Stephanie Lyden, MD, BS

Olivot JM, Mlynash M, Inoue M, Marks MP, Wheeler HM, Kemp S, et al. Hypoperfusion Intensity Ratio Predicts Infarct Progression and Functional Outcome in the DEFUSE 2 Cohort. Stroke. 2014;45:1018–1023.

In stroke care, it is important to understand the various factors that influence patients’ risk for infarct progression. In this regard, there has been increasing interest in understanding the collateral circulation. For example, in chronic vessel stenosis, ischemic preconditioning can cause collateral arborization that results in less than expected infarct size if an occlusion at that area of stenosis occurs. Additionally, in patients with large vessel occlusion who do not achieve recanalization, adequate collateral circulation may play a role in reducing infarct size. The use of perfusion imaging has contributed to a better understanding of the collateral circulation.

This study aimed to evaluate the association between the severity of perfusion-weighted imaging abnormalities, using a hypoperfusion intensity ratio (HIR), on infarct progression and functional outcome in the Diffusion and Perfusion Imaging Evaluation for Understanding Stroke Evolution Study 2 (DEFUSE 2). HIR was defined as the proportion of TMax >6 s lesion volume with a Tmax >10 s delay and was dichotomized based on its median value (0.4) into low versus high subgroups and quartiles. Another way this definition was explained is that it is the Tmax 10/6 s ratio and assessed within 4.9 [+/- 2.6] hours after stroke onset. Initial infarct size was determined using diffusion weighted (DWI) imaging in patients who presented within 12 hours of stroke onset in whom endovascular treatment was anticipated. At day 5 from stroke onset of symptoms, final infarct volume was determined using the fluid attenuated inversion recovery (FLAIR) sequence on magnetic resonance imaging (MRI) of the brain. Total infarct growth was determined by the difference between final infarct volume and initial infarct volume. Baseline DWI lesion volume divided by the delay from symptom onset to baseline MRI of the brain calculated the initial infarct growth velocity. Conventional angiography was used to help determine good or poor collateral flow. A modified Rankin Scale ≤ 2 at 90 days was considered a good functional outcome.

Ninety-nine patients were included. Baseline DWI, perfusion-weighted imaging and final infarct volumes increased with HIR quartiles (P<0.01). A high HIR was felt to predict poor collaterals. Patients with a high HIR were found to have greater initial infarct growth velocities and total infarct growth (P<0.001). A low HIR was associated with a good functional outcome after confounders, such as DWI volume, age and reperfusion status, was accounted for (Odds ratio = 4.4; 95% CI, 1.3-14.3; P =0.014).

HIR was noted in this article to also be associated with the severity of stroke at baseline (larger ischemic lesion and National Institute of Health Stroke Scale). It was also felt to be more severe in patients with a proximal vessel occlusion.

A limitation of this study is that the results are reflective of a highly selected patient population enrolled in the DEFUSE 2 trial. Additionally, the fact that final infarct volume was determined at day 5 from onset of stroke symptoms could have led to overestimation of infarct volume due to edema at that time point.

One conclusion of the study was that a high HIR on baseline MRI was felt to be a measure to predict more rapid growth of the ischemic core and thereby affect treatment decisions. Altogether, the results of this study suggest that HIR could be a potential tool to help provide an estimate of collateral flow, clinical outcome and infarct growth due to failure of collateral blood flow.