Stroke Mechanisms in Symptomatic Intracranial Atherosclerotic Disease

Abstract

Background and Purpose— In patients with symptomatic intracranial atherosclerotic stenosis, identifying the underlying stroke mechanisms may inform secondary prevention. We aimed to propose reproducible classification criteria for stroke mechanisms based on routine neuroimaging in symptomatic intracranial atherosclerotic stenosis and explore their clinical implications. Methods— We recruited patients with acute ischemic stroke attributed to 50% to 99% intracranial atherosclerotic stenosis in anterior circulation from 2 centers. Two investigators independently classified probable stroke mechanisms as parent artery atherosclerosis occluding penetrating artery, artery-to-artery embolism, hypoperfusion, and mixed mechanisms, with prespecified criteria based on infarct topography and magnetic resonance/computed tomography angiography. These stroke mechanisms were correlated with features of the patients at baseline and recurrent ischemic stroke in the same territory or relevant transient ischemic attack within 1 year. Results— Among 153 patients recruited, the most common stroke mechanisms were isolated hypoperfusion (35.3%) and mixed mechanism of artery-to-artery embolism and hypoperfusion (37.3%) that was associated with higher incidence of dyslipidemia ( P =0.045) and hypertension ( P =0.033) than patients with other stroke mechanisms. The proposed criteria showed substantial to excellent intrarater and interrater reproducibilities (κ, 0.791–0.908). Overall, 31 patients received interventional treatment of the diseased intracranial artery; 122 received medical treatment, among whom a mixed mechanism of artery-to-artery embolism and hypoperfusion at baseline was associated with higher risk of ischemic stroke in the same territory within 1 year (24.4% versus 7.8%; hazard ratio, 3.40; 95% CI, 1.25–9.20; log-rank P =0.010) than other mechanisms combined. Conclusions— Artery-to-artery embolism and hypoperfusion commonly coexist in ischemic stroke attributed to intracranial atherosclerotic stenosis, which may be associated with higher risk of stroke relapse.

Plaque morphology in acute symptomatic intracranial atherosclerotic disease

“…22 The higher cumulative infarction downstream of ulcerative plaques might suggest repetitive artery-to-artery thromboembolism. 25 This observation might explain the efficacy of dual antiplatelet regimen during acute stage of ICAD 26 27 and a potential therapeutic application of blood flow augmentation in clearing the stranded emboli at the watershed regions. 28 Basal ganglia or brainstem lacunar syndrome had been common in ICAD patients with infarct topography resembling small vessel disease.…”

“…29 With 3DRA, we revealed the frequent coexistence of adjoining BAD within the perforator-rich stenotic segments, constituting a competing stroke mechanism: parent artery atherosclerosis occluding branch/perforator. 25 In fact, understanding the spatial relationship between parent artery and branches/perforators might have further clinical implications. First, ostial involvement of branches/perforators might highlight the risk of branch jailing by 'snow-plow effect' during intracranial angioplasty/stenting.…”

Intracranial Atherosclerosis Coexisting With White Matter Hyperintensities May Predict Unfavorable Functional Outcome in Patients With Acute Cerebral Ischemia

“…Different pathogenesis has different recurrence risk. Previous reports showed that ICAS with multiple infarctions (indicated by an artery to artery mechanism) (17), borderzone infarcts and impaired collateral flow (hemodynamic markers) (18), or a mixed mechanism of artery to artery embolism and hypoperfusion (19) were more likely to have recurrent stroke. WMHs are often considered to be a consequence of chronic hypoperfusion (20).…”

Intracranial Atherosclerotic Stenoses: Pathophysiology, Epidemiology, Risk Factors and Current Therapy Options

“…Of note, a combination of more than one mechanism is also possible [ 32 – 34 ]. For example, impaired washout of emboli may occur in the case of embolism and hypoperfusion with/without poor collaterals combined [ 35 ].…”