Vertebral Artery Reconstruction for Vertebrobasilar Ischemia



Vertebral Artery Reconstruction for Vertebrobasilar Ischemia



Ramon Berguer


Vertebrobasilar ischemia (VBI) is a syndrome with different etiologies. The term insufficiency, which is still commonly used, should be abandoned because it implies only a low-flow condition affecting the vertebrobasilar territory and ignores the important mechanism of microembolization that constitutes approximately a third of the VBI pathology. Low-flow VBI is more often than not caused by a drop in systemic blood pressure, but it can also be the result of a mild drop in central aortic pressure compounded with severe stenosis or occlusion of the vertebral or basilar arteries. A patient may have a severe vertebral artery (VA) stenosis or occlusion but be free of symptoms because of flow compensation from the opposite vertebral artery or from the internal or external carotid arteries. Symptoms caused by vertebral artery dissection can be a result of both the low-flow mechanism (collapse of the true lumen by the dissecting hematoma) or microembolization (reentry of fragments of the dissecting hematoma into the true lumen through the distal tear of the dissection).


When considering low-flow VBI, it is important to bear in mind that a cause-and-effect relationship between the VA stenosis and the syndrome cannot be presumed until a number of medical entities have been ruled out as being causative factors. Treatment of low-flow VBI requires consideration of the different possible etiologies of this clinical entity, and to rule them out, the collaboration of a cardiologist, an otolaryngologist, and a neurologist are often needed.


Once the common medical causes of VBI have been ruled out, a computed tomography arteriogram (CTA) or a conventional arteriography is indicated. When an arteriogram is needed, special techniques and views are required.


The VA is conventionally divided into four segments:




Patient Evaluation


The syndrome of VBI is well defined even though its clinical manifestations are more ambiguous and less precise than those caused by ischemia of the anterior circulation. Standard neurologic textbooks give a detailed description. A brief listing of symptoms includes any or several of the following: dizziness, vertigo, diplopia, blurring of vision, tinnitus, perioral numbness, alternating paresthesias, and drop attacks.


The history should clarify the precise sequence of events that results in VBI. In most patients, the symptoms, particularly lightheadedness, appear on orthostatism when rising from bed or from a chair. Although this does not rule out a VA lesion as etiology, it draws attention to the possibility that one may be dealing with poor peripheral vasomotor control as seen in diabetics or in patients taking antihypertensive drugs experiencing autonomic dysfunction.


Concurrence of palpitation during attacks of VBI suggests a cardiac arrhythmia causing a temporary drop in cardiac output and hypotension. Vertigo or syncope triggered by neck rotation or extension suggest extrinsic compression of a VA in its bony cervical course (segments V2 and V3) and requires a specific arteriography technique—dynamic angiography—to demonstrate this mechanism. Carotid symptoms are uncommon in patients experiencing VBI. When they do occur, it is usually a case of bilateral internal carotid artery (ICA) occlusion and an anterior circulation dependent on posterior (basilar) inflow.


Examination of the patient must include the taking of bilateral brachial pressures. A difference greater than 25 mm Hg suggests a subclavian artery stenosis or occlusion and the possibility of subclavian steal syndrome. A drop in brachial pressure after the patient stands briskly shows that an orthostatic component is present. A 25 mm Hg drop in systolic pressure after briskly standing up is the arbitrary indicator of significant orthostatic hypotension.


Supraclavicular bruits can suggest subclavian or VA disease but have no specificity, and the absence of bruits has no clinical significance. A dampened and delayed radial pulse in one wrist is evidence of a lengthened and narrowed pulse pathway associated with a subclavian steal syndrome.


Vertigo and nystagmus provoked by brisk head rotation to both sides suggests labyrinthine dysfunction. Slow rotation to one side that, after a delay of 1 to 2 seconds, results in dizziness, dysequilibrium, or syncope suggests external compression of the VA by bone (bow hunter syndrome).


Duplex scanning of both carotid and vertebral arteries is indicated in all cases. Holter monitoring of cardiac rhythm is indicated if cardiac arrhythmia is suspected. The antihypertensive drugs the patient is taking and their dosage should be reviewed. In specific cases (symptoms induced by brisk shaking of the head), labyrinthine function tests are indicated.


The primary imaging tool for vertebral artery disease is a CTA of the head and neck. CTA displays stenosis, dissection, occlusion, and false aneurysm of the VA and will give information on the status of the posterior communicating and basilar arteries. The search for infarctions in the brain stem or cerebellum requires magnetic resonance imaging (MRI) because computed tomography (CT) cannot resolve the small infarcts occurring in the brain stem. The brain stem is surrounded by dense bone that causes diffraction artifacts.


The standard arteriogram includes at least an intraarterial digital view of the arch in both the right and the left posterior oblique projections and selective injections of both carotids and the left subclavian arteries. The vertebrobasilar system must be displayed in its entirety from the origin of the VA to the top of the basilar artery. There is no reason to selectively catheterize a VA, a procedure that can result in a dissection.


Arch views will document if the left VA originates from the arch (7%). The point of entrance of the VA into the cervical vertebral canal should be determined because this information is relevant to the choice of operation. Vertebral arteries are usually of different size, and deciding which one is dominant is important because the latter will be the one chosen for reconstruction in patients with low-flow symptoms. The left VA is more commonly the dominant one. Incomplete or hypoplastic vertebrals that terminate in a posteroinferior cerebellar artery are not uncommon (7%). These arteries do not contribute to basilar flow. When quantifying disease in both VA in order to make a surgical decision, these incomplete arteries are considered occluded.


The most common and most easily missed atherosclerotic lesion of the VA is a short and severe stenosis at its origin. The entire lesion may be obscured by the superimposition of the subclavian artery. This requires additional oblique views to throw off the first segment of the subclavian artery that obscures the origin of the VA.


If one or both vertebral arteries are occluded, demonstration of their reconstitution at V3 is sought in subtracted and delayed views. This provides essential information in the planning stage of a VA reconstruction because demonstration of reconstituted V3 and V4 segments distal to a proximally occluded VA makes it technically possible to bypass the artery at the C2–C1 level to provide new basilar artery inflow.


At, or just distal to, the level of the atlanto-occipital membrane, the VA can have a short stenosis difficult to discern in the usual arteriographic views. It is important not to overlook these stenoses because, when they are critical, they contraindicate a proximal VA reconstruction. The basilar artery in the lateral projection is overlain by the temporal bone and in the Towne anteroposterior (AP) projection is foreshortened. Its normalcy needs to be assessed because severe disease of the basilar artery contraindicates any VA reconstruction.


In patients with rotational symptoms, additional views (dynamic arteriography) are indicated. These are done by selective subclavian injections with rotation-extension of the head while inducing axial compression of the latter to show the interruption of VA flow, usually in the V3 segment (bow hunter syndrome).

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Aug 25, 2016 | Posted by in CARDIOLOGY | Comments Off on Vertebral Artery Reconstruction for Vertebrobasilar Ischemia

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