Surgical and Endovascular Management of Vertebrobasilar Atherosclerosis

Epidemiology and Natural History

Atherosclerotic disease of the vertebrobasilar system accounts for 25–35% of ischemic events in the posterior circulation . Patients presenting with posterior circulation TIA or stroke in the presence VBA are at significantly greater risk of developing recurrent events than symptomatic lesions affecting the anterior lesion . A review of patients suffering VBA found 46% of patients presenting with stroke or TIA suffered a recurrent event during the following 23 months, while a systematic review of symptomatic VBA found recurrent stroke risk to be as high as 33% within the first 90-days after initial event .

Anatomical Features of the Vertebrobasilar System

Each vertebral artery (VA) arises as the first branch from their respective subclavian artery. The extraosseous segment (V1) of the VA extends from the origin, behind the anterior scalene, to its entrance of the transverse foramen of the 6th cervical vertebra. The foraminal segment (V2) courses through the transverse foramina of C6 through C1, providing segmental branches to the spinal cord and musculature until it emerges beside the lateral mass of the atlas. The extraspinal segment (V3) then forms a posterior-medial loop around the atlantooccipital articulation, coursing on the superior surface of the arch of the atlas. The intracranial segment (V4) begins where the artery penetrates the dura, and fuses with the contralateral VA to form the basilar artery, ventral to the pontomedullary junction.

The normal diameter of the VA lumen is 3–5 mm, with unilateral hypoplasia of the right VA (diameter ≤2 mm) in 75–85% of cases where the vertebral arteries are asymmetric with respect to size . The basilar artery is typically 3–4 mm in diameter and provides nearly 20 paramedian and circumflex perforating arteries to the pons and midbrain. The vertebrobasilar circulation irrigates the entire brain stem, cerebellum, occipital lobes, and part of the temporal lobes.

The intracranial arteries lack external elastic lamina, have thin adventitia, and are suspended within the leptomeninges, making them susceptible to injury from both endoluminal and microsurgical manipulation. Intracranial arteries also have well-developed internal elastic lamina and circularly arranged smooth muscle which can be damaged by over-dilation, possibly contributing to greater recoil following angioplasty. Numerous perforating arteries arise from the vertebrobasilar system that can be damaged and/or occluded by displacement of the atheromatous plaque during angioplasty and stent deployment or during microsurgical dissection and vessel manipulation.

There are several collateral pathways to the vertebrobasilar system that may compensate for flow-limiting disease, including leptomeningeal collaterals, persistent carotid-vertebrobasilar anastomoses, and external carotid artery (ECA)-segmental VA anastomoses. However, the existence and hemodynamic capacity of these collaterals greatly varies between individuals. Anatomical variants that could potentially limit compensatory flow to the vertebrobasilar territory in the setting of VBA include hypoplasia or absence of the contralateral VA, posterior communicating arteries, and P1 segment of the PCAs .

Pathophysiological Features of Vertebrobasilar Atherosclerosis

VBA produces ischemic stroke through three primary mechanisms, (1) distal embolization, (2) occlusive disease at perforator ostia, and (3) hemodynamic failure . Coexistence of embolism and hemodynamic failure portends a particularly poor prognosis . Beyond conventional atherosclerotic risk factors, several pathophysiological characteristics contribute to the risk of stroke recurrence in VBA and have serious implications regarding tailoring treatment to the underlying disease.

The morphology of atherosclerotic lesions plays a significant role in both risk and timing of recurrent stroke. Thromboembolism from unstable atheroma rupture is considered to be an important mechanism of stroke in VBA . Radiographic patterns suggestive of a thromboembolic mechanism include branch-vessel territory infarcts and/or perforator infarcts adjacent to the plaque. The existence of a period of thromboembolic lability in VBA has been supported by detection of emboli distal to the stenosis in patients presenting after stroke or TIA . A systematic review investigating the timing of recurrent stroke in symptomatic VBA found the risk of recurrence within 30 days to be 33% suggesting a period of increased thromboembolic lability or hemodynamic instability in the weeks following plaque rupture . Complicating intervention, unstable atherosclerotic lesions have also been cited as potential causes of the high periprocedural stroke and death rates that occur with early endovascular therapy for VBA .

Severity of stenosis is a traditional surrogate for hemodynamic status and has been associated with increased risk of stroke recurrence. The Oxford Vascular Study group found stenosis ≥50% in VBA to be associated with 3 times greater risk of recurrent stroke and/or TIA (up to 46% of patients) independent of cardiovascular risk factors, while the WASID study found twice the risk of stroke recurrence in those with >70% stenosis . Conversely, other studies have found that stenosis >70% was not associated with risk of stroke recurrence, suggesting stenosis alone might be an insufficient surrogate of hemodynamic impairment . The GESICA study analyzed patients with ≥50% stenosis and found that in patients suspected of having hemodynamic insufficiency based on symptomatology (multiple recurrent events, dependency of symptoms on body position, exercise, and so on) 61% developed recurrent TIA or stroke (vs. 32% of those without) . The VERiTAS Study Group evaluated distal flow status in VBA using phase-contrast quantitative MRA (QMRA) and found that although parent vessel flow diminishes above 80% stenosis, hemodynamic insufficiency in the vascular territory supplied by the stenosed vessel was not well predicted by severity of stenosis . These data support the idea that the hemodynamic consequences of high-grade intracranial stenosis are primarily determined by the presence and vigor of posterior circulation collaterals.