Management of Vertebral Artery Origin Stenosis
Most posterior circulation strokes are embolic, not hemodynamic.
The first-line treatment of vertebral artery stenosis is usually medical, using a combination of antiplatelet agents, statins, and risk factor reduction.
Endovascular revascularization should be considered for symptomatic lesions with greater than 50% stenosis in patients who fail medical management.
The use of balloon-mounted, medicated stents may help prevent restenosis after endovascular vertebral artery origin revascularization.
Distal embolic protection during angioplasty and stenting of the vertebral artery origin may reduce the risk of embolic complications.
The vertebral artery (VA) origin is the most common site of atherosclerosis in the posterior circulation. Artery-to-artery emboli from VA-origin lesions are responsible for most posterior circulation strokes. The management of VA-origin stenosis (VAOS) is usually medical, consisting of antiplatelet agents, statins, and lifestyle modification. In patients who fail medical management, surgical revascularization procedures such as vertebral endarterectomy and transposition can help improve flow and reduce the risk of emboli to the posterior circulation, but these procedures are associated with potentially significant surgical morbidity.
Endovascular interventions such as angioplasty and stenting offer an alternative, minimally invasive way to open a stenotic vertebral artery origin. Although the long-term patency of these interventions is still being examined, the technology and techniques used to treat these lesions is continually evolving. This chapter discusses the natural history of vertebral origin stenosis, presents the available treatment options, and describes the indications and techniques used for endovascular treatment of these lesions.
Due to the difficulty of imaging the VA origin noninvasively, the incidence of VAOS in the general population has not been determined. In patients with vascular risk factors, approximately 2% will have VAOS and nearly 7% will have one occluded or congenitally absent VA.1 In patients who have sustained a posterior circulation stroke or transient ischemic attack (TIA), over 30% will have a high-grade lesion of one or both VA origins. Overall, nearly 10% of all posterior circulation strokes can be attributed to VAOS.2
♦ Risk Factors
The New England Medical Center Posterior Circulation Registry2 identified hypertension (75%), smoking (50%), and coronary artery disease (48%) as the most common risk factors shared among patients with VAOS. Other risk factors associated with peripheral vascular disease, such as diabetes and hyperlipidemia, were less frequently associated with VAOS.2 , 3 It has been observed that VAOS is more common in Caucasian men than in other demographic groups.4
In greater than 90% of cases, VAOS causes posterior circulation strokes by artery-to-artery embolization. Common ischemic symptoms associated with extracranial VA disease include vertigo, diplopia, vision loss, perioral paresthesias, tinnitus, headache, and ataxia.5 Symptoms are often vague, overlooked, or attributed to a more benign disease process. Catastrophic stokes from large emboli can result in hemiparesis, locked-in syndrome, coma, or death. Less commonly, patients with VAOS can experience posterior circulation TIA symptoms related to transient relative posterior circulation hypoperfusion. In these patients, orthostatic hypotension and anatomic obstructions may incite or exacerbate symptoms.
♦ Natural History
Isolated, asymptomatic atherosclerotic lesions of VA origin may have a benign natural history.3 Moufarrij and colleagues3 followed 89 patients with VAOS for an average of 4.6 years. During that time only two patients had a posterior circulation stroke. On the other hand, the 5-year survival rate of these patients was only 60% compared with 87% for age-matched controls. The increased mortality of VAOS patients in this series was attributed to a greater degree of generalized vascular disease, with most patients dying from either cardiac disease (53%) or anterior circulation hemispheric strokes (20%).
Considering the literature on symptomatic carotid lesions, it might be assumed that symptomatic lesions of VA origin might have a more aggressive course than asymptomatic lesions. There is no definitive literature, however, supporting that assumption. The Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS)6 is the only randomized trial to date comparing endovascular treatment of symptomatic VA stenosis to medical treatment. In a mean follow-up of 4.7 years, not a single patient in either treatment arm had a posterior circulation stroke. The authors concluded that even symptomatic VAOS may have a benign course and that endovascular treatment was not shown to be superior to medical management.7
♦ Medical Treatment of Vertebral Origin Stenosis
Blood Pressure Management
There is strong evidence that even a modest reduction of systemic hypertension can substantially reduce the risk of secondary stroke. For instance, in the PROGRESS (Perindopril pROtection aGainst REcurrent Stroke Study) trial, a combination of an angiotensin-converting enzyme (ACE) inhibitor with a thiazide diuretic resulted in a decrease in the average blood pressure by 12/5 and reduced the risk of recurrent stroke by 43%.7
Patients with acute stroke often present with hypertension that slowly resolves over the first 24 to 48 hours. Castillo et al8 observed that the average blood pressure during the first 24 hours of stroke has a U-shaped effect on outcome, with the best outcomes associated with a systolic blood pressure of 180 mm Hg. Patients with blood pressures 20 mm Hg higher or lower than 180 mm Hg had substantially larger stoke volumes and worse neurologic outcomes. Based on these observations, acutely lowering the systolic blood pressure below 180 mm Hg is not recommended during the first 24 hours after a stroke. However, it is important to consider lowering systolic blood pressure below 180 mm Hg in patients receiving intravenous thrombolytics, as blood pressures over 185/110 mm Hg have been associated with a significant in crease in cerebral hemorrhage.9
There are two large trials that suggest that the use of a statin can reduce the risk of both primary and secondary stroke. In the Heart Protection Study (HPS), 20,536 patients with stroke risk factors such as hypertension, vascular disease, and diabetes were randomly assigned to receive 40 mg of simvastatin or placebo. At the end of the 5-year follow-up period, the risk of primary stroke was 25% lower in the treatment group. In the Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) trial,10 patients with a history of stroke or TIA within 6 months were randomly assigned to treatment with either 80 mg of atorvastatin or placebo. In the 5-year follow-up period there was an 18% relative reduction in the risk of secondary stroke in patients treated with atorvastatin. Interestingly, there was an increase in the relative risk of hemorrhagic stroke among statin users that was not observed in the HPS trial.
Based on the data from these two studies, statins should be used in all patients with risk factors for ischemic stroke including VAOS. Statins, in addition to lowering total body cholesterol, may help stabilize plaque, halt or reverse atherosclerosis, and improve arterial endothelial function. In addition, statins significantly lower the risk of cardiac events in patients with vascular risk factors, a major source of morbidity and mortality in this patient population.
♦ Revascularization of Vertebral Artery Origin Stenosis
In experienced hands, VA revascularization can be done with acceptable risk.11 Perioperative mortality and stroke during revascularization is uncommon (<2%).11 Nevertheless, surgical morbidity from these procedures is common. In a recent series of 29 patients who underwent proximal VA revascularization either by transposition or endarterectomy, 48% of patients sustained some sort of surgical approach morbidity such as Horner’s syndrome, recurrent laryngeal nerve injury, or chylothorax.12 Despite its high morbidity rate, surgical revascularization is still a reasonable option in patients who fail medical management and who are poor candidates for an endovascular approach. It is also notable that surgical revascularization carries an 80% 5-year patency rate,11 considerably better than what has been reported in most endovascular series to date.
♦ Endovascular Revascularization of Vertebral Artery Origin Stenosis
Vertebral artery origin atherosclerosis, like carotid artery disease, is often a marker of systemic vascular disease. Not surprisingly, the cause of death in most VAOS patients, even symptomatic ones, is cardiac disease. A careful history and physical examination often uncover other health issues such as congestive heart failure or angina that may require additional workup, optimization, and planning prior to an invasive procedure. Palpation of the femoral and peripheral pulses, including an Allen test, helps to identify potential problems with percutaneous access. Physiologic testing of heart function is often important in preoperative preparation before a stent is placed.
Noninvasive Vessel Imaging
The diagnosis of VAOS is usually made on the basis of noninvasive vessel imaging. Color duplex imaging can diagnose lesions at the vertebral artery origin,13 but does not provide the anatomic detail required for planning a revascularization procedure. Computed tomography angiography (CTA) and magnetic resonance angiography (MRA) are also capable of visualizing the VA origin. A comparison of various noninvasive imaging techniques14 determined that contrastenhanced MRA is more sensitive and specific than CTA in evaluating VAOS. In practice, however, noninvasive imaging is often marred by artifact from tissue and bone in the chest wall and calcifications within the atherosclerotic plaque.
The role of perfusion imaging in the management of VAOS remains undefined. Because most patients have redundant blood supply to the basilar artery from the contralateral VA, it is relatively uncommon for patients with VA stenosis to have a hemodynamic stroke. Rather, most posterior circulation strokes are due to artery-to-artery emboli from the plaque itself. Perfusion imaging is potentially useful in patients with a hypoplastic or stenotic contralateral VA if a hemodynamic syndrome is suspected. Nevertheless, only a handful of case reports in the literature describe the use and utility of computed tomography (CT) perfusion imaging in the posterior circulation.
A complete diagnostic cerebral angiogram often yields information helpful in medical decision making. The goals of angiography include the following:
Visualizing and measuring the degree of stenosis and tortuosity of the VA origin
Characterizing collateral flow pathways to the posterior circulation
Finding suitable donor and recipient vessels for open surgical bypass in the event that endovascular revascularization fails
Identifying anatomic variants or other vascular lesions that might contribute to posterior circulation ischemia.
All patients being prepared for VA stent placement require dual antiplatelet therapy, usually with aspirin and clopidogrel. In patients undergoing elective procedures the patient is started on 75 mg of clopidogrel and 325 mg of aspirin 1 week prior to the procedure. Based on the American College of Surgery (ACS) literature, patients who require more urgent treatment should be loaded with 300 mg of clopidogrel at least 8 hours prior to stenting. Alternatively, 600 mg of clopidogrel at least 3 hours prior to the procedure is effective.15 Platelet aggregation studies may be useful in identifying patients who may be nonresponders to aspirin or clopidogrel, although they are not routinely available in all centers and their utility remains controversial.
Vertebral artery origin stenting can often be performed with the patient under moderate conscious sedation. Although most patients tolerate VA-origin angioplasty and stenting under conscious sedation, it is not the best choice in all patients. General anesthesia should be considered for patients with congestive heart failure (CHF), dementia, or even severe lumbar spine disease who cannot lie flat comfortably for at least 1 hour. General anesthesia with neurophysiologic monitoring may also be a good choice for patients with poor collateral flow who may not tolerate temporary occlusion of the VA during angioplasty. If general anesthesia is selected, then somatosensory evoked potentials (SSEPs), motor evoked potentials (MEPs), and electroencephalogram (EEG) monitoring are an option to assess the presence of ischemia. A blood pressure cuff should be placed on the ipsilateral arm, so that it can be inflated during the subclavian injections to improve visualization of the VA if necessary.
The most convenient access point is generally the common femoral artery, although radial or brachial access can be used if femoral access is impossible or the VA anatomy is not favorable for a femoral approach. Often, patients with VA stenosis have other manifestations of peripheral vascular disease (Fig. 33.1). A 6-French (F), 10- or 25-cm groin sheath is usually sufficient for access if a guide catheter will be used. In patients with very tortuous anatomy an 80-cm Raabe guide sheath (Cook Medical, Bloomington, IN) parked just proximal to the VA origin in the subclavian artery provides additional support.
Intravenous heparin (usually 70 units/kg) is given to all patients after arterial access is secured. The activated clotting time (ACT) is measured with a Hemochron ACT analyzer (ITC Nexus Dx, Edison, NJ) 15 minutes after heparin administration. Patients are re-bolused with intravenous heparin hourly as needed to maintain the ACT between 250 and 300 seconds.16
Guide Catheter Placement
A 6F guide catheter (or guide sheath) on a continuous heparinized saline flush is navigated into the subclavian artery just proximal to the VA origin. A preprocedure angiogram of the entire length of the VA should be performed to verify balloon and stent measurements as well as to identify more distal disease. Cerebral angiography should also be performed to assess blood flow and define the baseline anatomy should an embolus occur.
On occasion, aortic arch anatomy may not provide adequate support for the guide catheter in the proximal subclavian artery. If this occurs, a “buddy wire” can provide additional support. In this technique an 0.018- or 0.014-inch wire is passed through the guide sheath and into the brachial artery. The wire is then left in place throughout the procedure to help prevent the guide catheter from slipping back into the arch (Fig. 33.2). A guide catheter can also be passed through a guide sheath in a coaxial arrangement to improve stability if necessary.