8 Vertebrobasilar Stenosis and Insufficiency
Abstract
Symptomatic basilar and vertebral artery stenosis is a particularly morbid disease with an extremely poor natural history. Posterior circulation ischemia (PCI) accounts for 25 to 30% of all ischemic infarctions. Symptoms of vertebrobasilar insufficiency (VBI) can be nonspecific or nonfocal and diagnosis could be difficult to make. PCI symptoms or VBI should undergo a complete stroke workup, including MRI of the brain and CTA of the neck and head. Diagnostic cerebral angiography should also be obtained to document the degree and location of the stenosis, collateral circulation, and proximal endovascular access if an intervention is planned. The first line of treatment is optimal medical therapy including antiplatelet agents. Additional treatments should be considered if medical management fails as documented with progressive clinical strokes, silent ischemia, or hemodynamic failures. Endovascular submaximal balloon angioplasty (SBA) consists of progressive dilation of the intracranial stenosis with a semicompliant intracranial balloon. If the intracranial stenosis is recurrent, one should consider intracranial stenting. SBA is a relatively safe procedure; however, it is not free from complications that usually occur secondary to a poor understanding of the lesion anatomy, technical mishaps during navigation of the lesion or during angioplasty, inadequate platelet aggregation or anticoagulation, or residual flow issues due to stenosis or dissection. Bypass revascularization is not a common practice for VBI and it is limited to tertiary centers. These strategies should not be ignored and should take a very specialized location within the overall algorithm of VBI treatment.
Introduction
Intracranial atherosclerotic disease (ICAD) of the major intracranial arteries (carotid, middle cerebral, vertebral, or basilar) is a major cause of stroke and is associated with a high risk of recurrent stroke. The Comparison of Warfarin and Aspirin for Symptomatic Intracranial Arterial Stenosis (WASID) trial demonstrated that symptomatic intracranial basilar or vertebral artery (VA) stenosis is a particularly morbid disease with an extremely poor natural history. The Stenting versus Aggressive Medical Therapy for Intracranial arterial Stenosis (SAMMPRIS) and other randomized controlled trials have demonstrated that the first line of treatment for severe, symptomatic intracranial stenosis is medical treatment with antiplatelet agents; however, in select patients who fail medical therapy and have progressive transient ischemic attacks (TIAs) or stroke, there is a role for endovascular management with angioplasty and/or intracranial stenting.
Major controversies in decision making addressed in this chapter include:
Whether treatment is indicated or not in vertebrobasilar stenosis.
Drug selection and dosing regimens for medical treatment of intracranial vertebrobasilar stenosis.
Medical versus interventional treatment for intracranial vertebrobasilar stenosis.
Technical nuances for intracranial angioplasty and stenting.
Role of cerebrovascular surgery or bypass procedures for vertebrobasilar insufficiency (VBI).
Whether to Treat
In all patients with symptomatic stenosis of ≥70% of the vertebral and/or basilar arteries therapy should be instituted ( 1 , 2 in algorithm ). Therapy includes general cardiovascular risk reduction including weight loss, exercise, antihypertensive therapies, smoking cessation, strict diabetic control (if present), and high-dose statin therapy. Patients should also receive treatment with dual-antiplatelet therapy.
Endovascular treatment with intracranial angioplasty and stenting should be considered in patients who fail conservative management. Patients with a documented infarction in the vascular territory served by a severely stenotic vessel while on dual-antiplatelet therapy have a 35% stroke risk at 2 years ( 3, 4, 6, 7 in algorithm ). Patients with vulnerable plaques and/or poor collateral circulation are also considered to be in this high-risk category. Recently, using quantitative magnetic resonance angiography (MRA) evaluation of distal flow in vertebrobasilar disease, Amin-Hanjani et al found patients with greater than 20% reduction in distal flow from normal values had 70 and 78% event-free survival rates at 12 and 24 months compared with patients with preserved distal flow whose event-free rates were 96 and 87%, respectively. Thus, in patients who have been quoted as failed conservative management, the reported periprocedural morbidity and mortality of an intracranial stent, and/or angioplasty may be justified ( 3, 4, 6, 7 in algorithm ).
Conservative Treatment
Current evidence supports the use of aspirin and clopidogrel (Plavix). A typical regimen for initiating therapy would be a 650-mg loading dose of aspirin and 300-mg loading dose of clopidogrel, followed by aspirin 325 mg and clopidogrel 75 mg daily ( 1 , 2 in algorithm ).
Clopidogrel is a prodrug that is absorbed through the intestine and relies on conversion to an active metabolite via enzymes in the cytochrome P450 pathway. Clopidogrel irreversibly binds the platelet P2Y12 receptor, inhibiting ADP-mediated platelet activation and aggregation. The pharmacological response to clopidogrel is variable, with 20 to 40% of patients being classified as nonresponders because of low inhibition of ADP-induced platelet activation. This is believed to be due to polymorphisms in the CYP2C19 and CYP2C9 protein-coding genes.
The VerifyNow P2Y12 assay (Accumetrics Inc., San Diego, CA) is one test established to theoretically access the adequacy of platelet inhibition by clopidogrel. The VerifyNow assay is a point-of-care device that measures platelet aggregation as a function of light absorbance. This assay has been shown to be equivalent to other methods for assessing inhibition of platelet aggregation. Glycoprotein IIb/IIIa inhibitors tirofiban (Aggrastat) or eptifibatide (Integrilin) will yield abnormal and unreliable VerifyNow results for 2 days following administration and abciximab (ReoPro) will adversely affect the assay for 2 weeks. Patients with some inherited platelet disorders (e.g., von Willebrand factor deficiency) will not yield reliable test results as well.
Prasugrel (Effient) is a newer third-generation thienopyridine-like clopidogrel that does not rely on hepatic prodrug activation. Ticagrelor (Brilinta) is a different class Cyto-pentyl-triazolopyrimidine that in contrast to the thienopyridines reversibly inhibits the P2Y12 component of ADP receptor with similar effects on platelet inhibition. It is important to consider that no data currently support the safety or efficacy of prasugrel for the treatment of intracranial stenosis and its use carries a technical contraindication in patients with history of stroke. Additionally, there are case reports that suggest there may be an increased risk of hemorrhagic complications with the use of prasugrel and aspirin in neurointerventional procedures, but that does not reflect the authors’ current experience.
Anatomical Considerations
The VA originates from the first segment of the subclavian arteries, and in about 4% of people they will come off of the aortic arch. The VA has four different segments (▶ Fig. 8.1 ). The most common site of stenosis is at the VA ostium (see Chapter 9); however, plaque formation and stenosis can occur at any level of the posterior circulation. VAs can present different degrees of tortuosity and catheterization from a femoral approach can be challenging: sometimes, a radial or brachial approach is necessary. We suggest obtaining a computed tomography angiography (CTA) in all patients, to have a better understating of the anatomy prior to any interventions.
Collaterals play an important role in any stenoocclusive disease. Therefore, a full six-vessel cerebral angiography should be performed. Arterial branches from the external carotid artery (ECA; e.g., occipital artery [OA]) or subclavian artery (e.g., thyrocervical or costocervical branches) can supply the posterior circulation in chronic VA stenosis or occlusion. It is important to know the degree of contribution from anterior circulation through posterior communicating arteries (PCoAs). The VA can end in posterior inferior cerebellar artery (PICA) and contribute little or nothing to the contralateral side or basilar artery. This configuration rests the entirety of the basilar artery perfusion on one VA if no PCoAs are present.
The basilar and V4 vertebral segments can become extremely tortuous especially in the setting of long-standing hypertension; this only adds to the difficulty of endovascular treatment. The basilar artery is not an uncommon place for fenestrations to occur and these can make endovascular procedures more difficult. Although rare, beware for rare variants such as pro-atlantal or persistent fetal vessels, which can receive all, or most, of their supply from the anterior circulation and care should be taken, as carotid injury can have devastating consequences in this scenario.
Workup
Clinical Evaluation
Patients with VBI or posterior circulation ischemic symptoms should undergo a complete stroke workup. Cardiogenic etiologies of VBI must be considered and a thorough cardiovascular evaluation should be undertaken. High-grade intracranial stenosis can be dependent on adequate cardiac output. In patients with high-grade intracranial stenosis and concomitant cardiac dysfunction (e.g., dysrhythmia, atrial fibrillation), or hemodynamic instability (e.g., orthostatic hypotension), variations in perfusion pressure can produce symptoms in patients, and patient history should attempt to clarify the etiology of the symptoms.
Imaging
In the absence of magnetic resonance imaging (MRI) and documented recurrent diffusion-weighted imaging (DWI)-proven ischemia in patients who will be deemed a medical treatment failure, additional steps should be taken (e.g., loop recorders, tilt-table testing, sleep apnea testing) to clarify presenting complaints. Careful attention also should be paid during follow-up to the interval development of additional silent ischemic “hits,” which can be seen with meticulous comparisons of T2-weighted–fluid-attenuated reversion recovery (FLAIR) sequences on MRI examinations over time. We consider the appearance of new T2/FLAIR lesions referable to the stenotic lesion to represent failure of medical therapy and intervention should now be considered ( 2 in algorithm ).
In most instances, noninvasive imaging (i.e., MRA or CTA) is sufficient to establish a diagnosis of ICAD and guide initial treatment medical management; however, formal cerebral digital subtraction angiography (DSA) is also justifiable in the early stages to document the degree and location of stenosis as CTA will frequently overestimate the degree of a stenosis, and both CTA and MRA can be subject to artifact in evaluating the lower cervical vessels. This also allows for the documentation of collateral circulation, as well as proximal access issues, should intervention be entertained. It is important to remember that many of these patients will harbor tandem cervical and/or great vessel lesions, which may be treated more easily and can be obscured by artifact on noninvasive imaging studies. We strongly recommend thoroughly studying patients with ICAD and VBI to elucidate the likely etiology of the presenting event, as the probability of additional future presentations is high.
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