Impact of collateral flow on tissue fate in acute ischaemic stroke
- O Y Bang1,
- J L Saver2,
- B H Buck3,
- J R Alger2,
- S Starkman2,4,
- B Ovbiagele2,
- D Kim2,
- R Jahan5,
- G R Duckwiler5,
- S R Yoon5,
- F Viñuela5,
- D S Liebeskind2
- 1Department of Neurology, Samsung Medical Centre, Sungkyunkwan University, Seoul, South Korea
- 2Departments of Neurology, UCLA Stroke Center, University of California, Los Angeles, California, USA
- 3Division of Neurology, Department of Medicine, University of Alberta, Canada
- 4Department of Emergency Medicine, UCLA Stroke Center, University of California, Los Angeles, California, USA
- 5Department of Radiology, UCLA Stroke Center, University of California, Los Angeles, California, USA
- Dr D S Liebeskind, UCLA Stroke Center, 710 Westwood Plaza, Los Angeles, CA 90095, USA; davidliebeskind{at}yahoo.com
- Received 22 August 2007
- Revised 14 November 2007
- Accepted 15 November 2007
- Published Online First 12 December 2007
Abstract
Background: Collaterals may sustain penumbra prior to recanalisation 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 ischaemia. 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 ≥4 s (severe delay) and Tmax ≥2 but <4 s (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 pretreatment 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 non-recanalisation 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 recanalisation therapy. These angiographic and MRI parameters provide complementary information about residual blood flow that may help guide treatment decision making in acute cerebral ischaemia.
Footnotes
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Competing interests: None.
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Ethics approval: The local institutional review board approved the study.







