Risk factors of late lesion growth after acute ischemic stroke treatment

 Well, your description of late(1 day to 1 week) is precisely the

5 causes of the neuronal cascade of death in the first days. This has been known for over a decade since the Rockefeller University described it in 2009. Why don't you solve that goddamn problem? This did nothing that wasn't known before.

Risk factors of late lesion growth after acute ischemic stroke treatment

Praneeta Konduri^1,2*, Amber Bucker³, Anna Boers^1,4, Bruna Dutra^1,2, Noor Samuels^5,6,7, Kilian Treurniet^2,8, Olvert Berkhemer^2,5,6, Albert Yoo⁹, Wim van Zwam¹⁰, Robert van Oostenbrugge¹¹, Aad van der Lugt⁵, Diederik Dippel⁶, Yvo Roos¹², Joost Bot¹³, Charles Majoie², Henk Marquering^1,2 and the MR CLEAN Trial Investigators (Multicenter Randomized Clinical Trial of Endovascular Treatment for Acute Ischemic Stroke in the Netherlands)

• ¹Department of Biomedical Engineering and Physics, Amsterdam UMC, Location AMC, Amsterdam, Netherlands
• ²Department of Radiology and Nuclear Medicine, Amsterdam UMC, Location AMC, Amsterdam, Netherlands
• ³Department of Radiology, University Medical Center Groningen, Groningen, Netherlands
• ⁴Nico-Lab, Amsterdam, Netherlands
• ⁵Department of Radiology and Nuclear Medicine, Erasmus MC, University Medical Center, Rotterdam, Netherlands
• ⁶Department of Neurology, Erasmus MC University Medical Center, Rotterdam, Netherlands
• ⁷Department of Public Health, Erasmus MC, University Medical Center, Rotterdam, Netherlands
• ⁸Department of Radiology, Haaglanden Medisch Centrum, The Hague, Netherlands
• ⁹Department of Radiology, Texas Stroke Institute, Dallas-Fort Worth, Dallas, TX, United States
• ¹⁰Department of Radiology and Nuclear Medicine, Maastricht University Medical Center and Cardiovascular Research Institute Maastricht (CARIM), Maastricht, Netherlands
• ¹¹Department of Neurology, Maastricht University Medical Center and Cardiovascular Research Institute Maastricht (CARIM), Maastricht, Netherlands
• ¹²Department of Neurology, Amsterdam UMC, Location AMC, Amsterdam, Netherlands
• ¹³Department of Radiology and Nuclear Medicine, Amsterdam UMC, Vrije Universiteit van Amsterdam, Amsterdam, Netherlands

Background: Even days after treatment of acute ischemic stroke due to a large vessel occlusion, the infarct lesion continues to grow. This late, subacute growth is associated with unfavorable functional outcome. In this study, we aim to identify patient characteristics that are risk factors of late, subacute lesion growth.

Methods: Patients from the MR CLEAN trial cohort with good quality 24 h and 1-week follow up non-contrast CT scans were included. Late Lesion growth was defined as the difference between the ischemic lesion volume assessed after 1-week and 24-h. To identify risk factors, patient characteristics associated with lesion growth (categorized in quartiles) in univariable ordinal analysis (p < 0.1) were included in a multivariable ordinal regression model.

Results: In the 226 patients that were included, the median lesion growth was 22 (IQR 10–45) ml. In the multivariable model, lower collateral capacity [aOR: 0.62 (95% CI: 0.44–0.87); p = 0.01], longer time to treatment [aOR: 1.04 (1–1.08); p = 0.04], unsuccessful recanalization [aOR: 0.57 (95% CI: 0.34–0.97); p = 0.04], and larger midline shift [aOR: 1.18 (95% CI: 1.02–1.36); p = 0.02] were associated with late lesion growth.

Conclusion: Late, subacute, lesion growth occurring between 1 day and 1 week after ischemic stroke treatment is influenced by lower collateral capacity, longer time to treatment, unsuccessful recanalization, and larger midline shift. Notably, these risk factors are similar to the risk factors of acute lesion growth, suggesting that understanding and minimizing the effects of the predictors for late lesion growth could be beneficial to mitigate the effects of ischemia.

Introduction

Treatment of acute ischemic stroke (AIS) is strongly focused on the acute phase. However, even after treatment, both successful and unsuccessful, the volumetric increase of infarct related lesions, occurs between 24 h and 1 week after treatment. Although commonly unrecognized, this late lesion growth in the subacute period (i.e., after 24 h of stroke onset) is associated with unfavorable functional outcome (1–6). This suggests that secondary treatment even 24 h after stroke onset can be beneficial to alleviate the effects of ischemia. Infarct-related lesion growth is caused by a combination of edema formation and true infarct progression. Lesion growth is a dynamic and often an irreversible process (7, 8). Both ischemia and post-ischemic reperfusion lead to a cascade of pathophysiological processes, which results in poor prognosis (9). Although several risk factors for early, acute lesion growth between pre and post treatment time-points have been identified in literature (10–13). risk factors for late lesion growth after treatment are understudied.

The aim of this study is to perform an exploratory analysis of associations between baseline, imaging, and (post-) treatment characteristics and late lesion growth after treatment in patients with acute ischemic stroke due to a large vessel occlusion.

More at link.