Abstract TMP10: A 4D Patient-specific Metamorphosis-based Method to Model Ischemic Stroke Lesion Evolution from Acute Diffusion-weighted to Final T2-defined Outcome
There is considerable interest in how well acute DWI can predict the infarct on final T2-w imaging at >1month after stroke. We estimated the 4D dynamic change, from the acute DWI to the final T2-w lesion, to assess DWI predictive ability. Our model dynamically simulates the evolution of uni- or multi-component lesions.
We applied a 4D metamorphosis, modeling the morphogenesis of the acute (<6hr) DWI lesion boundary into that of the final (90 day) T2-w in 10 representative patients, dividing the 90 days into 10 equal intervals. We estimated the mean contraction and expansion deformation velocities that drive change in the acute DWI to the final T2-w boundary, focusing on areas where the DWI volume differed from the final T2-w volume (DWI\T2).
In DWI\T2, over the 10 patients, time-evolving contraction velocity values show a rapid decrease from 0.206+/-0.0091 (mean over time, mm/9days +/- sd) to 0.00097+/-0.001 with time, indicating that contracting DWI\T2 areas were very dynamic acutely and rapidly slowed. Expansion areas displayed a rapid and quasi-monotonic fall from 0.025+/-0.01 to 0.00075+/-0.00028 showing that some parts of DWI tissue had an early high expansion velocity which slowed with time, leading to appearance of newly infarcted areas not present in the acute DWI. A high correlation index (r=0.72, p<0.001) between contraction (also expansion) velocity curves of all patients shows that the 4D evolution patterns of DWI\T2 were similar between patients.
Our imaging derived 4D model of acute DWI-final T2-W lesion evolution shows a consistent pattern, with both ‘recovery’ and ‘new’ infarct happening rapidly at early time points. This confirms that a) acute DWI lesion includes salvageable tissue and is not all statically dead, b) acute DWI lesion does not include all final T2-w dead tissue and c) the method can accurately assess and quantify early treatment response, eg in clinical trials.
- © 2012 by American Heart Association, Inc.