Abstract DP023: Quantitative Biomarker Profiling of No-Reflow Regions Following Excellent Reperfusion

Background: Despite successful macrovascular reperfusion following endovascular treatment patients with large vessel occlusion (LVO) acute ischemic stroke (AIS), persistent microvascular hypoperfusion known as “no-reflow” can occur in 20–30% of patients and is associated with poor outcomes. We aimed to characterize the MRI biomarker profile of no-reflow regions on posttreatment MRI and evaluate the predictive value of individual and combined parameters. Methods: In this retrospective study, patients were included if they had anterior circulation LVO-AIS, who achieved excellent reperfusion (TICI ≥2c) and had posttreatment MRI including dynamic susceptibility contrast (DSC) perfusion within 48 hrs of reperfusion. DSC was processed with a novel vascular model using Bayesian voxel-wise transit time distribution to generate perfusion maps including capillary transit-time heterogeneity (CTH) and cerebral metabolic rate of oxygen (CMRO 2 ). Final infarct was segmented on diffusion-weighted MRI. Segmentation masks and perfusion maps were coregistered via linear registration, and voxel values extracted. All voxel values were normalized to median value of contralateral region-of-interest to calculate relative measures. No-reflow was defined as voxel values with relative CBV (rCBV) and CBF (rCBF) ≥15% below contralateral median. Group comparisons, multivariate logistic regression, and ROC analyses were performed. Results: A total of 53 patients met the inclusion criteria. Among 42,761 voxels defined as infarction on final MRI, a total of 14,765 (34%) designated as no reflow voxels. Ischemic tissue with no-reflow had significantly higher rCTH and Tmax, and significantly lower rCMRO 2 (all p < 0.001) compared to the completely reperfused tissue. In multivariable logistic regression, lower rCMRO 2 (OR = 0.14; 95% CI, 0.14–0.15; p < 0.001), longer Tmax (OR = 0.99; 95% CI, 0.98–1; p=0.04), and higher rCTH (OR = 2.4; 95% CI, 2.3–2.5; p < 0.001) were independently associated with no-reflow. The combined model of these 3 predictors demonstrated good discriminative performance (AUC = 0.87; 95% CI, 0.86–0.87). The optimal Youden threshold corresponded to rCMRO 2 ≤ 0.98, Tmax ≥ 0.2, and rCTH ≥ 1.2, yielding a sensitivity of 80% and specificity of 78%. Conclusion: No-reflow regions exhibit a distinctive MRI biomarker profile of elevated Tmax and CTH, as well as reduced CMRO 2 . A combined multi-parametric model provides superior discrimination compared to individual predictors.

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Journal
Stroke
Published
2026-01-29
DOI
https://doi.org/10.1161/str.57.suppl_1.dp023
Primary Topic
Acute Ischemic Stroke Management
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article
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article

Abstract DP023: Quantitative Biomarker Profiling of No-Reflow Regions Following Excellent Reperfusion

Corey W Arnold, L Savastano, Matthew R. Amans, Kambiz Nael et al.
Stroke
Acute Ischemic Stroke Management
article

Abstract DP023: Quantitative Biomarker Profiling of No-Reflow Regions Following Excellent Reperfusion

Corey W Arnold, L Savastano, Matthew R. Amans, Kambiz Nael, Ethan A. Winkler, Mersedeh Bahr Hosseini, Daniel L. Cooke, Mona Asghariahmadabad, D Liebeskind, Wade Smith, Ameera Ismail, Jeffrey Saver, Christopher Hess, Steven Hetts, Anthony Kim, Nerissa Ko, Andy Josephson, Kevin Mahmoudi
article en

Abstract

Background: Despite successful macrovascular reperfusion following endovascular treatment patients with large vessel occlusion (LVO) acute ischemic stroke (AIS), persistent microvascular hypoperfusion known as “no-reflow” can occur in 20–30% of patients and is associated with poor outcomes. We aimed to characterize the MRI biomarker profile of no-reflow regions on posttreatment MRI and evaluate the predictive value of individual and combined parameters. Methods: In this retrospective study, patients were included if they had anterior circulation LVO-AIS, who achieved excellent reperfusion (TICI ≥2c) and had posttreatment MRI including dynamic susceptibility contrast (DSC) perfusion within 48 hrs of reperfusion. DSC was processed with a novel vascular model using Bayesian voxel-wise transit time distribution to generate perfusion maps including capillary transit-time heterogeneity (CTH) and cerebral metabolic rate of oxygen (CMRO 2 ). Final infarct was segmented on diffusion-weighted MRI. Segmentation masks and perfusion maps were coregistered via linear registration, and voxel values extracted. All voxel values were normalized to median value of contralateral region-of-interest to calculate relative measures. No-reflow was defined as voxel values with relative CBV (rCBV) and CBF (rCBF) ≥15% below contralateral median. Group comparisons, multivariate logistic regression, and ROC analyses were performed. Results: A total of 53 patients met the inclusion criteria. Among 42,761 voxels defined as infarction on final MRI, a total of 14,765 (34%) designated as no reflow voxels. Ischemic tissue with no-reflow had significantly higher rCTH and Tmax, and significantly lower rCMRO 2 (all p < 0.001) compared to the completely reperfused tissue. In multivariable logistic regression, lower rCMRO 2 (OR = 0.14; 95% CI, 0.14–0.15; p < 0.001), longer Tmax (OR = 0.99; 95% CI, 0.98–1; p=0.04), and higher rCTH (OR = 2.4; 95% CI, 2.3–2.5; p < 0.001) were independently associated with no-reflow. The combined model of these 3 predictors demonstrated good discriminative performance (AUC = 0.87; 95% CI, 0.86–0.87). The optimal Youden threshold corresponded to rCMRO 2 ≤ 0.98, Tmax ≥ 0.2, and rCTH ≥ 1.2, yielding a sensitivity of 80% and specificity of 78%. Conclusion: No-reflow regions exhibit a distinctive MRI biomarker profile of elevated Tmax and CTH, as well as reduced CMRO 2 . A combined multi-parametric model provides superior discrimination compared to individual predictors.

StrokeVol. 57(Suppl_1)
City College of San Francisco (US), UCLA Health (US), Hillsborough Hospital (CA), University of California System (US), Electronic Sensor Technology (United States) (US), Brunel University of London (GB)
No poverty
Openalex Percentile: Top 72%
Acute Ischemic Stroke Management
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