Evidence Behind Modern Stroke Practice

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1. How to read this evidence

• Randomized trials can estimate comparative treatment effects within the patients and workflows studied.
• Registries and cohorts can reveal safety, feasibility, prognosis, and real-world patterns, but they cannot by themselves prove that one treatment is superior to another.
• Guidelines translate a dated evidence base into recommendations; they are not interchangeable with the original studies.
• My Clinical Perspective is explicitly labeled expert interpretation by Morteza Modaber, M.D. It is evidence-informed opinion, not a guideline or institutional protocol.

02

2. Selected Late-Window Anterior-Circulation Thrombectomy

How did DAWN and DEFUSE 3 establish thrombectomy benefit in selected patients presenting beyond 6 hours without creating one blended selection protocol?

Current guideline context

The 2026 AHA/ASA acute ischemic stroke guideline identifies DAWN and DEFUSE 3 as randomized evidence establishing thrombectomy benefit after 6 hours in patients selected for limited predicted core and salvageable tissue. It states that advanced CT or MR imaging can be useful for thrombectomy evaluation from 6 to 24 hours when immediately available. [1]

DAWN

DAWN randomized 206 patients with intracranial ICA or proximal MCA occlusion, last known well 6-24 hours, and an age-adjusted clinical-core mismatch to thrombectomy plus standard care or standard care alone. Functional independence at 90 days was 49% versus 13%; symptomatic intracranial hemorrhage and mortality did not differ significantly. Early stopping and narrow RAPID-based mismatch criteria limit extrapolation beyond the enrolled population. [3]

Study design: randomized-controlled-trial.

What changed in practice: Established efficacy of thrombectomy in a narrowly selected clinical-core mismatch population up to 24 hours after last known well.

Key boundary: The trial stopped early and used narrow age-, deficit-, core-volume-, anatomy-, and automated-imaging criteria that should not be generalized into broader late-window eligibility.

DEFUSE 3

DEFUSE 3 randomized 182 patients with proximal anterior-circulation occlusion 6-16 hours after last known well, an ischemic core below 70 mL, a perfusion-to-core ratio at least 1.8, and at least 15 mL of penumbra. Thrombectomy improved 90-day disability and functional independence (45% versus 17%); symptomatic hemorrhage did not differ significantly. Early stopping and RAPID-based selection limit broader extrapolation. [4]

Study design: randomized-controlled-trial.

What changed in practice: Extended thrombectomy evidence to a perfusion-core mismatch population through 16 hours, including patients who did not meet DAWN criteria.

Key boundary: The trial stopped early, required automated perfusion selection at experienced U.S. centers, and enrolled a selected population with limited core and substantial salvageable tissue.

What the studies establish together

DAWN and DEFUSE 3 provide complementary randomized evidence that selected patients with proximal anterior-circulation occlusion can benefit from thrombectomy after 6 hours. DAWN used age-adjusted clinical-core mismatch through 24 hours; DEFUSE 3 used a perfusion-core mismatch through 16 hours and included a broader range of core volumes and deficit severities. Their findings support trial-informed selection, not a single eligibility rule assembled from both protocols.

Cross-trial comparisons require caution because:

• DAWN used age- and NIHSS-dependent core-volume thresholds, whereas DEFUSE 3 used core volume, mismatch ratio, and minimum penumbral volume.
• The time windows differed: 6-24 hours in DAWN and 6-16 hours in DEFUSE 3.
• DAWN had coprimary utility-weighted disability and functional-independence outcomes; DEFUSE 3 used an ordinal modified Rankin Scale shift as its primary outcome.
• Both trials stopped early and depended on highly selected imaging-defined populations, limiting extrapolation to patients outside their enrollment boundaries.

Current practical conclusion

Evidence basis: guideline-aligned.

Selected late-window thrombectomy is evidence-based for eligible proximal anterior-circulation occlusion. Evaluation should preserve the actual clinical, anatomic, time, and imaging boundaries of the supporting trials; DAWN and DEFUSE 3 criteria should not be blended into a synthetic protocol.

Important evidence gaps

• The trials do not establish benefit for every patient presenting 6-24 hours after last known well; uncertainty remains outside their selected anatomy, core-volume, deficit, and salvageable-tissue boundaries and across imaging workflows not tested in the trials.

My Clinical Perspective

DAWN and DEFUSE 3 were pivotal trials that expanded mechanical-thrombectomy eligibility for many patients who previously would not have been treated. Their lasting contribution is not simply a longer clock window, but proof that selected patients can retain clinically meaningful salvageable tissue well beyond 6 hours.

In practice, however, automated estimates of ischemic core can be interpreted too rigidly. The commonly used CT-perfusion threshold of relative CBF below 30% is an operational imaging estimate, not a histologic demonstration that every included voxel is already dead. I prefer the term likely irreversibly injured tissue because it is more faithful to the uncertainty of a probabilistic measurement. Early-window studies of the “ghost core” show that CT perfusion can overestimate final infarction, particularly when imaging occurs very early and reperfusion is rapid [6]. More recent randomized large-core trials, including SELECT2, also demonstrate that a large estimated core does not automatically eliminate treatment benefit [5].

That does not mean core volume is unimportant. Large-core and trial-ineligible cohorts generally have worse absolute outcomes and may have greater hemorrhagic risk; in the BEST cohort, patients with ASPECTS below 6 had substantially poorer outcomes and more symptomatic hemorrhage [8]. The practical lesson is therefore not to ignore core, but to avoid treating a single perfusion threshold as a biologic bright line—especially in an early-presenting patient with a technically favorable occlusion and an opportunity for rapid reperfusion.

Outcome heterogeneity also shows why last-known-well time is necessary but incomplete. Some carefully selected patients near 24 hours obtain substantial benefit, whereas some patients treated much earlier still progress rapidly or have poor outcomes. AURORA found thrombectomy benefit across the 6-to-24-hour treatment terciles in patients with defined clinical or perfusion mismatch, but did not establish the same benefit in patients with an undetermined imaging profile [7]. This supports tissue- and patient-based selection within evidence boundaries; it does not make time biologically irrelevant.

Collateral circulation and the mechanism of large-vessel occlusion may help explain part of this heterogeneity, including differences in infarct growth, reperfusion durability, hemorrhagic risk, and functional outcome. Current eligibility frameworks do not use etiology or collateral grade as decisive standalone criteria. Observational evidence supports their prognostic importance, but the interaction between etiology and collateral effect remains inconsistent; a recent multicenter registry suggested different patterns in large-artery atherosclerosis and cardioembolism but found no significant formal interaction [9]. I therefore view collateral status and occlusion mechanism as clinically important modifiers and research priorities, not yet validated replacements for established thrombectomy selection criteria.

Evidence balance. Supportive evidence includes early-window core overestimation, randomized benefit in selected large-core patients, and persistent benefit across late-window terciles in mismatch-selected patients. Countervailing evidence is that large core remains a marker of poorer prognosis and higher complication risk, while benefit outside validated mismatch profiles is less certain.

References: [3] DAWN, doi:10.1056/NEJMoa1706442. [4] DEFUSE 3, doi:10.1056/NEJMoa1713973. [5] SELECT2, doi:10.1056/NEJMoa2214403. [6] García-Tornel et al., doi:10.1161/STROKEAHA.120.031800. [7] AURORA pooled analysis, doi:10.1001/jamaneurol.2021.2319. [8] BEST cohort, doi:10.1093/neuros/nyz485. [9] Leng et al., doi:10.1177/17474930251324463.

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3. Selective Short-Term Dual Antiplatelet Therapy

How did CHANCE, POINT, and THALES shape selective short-term dual antiplatelet therapy after minor noncardioembolic stroke or high-risk TIA?

Current guideline context

The 2026 AHA/ASA guideline recommends early aspirin-clopidogrel dual antiplatelet therapy for 21 days, followed by single antiplatelet therapy, in patients with minor noncardioembolic stroke (NIHSS 3 or less) or high-risk TIA (ABCD2 4 or greater) within 24 hours who did not receive thrombolysis. A 30-day ticagrelor-aspirin regimen may be considered for selected patients meeting the broader THALES-type risk criteria. [1]

CHANCE

CHANCE randomized 5,170 patients in China with minor stroke (NIHSS 3 or less) or high-risk TIA (ABCD2 4 or greater) within 24 hours to clopidogrel plus aspirin for 21 days, then clopidogrel alone, or aspirin alone. Ninety-day stroke was 8.2% versus 11.7%, with moderate or severe hemorrhage 0.3% in both groups. Geography and regimen limit direct generalization. [10]

Study design: randomized-controlled-trial.

What changed in practice: Supported early, time-limited aspirin-clopidogrel therapy after minor stroke or high-risk TIA.

Key boundary: The trial was conducted exclusively in China, and its 21-day dual-therapy regimen followed by clopidogrel monotherapy should not be treated as equivalent to longer dual therapy.

POINT

POINT randomized 4,881 international patients with minor stroke or high-risk TIA within 12 hours to clopidogrel plus aspirin for 90 days or aspirin alone. Major ischemic events fell from 6.5% to 5.0%, while major hemorrhage rose from 0.4% to 0.9%. Early termination, 29% drug discontinuation, and exclusion of cardioembolic, reperfusion-treated, and more severe strokes limit generalization. [11]

Study design: randomized-controlled-trial.

What changed in practice: Confirmed an early ischemic benefit in an international population while demonstrating that prolonged dual therapy carries continuing bleeding risk.

Key boundary: The trial excluded moderate-to-severe stroke, cardioembolic stroke, and candidates for thrombolysis or thrombectomy; 29% permanently discontinued study medication before follow-up ended.

THALES

THALES randomized 11,016 patients with noncardioembolic stroke (NIHSS 5 or less) or qualifying high-risk TIA within 24 hours to ticagrelor plus aspirin for 30 days or aspirin alone. Stroke or death was 5.5% versus 6.6%, but severe bleeding was 0.5% versus 0.1%, with no significant disability difference. Excluded reperfusion-treated, cardioembolic, and more severe strokes limit applicability. [12]

Study design: randomized-controlled-trial.

What changed in practice: Provided evidence for a distinct ticagrelor-aspirin option in selected mild-to-moderate stroke or high-risk TIA populations.

Key boundary: The trial excluded more severe, cardioembolic, later-presenting, and reperfusion-treated patients, and its agent, population, duration, endpoints, and bleeding definition differ from CHANCE and POINT.

What the studies establish together

CHANCE and POINT support early aspirin-clopidogrel therapy in minor stroke or high-risk TIA, but their loading doses and exposure to dual therapy differed: 21 days in CHANCE and 90 days in POINT. POINT showed major bleeding continuing across the longer treatment period. THALES tested a different P2Y12 inhibitor, included NIHSS scores up to 5 and different TIA criteria, and balanced a smaller reduction in stroke or death against more severe bleeding. These trials support selective, time-bounded regimens rather than interchangeable dual antiplatelet therapy.

Cross-trial comparisons require caution because:

• CHANCE enrolled only in China; POINT and THALES were international.
• CHANCE and POINT tested clopidogrel, while THALES tested ticagrelor.
• Dual-therapy duration was 21 days in CHANCE, 90 days in POINT, and 30 days in THALES.
• Enrollment timing, NIHSS and TIA thresholds, loading doses, efficacy endpoints, and bleeding definitions differed.
• None of the three trials represented patients receiving thrombolysis or thrombectomy, cardioembolic stroke, or more severe stroke.

Current practical conclusion

Evidence basis: guideline-aligned.

Dual antiplatelet therapy is an early, selective, and time-limited strategy for defined noncardioembolic minor stroke or high-risk TIA populations. Aspirin-clopidogrel for 21 days has the strongest guideline support; ticagrelor-aspirin for 30 days is a distinct option for selected patients, with bleeding risk weighed explicitly.

Important evidence gaps

• The pivotal trials do not establish these regimens for cardioembolic stroke, more severe stroke, patients receiving acute reperfusion therapy, or treatment initiated beyond their enrollment windows; direct comparisons between clopidogrel- and ticagrelor-based regimens are not provided by these trials.

My Clinical Perspective

CHANCE, POINT, and THALES established that selected patients with minor noncardioembolic stroke or high-risk TIA have a modestly better early outcome with short-term dual antiplatelet therapy than with aspirin alone. Their benefit is real, but the treatment effect is accompanied by bleeding risk and applies to the populations and regimens actually studied [P-DAPT-01–P-DAPT-03].

These trials were not entirely mechanism-agnostic: they excluded clear cardioembolic indications, and THALES incorporated atherosclerotic-risk criteria. Nevertheless, enrollment was driven mainly by clinical severity and risk scores—particularly NIHSS and ABCD2—rather than by a complete mechanistic and tissue-based characterization of every event. That matters because NIHSS is not anatomically neutral. It can underestimate posterior-circulation deficits [16] and systematically assigns lower scores to some right-hemisphere strokes than to left-hemisphere strokes of comparable clinical consequence [17]. A low NIHSS therefore should not be treated as synonymous with a small infarct, low disability, or low hemorrhagic risk.

This creates a clinically important uncertainty for patients with a low NIHSS but a substantial posterior-circulation or right-hemisphere infarct, particularly when edema, mass effect, or hemorrhagic transformation is a concern. The pivotal DAPT trials did not provide a sufficiently powered tissue-volume, hemisphere, or posterior-circulation analysis to show that these patients benefit less. I would therefore frame reduced benefit in this subgroup as a plausible safety concern—not an established treatment interaction—and would weigh infarct size, location, mechanism, and bleeding risk in addition to the numerical NIHSS.

Intracranial atherosclerosis is another area where mechanism may matter. Patients with ICAS have higher recurrence risk, but the CHANCE ICAS subgroup did not show a statistically significant interaction proving that ICAS patients derive a larger relative benefit from aspirin-clopidogrel [13]. In THALES, ipsilateral atherosclerotic stenosis identified a higher-risk group with a larger absolute risk reduction, yet the treatment-by-stenosis interaction was again not significant [14]. INSPIRES adds stronger support for initiating clopidogrel-aspirin within 72 hours in mild stroke or high-risk TIA of presumed atherosclerotic cause, but it still used aspirin for 21 days and does not establish that extending dual therapy beyond the usual short course is beneficial [15].

My clinical view is therefore that nonsevere ICAS may identify patients with more to gain in absolute terms, but current evidence does not reliably define which degree, distribution, or plaque mechanism should receive a longer DAPT course. Any extension beyond evidence-based short-term regimens remains an individualized, unproven decision with accumulating hemorrhagic risk rather than an evidence-based default.

Evidence balance. Supportive evidence confirms early DAPT benefit and the limitations of NIHSS in posterior and right-hemisphere stroke; atherosclerotic populations may have greater absolute recurrence reduction. Countervailing evidence is that subgroup interaction tests have not proved a larger relative DAPT effect in ICAS, and no pivotal trial establishes less benefit in low-NIHSS posterior/right-hemisphere infarction or supports routine prolonged DAPT for nonsevere ICAS.

References: [10] CHANCE, doi:10.1056/NEJMoa1215340. [11] POINT, doi:10.1056/NEJMoa1800410. [12] THALES, doi:10.1056/NEJMoa1916870. [13] CHANCE ICAS subgroup, doi:10.1212/WNL.0000000000001972. [14] THALES atherosclerotic subgroup, doi:10.1161/STROKEAHA.120.032239. [15] INSPIRES, doi:10.1056/NEJMoa2309137. [16] POST-NIHSS, PMID 34905944. [17] Fink et al., doi:10.1161/STROKEAHA.108.523365.

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4. Symptomatic Intracranial Atherosclerotic Disease: Medical Therapy and Stenting Evidence

How should randomized SAMMPRIS evidence and the later WEAVE/WOVEN registry experience be interpreted without treating them as equivalent?

Current guideline context

The 2021 AHA/ASA secondary-prevention guideline prefers aggressive medical management and short-term dual antiplatelet therapy for severe symptomatic intracranial stenosis and states that angioplasty and stenting should not be initial treatment. For recurrent events despite medical therapy and risk-factor control, the usefulness of angioplasty or stenting remains unknown. [2]

SAMMPRIS final results

SAMMPRIS randomized 451 patients with recent TIA or stroke from 70%-99% intracranial stenosis to aggressive medical management or the same therapy plus Wingspan stenting. Stroke or death by 30 days was 5.8% versus 14.7%, and the medical-management advantage persisted over median 32.4-month follow-up. The unmasked trial faced procedural-experience concerns, but no prespecified subgroup benefited from stenting. [18]

Study design: randomized-controlled-trial.

What changed in practice: Established aggressive medical management as superior to Wingspan stenting for the randomized population, driven by early procedural harm without later compensating benefit.

Key boundary: The trial was not double-masked; procedural experience and timing were debated, but no prespecified subgroup benefited from stenting.

WEAVE

WEAVE prospectively enrolled 152 strictly on-label patients with 70%-99% symptomatic intracranial stenosis, recurrent territorial strokes despite medical therapy, and stenting at least 8 days after the last stroke. The adjudicated 72-hour stroke, bleed, or death rate was 2.6%. Its single-arm design, experienced operators, narrow selection, early stopping, and short safety window cannot establish efficacy versus aggressive medical management. [19]

Study design: prospective-registry.

What changed in practice: Showed that strictly on-label Wingspan use could achieve lower periprocedural event rates in highly selected patients treated by experienced operators.

Key boundary: The registry assessed only periprocedural safety, stopped after interim analysis, and cannot establish comparative efficacy against aggressive medical management.

WOVEN

WOVEN followed 129 of 152 WEAVE patients from 12 of 24 sites after on-label Wingspan stenting. Including periprocedural events, stroke or death occurred in 8.5% by one year; seven delayed strokes and no later deaths were recorded. Incomplete site participation, 85% cohort follow-up, chart-review ascertainment, nonstandardized imaging, and no medical control prevent randomized efficacy conclusions. [20]

Study design: retrospective-registry.

What changed in practice: Extended the selected WEAVE cohort's safety description to one year and documented delayed stroke and restenosis experience.

Key boundary: Follow-up included 85% of the original cohort from half the sites, used chart review without a control arm, and lacked standardized longitudinal risk-factor and imaging follow-up.

What the studies establish together

SAMMPRIS randomized aggressive medical management against Wingspan stenting and found higher early harm without later compensating benefit from stenting. WEAVE and WOVEN subsequently described lower periprocedural and one-year event rates under narrower on-label selection, delayed treatment, and experienced-operator conditions. That registry experience supports feasibility and safety assessment in a selected subgroup, but the absence of a randomized medical comparator means it neither reverses SAMMPRIS nor proves that stenting improves outcomes.

Cross-trial comparisons require caution because:

• SAMMPRIS was randomized; WEAVE was a single-arm prospective postmarket registry and WOVEN was observational follow-up of that registry.
• WEAVE/WOVEN applied narrower on-label criteria, later procedure timing, and experienced-operator conditions that differed from SAMMPRIS.
• WEAVE's primary window was 72-hour procedural safety, whereas SAMMPRIS tested a composite clinical endpoint over randomized follow-up.
• WOVEN included 129 of 152 WEAVE patients from 12 of 24 sites and had no concurrent medical control.
• Numerical event-rate comparisons across these designs cannot establish relative efficacy.

Current practical conclusion

Evidence basis: guideline-aligned.

Aggressive medical management remains first-line treatment for symptomatic severe intracranial atherosclerotic stenosis. Wingspan registry results suggest improved procedural safety under strict selection and experienced care, but do not establish superiority or noninferiority to contemporary medical management; use after recurrent events remains an unresolved, highly selected question.

Important evidence gaps

• Whether modern, strictly on-label Wingspan stenting improves outcomes over contemporary aggressive medical management in true medical failures remains unproven and requires a randomized comparison.

My Clinical Perspective

My clinical dilemma in symptomatic intracranial atherosclerotic disease is what it means to wait for “medical failure.” Subtle recurrent symptoms may be missed by patients, families, and clinicians, and serial perfusion imaging is not always practical or reimbursed. In some patients, the first unmistakable failure may already represent a disabling territorial infarction, after which delayed revascularization offers little salvageable tissue.

The evidence nevertheless does not support routine preemptive Wingspan stenting. SAMMPRIS established aggressive medical management as first-line therapy because early harm from stenting was not offset by later benefit [18]. WEAVE showed that strict on-label selection, delayed treatment, and experienced operators can substantially improve procedural safety, but it was a single-arm safety registry rather than a comparison with medical therapy [19]. CASSISS is an important counterweight: even with refined selection and experienced centers, stenting did not improve outcomes over medical therapy [21]. These findings mean that identifying a high-risk mechanism is not the same as proving that stenting that mechanism improves outcome.

I do believe the mechanism of the presenting stroke deserves more attention than the percentage of stenosis alone. A borderzone pattern with poor collaterals may suggest hemodynamic compromise, whereas scattered cortical infarcts may suggest artery-to-artery embolism from an unstable plaque. A SAMMPRIS post hoc analysis supports the prognostic value of this distinction: borderzone infarction, especially with impaired collaterals, was associated with a high risk of recurrent territorial stroke despite aggressive medical therapy [22].

The distinction is not deterministic. Emboli preferentially lodge in low-flow borderzone regions, and hypoperfusion can impair embolic washout; both mechanisms may coexist in the same patient. MyRIAD found recurrent infarcts commonly had mixed patterns, and its tested flow, perfusion, vasoreactivity, and embolic biomarkers did not yield a single validated rule for selecting an intervention [23]. I would therefore avoid assuming that every watershed infarct represents pure low-flow failure or that every plaque-related embolic pattern will reliably respond to medical therapy.

High-resolution vessel-wall MRI may eventually improve this mechanistic assessment by identifying plaque enhancement, burden, remodeling, or intraplaque hemorrhage. Prospective observational data associate plaque enhancement with recurrence [24], but these markers are not standardized, universally available, or validated as thresholds for stenting. They currently support risk stratification and closer follow-up more than they direct a specific procedure.

The field is also evolving beyond the original Wingspan question. BASIS reported benefit from submaximal balloon angioplasty plus aggressive medical management in a selected Chinese population, but procedural complications occurred and the findings cannot be assumed to apply to Wingspan stenting, other populations, or preemptive treatment before medical failure [25].

My practical position is that aggressive medical therapy remains the default, while recurrent symptoms, infarct pattern, collateral status, perfusion impairment, plaque features, and adherence should be assessed together to identify exceptionally high-risk patients for multidisciplinary consideration or clinical trials. The current evidence supports better mechanistic surveillance; it does not yet provide a validated trigger for prophylactic stenting.

Evidence balance. Supportive evidence shows that borderzone infarction with poor collaterals and certain vessel-wall features identify higher recurrence risk, and modern carefully selected interventions may be safer than early Wingspan experience. Countervailing evidence from randomized stenting trials does not show benefit over aggressive medical therapy, and no imaging mechanism has yet been validated as a treatment-selection rule.

References: [18] SAMMPRIS final results, doi:10.1016/S0140-6736(13)62038-3. [19] WEAVE, doi:10.1161/STROKEAHA.118.023996. [21] CASSISS, doi:10.1001/jama.2022.12000. [22] Wabnitz et al., doi:10.1161/STROKEAHA.118.020840. [23] MyRIAD, doi:10.1016/j.jstrokecerebrovasdis.2020.105504. [24] Gómez-Vicente et al., doi:10.1111/jon.13077. [25] BASIS, doi:10.1001/jama.2024.12829.

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5. Practical reading across the three evidence families

• Preserve the inclusion boundaries and treatment details of each pivotal trial.
• Do not combine different trial criteria into a synthetic protocol that was never tested.
• Distinguish comparative efficacy evidence from registry evidence showing procedural safety or feasibility.
• Use imaging, mechanism, and anatomy as clinical context without presenting unvalidated markers as established treatment-selection rules.
• When evidence is incomplete, label the uncertainty rather than converting a plausible mechanism into a recommendation.

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References

1. [G-AIS-2026] Prabhakaran S, et al. 2026 Guideline for the Early Management of Patients With Acute Ischemic Stroke. Stroke. 2026;57:e00-e00.
2. [G-SP-2021] Kleindorfer DO, et al. 2021 Guideline for the Prevention of Stroke in Patients With Stroke and Transient Ischemic Attack. Stroke. 2021;52:e364-e467.
3. [P-EVT-01] Nogueira RG, et al; DAWN Trial Investigators. Thrombectomy 6 to 24 Hours after Stroke with a Mismatch between Deficit and Infarct. N Engl J Med. 2018;378:11-21.
4. [P-EVT-02] Albers GW, et al; DEFUSE 3 Investigators. Thrombectomy for Stroke at 6 to 16 Hours with Selection by Perfusion Imaging. N Engl J Med. 2018;378:708-718.
5. [P-EVT-03] Sarraj A, et al; SELECT2 Investigators. Trial of Endovascular Thrombectomy for Large Ischemic Strokes. N Engl J Med. 2023;388:1259-1271.
6. [P-EVT-04] García-Tornel Á, et al. Ischemic Core Overestimation on Computed Tomography Perfusion. Stroke. 2021;52:1751-1760.
7. [P-EVT-05] Albers GW, et al; AURORA Investigators. Assessment of Optimal Patient Selection for Endovascular Thrombectomy Beyond 6 Hours After Symptom Onset. JAMA Neurol. 2021;78:1064-1071.
8. [P-EVT-06] Siegler JE, et al. Thrombectomy in DAWN- and DEFUSE-3-Ineligible Patients: A Subgroup Analysis From the BEST Prospective Cohort Study. Neurosurgery. 2020;86:E156-E163.
9. [P-EVT-07] Leng X, et al. Collaterals and Outcomes After Endovascular Treatment in Acute Large Vessel Occlusion: Disparity by Stroke Etiologies. Int J Stroke. 2025;20:864-873.
10. [P-DAPT-01] Wang Y, et al; CHANCE Investigators. Clopidogrel with Aspirin in Acute Minor Stroke or Transient Ischemic Attack. N Engl J Med. 2013;369:11-19.
11. [P-DAPT-02] Johnston SC, et al; POINT Investigators. Clopidogrel and Aspirin in Acute Ischemic Stroke and High-Risk TIA. N Engl J Med. 2018;379:215-225.
12. [P-DAPT-03] Johnston SC, et al; THALES Investigators. Ticagrelor and Aspirin or Aspirin Alone in Acute Ischemic Stroke or TIA. N Engl J Med. 2020;383:207-217.
13. [P-DAPT-04] Liu L, et al. Dual Antiplatelet Therapy in Stroke and ICAS: Subgroup Analysis of CHANCE. Neurology. 2015;85:1154-1162.
14. [P-DAPT-05] Amarenco P, et al. Ticagrelor Added to Aspirin in Acute Nonsevere Ischemic Stroke or Transient Ischemic Attack of Atherosclerotic Origin. Stroke. 2020;51:3504-3513.
15. [P-DAPT-06] Gao Y, et al; INSPIRES Investigators. Dual Antiplatelet Treatment up to 72 Hours after Ischemic Stroke. N Engl J Med. 2023;389:2413-2424.
16. [P-DAPT-07] Alemseged F, et al. Posterior National Institutes of Health Stroke Scale Improves Prognostic Accuracy in Posterior Circulation Stroke. Stroke. 2022;53:1247-1255.
17. [P-DAPT-08] Fink JN, et al. Does Hemispheric Lateralization Influence Functional and Cardiovascular Outcomes After Stroke? Stroke. 2008;39:3335-3340.
18. [P-ICAS-01] Derdeyn CP, et al; SAMMPRIS Investigators. Aggressive Medical Treatment With or Without Stenting in High-Risk Patients With Intracranial Artery Stenosis: Final Results. Lancet. 2014;383:333-341.
19. [P-ICAS-02] Alexander MJ, et al. WEAVE Trial: Final Results in 152 On-Label Patients. Stroke. 2019;50:889-894.
20. [P-ICAS-08] Alexander MJ, et al. The WOVEN Trial: Wingspan One-Year Vascular Events and Neurologic Outcomes. J Neurointerv Surg. 2021;13:307-310.
21. [P-ICAS-03] Gao P, et al; CASSISS Trial Investigators. Effect of Stenting Plus Medical Therapy vs Medical Therapy Alone on Risk of Stroke and Death in Patients With Symptomatic Intracranial Stenosis. JAMA. 2022;328:534-542.
22. [P-ICAS-04] Wabnitz AM, et al; SAMMPRIS Investigators. Hemodynamic Markers in the Anterior Circulation as Predictors of Recurrent Stroke in Patients With Intracranial Stenosis. Stroke. 2019;50:143-147.
23. [P-ICAS-05] Romano JG, et al; MyRIAD Investigators. Infarct Recurrence in Intracranial Atherosclerosis: Results From the MyRIAD Study. J Stroke Cerebrovasc Dis. 2021;30:105504.
24. [P-ICAS-06] Gómez-Vicente B, et al. Intracranial Atherosclerotic Plaque Enhancement and Long-Term Risk of Future Strokes. J Neuroimaging. 2023;33:289-301.
25. [P-ICAS-07] Sun X, et al; BASIS Investigators. Balloon Angioplasty vs Medical Management for Intracranial Artery Stenosis. JAMA. 2024;332:1059-1069.