Border Zone Infarcts Research Articles

Acute Border Zone Infarcts in Hypereosinophilic Syndrome

Acute Border Zone Infarcts in Hypereosinophilic Syndrome

Spontaneous calcified cerebral emboli: a comprehensive review and proposed diagnostic criteria.

Spontaneous calcified cerebral emboli (SCCE) secondary to aortic valve calcification are a rare and underreported cause of acute ischaemic stroke. Only five cases of SCCE secondary to bicuspid aortic valve calcification have been reported in the literature. This review includes a unique case example of acute ischaemic stroke secondary to SCCE, as the first manifestation of a calcified bicuspid aortic valve. This is the first clinical case of calcified cerebral emboli (CCE) associated with borderzone infarction ('cortical ribbon sign'). Whilst previously assumed that most CCE are secondary to iatrogenic causes, recent literature suggests the majority of CCE are spontaneous and clinically silent. Despite CT imaging widely considered the 'gold standard' for diagnosis, CCE are frequently misdiagnosed and missed entirely. Misdiagnosis of CCE may have catastrophic consequences due to the high risk of recurrence and missed opportunity to prevent neurological disability and death. This review presents a revised CCE diagnostic criteria, using evidence that has emerged over the last decade to create both Compulsory (Major) and Supporting (Minor) criteria. Current CCE management is not evidence based and remains largely speculative. SCCE may be the first manifestation of cardiac or vascular disease and diagnosis should trigger aggressive treatment of emboligenic sources. Future epidemiological studies, analysing symptomatic and asymptomatic SCCE patients, would be beneficial in providing accurate quantification of disease burden. Other future research directions include exploring intracranial stenting for CCE revascularisation and cerebral intravascular lithotripsy.

Clinical characteristics and imaging patterns of cerebral infarction with outcomes of carotid artery stenting in symptomatic carotid stenosis: An eight-year journey

Objectives: Carotid artery stenting (CAS) for symptomatic carotid stenosis (SCS) has emerged as an attractive option in recent times. CAS and topographical patterns of stroke in symptomatic stenosis have been inadequately addressed. With this objective, we conducted a study to analyze infarct patterns and complications of carotid stenting and determine outcome predictors after stenting. Materials and Methods: A single-center retrospective study from January 01, 2015, to December 31, 2022, on patients with SCS, who underwent carotid stenting with at least six months of follow-up was conducted. Infarct patterns, angiographic findings, procedural complications, and outcomes (favorable [modified Rankin scale (mRS) ≤2] or unfavorable [mRS >2]) were recorded. Chi-square, analysis of variance for qualitative and quantitative variables was employed. Significant variables on univariate analysis were entered into regression and outcome predictors were determined. Results: Ninety-six records were included in the study. Forty-six (47.91%), 12 (12.50%), and 38 (39.58%) patients had territorial infarcts (TIs), border-zone infarcts (BZIs), and mixed infarcts (MIs). National Institutes of Health Stroke Scale (NIHSS) <5 and transient ischemic attack (TIA) were significant (P < 0.05) while the circle of Willis anomalies were comparable in TI versus BZI versus MI. Bradycardia (54.16%) and vessel spasm (19.79%) were noted during stenting. Successful revascularization (residual stenosis <20%) was achieved in 97.87%. Procedural complications were comparable in TI versus BZI versus MI. Minor cerebral hyperperfusion syndrome (CHS) with headache (9.57%), seizure (2.12%) peaking between 6 and 12 h, and severe with basal ganglia hemorrhage and death occurred. There were no major strokes. 64.13% and 75.28% achieved a favorable mRS at one and six months, respectively. NIHSS ≤10, early intervention (≤ 2 weeks), absence of diabetes, hypertension, or ischemic heart disease were significant (P < 0.05) for a favorable outcome. NIHSS ≤10, absence of hypertension at one month and NIHSS ≤10, absence of diabetes at six months were predictors of a favorable outcome. Conclusion: Severe carotid disease predisposed to CHS. Overall, CAS was a safe and effective procedure with 74.15% achieving favorable outcomes at six months.

Clinical implications of haemodynamics in symptomatic intracranial atherosclerotic stenosis by computational fluid dynamics modelling: a systematic review

BackgroundRecently, computational fluid dynamics (CFD) has been used to simulate blood flow of symptomatic intracranial atherosclerotic stenosis (sICAS) and investigate the clinical implications of its haemodynamic features, which were systematically...

Development and validation of a SCORing systEm for pre-thrombectomy diagnosis of IntraCranial Atherosclerotic Disease (Score-ICAD)

BackgroundEarly identification of intracranial atherosclerotic disease (ICAD) may impact the management of patients undergoing mechanical thrombectomy (MT). We sought to develop and validate a scoring system for pre-thrombectomy diagnosis of...

Characteristics of Atherosclerotic Plaques and Stroke Mechanism in Patients with Border-Zone Infarcts: A High-resolution Magnetic Resonance Imaging Study

BackgroundRelatively little is known about the plaque characteristics of border-zone infarcts and how they differ between cortical border-zone (CBZ) and internal border-zone (IBZ) infarcts. MethodsWe conducted a prospective observational cohort study of patients of intracranial atherosclerotic disease who underwent high-resolution magnetic resonance imaging (HR-MRI) examination. Individuals with border-zone infarcts in the middle cerebral artery (MCA) territory, detected by diffusion-weighted imaging, were enrolled. Plaque morphological and compositional parameters of both IBZ and CBZ groups were compared. Independent predictors were identified using a binary logistic regression model, and the sensitivity and specificity of the model were assessed using a receiver operating characteristic curve. Kaplan-Meier survival analysis further explored differences in stroke recurrence between BZ patients with mono or dual antiplatelet therapy. ResultsWe reviewed 101 symptomatic patients with border-zone infarcts (BZ) within the MCA territory in the study. Out of the patients meeting the imaging eligibility criteria, we detected 34 cases with isolated IBZ, 23 cases with isolated CBZ, and 6 cases with both IBZ and CBZ infarcts. Those with IBZ infarcts had a higher plaque burden than those without (p<0.001), and those with CBZ infarcts exhibited a complicated plaque less frequently than those without (37.9% vs 67.6%, p=0.018). In those with isolated IBZ or CBZ infarcts, plaque burden was independently associated with isolated IBZ infarcts (odd ratio=1.08; 95% CI, 1.02-1.15; p=0.023). During the median follow-up period of 37 (27, 50) months, 13.8% of patients receiving early dual antiplatelet treatment and 30.4% of those on single antiplatelet therapy experienced stroke recurrence (p=0.182). ConclusionsIntracranial atherosclerotic plaque morphology and composition differ between patients with IBZ and those with CBZ infarcts. Higher plaque burden is more associated with IBZ infarcts.

Cerebrovascular disease in patients with antiphospholipid antibody syndrome: a transcranial Doppler and magnetic resonance imaging study.

Transcranial Doppler (TCD) and brain MRI may be useful in evaluating patients with APS, helping to stratify the risk of cerebrovascular ischaemic events in this population. This study aimed to assess the frequency of brain MRI abnormalities in patients with primary antiphospholipid syndrome, secondary antiphospholipid syndrome and SLE and correlate to TCD findings. The study, conducted over four years at two autoimmune disease referral centres, included 22 primary antiphospholipid syndrome patients, 24 secondary antiphospholipid syndrome patients, 27 SLE patients without APS and 21 healthy controls. All participants underwent TCD to assess cerebral haemodynamics, detect microembolic signals and evaluate right-to-left shunts, followed by brain MRI and magnetic resonance angiography. MRI scans were reviewed for acute microembolism, localized cortical infarctions, border infarctions, lacunar infarctions, ischaemic lesions, white matter hyperintensity, micro and macro haemorrhages and arterial stenosis ≥50% of the cervical carotid artery, by two neuroradiologists blinded to the clinical data. Brain MRI findings were similar between the groups, except for lacunar infarction, more frequent in patients with secondary antiphospholipid syndrome (P = 0.022). Patients with intracranial stenosis detected by TCD had a higher frequency of territorial infarction (40% vs 7.5%, P = 0.02), lacunar (40% vs 11.3%, P = 0.075) and border zone infarcts (20% vs 1.9%, P = 0.034). Patients with intracranial stenosis presented a higher frequency of territorial, lacunar and border zone infarcts, suggesting that evaluating the intracranial vasculature should not be neglected in patients with APS and stroke.

Abstract 87: Predictive Scoring System for Pre-Thrombectomy Diagnosis of Intracranial Atherosclerotic Disease LVOS

Introduction: Early identification of intracranial atherosclerotic disease (ICAD) underlying large vessel occlusion strokes (LVOS) may allow for mechanical thrombectomy (MT) optimization. We sought to create a pre-procedural scoring system to predict ICAD. Methods: Retrospective analysis of prospectively collected MT databases from 2 comprehensive stroke centers (derivation and validation) including patients with anterior circulation LVOS. ICAD cases were matched for age / sex (1:1) to non-ICAD controls and stepwise logistic regression utilized for various clinical and radiological (NCCT, CTA and CTP) variables. Calibration slope / intercept as well as the area under curve (auROC) were assessed. Results: Of 2870 MTs within the study period, 174 anterior circulation ICAD (6.6%) were matched with 174 controls (n=348) in the derivation cohort. Multivariable analysis β coefficients lead to a 20 point-scale: absence of AF (5), vascular risk factor burden (1 for each: hypertension, diabetes, smoking, hyperlipidemia), CTA multifocal ICAD (3), absence of cortical infarcts (3), presence of borderzone infarct (3), calcium at the siphon (2). The validation cohort comprised 75 ICAD patients (6.9% of 1359 MTs) and 75 controls. AuROC for the derivation cohort was 0.88(0.84-0.91) while for the validation cohort 0.82(0.73-0.89). Calibration slope and intercept showed a good fit for the development cohort although with overestimated risk for the validation cohort. After intercept adjustment, the overestimation was corrected (intercept 0; 95%CI -0.5-0.5 / slope 0.8 95%CI 0.5-1.1). In the full cohort (n=498), ≥ 11 points showed the best performance for distinguishing ICAD from non-ICAD patients, with a sensitivity 0.71 (0.65-0.78) and specificity 0.82 (0.77-0.87), a positive likelihood ratio of 3.92 (2.92, 5.28) and a negative LR of 0.35 (0.28, 0.44). Scores ≥ 12 showed 90% specificity, although sensitivity of 63% (55%-69%). Conclusion: We developed a predictive scoring system for pre-procedural diagnosis of ICAD LVOS with satisfactory discrimination and calibration based on clinical and non-invasive radiological data.

Abstract 223: Pre‐Thrombectomy Diagnosis of Large Vessel Occlusion with Underlying Intracranial Atherosclerotic Disease

Introduction Intracranial atherosclerotic disease (ICAD) is one of the leading causes of ischemic stroke. We sought to identify variables associated with ICAD underlying large vessel occlusion strokes (LVOS) to facilitate pre‐procedural diagnosis. Methods Retrospective analysis of a prospectively collected thrombectomy single comprehensive stroke center database. Inclusion criteria: anterior circulation occlusion involving the intracranial ICA, MCA‐M1/M2/M3 or ACA(A1‐A2‐A3). ICAD cases were matched for age and sex in a 1:1 ratio to non‐ICAD controls. Results A total of 348 patients were included in the analysis. Patients with ICAD more frequently presented with vascular risk factors. ICAD LVOS showed less frequent atrial fibrillation(AF)(4%vs31%,P=0.001), and lower baseline NIHSS(14vs17,P=0.002) compared to the non‐ICAD group. The ICAD group less frequently showed hyperdense vessel sign and territorial cortical infarcts, but presented more frequently borderzone, deep subcortical and bilateral infarcts on CT compared to the non‐ICAD group. ICAD strokes had higher ASPECTS, and more frequently had calcifications at the carotid siphon as well as multifocal intracranial stenosis on CTA. CTA collaterals scores were comparable between groups. The ICAD group had lower median infarct core volume (1vs12 ml;P&gt;0.001), Tmax&gt;4s (249vs276 ml;P&gt;0.003), and Tmax&gt;6s (97vs140 ml;P&lt;0.003) and higher Tmax&gt;4:6 s ratio (2vs1;P=0.007) on CTP compared to non‐ICAD group. On multivariable analysis, absence of AF, absence of cortical infarcts, presence calcium at ipsilateral carotid siphon, cerebrovascular stroke risk factors burden (DM‐HTN‐Hyperlipidemia‐smoking), borderzone infarcts either (superficial cortical or Internal deep border zone), and multifocal intracranial stenosis were independent factors associated with ICAD. The model (table 1) by AUC for the whole model had sensitivity of 88% [P=&lt;0.001,95%CI(0.84‐0.91)]. Conclusion In patients with anterior circulation LVO strokes, our study suggests that presence of CVS risk factors burden, calcium at carotid siphon, borderzone infract pattern, absence of territorial cortical infarct pattern, multifocal intracranial stenosis, and absence of AF were predictors for ICAD. Additional validation is warranted

Cerebral hemodynamics and stroke risks in symptomatic intracranial atherosclerotic stenosis with internal versus cortical borderzone infarcts: A computational fluid dynamics study

There may be different mechanisms underlying internal (IBZ) and cortical (CBZ) borderzone infarcts in intracranial atherosclerotic stenosis. In 84 patients with symptomatic, 50-99% atherosclerotic stenosis of M1 middle cerebral artery (MCA-M1) with acute borderzone infarcts in diffusion-weighted imaging, we classified the infarct patterns as isolated IBZ (n = 37), isolated CBZ (n = 31), and IBZ+CBZ (n = 16) infarcts. CT angiography-based computational fluid dynamics models were constructed to quantify translesional, post-stenotic to pre-stenotic pressure ratio (PR) in the MCA-M1 lesion. Those with IBZ infarcts were more likely to have a low PR (indicating impaired antegrade flow across the lesion) than those without (p = 0.012), and those with CBZ infarcts were more likely to have coexisting small cortical infarcts (indicating possible embolism) than those without (p = 0.004). In those with isolated IBZ or CBZ infarcts, low PR was independently associated with isolated IBZ infarcts (adjusted odds ratio = 4.223; p = 0.026). These two groups may also have different trajectories in the stroke risks under current medical treatment regimen, with a higher risk of same-territory ischemic stroke recurrence within 3 months in patients with isolated IBZ infarcts than isolated CBZ infarcts (17.9% versus 0.0%; log-rank p = 0.023), but similar risks later in 1 year.

Posterior Reversible Leucoencephalopathy Syndrome: Case Series, Comments, and Diagnostic Dilemma.

To report a series of patients with clinical and radiological features suggestive of posterior reversible encephalopathy syndrome (PRES) related to diverse etiologies emphasizing its pathophysiological basis. Posterior reversible encephalopathy syndrome (PRES) may present with a broad range of clinical symptoms from headache and visual disturbances to seizure and altered mentation. Typical imaging findings include posterior-circulation predominant vasogenic edema. Although there are many well-documented diseases associated with PRES, the exact pathophysiologic mechanism has yet to be fully elucidated. Generally accepted theories revolve around disruption of the blood-brain barrier secondary to elevated intracranial pressures or endothelial injury induced by ischemia from a vasoconstrictive response to rising blood pressure or toxins/cytokines. While clinical and radiographic reversibility is common, long-standing morbidity and mortality can occur in severe forms. In patients with malignant forms of PRES, aggressive care has markedly reduced mortality and improved functional outcomes. Various factors that have been associated with poor outcome include altered sensorium, hypertensive etiology, hyperglycemia, longer time to control the causative factor, elevated C reactive protein, coagulopathy, extensive cerebral edema, and hemorrhage on imaging. Reversible cerebral vasoconstriction syndromes (RCVS) and primary angiitis of the central nervous system (PACNS) are invariably considered in the differential diagnosis of new cerebral arteriopathies. Recurrent thunderclap headache (TCH), and single TCH combined with either normal neuroimaging, border zone infarcts, or vasogenic edema, have 100% positive predictive value for diagnosing RCVS or RCVS-spectrum disorders. Diagnosis of PRES in some circumstances can be challenging and structural imaging may not be sufficient to distinguish it from other differential diagnostic considerations like ADEM. Advanced imaging techniques, such as MR spectroscopy or positron emission tomography (PET) can provide additional information to determine the diagnosis. Such techniques are more useful to understand the underlying vasculopathic changes in PRES and may answer some of the unresolved controversies in pathophysiology of this complex disease. Eight patients with PRES resulting from different etiologies varying from pre-eclampsia/eclampsia, post-partum headache with seizures, neuropsychiatric systemic lupus erythematosus, snake bite, Dengue fever with encephalopathy, alcoholic liver cirrhosis with hepatic encephalopathy, and lastly reversible cerebral vasoconstriction syndrome (RCVS). Additionally, a diagnostic dilemma between PRES and acute disseminated encephalomyelitis (ADEM) was notable in one patient. Some of these patients did not have or only very transiently had arterial hypertension. PRES may underlie the clinical conundrum of headache, confusion, altered sensorium, seizures, and visual impairment. PRES need not necessarily be always associated with high blood pressure. Imaging findings may also be variable. Both clinicians and radiologists need to familiarize themselves with such variabilities.

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

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. 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. 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. 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.

Conduction Velocity Dispersion Predicts Postinfarct Ventricular Tachycardia Circuit Sites and Associates With Lipomatous Metaplasia

BackgroundRegional myocardial conduction velocity (CV) dispersion has not been studied in postinfarct patients with ventricular tachycardia (VT). ObjectivesThis study sought to compare the following: 1) the association of CV dispersion vs repolarization dispersion with VT circuit sites; and 2) myocardial lipomatous metaplasia (LM) vs fibrosis as the anatomic substrate for CV dispersion. MethodsAmong 33 postinfarct patients with VT, we characterized dense and border zone infarct tissue by late gadolinium enhancement cardiac magnetic resonance, and LM by computed tomography, with both images registered with electroanatomic maps. Activation recovery interval (ARI) was the time interval from the minimum derivative within the QRS complex to the maximum derivative within the T-wave on unipolar electrograms. CV at each EAM point was the mean CV between that point and 5 adjacent points along the activation wave front. CV and ARI dispersion were the coefficient of variation (CoV) of CV and ARI per American Heart Association (AHA) segment, respectively. ResultsRegional CV dispersion exhibited a much larger range than ARI dispersion, with median 0.65 vs 0.24; P < 0.001. CV dispersion was a more robust predictor of the number of critical VT sites per AHA segment than ARI dispersion. Regional LM area was more strongly associated with CV dispersion than fibrosis area. LM area was larger (median 0.44 vs 0.20 cm2; P < 0.001) in AHA segments with mean CV <36 cm/s and CoV_CV >0.65 than those with mean CV <36 cm/s and CoV_CV <0.65. ConclusionsRegional CV dispersion more strongly predicts VT circuit sites than repolarization dispersion, and LM is a critical substrate for CV dispersion.

Transient Left MCA Syndrome Triggered by a Diagnostic Lumbar Puncture in a Case of Atypical Moyamoya Syndrome (P12-5.017)

<h3>Objective:</h3> Case report <h3>Background:</h3> No reported cases of transient ischemia are triggered by diagnostic lumbar puncture (LP). Here we present a suspected moyamoya syndrome with reversible ischemic event shortly following LP. <h3>Design/Methods:</h3> N/A <h3>Results:</h3> 48-year-old Asian woman presented to the emergency department after two weeks of gradually worsening left leg weakness &amp; numbness. She was diagnosed with subacute right MCA-ACA border-zone infarct on clinical assessment and MRI. Vessel imaging with CTA suggested widespread obstructive arteriopathy involving bilateral ACA and MCA while sparing the terminal ICA and posterior circulation, with extensive collateral development in lenticulostriate vasculature. Cerebral angiogram confirmed the CTA findings with no signs of diffuse atherosclerosis or inflammation, raising concern for Moyamoya syndrome despite the lack of ICA termini involvement. To rule out inflammatory etiology of arteriopathy, she underwent a diagnostic LP, and 24cc of clear fluid was collected, which was non-inflammatory. Towards the end of the procedure, she developed global aphasia, left-sided gaze deviation, right-sided hemiplegia &amp; homonymous hemianopsia, suggestive of left MCA syndrome, while being normotensive and in a supine position. CT perfusion map showed 131 mL of left MCA/ACA territory penumbra with no core infarct. She was placed in Trendelenburg position and resuscitated with fluids and phenylephrine to maintain high MAP goal. This was followed by rapid resolution of her left MCA syndrome within one hour. <h3>Conclusions:</h3> The proposed mechanism for transient left MCA syndrome during LP in our patient with likely atypical Moyamoya syndrome was likely due to a steal phenomenon characterized by shunting blood flow away from severely narrowed left MCA due to global intracranial vascular dilation secondary to ICP drop during LP. This is supported by complete resolution of symptoms within one hour, mainly due to repletion of drained CSF and position change, which restored ICP to exert resistance on other less stenosed intracranial vessels while supporting MAP. <b>Disclosure:</b> Dr. Bareja has nothing to disclose. Dr. Al Gburi has nothing to disclose. Dr. Shnawa has nothing to disclose.

Abstract WMP73: Border Zone Infarct Pattern Predicts Early Recurrence In Symptomatic Intracranial Atherosclerotic Disease: A Systematic Review And Meta-analysis

Introduction: Stroke secondary to intracranial atherosclerosis (ICAD) results in three distinct infarct patterns: (a) border zone infarcts (BZI) due to impaired distal perfusion (b) territorial infarcts due to distal plaque/thrombus embolization, and (c) perforator infarcts due to plaque progression. Previous studies indicate higher stroke recurrence in ICAD patients with BZI. Methods: This registered systematic review (CRD42021265230) comprised Medline and Web of Science search from inception to March 2022 for keywords (Intracranial Atherosclerosis OR Intracranial Stenosis) AND (Border zone OR Infarct Pattern) to identify papers and conference abstracts reporting initial infarct patterns and recurrence rates in patients with symptomatic ICAD. Sensitivity analyses were performed for studies including any BZI vs isolated BZI and those excluding posterior circulation strokes. The study outcome included neurological deterioration and/or stroke recurrence. For all outcome events, corresponding risk ratios (RR) and 95% confidence intervals (CI) were calculated. Risk of bias assessments will be presented. Results: Literature search yielded 4478 studies,11 met inclusion criteria (n=1315 patients, 354 with BZI, weighted proportions summarized in figure). The meta-analysis of these studies with moderate heterogeneity (I 2 =38.7%) demonstrated that RR of outcomes in BZI group compared to non-BZI group was 2.10 (95% CI 1.52-2.90). Limiting analysis to studies including any BZI, RR (and 95% CI) was 2.32 (1.58-3.40), and 3.25 (2.09-5.07) for studies only including anterior circulation strokes with low heterogeneity for both (I 2 =0%). A non-significantly high outcome rate was seen with isolated BZI (RR 2.29, 95% CI 0.94-5.62) but with moderate heterogeneity across studies (I 2 =70.25%). Conclusion: We demonstrate the presence of BZI secondary to symptomatic ICAD can be imaging biomarker to predict neurological deterioration and/or stroke recurrence.

Abstract WP141: The Combined Effect Of Blood Pressure And Translesional Pressure Ratio Impacts The Stroke Mechanisms Of Intracranial Atherosclerosis

Introduction: ICAS confers the greatest risk of stroke, but the pathophysiology of stroke mechanismremains unclear. Essentially, plaque rupture is a physical process of structural failuredue to destructive biomechanics, and hypoperfusion is due to low perfusion pressure,which act as 2 major stroke mechanisms in sICAS. Notably, blood pressure (BP)plays key role in determining both biomechanics and perfusion of ICAS. Hypothesis: ICAS could result in significant BP change which may further influence strokemechanism. High local pressure gradient across ICAS may cause plaque rupture andthe subsequent artery-to-artery embolism, whereas low perfusion pressure atpost-stenosis area may restrict perfusion and induce the subsequent borderzoneinfarcts (Fig) . Method: A total of 339 sICAS patients due to 50-99% stenosis in MCA or ICA were includedfrom CNSR3. By Newton-Krylov-Schwarz method, CFD models were built based onTOF-MRA (Fig) . Translesional pressure ratio (PR) across ICAS was calculated as:pressurepoststenotic/pressureprestenotic. SBP gradient was calculated as: SBPх(1-PR),indicating the SBP drop across ICAS. Perfusion pressure at post-stenosis area wascalculated as: MAPхPR. Results: After adjustment, high SBP gradient and low perfusion pressure was shown tocorrelate with cortical infarcts (p=0.041) and borderzone infarcts (borderlinesignificant, p=0.059) (Fig) . Between the 2 parameters, Pearson correlation coefficient=-0.854, p &lt;.0001. The cutoff of SBP gradient and perfusion pressure for the above 2stroke mechanisms was 14.4mmHg and 94.4mmHg, respectively. Conclusions: We demonstrated the hemodynamic hypothesis of stroke mechanism in sICAS thatartery-to-artery embolism and hypoperfusion could be attributed to the combinedeffect of blood pressure and translesional PR. Accordingly, a double-edged role of high BP level in sICAS may further surface, which can induce destructivebiomechanics but relieve hypoperfusion simultaneously.

Abstract WP97: Routine MRI Reveals Prior Stroke In The Same Vascular Territory In Half Of Patients Presenting With Acute Ischemic Stroke Due To Intracranial Atherosclerotic Disease

Introduction: In 2012, after SAMMPRIS demonstrated worse 30-day outcomes with Wingspan intracranial stent placement for intracranial atherosclerotic disease (ICAD), the FDA narrowed the “on-label” indication to a very specific subset of patients with symptomatic ICAD. The updated criteria require a prior stroke in the territory of the symptomatic vessel based on clinical history. Limitations in the accuracy of diagnosis of clinical stroke may be overcome with the use of MRI to identify any prior stroke - whether clinical or subclinical - which could expand the number of patients who are eligible for stenting. Methods: This was a retrospective analysis of consecutive cases of acute ischemic stroke attributable to ICAD with 50-99% stenosis in the symptomatic vessel from July 2019 - June 2022. MRI FLAIR sequences were reviewed for imaging evidence of prior infarction in the vascular territory of the symptomatic vessel. Subgroup analysis was performed based on stroke location, infarct pattern, degree of stenosis, and premorbid medication use. Results: 73 patients met inclusion criteria. Mean age was 72, and 41% were women. 37 patients (51%) exhibited MRI evidence of prior stroke in the same vascular territory. Of these, only 18/37 (49%) reported a prior clinical stroke. The frequency of prior stroke on MRI was similar with anterior (51%) and posterior (50%) circulation ICAD. Frequency of prior stroke based on infarct pattern was 64% for border zone infarction, 42% for thromboembolism, and 55% for branch atheromatous disease. Of the 31 patients who had degree of stenosis quantified on DSA, the frequency of prior infarction was 63% in patients with 70-99% stenosis versus 48% in those with &lt;70% stenosis. Only 1 patient (1.4%) met FDA on-label criteria for intracranial stenting. The most common reason for ineligibility was absent history of clinical stroke in the territory of the symptomatic vessel (75%). Conclusions: In patients presenting with acute stroke due to symptomatic ICAD, half exhibit MRI evidence of a prior stroke in the symptomatic arterial territory, and half of these prior strokes are not reported from clinical history. Routine MRI can be a valuable tool to identify prior stroke in the symptomatic territory, which may in turn expand therapeutic options for ICAD.

Etiopathology, Clinical and Imaging Characteristics of Border Zone Strokes.

A border zone infarct (BI) is defined as an infarction that is localized to watersheds or border zones in the brain. BI is further classified into cortical border zone infarct (CBZ) and internal border zone infarct (IBZ). This study was conducted to explore the clinical and radiological characteristics of BI. The study was conducted on eligible 400 acute ischemic stroke patients out of which 52 BI patients (diagnosed by the radiologist on DWI MRI images), patients >18 yrs of age were selected and divided into two groups of IBZ and CBZ infarct patients. The degree of intracranial and extracranial stenosis and characteristics on clinical presentation were assessed. The data were collected and analyzed using SPSS version 20.0 software at significance level p-value <0.05. 25% and 75% of CBZ and IBZ patients, respectively, had history of presyncope or syncope before stroke. On vascular evaluation, 3.9% and 51.9% were in MCA and ICA stenosis group, respectively. Evidence of cardio embolism was found in 17.3% of patients. 53.3% of CBZ and 53.8% of IBZ patients were in ICA stenosis group, and 6.7% of CBZ and 7.7% of IBZ patients were in MCA stenosis group, with a statistically insignificant relation (p-value >0.05). Association of BI with events causing hypotension or hypovolemia is well-established in our study, association of BI with large vessel atherosclerosis is common, and its contribution to CBZ and IBZ seems to be equal.

Borderzone infarction and recurrent stroke in intracranial atherosclerosis

BackgroundIntracranial stenosis (ICAS) is a common cause of stroke worldwide and patients with symptomatic ICAS exhibit a high rate of recurrence, particularly in the early period after the initial event. In this study, we aimed to study the association between borderzone infarct and recurrent ischemic stroke in patients hospitalized with symptomatic ICAS. MethodsThis is a retrospective single center study that included patients hospitalized with acute ischemic stroke in the setting of intracranial stenosis (50% or more and an acute ischemic stroke in the territory supplied by the stenosed artery) over a 32-month period. We excluded patients who did not receive a brain MRI or did not have an infarct on brain imaging. The primary predictor is infarct pattern (any borderzone vs. no borderzone infarct) and the primary outcome was recurrent cerebrovascular events (RCVE) within 90 days. We used unadjusted, and age and sex adjusted logistic regression models to determine associations between infarct pattern and RCVE at 90-days. ResultsAmong 99 patients who met the inclusion criteria (4 tandem), the mean age was 70.1 ± 11.2 years and 41.4% were women; 43 had borderzone infarcts and 19 had RCVE. In adjusted binary logistic regression analysis, borderzone infarct was associated with increased risk of RCVE (adjusted OR 4.00 95% CI 1.33-11.99, p=0.013). The association between borderzone infarction and RCVE was not different among anterior circulation ICAD (adjusted HR 2.85 95% CI 0.64-12.76, p=0.172) vs. posterior circulation ICAD (adjusted HR 6.69 95% CI 1.06-42.11, p=0.043), p-value for interaction = 0.592. ConclusionIn real world post-SAMMPRIS medically treated patients with ICAD, the borderzone infarct pattern was associated with 90-day RCVE. Borderzone infarcts are likely a surrogate marker of impaired distal blood flow, highlighting the importance of targeting stroke mechanisms and developing alternative treatment strategies for high-risk cohorts.

Border Zone Infarcts in the Setting of Eosinophilia.

HomeStrokeVol. 54, No. 2Border Zone Infarcts in the Setting of Eosinophilia No AccessCase ReportRequest AccessFull TextAboutView Full TextView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toNo AccessCase ReportRequest AccessFull TextBorder Zone Infarcts in the Setting of Eosinophilia Ulf Jensen-Kondering, Philipp Johannes Koch and Victoria Hagelstein Ulf Jensen-KonderingUlf Jensen-Kondering Correspondence to: Ulf Jensen-Kondering, MD, Department of Neuroradiology, University Hospital Schleswig-Holstein, Campus Lübeck, Ratzeburger Allee 160, Haus A, 23538 Lübeck, Germany. Email: E-mail Address: [email protected] https://orcid.org/0000-0002-0860-4410 Department of Neuroradiology (U.J.-K.), University Medical Center Schleswig-Holstein, Lübeck, Germany. Search for more papers by this author , Philipp Johannes KochPhilipp Johannes Koch Department of Neurology (P.J.K.), University Medical Center Schleswig-Holstein, Lübeck, Germany. Search for more papers by this author and Victoria HagelsteinVictoria Hagelstein Department of Dermatology (V.H.), University Medical Center Schleswig-Holstein, Lübeck, Germany. Search for more papers by this author Originally published12 Oct 2022https://doi.org/10.1161/STROKEAHA.122.040754Stroke. 2023;54:e36–e37"Border Zone Infarcts in the Setting of Eosinophilia." Stroke, 54(2), pp. e36–e37FootnotesFor Sources of Funding and Disclosures, see page e36.Correspondence to: Ulf Jensen-Kondering, MD, Department of Neuroradiology, University Hospital Schleswig-Holstein, Campus Lübeck, Ratzeburger Allee 160, Haus A, 23538 Lübeck, Germany. Email: Ulf.[email protected]de