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Impact of collateral flow on tissue fate in acute ischemic stroke
  1. Oh Young Bang (nmboy{at}unitel.co.kr)
  1. Department of Neurology, Samsung Medical Center, Sungkyunkwan University, Korea, Republic of
    1. Jeffrey L Saver (jsaver{at}ucla.edu)
    1. Departments of Neurology, University of California, Los Angeles, United States
      1. Brian H Buck
      1. Division of Neurology, Department of Medicine, University of Alberta, Canada, Canada
        1. Jeffry R Alger
        1. Departments of Neurology, University of California, Los Angeles, United States
          1. Sidney Starkman
          1. Departments of Emergency Medicine, University of California, Los Angeles, United States
            1. Bruce Ovbiagele
            1. Departments of Neurology, University of California, Los Angeles, United States
              1. Doojin Kim
              1. Departments of Neurology, Univesity of California, Los Angeles, United States
                1. Reza Jahan
                1. Departments of Radiology, University of California, Los Angeles, United States
                  1. Gary R Duckwiler
                  1. Departments of Radiology, University of California, Los Angeles, United States
                    1. Sa Rah Yoon
                    1. Departments of Radiology, University of California, Los Angeles, United States
                      1. Fernando Viñuela
                      1. Departments of Radiology, University of California, Los Angeles, United States
                        1. David S Liebeskind (davidliebeskind{at}yahoo.com)
                        1. Departments of Neurology, University of California, Los Angeles, United States

                          Abstract

                          Background: Collaterals may sustain penumbra prior to recanalization, yet the influence of baseline collateral flow on infarct growth following endovascular therapy remains unknown.

                          Methods: Consecutive patients underwent serial diffusion and perfusion MRI before and after endovascular therapy for acute cerebral ischemia. We assessed the relationship between MRI diffusion and perfusion lesion indices, angiographic collateral grade, and infarct growth. Tmax perfusion lesion maps were generated and diffusion-perfusion mismatch regions were divided into Tmax¡Ý4 sec (severe delay) and Tmax¡Ý2 but <4 sec (mild delay).

                          Results: Among 44 patients, collateral grade was poor in 7 (15.9%), intermediate in 20 (45.5%), and good in 17 (38.6%) patients. Although diffusion-perfusion mismatch volume was not different depending on the collateral grade, patients with good collaterals had larger areas of milder perfusion delay than those with poor collaterals (p=0.005). Among 32 patients who underwent day 3-5 post-treatment MRIs, the degree of pre-treatment collateral circulation (r=-0.476, p=0.006) and volume of diffusion-perfusion mismatch (r=0.371, p=0.037) were correlated with infarct growth. Greatest infarct growth occurred in patients with both nonrecanalization and poor collaterals. Multiple regression analysis revealed that pretreatment collateral grade was independently associated with infarct growth.

                          Conclusion: Our data suggest that angiographic collateral grade and penumbral volume interactively shape tissue fate in patients undergoing endovascular recanalization therapy. These angiographic and MRI parameters provide complementary information about residual blood flow that may help guide treatment decision-making in acute cerebral ischemia.

                          • Angiography
                          • Collaterals
                          • Magnetic resonance imaging
                          • Stroke, Ischemic
                          • Thrombolysis

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