Carotid Artery Atherosclerotic Disease

Stroke resulting from atherosclerosis is a common cause of death in the United States. It results in ~150,000 deaths per year.^1,2 Approximately 400,000 to 500,000 new strokes are reported annually with a 20 to 50% recurrence rate within 5 years.^1,3 Stroke is also the leading cause of long-term physical and intellectual disability among adults.⁴ Race, gender, and vascular risk factors may influence the distribution of atherosclerosis. Premenopausal women and Japanese, Chinese, Thai, and African-American populations are more likely to develop intracranial disease, whereas Caucasians and those with hypercholesterolemia are more likely to develop extracranial disease.⁵ The most common extracranial sites for atherosclerotic disease are the carotid bifurcation, the subclavian arteries, and the proximal vertebral arteries^6,7

The process of atherosclerosis is thought to occur at these sites secondary to the combined effects of turbulence, blood stagnation, hemodynamic sheer stress, and boundary separation.⁸ The ratio of internal carotid artery area to common carotid artery area and the bifurcation angle result in a geometry at the bifurcation that produces vortex flow and increased contact of atherogenic substances and platelets with the site of maximal plaque development.⁹ This current view of atherogenesis is referred to as the “response to injury” hypothesis.^10,11 According to this hypothesis, a variety of forces injures the endothelium, and the inflammatory response to this injury results in plaque development. Factors that may cause endothelial injury include hypercholesterolemia, cigarette smoking, hypertension, oxidative stress, advanced glycation end-products, and possibly infection.¹² Injury induces endothelial gene expression of platelet and leukocyte adhesion molecules and molecules involved in growth factor, cytokine, and coagulation protein synthesis.^13,14 Increased permeability secondary to endothelial injury allows monocytes and low-density lipoprotein to enter the intima. Monocytederived macrophages secrete mitogens that induce smooth muscle cell egress into the intima, with subsequent proliferation and extracellular collagen and proteoglycan synthesis. Oxidized lipoproteins fill macrophages turning them into foam cells that may rupture and release lipid and cytotoxic enzymes. This increases the fibroproliferative response of the smooth muscle cells.¹⁵ Also, injured endothelium is more thrombogenic secondary to decreased expression of nitric oxide, prostacyclin, and fibrinolytic and antithrombotic glycoproteins.¹⁴

Stroke is defined as a sudden, nonconvulsive, focal neurological deficit. It is characterized by a specific temporal profile that includes abrupt onset of a neurological deficit, followed by subsequent arrest, and then regression in all but the most severe strokes. The type of neurological deficit is dependent upon the involved vascular territory but can include hemiplegia, mental confusion, varied sensory deficits, aphasia, visual field defects, diplopia, dizziness, or dysarthria.¹⁶

Atherosclerotic narrowing and ulceration at the carotid bifurcation is a major cause of thromboembolic stroke. The results of several prospective, randomized trials for symptomatic and asymptomatic carotid occlusive disease have provided evidence-based data for treatment. By 1990, seven trials were planned or in progress. Four of these trials addressed asymptomatic carotid occlusive disease (the Carotid Artery Stenosis Asymptomatic Narrowing Operation Versus Aspirin [CASANOVA] study, the Mayo Asymptomatic Carotid Endarterectomy [MACE] study, the Veterans Administration Asymptomatic Stenosis Trial [VAAST], and the Asymptomatic Carotid Atherosclerosis Study [ACAS]). Patients could not have symptoms from ipsilateral cerebral ischemia secondary to carotid occlusive disease, although contralateral symptoms were permitted in VAAST and ACAS. The four trials used similar exclusion criteria. Patients with neurological (e.g., seizures, dementia), cardiac (e.g., atrial fibrillation, severe valvular disease), or general medical conditions (e.g., diabetes, renal failure) that might affect stroke outcome were also excluded.¹⁷ There is one asymptomatic carotid surgery randomized trial in the United Kingdom and Europe, the ACST trial.^18,18A

The CASANOVA study randomized patients from the general population to immediate surgery versus antiplatelet therapy alone and best medical management. The stenosis criterion was 50 to 90% by noninvasive testing or angiography. Both arms received best medical management including aspirin (1000 mg/d) and dipyridamole (225 mg/d). The follow-up was 3 years and the study size was 410 patients. Endpoints were death and stroke. Two hundred six patients were randomized to immediate surgery, and 204 patients were randomized to antiplatelet therapy alone. One hundred eighteen of the 204 patients in the nonsurgical arm had delayed endarterectomy during the follow-up period secondary to transient ischemic attack (TIA), progressive severe stenosis (>90%), bilateral stenosis (>50%), or contralateral stenosis (>50%). The study found no statistically significant difference in outcome between the surgical and nonsurgical arms (10.7% and 11.3%, respectively).¹⁹ The unusual study design of CASANOVA limits its statistical validity.

The MACE study enrolled 71 patients with >50% stenosis by noninvasive testing. The planned follow-up was 2 years. The nonsurgical arm received best medical management and aspirin (80 mg/d). The surgical arm did not receive aspirin. Only Mayo Clinic patients were randomized to the treatment arms. The study was terminated prematurely because of increased frequency of myocardial infarction in the surgical arm that did not receive aspirin. At termination, too few patients were enrolled to assess statistical significance. It was concluded that aspirin was appropriate for the perioperative and postoperative period unless contraindicated.²⁰

The VAAST enrolled only men from VA centers and randomized them to surgical and nonsurgical arms, both of which received best medical management and aspirin (1300 mg/d). The stenosis criterion was >50% by angiography. The follow-up was 5 years and the study population was 444 patients (211 of 444 surgical and 233 of 444 nonsurgical patients). Participating centers were screened for perioperative morbidity and mortality of >3%. At 4-year follow-up, the combined incidence of ipsilateral TIA or stroke was 8% and 20.6% for the surgical and nonsurgical arms, respectively (p <.001). The sample size was not large enough to show statistical significance for stroke alone.²¹

The ACAS randomized 1662 patients with >60% stenosis (by angiography or Doppler ultrasound) to surgery versus best medical management. All patients received daily aspirin (325 mg). Nonwhite populations comprised only 5% of the study group. The projected risk of ipsilateral stroke at 5 years (mean follow-up of 2.7 years) was 5.1% for the surgical group and 11% for medical management. This represented an overall relative risk reduction of 53%. This risk reduction was more apparent for men and independent of degree of stenosis or contralateral disease. The calculated stroke risk for the medical management arm was 2.2% per year. The perioperative risk of stroke and death was 2.3% plus an additional risk of 1.2% for arteriography. Surgical benefit was noted at 10 months postrandomization and remained statistically significant at 3 years.²² The European ACST also was a positive trial, confirming the benefit of surgery over medical therapy in a large number of asymptomatic patients.

Three trials focused on symptomatic carotid occlusive disease (the North American Symptomatic Carotid Endarterectomy Trial [NASCET], the Veterans Administration Symptomatic Stenosis Trial [VASST], and the European Carotid Surgery Trial [ECST]). All three of these trials were terminated early. NASCET and VAAST maintained that participating centers must have surgical morbidity rates of >6%. Inclusion criteria were relatively similar among the trials and included transient retinal ischemia, transient cerebral ischemia, or minor completed stroke within 120 days of randomization in the distribution of the carotid lesion.²³

The ECST stenosis criterion was 0 to 99%. The trial randomized 3018 patients, 1807 to surgery and 1211 to best medical management. The trial was terminated early at an interim analysis of 2200 patients. Follow-up was 5 years with a mean of 2.7 years for those with >30% stenosis and 3.0 years for those with >70% stenosis. Sample size was 374 for the >30% group and 395 for the >70% group. The primary endpoint was ipsilateral stroke. The mild stenosis group (>30%) revealed no statistically significant difference between surgical and nonsurgical arms with respect to stroke incidence. The severe stenosis group (>70%) revealed a benefit to the endarterectomy arm with a 10.3% total risk of stroke (i.e., 7.5% risk of stroke or death within 30 days plus an additional 2.8% risk of stroke) versus a 16.8% risk in the nonsurgical arm. The total 3-year risk of disabling or fatal stroke was 6.0% versus 11.0% in the surgical versus nonsurgical arms, respectively. Surgical benefit outweighed best medical management risk in patients with 70 to 80% stenosis. This benefit was realized 2- to 3-year status postrandomization.²⁴ The ECST data reanalysis using NASCET criteria revealed a significant surgical benefit for patients with 70% stenosis.

The NASCET was terminated early secondary to significant risk reduction in patients with >70% stenosis in the surgical arm. Six-hundred fifty-nine patients with symptomatic carotid stenosis between 70% and 99% were randomized to surgical (328 patients) and nonsurgical (331 patients) treatment arms. Ipsilateral stroke risk at 2-year follow-up was 9% for the surgical group versus 26% for the nonsurgical group. This represented a 71% relative risk reduction (p <.001), i.e., one stroke could be prevented for every 6 to 7 endarterectomies performed. A significant correlation was noted between severity of stenosis and surgical benefit. The protective effect of endarterectomy was durable over time and independent of age, gender, and stroke risk factors.²⁵ At 5-year follow-up for 2226 patients with 50 to 69% stenosis randomized to nonsurgical and surgical arms, the ipsilateral stroke rate was 22.2% versus 15.7% (nonsurgical vs. surgical, p =.045). Author estimates were that 15 endarterectomies would have to be performed to prevent one stroke in a 5-year period. Those individuals with >50% stenosis did not benefit from endarterectomy. Contralateral occlusion was a strong risk factor for stroke, though contralateral stenosis was not a risk factor.²⁶ The timing of the surgery did not affect surgical risk.

The VASST was terminated early secondary to preliminary results from the two aforementioned trials. Though 5000 patients were screened at 16 participating VA centers, only 193 men were randomized to best medical management (98 men) and surgical (91 men) treatment arms.²⁷ Angiography was performed on all patients and greater than two-thirds of the population had >70% stenosis. There was a mean follow-up of 11.9 months. Risk of stroke or crescendo TIA was 7.7% versus 19.4% (surgical vs. nonsurgical, p =.028). Surgical benefit in patients with >70% stenosis was 7.9% versus 25.6% (surgical vs. nonsurgical). Sample size at 50 to 69% stenosis was too small to draw any statistically significant conclusions. Surgical benefit was appreciated as soon as 2-month status postrandomization and was maintained throughout follow-up. Total perioperative risk was 5.5% (perioperative morbidity of 2.2% plus perioperative mortality of 3.3%).

The above studies provide convincing evidence for the surgical treatment of carotid occlusive disease in asymptomatic patients with >60% stenosis and symptomatic patients with >50% stenosis. Note, however, that surgical benefit for women in ACAS was not apparent and that nonwhite patients comprised only 5% of the study population. Also, ACAS and VAAST surgeons and patients were specifically selected for low surgical risk. In the symptomatic carotid stenosis trials, the benefit of endarterectomy was observed in the setting of low surgical risk. Surgical benefit in nonselected populations may be less predictable.

Endovascular techniques including angioplasty and stenting are alternatives to carotid endarterectomy for the treatment of carotid occlusive disease. Presently, endovascular techniques are indicated for patients who are not candidates for conventional open reconstruction. This may include patients with extremely high lesions and patients with medical contraindications to general anesthesia (pulmonary or cardiac). Some experts feel that recurrent carotid stenosis and patients with contralateral carotid occlusion are better treated by endovascular techniques; the senior author (CML) feels that in most cases these patients remain excellent surgical candidates and can be operated on without undue risk in our experience.

Several studies have demonstrated acceptable morbidity and mortality data for the use of carotid angioplasty and stenting in carotid stenosis. Diethrich et al reported on 110 patients (117 vessels), 79 of whom were asymptomatic and 31 of whom were symptomatic with stenosis greater than or equal to 70%.²⁸ Two major and five minor neurological events resulted from the procedure, together representing 6.4% of the study population. Five patients had transient ischemic attacks, with 1.8%, mortality. Asymptomatic occlusion occurred in 1.8%, and 2.7% ultimately required endarterectomy for failure or restenosis. Yadav et al reported on 107 patients, with 189 stents placed into 126 carotid arteries.²⁹ Mean stenosis was 78% preoperatively and 2% postoperatively. Eighty-two percent of these patients met NASCET criteria. There was a 10.8% complication rate for symptomatic patients and a 4% neurological event rate for asymptomatic patients. In follow-up, 4.9% experienced restenosis. The experience of Iyer³⁰ in 352 patients undergoing 384 procedures revealed a 0.7% major stroke rate, a 6% minor stroke rate, and 0.8% mortality. Nonneurological death occurred in 1.4%. Guterman and Hopkins³¹ relayed their experience with 96 high–medical-risk patients with unstable angina or restenosis after endarterectomy. Patients with long stenotic segments or high carotid bifurcations were also included. Angioplasty and stent placement was undertaken in 62 patients, with the remainder receiving angioplasty alone. Two deaths of cardiac origin, two minor strokes, and no major complications were reported. The experience of Rosenwasser and Shanno³² with 47 patients treated with angioplasty (45 of whom also had stents placed) revealed one major stroke 5 days postoperatively and one “cold foot” that resolved with heparin therapy. Sixty-three percent required temporary pacing during inflation (29 of 47 patients). Their indications for endovascular treatment of carotid occlusive disease were radiation-induced stenosis, recurrent stenosis, medically unstable patients (with cardiac or pulmonary risk factors), and lesions at C1–2 or long lesions extending into the petrous segment.

Complications of carotid endarterectomy include infection, bleeding, damage to local tissue structures (vessels, nerves, muscle), restenosis, myocardial infarction, stroke, and death. Complications applicable to endovascular techniques include pseudoaneurysm, arterial dissection or rupture, aberrant placement of prosthesis, infection, stroke, myocardial infarction, and death.

In conclusion, there is convincing evidence for the surgical treatment of carotid occlusive disease in asymptomatic patients with >60% stenosis and symptomatic patients with >50% stenosis. Though more studies need to be performed to define long-term benefit and durability of endovascular therapies for carotid occlusive disease, current studies are promising. For selected indications, e.g., radiation-induced stenosis, recurrent stenosis, medically unstable patients (with cardiac or pulmonary risk factors), and lesions at C1–2 or long lesions extending into the petrous segment, endovascular therapy is a viable alternative to surgical endarterectomy in selected centers with experienced teams.

Vertebral Artery Atherosclerotic Disease

Atherosclerosis of the vertebral artery may produce vertebrobasilar insufficiency (VBI) or stroke by way of embolism, hypoperfusion, or both. The diagnosis of VBI requires two or more of the following: bilateral sensory and/or motor symptoms occurring during the same event, diplopia, dysarthria, or homonymous hemianopsia. “Dizziness” not explained by orthostasis or inner ear pathology may be a symptom of VBI. Because the vertebral arteries exist as a pair, hypoperfusion typically results from bilateral vertebral atherosclerosis or unilateral atherosclerosis in combination with unilateral congenital hypoplasia or atresia.

The vertebral arteries arise from their respective subclavian arteries, with the left vertebral artery being dominant in ~50 to 60% of cases.³³ The vertebral arteries begin their ascent thru the transverse foramina at C6, and at the level of C2 break laterally to ascend thru the transverse foramina of C1. Once through the transverse foramina of C1 the vertebral arteries course posteriorly along the atlas before turning superiorly and medial to pierce the atlanto-occipital membrane and dura. The intracranial vertebral arteries give rise to the posterior inferior cerebellar arteries and the anterior spinal artery before joining as the basilar artery. The left vertebral artery has an aortic arch origin in ~5% of cases, and in some 40% of cases, the vertebral artery is hypoplastic.³⁴

A commonly used system for naming the vertebral artery was developed by Krayenbuhl and Yasargil.³⁵ The vertebral artery is divided into four portions, V1 to V4. Portion V1 is the first portion of the vertebral artery extending from its origin to the C6 transverse foramen. The second portion, V2, is intraosseous, extending from the transverse foramen of C6 to that of C2. Postion V3 portends to that portion of the vertebral artery between the transverse foramen of C2 and the point of posterior fossa entry by way of the foramen magnum. The fourth portion, or intracranial portion of the vertebral artery (V4), travels a short distance before joining its homologue to become the basilar artery. The above-described system of vertebral artery nomenclature facilitates discussion regarding anatomy and pathology and, germane to this chapter, areas of atherosclerosis and surgical treatment.

In Western society, atherosclerosis is ubiquitous. The atherosclerotic lesion begins as an intimal fatty streak, which evolves over time to become a fibrous plaque. The fibrous plaque may grow to occlude or stenose the arterial lumen, or the plaque may rupture causing thrombosis or embolization. Risk factors for the development of atheromatous disease include hyperlipidemia, cigarette smoking, diabetes, hypertension, obesity, and a sedentary lifestyle. As noted by Fisher et al, atherosclerosis seems to affect the V1 segment primarily; however, distal V4 segment disease is more commonly symptomatic.⁴ Subclavian steal of vertebral blood flow may occur if a flow-limiting atherosclerotic plaque extends into the proximal subclavian artery.

Very few published studies address the natural history of extracranial vertebral artery atherosclerotic occlusive disease. In 1984, Moufarrij et al published their data after following 96 patients with greater than 50% vertebral artery stenosis for approximately 4 years.³⁶ They concluded that proximal vertebral artery atherosclerotic stenosis was a relatively benign condition when not associated with basilar artery atherosclerosis.

Surgical treatment of extracranial vertebral artery atherosclerotic disease consists of endarterectomy, bypass grafting, or transposition. These surgical procedures are reserved typically for those individuals suffering from persistent vertebrobasilar insufficiency or transient ischemic attacks attributable to the vertebral artery. These procedures are made difficult by the relative inaccessibility and small size of the proximal vertebral artery, and as such are fraught with a relatively high morbidity and mortality. Published morbidity and mortality data for proximal vertebral artery reconstruction vary greatly, ranging between 1.9 and 20%.^37–39 Five-year patency rates vary between 75 and 80%.^37,38

Balloon angioplasty and stent-supported angioplasty are now being used with increasing frequency to treat symptomatic extracranial vertebral artery disease. Stentsupported angioplasty utilizes the intraluminal rigidity of a stent to prevent elastic recoil and early restenosis. In 1996, a review of 268 vertebral balloon angioplasties performed by Kachel⁴⁰ reported an overall success rate of 95%, no mortality, and 0.7% morbidity. Although no longterm outcome studies exist for vertebral stent-supported angioplasty, the short-term results are promising.

Those patients with vertebrobasilar insufficiency or transient ischemic attacks attributable to the extracranial vertebral arteries are candidates for open surgical or endovascular revascularization procedures. Although no randomized prospective trial has compared the therapeutic efficacy of medical (platelet inhibitors and systemic anticoagulation) versus surgical versus endovascular treatment of symptomatic vertebral disease, the Warfarin-Aspirin Symptomatic Intracranial Disease Study⁴¹ found that patients with a symptomatic stenosis of a major intracranial vessel had fewer strokes when taking Warfarin than when taking aspirin, and the results from this study are extrapolated to justify systemic anticoagulation in those with symptomatic extracranial atherosclerotic disease of the vertebral arteries. Certainly, surgical or endovascular procedures should be considered in those patients with a symptomatic stenosis of an extracranial vertebral artery who fail to respond to medical management.

Patients who are too medically ill to undergo general anesthesia may be better candidates for long-term systemic anticoagulation or endovascular revascularization. There are no absolute contraindications to endovascular treatment of a symptomatic vertebral artery stenosis; however, a recent posterior circulation stroke associated with a tight vertebral artery stenosis is a temporary contraindication to surgical or endovascular revascularization secondary to concern of reperfusion hyperemia and the potentially disastrous consequence of hemorrhagic stroke conversion.

The diagnosis of vertebral artery stenosis or occlusion is confirmed with conventional angiography. Contrastenhanced magnetic resonance angiography is constantly improving with the use of new pulse-sequences and software⁴²; however, conventional angiography remains the definitive test in those patients suspected to have stenotic vertebral arteries. Duplex ultrasound screening of the proximal vertebral arteries is relatively unreliable.⁴³

As mentioned above, the therapeutic options for symptomatic stenosis of the vertebral artery include medical, surgical, and endovascular management. The modality of choice should be tailored to individual patient needs and expectations, and typically, even with endovascular and surgical revascularization procedures, antiplatelet drugs or anticoagulants are used in the short term. Obviously, long-term systemic anticoagulation with Warfarin is associated with significant morbidity and mortality, and the risks and benefits of any treatment modality must be discussed thoroughly with the patient. A long-term, multicenter, prospective, randomized trial is needed to establish reliable data and scientifically based recommendations regarding the treatment of extracranial vertebral artery atherosclerotic disease.

Potential complications of surgical revascularization include death, damage to soft tissues, infection, bleeding, stroke, and early restenosis or occlusion. Endovascular revascularization carries similar risks; however, complications related to arterial access (hematoma, infection, pseudoaneurysm) are included.

Iatrogenic dissection has been described with endovascular techniques; however, if evident at the time of treatment, placement of additional stents across the dissection is usually curative.³⁹

Extracranial Vertebral and Carotid Artery Dissection

Carotid and vertebral artery dissection occurs spontaneously or following trauma; it is characterized by bleeding into the tunica media. Carotid dissection is more common than vertebral artery dissection.⁴⁴ Arterial dissection is a relatively common cause of stroke in the young, although dissections may occur at any age. Both vertebral and carotid dissection may be associated with headache (commonly ipsilateral), transient ischemic attack, stroke, or a palpable pulsatile mass in cases of pseudoaneurysm formation. Dissection may be asymptomatic and found incidentally on radiographic studies, or it may be symptomatic. Vessel stenosis and thromboembolism typically results from bleeding between the intima and media, or alternatively, pseudoaneurysm formation may follow bleeding between the media and adventitia.

Spontaneous dissection occurs more commonly in those predisposed by various disease states including fibromuscular dysplasia,⁴⁵ Marfan’s syndrome, atherosclerosis, and various arteritides. Dissections may also follow relatively innocuous trauma such as sneezing, coughing, or shaving. Iatrogenic dissection following arterial catheterization is well described.³⁹

The natural history of extracranial carotid and vertebral dissection is largely unknown because those with asymptomatic lesions rarely seek medical attention, and those with symptomatic dissections are treated via a medical, surgical, or endovascular route. It is generally held that thrombus within the tunica media resolves over several weeks and that the arterial lumen returns to its normal size spontaneously.

Dissection of the vertebral artery should be suspected in those complaining of severe spontaneous or posttraumatic neck pain associated with signs and symptoms of posterior circulation stroke or transient ischemia. A history of whiplash, a blow to the back of the neck, chiropractic manipulation, or cervical spine fracture should trigger suspicion of vertebral artery dissection. Vertebral artery dissection-induced pseudoaneurysms may produce a cervical radiculopathy, as described by Fournier et al. As mentioned above, carotid artery dissection may be associated with signs and symptoms of stroke or transient ischemia.⁴⁶ A patient with a Horner’s syndrome complaining of headache should be considered to have carotid artery dissection until proven otherwise.

Arch and four-vessel cerebral angiography is the diagnostic modality of choice; however, duplex ultrasound, magnetic resonance imaging, and computed tomography are reasonable alternatives if contraindication exists to conventional angiography. Duplex ultrasonography should not be relied upon in cases of potential vertebral dissection, as the proximal vertebral artery is not well visualized with ultrasound.⁴³ Angiography classically reveals an area of severe narrowing or occlusion following a gradually tapered lumen. Extracranial carotid artery dissections usually begin distal to the carotid sinus and extend for a variable distance before ending proximal to the petrous carotid.⁴⁷ Vertebral artery dissections most commonly occur between the C2 vertebral body and the skull base (V3 segment).

In cases of vertebral or carotid artery dissection, medical management consisting of systemic anticoagulation should be started on an emergent basis. Typically, heparin provides immediate anticoagulation while oral anticoagulants are allowed to take effect. Systemic anticoagulation is contraindicated in those with stroke. Three to six months of anticoagulation is usually sufficient prophylaxis against propagation of intramural thrombus and distal embolization.

Endovascular and surgical therapeutic modalities are reserved for those patients with dissection who remain symptomatic despite systemic anticoagulation. In cases of carotid dissection or pseudoaneurysm unresponsive or partially responsive to maximal medical therapy, attempts at open surgical bypass, external carotid to internal carotid bypass (EC-IC bypass) combined with internal carotid ligation, or internal carotid ligation alone may be made. Most of these surgical procedures are treacherous given the relative inaccessibility of the high cervical carotid artery and the friable nature of pseudoaneurysms. Muller et al reviewed 50 surgeries performed for symptomatic carotid artery dissection or pseudoaneurysm formation.⁴⁸ Forty-nine surgeries were performed for chronic symptomatology despite at least 6 months of anticoagulation, and one surgery was performed on a semi-emergent basis of fluctuating neurological symptoms. In their series one patient died of intracranial bleeding, five patients suffered the development of recurrent minor stokes, and 58% developed cranial nerve deficits, which, in most cases, were temporary.

Medically intractable vertebral dissections and pseudoaneurysms may also be treated surgically.^37,38 Ligation of the vertebral artery may be performed with or without bypass. Test balloon occlusion may help predict which patients have adequate collateral blood flow to withstand ligation of the carotid or vertebral arteries. Surgical ligation of the vertebral artery should take a common-sense approach with regard to the posterior inferior cerebellar artery (PICA). If the PICA takes off distal to the problematic area, then the dissection or pseudoaneurysm may be trapped between two ligatures. If the PICA originates within the area of dissection or pseudoaneurysm, one ligature may be placed just proximal to the PICA origin. In both of the above cases, the posterior inferior cerebellar artery will fill in a retrograde fashion from the contralateral vertebral artery.

Endovascular treatment of carotid and vertebral artery dissection and pseudoaneurysm has become feasible with the advent and optimization of coils and stents.^49–51 Saito et al described the endovascular treatment of a spontaneous carotid artery dissection with symptomatic pseudoaneurysm formation.⁵⁰ In their report, a selfexpanding stent was used to cover the pseudoaneurysm neck while coils were passed through the stent into the pseudoaneurysm. Arteriography performed 4 months later confirmed thrombosis of the pseudoaneurysm with preservation of internal carotid artery blood flow. The patient reported symptomatic improvement. In 1999, Liu et al reported their 8-year experience of treating seven patients with symptomatic carotid artery dissections or pseudoaneurysms with stents.⁴⁹ Four patients received stents for large, nonhealing, pseudoaneurysms, and three patients received stents for severe preocclusive stenosis. In their series, no deaths or significant morbidity occurred; however, one patient developed asymptomatic occlusion of the treated carotid artery, and one patient required coil embolization of a persistent pseudoaneurysm. Use of stent-supported angioplasty is also well described in the treatment of noncarotid xtracranial cerebrovascular disease^40,52 and dissection.³⁹

Again, no long-term, prospective, randomized study has compared the efficacy and complication rates for the surgical and endovascular treatment of carotid and vertebral artery dissection and dissection-induced pseudoaneurysm; however, the seemingly good results and low complication rates associated with endovascular treatment modalities are impressive and should warrant the strong consideration for endovascular treatment to be the modality of choice.

Miscellaneous Lesions of the Extracranial Vertebral and Carotid Arteries

Fibromuscular dysplasia (FMD) is an idiopathic angiopathy that may affect the extracranial vertebral and carotid arteries. Pathologically, FMD is characterized by fibrous thickening of the arterial tunica media. Fibromuscular dysplasia affects the arterial wall intermittently giving an angiogram the classic “string-of-beads” appearance, and like carotid artery dissections, FMD typically affects the internal carotid artery at least 2 cm distal to the common carotid bifurcation. The carotid artery is affected in ~75% of cases, and the vertebral artery is affected in up to 25% of cases. Bilateral involvement occurs in 60 to 75% of all cases.⁵³ Fibromuscular dysplasia of the extracranial carotid and vertebral arteries predisposes to dissection, pseudoaneurysm formation, stenosis, and thromboembolic phenomena. Cases of symptomatic stenosis secondary to fibromuscular dysplasia have traditionally been treated surgically with the graduated internal dilation technique⁵⁴; however, in recent times endovascular stent-supported angioplasty has proven to be effective in cases of simple stenosis and in cases of FMD-induced pseudoaneurysms.⁵⁵

Carotid artery injury secondary to penetrating neck wounds is a significant cause for morbidity and mortality in the urban young. Carotid artery laceration or transaction may be accompanied by exsanguination, or lesser injury may cause thrombosis, dissection, or pseudoaneurysm formation. Those patients who are hemodynamically unstable from a carotid artery injury should be taken immediately to the operative suite for repair, reconstruction, or ligation of the damaged artery. Patients with no neurological deficit, or with a noncoma deficit, should preferentially undergo carotid repair or reconstruction instead of ligation.⁵⁶ Comatose individuals may have the carotid artery ligated, and hemodynamically stable patients suspected to have a carotid injury should undergo angiography prior to neck exploration.

Head and neck neoplasms that affect the extracranial carotid or vertebral arteries should be removed if possible, by dissecting the tumor off the vessel. If tumor invasion of the arterial wall has occurred, then various reconstructions may be employed. Preoperative test balloon occlusion of the extracranial vessels coupled with intraoperative monitoring may provide invaluable information in difficult cases when sacrifice of an artery is considered. Carotid body tumors arise from paraganglion cells; they are typically benign and slow growing. Surgical resection of these tumors classically is associated with a relatively high morbidity and mortality.

References

1. American Heart Association. Heartfacts: 1994 Cardiovascular Statistics. Dallas: American Heart Association; 1994

2. Blatter DD, Bahr AL, Parker DL, et al. Cervical carotid MR angiography with multiple overlapping thin-stab acquisition: comparison with conventional angiography. AJR Am J Roentgenol 1993;161:1269–1277

3. Zwiebel WJ. Duplex sonography of the cerebral arteries: efficacy, limitations, and indications [comments]. AJR Am J Roentgenol 1992;158:29–36

4. Fleck JD, Biller J, Loftus CM. Medical and surgical management of stroke and extracranial carotid artery disease. In: Grossman RG, Loftus CM, eds. Principles of Neurosurgery, ed 2. New York: Lippincott-Raven; 1999:271

5. Caplan LR, Gorelick PB, Hier DB. Race, sex, and occlusive cerebrovascular disease: a review. Stroke 1986;17:648–655

6. Fisher CM, Gore I, Okabe N, et al. Atherosclerosis of the carotid and vertebral arteries—extracranial and intracranial. J Neuropathol Exp Neurol 1965;24:455–476

7. Hutchinson HC, Yates PO. Carotico-vertebral stenosis. Lancet 1957;1:2–8

8. Warlow C. Disorders of the cerebral circulation. In: Walton J, ed. Brain’s Diseases of the Nervous System, ed 10. Oxford: Oxford University Press; 1993:217

9. Fisher M, Fieman S. Geometric factors of the bifurcation in carotid atherogenesis. Stroke 1990;21:267–271

10. Fuster V, Badimon L, Badimon JJ, et al. The pathogenesis of coronary artery disease and the acute coronary syndromes. N Engl J Med 1992;326:242–250

11. Ross R. The pathogenesis of atherosclerosis: a perspective for the 1990s. Nature 1993;362:801–809

12. Drexler H. Endothelial dysfunction: clinical implications. Prog Cardiovasc Dis 1997;39:287–324

13. Cybulsky MI, Gimbrone MA. Endothelial expression of a mononuclear leukocyte adhesion molecule during atherogenesis. Science 1991;251:788–791

14. O’Brien KD, McDonald TO, Chait A, et al. Neovascular expression of E-selectin, intracellular adhesion molecule-1, and vascular cell adhesion molecule-1 in human atherosclerosis and their relation to intimal leukocyte content. Circulation 1996;93:672–682