Borderzone Infarcts and Recurrent Cerebrovascular Events in Symptomatic Intracranial Arterial Stenosis: A Systematic Review and Meta-Analysis

Abstract

Background and Purpose Intracranial arterial stenosis (ICAS)-related stroke occurs due to three primary mechanisms with distinct infarct patterns: (1) borderzone infarcts (BZI) due to impaired distal perfusion, (2) territorial infarcts due to distal plaque/thrombus embolization, and (3) plaque progression occluding perforators. The objective of the systematic review is to determine whether BZI secondary to ICAS is associated with a higher risk of recurrent stroke or neurological deterioration.Methods As part of this registered systematic review (CRD42021265230), a comprehensive search was performed to identify relevant papers and conference abstracts (with ≥20 patients) reporting initial infarct patterns and recurrence rates in patients with symptomatic ICAS. Subgroup analyses were performed for studies including any BZI versus isolated BZI and those excluding posterior circulation stroke. The study outcome included neurological deterioration or recurrent stroke during follow-up. For all outcome events, corresponding risk ratios (RRs) and 95% confidence intervals (95% CI) were calculated.Results A literature search yielded 4,478 records with 32 selected during the title/abstract triage for full text; 11 met inclusion criteria and 8 studies were included in the analysis (n=1,219 patients; 341 with BZI). The meta-analysis demonstrated that the RR of outcome in the BZI group compared to the no BZI group was 2.10 (95% CI 1.52–2.90). Limiting the analysis to studies including any BZI, the RR was 2.10 (95% CI 1.38–3.18). For isolated BZI, RR was 2.59 (95% CI 1.24–5.41). RR was 2.96 (95% CI 1.71–5.12) for studies only including anterior circulation stroke patients.Conclusion This systematic review and meta-analysis suggests that the presence of BZI secondary to ICAS may be an imaging biomarker that predicts neurological deterioration and/or stroke recurrence.

Emergent Large Vessel Occlusion due to Intracranial Stenosis: Identification, Management, Challenges, and Future Directions

“…A post hoc analysis from the SAMMPRIS trial (Stenting Versus Aggressive Medical Therapy for Intracranial Arterial Stenosis) showed that infarct pattern is a strong predictor of recurrent stroke in symptomatic ICAS patients. 9 Among 101 patients, there were more recurrent strokes in the territory with BZI compared with non-BZI patients (14/53 [ 39 The use of perfusion imaging has also been suggested to predict risk of early stroke recurrence in ICAS patients. 40,41 A single-center study evaluated the association between impaired perfusion and early stroke recurrence in patients with symptomatic ICAS.…”

Hemodynamic Impairment of Blood Pressure and Stroke Mechanisms in Symptomatic Intracranial Atherosclerotic Stenosis

“…ntracranial atherosclerotic stenosis (ICAS) is emerging as a compelling cause of ischemic stroke and is associated with a poor prognosis. [1][2][3] The stroke mechanisms of symptomatic ICAS include artery-to-artery embolism, hypoperfusion, branch atheromatous disease, and large vessel occlusion, where artery-to-artery embolism is a result of plaque rupture and hypoperfusion is consequent to compromised blood flow, [4][5][6] which often coexist. 4 From a physics standpoint, hemodynamic impairment may have a significant influence on the stroke mechanism of atherosclerotic origin.…”

“…[1][2][3] The stroke mechanisms of symptomatic ICAS include artery-to-artery embolism, hypoperfusion, branch atheromatous disease, and large vessel occlusion, where artery-to-artery embolism is a result of plaque rupture and hypoperfusion is consequent to compromised blood flow, [4][5][6] which often coexist. 4 From a physics standpoint, hemodynamic impairment may have a significant influence on the stroke mechanism of atherosclerotic origin. [7][8][9] For example, a heightened mechanical burden has the potential to induce deformation and mechanical disruption of plaque, while low perfusion pressure may lead to hypoperfusion.…”