Major Infarct Growth Beyond 3-6 Hours is Associated with Failure of Collateral Circulation

  • Dr Bruce Campbell, Department of Medicine and Neurology, Royal Melbourne Hospital, University of Melbourne, Australia
  • Dr Soren Christensen, Department of Radiology, Royal Melbourne Hospital, University of Melbourne, Australia
  • Prof Patricia Desmond, Department of Radiology, Royal Melbourne Hospital, University of Melbourne, Australia
  • A/Prof Mark Parsons, Department of Neurology and Hunter Medical Research Institute, John Hunter Hospital, University of Newcastle, Australia
  • Prof P Alan Barber, Department of Neurology, Auckland Hospital, Auckland, New Zealand
  • Deidre A. De Silva, Singapore
  • Prof Christopher Levi, Department of Neurology and Hunter Medical Research Institute, John Hunter Hospital, University of Newcastle, Australia
  • Prof Christopher Bladin, Australia
  • Prof Geoffrey Donnan, Florey Neuroscience Institutes, University of Melbourne, Australia
  • Prof Stephen Davis, Department of Medicine and Neurology, Royal Melbourne Hospital, University of Melbourne, Australia

Objective: Without reperfusion, recruitment of ischemic penumbra into the infarct core is generally considered to progress relentlessly until completion. We hypothesized that dynamic shifts in hypoperfusion severity reflect the failure of collateral circulation and contribute to infarct growth, especially with increasing time after stroke onset.
Methods: The EPITHET imaging database of ischemic stroke patients imaged between 3-6 hours of symptom onset was visually reviewed to delineate patients with major infarct growth (recruitment of additional infarcted brain tissue between acute and day 3-5 MRI scans) from those with apparent growth due to edema. Reperfusion was defined as >50% reduction in Tmax>2sec perfusion lesion volume from acute to day 3-5 scans.
Results: Major infarct growth was identified in 21/80 patients; 6/51 (12%) with reperfusion vs 15/29 (52%) without (p<0.001). Amongst 29 patients without reperfusion, those with major growth developed increased mean Tmax severity between acute and day 3-5 scans, compared to stable patients where severity decreased (median change +1.34sec vs -2.88sec, p=0.004). The proportion of perfusion lesion with severe hypoperfusion (Tmax>14sec) also diverged between the two groups (p=0.008).This corresponded to visually evident alterations in leptomeningeal collateral flow between acute and day 3-5 T2*perfusion source images.
Conclusions: The degree of infarct growth in the absence of reperfusion varies considerably. The presence or absence of major growth is associated with increased or decreased perfusion severity over time respectively. These dynamic changes likely represent fluctuations in collateral circulation, emphasising the importance of understanding determinants of collateral flow.