Complication of Endovascular Treatment of Intracranial Stenosis

Introduction

Intracranial atherosclerotic disease (ICAD) is defined as atherosclerosis of the large intracranial arteries, namely the intracranial internal carotid artery (ICA), intracranial vertebral and basilar arteries, middle, anterior and posterior cerebral arteries, and their cortical branches (up to M3, A3, or P3 segments). Atherosclerotic disease of the small perforator and penetrating arteries is termed as small vessel (or small artery) disease. The term intracranial stenosis (ICS) usually denotes atherosclerotic narrowing of the main segments of the intracranial arteries involving the intracranial ICA, proximal segments of middle cerebral artery (MCA) (M1), anterior cerebral artery (ACA) (A1), posterior cerebral artery (PCA) (P1), basilar artery (BA), and the distal segment of vertebral artery (V4).

ICAD is a major cause of ischemic stroke accounting for up to 10% of strokes in the United States and as many as 30% in Asian, Hispanic, and African American communities. After one symptomatic event, the risk of recurrent stroke may be as high as 15% per year. Treatment with aspirin (or warfarin) in addition to other risk factor modification reduces the risk but the risk may still be as high as 22% at 2 years despite therapy. Multiple randomized clinical trials including SAMMPRIS (Stenting and Aggressive Medical Management for Preventing Recurrent Stroke in Intracranial Stenosis) and VISSIT (The Vitesse Intracranial Stent Study for Ischemic Stroke Therapy) have evaluated the outcome after medical management alone and with percutaneous angioplasty and stenting. In spite of all efforts, management of ICAD is still challenging and optimal treatment modality is still unclear.

Pathophysiology of Strokes in Intracranial Stenosis

It is imperative to understand the pathophysiology of strokes in ICAD patients to perceive the complications associated with its treatment. ICS can produce symptoms through the following mechanisms :

• artery-to-artery emboli

• hemodynamic insufficiency

• acute thrombotic occlusion (unstable plaque)

• branch (perforator) occlusive disease

The literature tends to be unclear regarding in-depth descriptions of these pathophysiologic mechanisms in individual patients. This is particularly relevant in the case of branch occlusive disease (BOD). This entity is often mistakenly identified as small vessel disease while in reality it is ICAD that incorporates the perforator origins. The plaques in these cases have been identified on high resolution MRI to be unstable, despite a relatively smaller extent of luminal stenosis. This has potential implications in interpreting data from stenting trials. MRI in such cases shows small deep “lacunar” infarcts. The phenomenon of hypoperfusion from severe stenosis is well described and occurs as a result of exhausted cerebrovascular reserve in the affected vascular territory. Patients typically develop orthostatic or exercise/stress-related ischemic symptoms. MRI reveals multiple water-shed cortical infarcts in the affected arterial territory. Patients with ICS who have hypoperfusion symptoms have a higher recurrent stroke risk than those without. Although SAMMPRIS failed to identify these patients as benefiting from stenting, well-designed prospective single center studies have shown impressive reduction in recurrent ischemic events in such patients following extracranial–intracranial (EC–IC) bypass. Finally, one of the important causes of stroke in ICAD patients is the artery-to-artery embolism in which small emboli formed de novo because of relative stasis or plaque rupture may travel along the gradient to smaller distal territories to produce focal strokes.

All three of these pathomechanisms produce distinct stroke patterns and have different therapeutic and prognostic implications. For example, perforator related strokes are usually located in the subcortical or basal ganglia region, hypoperfusion strokes affect the water-shed areas, and artery-to-artery embolic strokes affect distal small vascular territories. Hypoperfusion related border-zone infarct was the most common pattern observed in the SAMMPRIS trial in contrast to the territorial strokes from artery-to-artery emboli seen in the WASID (Warfarin Aspirin Symptomatic Intracranial Disease) trial. Nevertheless, the stroke pattern in ICAD patients can be mixed, involving more than one pathomechanism.