the 0.014 inch guidewire was placed into the inferior limb of M1, and (similar to the superior limb) mechanical disruption of the clot successfully recanalized the vessel obviating the need for mechanical thrombectomy. Final angiography confirmed the patency of both the superior and the inferior limbs of M1 (Figure 46.7).
By the following morning, the patient had significant improvement in her right-side extremity strength, with both upper and lower limbs demonstrating 4/5 strength. She had mild dysarthria but was able to speak. Her NIHSS score had improved to 8 (moderate impairment). Following a course of inpatient rehabilitation she was discharged, and she returned to independent living.
Illustrative Points
Both patients presented with profound neurologic deficits likely to result in severe disability, and both were dramatically improved after CBT reperfusion therapy. Common features associated with stroke lesions include a large clot burden,
organized thrombus, or embolization of atherothrombotic material that may render these intracerebral occlusions less responsive to thrombolysis than acute thrombi associated with myocardial infarction.
organized thrombus, or embolization of atherothrombotic material that may render these intracerebral occlusions less responsive to thrombolysis than acute thrombi associated with myocardial infarction.
 Figure 46.2 The merci concentric retriever system (Concentric Medical, Mountain View, CA). |
It is important to recognize the similarities and understand the fundamental differences between ischemic stroke and heart attack. Both represent ischemic events, but heart attack is usually the result of plaque rupture and in-situ thrombosis, whereas ischemic strokes more often result from atherothrombotic embolism.19 The treatment goal for both is safe and rapid reperfusion in order to restore blood flow to the ischemic tissue.
Our second case involved CBT as “rescue” therapy after failure to respond to intravenous thrombolytic therapy. Despite her early presentation, lytic therapy was not successful. Data from NINDS suggest that thrombolytic failure is not infrequent20 and that large vessel occlusions are less likely to recanalize with lytic therapy alone.21,22 Catheter-based therapy with adjunctive mechanical thrombectomy or mechanical clot disruption with angioplasty techniques offers the potential for successfully opening occlusions resistant to thrombolysis.
 Figure 46.3 The retrieval catheter (Retriever, Concentric Medical, Mountain View, CA) engaged in left MCA embolus (arrow). |
CBT has become the treatment of choice for large disabling strokes within 6 hours of onset, in patients who are not candidates for IV thrombolytic therapy. With proper patient selection and technique, the outcome of CBT patients who are not candidates for lysis can be as good as that of patients who receive lysis. Recent data has suggested that CBT for large-vessel strokes can be performed by experienced cardiologists working with neurologists and/or neuroradiologists. It is important to remember that the anatomy, pathology, and treatment of acute stroke are different from those of AMI. Intracranial hemorrhage, the most common serious complication of stroke intervention, is usually fatal if it occurs in this setting.
 Figure 46.4 Cerebral angiography following removal of the embolus with restored patency of MCA (arrow). |
 Figure 46.5 A filling defect is seen at the first MCA bifurcation with occlusion of superior branch and decreased flow in the inferior branch of the bifurcation (arrow). |
 Figure 46.7 Final angiogram after mechanical disruption of the embolus with restoration of normal flow in both superior and inferior branches of the MCA (arrows). |
 Figure 46.6 Microcatheter placed distal to superior MCA bifurcation obstruction confirming the intraluminal position of the catheter and distal patency of the artery (arrow). |
Both cases highlight the magnitude of benefit that can result from CBT in patients with disabling stroke. With the support of a multidisciplinary and cooperative stroke team, qualified physicians can effectively supplement the severe work force shortage of neurointerventionalists.
ELECTIVE INTRACRANIAL ANGIOPLASTY
Approximately 1 in 10 strokes is owing to intracranial atherosclerotic disease,23 with a higher incidence of the latter seen in Asians24 and African Americans.25 The initial treatment for patients with symptomatic >50% intracranial artery stenoses (IAS) is antithrombotic therapy.26
The Warfarin-Aspirin Symptomatic Intracranial Disease (WASID) trial demonstrated that aspirin was the preferred initial therapy over warfarin owing to an increase in adverse events with warfarin. In the WASID trial, 18% of patients had a recurrent stroke within 18 months despite “best” medical therapy, and of these strokes the majority (73%) occurred in the same territory as that of the previous stroke and almost half were disabling.27 In the Groupe d’Etude des Stenoses Intra-Craniennes Atheromateuses symptomatiques (GESICA) study, symptomatic patients had a 38% risk of a transient ischemic attack (TIA) or stroke at 2 years of follow-up. Surgical extracranial-to-intracranial (EC-IC) bypass failed to reduce the rates of recurrent stroke, and this approach has been abandoned.28
Patients with symptomatic IAS on anti-thrombotic therapy have a 2-year risk that ranges from 1:5 to 1:2 for recurrent stroke.26,29,30 Because of these very high recurrent stroke rates despite “best” medical therapy and the failure of surgical options, the use of catheter-based therapies has been explored.31 Early case reports and single-center series have suggested the safety and efficacy of intracranial angioplasty with or without stent placement.12,32,33
The continuous development of smaller, more flexible, and more deliverable interventional equipment has improved our access to intracranial lesions and lessened the technical challenges associated with intracranial CBT. Three stent systems are currently FDA approved for intracranial use: (i) Neuroform (Boston Scientific, Natick, MA), (ii) Wingspan (Boston Scientific, Natick, MA), and (iii) Enterprise (Codman Neurovascular/Cordis, Raynham, MA). The periprocedural risks of stroke or death with intracranial CBT have averaged about 10% (116/1138) across multiple series34, 35, 36, 37, 38, 39, 40, 41, 42 with a median of 7.7% reported in a systematic review of 1,177 published procedures.43 A drawback of current stent devices used for IAS is the reported in-stent restenosis (ISR) incidence of 25% to 35%.44
Our experience at the Ochsner Clinic Foundation with CBT in 89 symptomatic patients with 99 (≥70% diameter) IAS treated by interventional cardiologists in cooperation with their neurology and neuroradiology colleagues has demonstrated a procedure success rate of 96/99 (97%) of the lesions and a rate of in-hospital periprocedural stroke and/or death of 3%. Our 1-year (5.7%) and 2-year (13.5%) risk of stroke or vascular death compares very favorably with the results of “best” medical therapy reported in the WASID trial of 15% at 1 year and 20% at 2 years.26
A recent setback for CBT in symptomatic IAS patients was the publication of the Stenting and Aggressive Medical Management for Preventing Recurrent stroke in Intracranial Stenosis (SAMMPRIS) clinical trial (gov number NCT00576693). This trial compared intracranial primary stenting performed by neuroradiologists to medial therapy, and was stopped early for safety reasons. After 451 patients underwent randomization, the 30-day rate of stroke or death was 14.7% in the CBT group and 5.8% in the medical-management group45 (P = 0.002). Several significant concerns have been raised about the quality of data in this trial, and perhaps some methodological shortcomings that led to such very high periprocedural complication rates include (i) the choice of self-expanding stents (Wingspan, Boston Scientific, Watertown, MA), (ii) prohibition of poststent dilation, and (iii) a concern over the clinical skills of the operators.46
The natural history of patients with severe symptomatic IAS who have failed antithrombotic therapy is not very encouraging, and the relatively low complication rate for CBT in experienced hands makes it a reasonable alternative. However, the recent publication of the large, randomized SAMMPRIS trial should give us reason to redefine our patient selection criteria, rethink stent placement, reevaluate who performs the procedure and include high-volume coronary interventionalists, and refine the procedural techniques to minimize periprocedural complications.
Ultimately, the decision to proceed with CBT for symptomatic IAS patients requires balancing the procedure risks with the natural history of the disease on a case-by-case basis. Patients at the highest risk for recurrent stroke should be selected by lesion severity, lesion location, and documented failure of antithrombotic therapy. The natural history of such patients suggests that the recurrent stroke rates are high (20 to 55%), especially for restenoses29 (>70%). There is a need for newer, more flexible, self-expanding stents with better coverage and radial force and perhaps a role for drug-coated coronary balloons to improve the outcome of angioplasty in the intracranial circulation.
CASE 46.3
This 35-year-old woman presented with a 2-month history of left hemispheric stroke manifested by aphasia and right-side weakness. After her stroke, she sustained three more transient episodes of right-side weakness and aphasia, consistent with TIAs in the same distribution. Magnetic resonance imaging (MRI) revealed a stroke in the left MCA distribution, and magnetic resonance angiography (MRA) showed high-grade bilateral stenosis. Her exam was remarkable for expressive aphasia. She was referred by neurology for angiography and treatment.
Four-vessel selective cerebral angiography was performed using a 4F Berenstein catheter. This revealed a critical left MCA stenosis in the most proximal segment (M1; Figure 46.8A) and a normal right MCA (in contradiction to the MRA findings). There were no collaterals from the vertebral artery, indicating an absence of the left posterior communicating artery.
Intervention was performed with a 6F multipurpose coronary guiding catheter placed into the distal extracranial left internal carotid artery (ICA) just below the base of the skull. Using digital subtraction angiography with road mapping, a hydrophilic coronary guidewire (Whisper™ wire) was advanced across the critical stenosis in the left MCA. The lesion was dilated with a 2.0 × 15 mm coronary balloon at 10 atmospheres (atm). Angiography revealed an excellent balloon result, so the guidewire was removed and angiography was repeated. Because of a small dissection at the site of the lesion (Figure 46.8B), we attempted to advance a coronary stent; however, this would not traverse the bony intracranial portion of the ICA and the procedure was terminated. The patient’s aphasia improved but did not resolve completely by the morning after the procedure, and she was discharged on ASA and clopidogrel.
CASE 46.4
This 63-year-old female patient was referred by her neurologist because of recurrent episodes of dizziness, weakness, and diplopia 10 days after suffering a posterior circulation stroke. Her exam was consistent with a cerebellar stroke (unable to stand, diplopia, and weakness). MRI
showed pontine and basal ganglia infarctions with ischemia in the visual cortex. MRA revealed high-grade stenosis of the basilar artery.
showed pontine and basal ganglia infarctions with ischemia in the visual cortex. MRA revealed high-grade stenosis of the basilar artery.
 Figure 46.8 A. Critical stenosis (arrow) of the left M1 segment of the middle cerebral artery. B. After balloon angioplasty, there is a small dissection that does not appear to be flow-limiting. The small superior side branches arising from the M1 segment are the lenticulostriate arteries. Occlusion of these small end arteries by stenting can lead to a large stroke. |
After premedication with aspirin and a clopidogrel loading dose of 300 mg, vertebrobasilar angiography was performed with a 6F headhunter catheter, demonstrating critical stenosis of the mid-basilar artery (Figure 46.9) with a stenosis in the V4 segment (intracranial portion) of the left vertebral artery.
Intervention was performed with a 6F Soft-tipped (Envoy, Cordis Corp, Miami, FL) guiding catheter and a hydrophilic coronary wire (Choice PT floppy). A Rapid Transit catheter (Cordis) was advanced distal to the lesion over the hydrophilic wire, which was exchanged for a balanced middleweight (BMW, Abbott) coronary guidewire. The basilar artery stenosis was dilated with a 3.0 mm × 15 mm coronary balloon at 8 atm. Post-PTA angiography demonstrated 20% residual stenosis (Figure 46.9B). Stenting was not performed because of the risk of embolizing or “snow-plowing” atheromatous debris into the pontine branches that arise from the basilar artery at the stenosis. The patient had no subsequent events and remained asymptomatic at 2-year follow-up.
Illustrative Points
Intracranial intervention, both elective and emergency, is a field in its early development where collaboration between neurology, neuroradiology, and cardiology is important. These cases illustrate how patients with recurrent focal symptoms may benefit from angiography and intervention even if the duplex examination shows no cervical carotid stenosis. Lesions of the aorto-ostial common carotid artery and the intracranial carotid or vertebral arteries can be missed by carotid duplex examination.
CTA and MRA may also under- or overestimate the percent diameter stenosis, so invasive digital subtraction angiography remains the gold standard. Stenting is performed in a provisional manner because (i) many intracranial lesions are not stentable with current devices because of tortuosity in the target vessel, and (ii) side-branch occlusion of the small branches, especially of MCA (lenticulostriate arteries) and the basilar artery (pontine perforators), can lead to a major stroke, which may be more likely with stents than with PTA alone.
AORTIC ARCH AND CERVICAL VESSELS
Extracranial Carotid Artery Intervention
The majority of patients with internal carotid atherosclerotic narrowing are asymptomatic. The annual risk of stroke is between 1% and 4.3% for asymptomatic patients with ≥50% stenosis of the carotid artery.47,48 If there is plaque ulceration, the risk of stroke, in asymptomatic patients, increases to 7.5% per year. Symptomatic patients have a worse prognosis as compared to asymptomatic patients.
A transient ischemic attack (TIA), defined in the past as a neurologic event lasting <24 hours, predicted a 15% risk of stroke at 1 month and a 30% risk of TIA, stroke or death within 3 months.49,50
A transient ischemic attack (TIA), defined in the past as a neurologic event lasting <24 hours, predicted a 15% risk of stroke at 1 month and a 30% risk of TIA, stroke or death within 3 months.49,50
 Figure 46.9 A. Intracranial angioplasty. Critical stenosis in the basilar artery located just distal to the anterior inferior cerebellar artery (arrow). B. Angiogram after balloon angioplasty with a coronary system, showing significant improvement. |
Large randomized trials begun in the 1990s demonstrated superiority of carotid endarterectomy (CEA) versus antiplatelet therapy (aspirin) for stroke prevention in both symptomatic and asymptomatic patients.51, 52, 53, 54 Symptomatic patients have much more to gain from revascularization than do asymptomatic patients. This places a premium on reducing perioperative stroke and death to less than 3% in asymptomatic patients who are likely to live for 5 years. For symptomatic patients there was greater benefit with increasing severity of the stenosis above 50% diameter stenosis. However, in asymptomatic patients, the benefit was equal for moderate (60% to 79%) or severe (80% to 99%) lesions.55 There is a paradox, however, for very tight lesions, or near-occlusions, defined in the European Carotid Surgery Trial (ECST) as a severe stenosis with evidence of reduced flow in the distal carotid artery and evidence of narrowing of the poststenotic carotid artery. These patients did not benefit from CEA.53,56
Carotid artery stenting with embolic protection devices began with registry trials in the late 1990s in patients considered to be at increased risk for CEA57, 58, 59, 60, 61, 62, 63, 64, 65 (Table 46.1). The Stenting and Angioplasty with Protection in Patients at High
risk for Endarterectomy (SAPPHIRE) trial is the only randomized multicenter trial comparing CEA and CAS in patients at increased risk for surgery.66 The 1-year primary endpoint for CEA was 20.1% and 12.2% for CAS (ARR 7.9%, 95% CI: 16.4% to 0.7%, P = 0.004 for noninferiority). Multiple registry trials to obtain FDA approval for CAS systems have shown continued improvement in outcomes with increasing experience (Figure 46.10). Currently, CAS is the preferred therapy for high surgical risk patients who require revascularization to prevent stroke and who have suitable anatomy for CAS (Table 46.2).
risk for Endarterectomy (SAPPHIRE) trial is the only randomized multicenter trial comparing CEA and CAS in patients at increased risk for surgery.66 The 1-year primary endpoint for CEA was 20.1% and 12.2% for CAS (ARR 7.9%, 95% CI: 16.4% to 0.7%, P = 0.004 for noninferiority). Multiple registry trials to obtain FDA approval for CAS systems have shown continued improvement in outcomes with increasing experience (Figure 46.10). Currently, CAS is the preferred therapy for high surgical risk patients who require revascularization to prevent stroke and who have suitable anatomy for CAS (Table 46.2).
Table 46.1 Features that Increase the Risk of Carotid Endarterectomy (CEA) | ||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
|
High cervical or intrathoracic lesion
Age ≥80 y
Prior radical neck surgery or radiation
Class III/IV congestive heart failure
Contralateral carotid artery occlusion
Class III/IV angina pectoris
Prior ipsilateral CEA
Left main coronary disease
Contralateral laryngeal nerve palsy
Multivessel coronary artery disease
Tracheostoma
Planned surgery (<30 days)
LV ejection fraction ≤ 30%
Recent (≤30 d) myocardial infarction
Severe lung disease
Severe renal disease Figure 46.10 Multiple registry trials to obtain FDA approval of CAS systems have shown continued improvement in outcomes with increasing experience. |
Four large randomized controlled trials have recently compared CAS to CEA in usual or average surgical risk patients. Three European trials [SPACE,67 EVA-3S,68 and ICSS69] enrolled symptomatic patients with inexperienced CAS operators and who had no requirement for embolic protection devices (EPD). The largest randomized trial to compare CEA to CAS was the Carotid Revascularization Endarterectomy and Stenting Trial (CREST), which was based in the United States and Canada.70 CREST required stent operators to qualify by experience to gain entry into the trial, required that EPDs be used, and enrolled both symptomatic and asymptomatic patients. CREST enrolled 2,502 average surgical risk symptomatic (53%) and asymptomatic (47%) patients. Patients were followed out up to 4 years without any difference in the rates of the primary endpoint between CAS (7.2%) and CEA (6.8%) with a hazard ratio of 1.11 (95% CI: 0.81 to 1.51; P = 0.51). There
was an excess of minor strokes with CAS (4.1%) as compared to CEA (2.3%), but there was no difference in major strokes (CAS 0.9% versus CEA 0.7%). The CEA group had twice as many MIs (2.3%) as compared to CAS (1.1%). Cranial nerve palsy occurred in 4.8% of the CEA patients. There was an age effect with younger patients (<69 years) doing better with CAS and older patients doing better with CEA. The recent multisociety guideline document has endorsed CAS as Level I indication for usual-risk symptomatic patients.71
was an excess of minor strokes with CAS (4.1%) as compared to CEA (2.3%), but there was no difference in major strokes (CAS 0.9% versus CEA 0.7%). The CEA group had twice as many MIs (2.3%) as compared to CAS (1.1%). Cranial nerve palsy occurred in 4.8% of the CEA patients. There was an age effect with younger patients (<69 years) doing better with CAS and older patients doing better with CEA. The recent multisociety guideline document has endorsed CAS as Level I indication for usual-risk symptomatic patients.71
Table 46.2 Features that Increase the Risk of Carotid Stenting (CAS) | |||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
|
Age ≥80 y
Complex aortic arch
Operator inexperience
Symptomatic
Tortuosity
No emboli protection device
Decreased cerebral reserve
Calcification
Time delay from symptom onset
Hypercoagulable state
Intraluminal thrombus
Open cell stents
Severe renal disease
Echo lucent plaque
Vascular access difficulty
Increased bleeding riskCASE 46.5
This 80-year-old woman presented with right hemispheric TIAs manifested by left-sided weakness. She had a history of hyperlipidemia, three-vessel coronary artery disease, a permanent pacemaker, and prior coronary stenting. At the time of evaluation she had stable angina with exertion. Her physical examination was remarkable for a loud right carotid bruit and a normal neurologic exam. A carotid duplex examination revealed 80% to 99% stenosis of the right internal carotid artery (ICA) and 40% to 59% stenosis of the left ICA. Carotid angiography confirmed a severe (90%) right ICA stenosis (Figure 46.11A) and a mild (50%) left ICA stenosis. Vertebral angiography was unremarkable. She was referred for carotid angioplasty and stenting. Because of her age, she was considered as high-risk for CEA, and with a >70% symptomatic stenosis, she met Medicare appropriateness criteria for CAS.
 Figure 46.11 A. A lateral digital subtraction angiogram of the common carotid artery and its branches demonstrates minor plaquing in the common carotid just before the bifurcation and critical stenosis of the right internal carotid artery 1.0 cm beyond the bifurcation. B. After stenting, there is still 10% to 20% residual stenosis in the internal carotid artery. Aggressive dilating and trying to achieve a perfect result is not recommended because of the risk of distal embolization and stroke. |
After pretreatment with aspirin (81 mg/day) and clopidogrel (75 mg/day) for at least a week prior to the procedure, she was brought to the catheterization laboratory. Right common femoral access was obtained, and she was administered 5,000 Units of intra-arterial heparin. A 5F Vitek catheter was placed into the innominate artery and advanced over an extra stiff 0.035 inch Glidewire (Terumo) into the right common carotid artery, and then over the Glidewire it was placed into the right external carotid artery. The Glidewire was exchanged for an extra stiff 0.035 inch Amplatz exchange wire, and a 6F Shuttle sheath (Cook) was advanced into the right
common carotid artery. Her activated clotting time (ACT) was 275 seconds.
common carotid artery. Her activated clotting time (ACT) was 275 seconds.
An angiographic roadmap was made using digital subtraction and a 12 inch image intensifier. AP and Lateral views were obtained of the common carotid bifurcation and the right cerebral circulation. The right internal carotid artery lesion was crossed with an AngioGuard distal protection device (Cordis), and the lesion was predilated with a 4.0 × 30 mm balloon. During the inflation, the patient developed transient bradycardia and hypotension, which resolved after balloon deflation. Prior to stent deployment she was pretreated with 1.0 mg of atropine. A 9.0 × 40 mm self-expanding nitinol stent was then deployed across the carotid bifurcation. The stent was postdilated to 8 atm with a 5.0 × 20 mm balloon, and the patient again developed bradycardia and hypotension that required treatment with neosynephrine and 250 mL of saline intravenously. The distal protection device was retrieved, and final angiography was performed, including AP and lateral views of the cerebral circulation. There was <30% residual stenosis at the angioplasty site (Figure 46.11B).
After the procedure, she again developed transient hypotension that responded to volume expansion, atropine, and neosynephrine. Oral midodrine was begun in the recovery room. Her neurological exam was normal; the patient was discharged the next morning and the midodrine was tapered over 4 days. She remained asymptomatic and had no evidence of restenosis at 1 year by carotid duplex examination.
Illustrative Points
For symptomatic (>50%) and asymptomatic (>70% to 80%) carotid stenosis there are seven CAS systems approved for use by the FDA for high surgical risk patients and one CAS system, for usual surgical risk patients. The most recent multisocietal guideline document makes CAS the preferred treatment for selected high surgical risk patients and a Level I indication for symptomatic >50% diameter stenosis patients.
Self-expanding stents with embolic protection devices are preferred for the carotid bifurcation because of the risk of crushing associated with balloon expandable stents. These stents can be delivered through either a 6F sheath or an 8F guiding catheter. There seems to be no evidence favoring one type of stent over another—closed-cell versus open-cell or stainless steel versus nitinol. There are no data supporting the use of “tapered” stents over nontapered stents in the carotid artery. The choice of delivery mode depends upon the operator’s preference and the presence or absence of tortuosity in the common carotid artery. The nonkinking 6F sheaths have an outer diameter approximately the same as that of an 8F guiding catheter, so the size of the access site hole is similar for both.
The emergence of proximal protection devices has raised the bar for embolic protection. Comparative studies demonstrate less evidence of cerebral embolism with proximal protection systems as compared to distal filters, but proximal protection systems increase the complexity of the case, while filters are very user friendly.72
Unlike in coronary artery stenting, the goal is not a perfect angiographic result after carotid stenting. The main risk of this carotid intervention is distal embolization because of the large plaque burden, so great care is taken not to overdilate the carotid plaque any more than is necessary to achieve a <30% lesion. Many operators will prefer to avoid poststent balloon expansion if possible. Using a technique of underdilation of self-expanding stents, a target lesion revascularization rate of <5% can be expected.
Hypotension and bradycardia with predilation of the carotid stenosis is a marker for hemodynamic instability with stent placement owing to stimulation of the carotid body. Hypotension occurring hours following carotid stenting may signify access site bleeding. This generally responds to volume expansion, although atropine and alpha agonists such as neosynephrine and midodrine are employed when volume expansion alone is not sufficient.
Vertebral Artery Intervention
Approximately 20% to 25% of ischemic strokes involve the posterior circulation and the vertebrobasilar system.73, 74, 75 The prognosis for patients with posterior circulation atherosclerotic disease is poor, with occlusion or thrombosis associated with 80% to 100% mortality.76 Medically refractory, symptomatic vertebral artery disease carries a 5% to 11% incidence of stroke or death at 1 year.77, 78, 79, 80 Transient ischemic attacks owing to extracranial vertebral disease are associated with a stroke rate of 30% at 5 years.80, 81, 82
Revascularization of the vertebral arteries is indicated only for symptomatic patients. Typical symptoms include vertebrobasilar insufficiency (VBI), namely, dizziness, ataxia, visual disturbances, confusion, or coma. When assessing a patient with significant stenosis of a vertebral artery, the interventionalist should always determine the patency of the contralateral vertebral artery, the dominance of the diseased vertebral artery, and the amount of blood supplied to the vertebrobasilar system by the carotid arteries.
Depending upon the location of the stenosis, treatment options for vertebral artery stenosis may include balloon angioplasty with or without stent placement83 and surgery involving transplantation of the vertebral arteries onto the carotid artery or bypass grafting from the subclavian to the vertebral artery.84
Lesions located at the ostium (V0) or proximal (V1), mid (V2-3), or distal (V4) segments of the vertebral artery can be approached percutaneously.83,85 We prefer primary balloonexpandable stent placement for V0 and V1 lesions to scaffold the lesions and minimize elastic recoil. Lesions located more distally may be treated with balloon angioplasty with provisional balloon-expandable or self-expanding stents, depending upon the angiographic results and the tortuosity of the vessel. Lesions at the vertebrobasilar junction (V4) and in the basilar artery have a higher complication rate and are the most prone to dissection, occlusion, and perforation, and stroke.86
We have recently reported the largest single-center series of vertebral artery intervention in 105 consecutive
symptomatic patients83 (112 arteries, 71% male). Technical and clinical success was achieved in 105 (100%) and 95 (90.5%) patients, respectively. One-year follow-up was obtained in 87 (82.9%) patients, of which 69 patients (79.3%) remained symptom-free. At 1 year, six patients (5.7%) had died and five patients (5%) had a posterior circulation stroke. Target vessel revascularization (TVR) occurred in 7.4% at 1 year. At a median follow-up of 29.1 months (IQR 12.8 to 50.9 months), 71.4% were alive, 13.1% underwent TVR, and 70.5% remained symptom-free. Our data demonstrate that vertebral stent placement in symptomatic patients in experienced hands can be accomplished with a very high success rate (100%), with few periprocedural complications, and is associated with durable symptom resolution. We concluded that stenting of atherosclerotic vertebral artery disease is a safe and effective treatment and should be considered first-line therapy for this disease.
symptomatic patients83 (112 arteries, 71% male). Technical and clinical success was achieved in 105 (100%) and 95 (90.5%) patients, respectively. One-year follow-up was obtained in 87 (82.9%) patients, of which 69 patients (79.3%) remained symptom-free. At 1 year, six patients (5.7%) had died and five patients (5%) had a posterior circulation stroke. Target vessel revascularization (TVR) occurred in 7.4% at 1 year. At a median follow-up of 29.1 months (IQR 12.8 to 50.9 months), 71.4% were alive, 13.1% underwent TVR, and 70.5% remained symptom-free. Our data demonstrate that vertebral stent placement in symptomatic patients in experienced hands can be accomplished with a very high success rate (100%), with few periprocedural complications, and is associated with durable symptom resolution. We concluded that stenting of atherosclerotic vertebral artery disease is a safe and effective treatment and should be considered first-line therapy for this disease.
CASE 46.6
A 66-year-old man presented with recurrent episodes of dizziness (vertigo) that was orthostatic and associated with diplopia over a 2-month period. His history was remarkable for hyperlipidemia, systemic atherosclerosis, prior myocardial infarction, coronary artery bypass surgery, carotid stenting, and lower extremity percutaneous intervention. His physical examination revealed a right carotid bruit and a right supraclavicular bruit. His neurologic examination was normal. A color-flow Doppler examination of the carotid and vertebral vessels revealed no significant carotid stenosis and high velocities at the origin of both vertebral arteries consistent with stenosis with antegrade flow. He was referred for aortic arch and four-vessel selective cerebral angiography, and possible intervention.
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