Hypoperfusion intensity ratio predicts infarct progression and functional outcome in the DEFUSE 2 Cohort

Abstract

Background and purpose: We evaluate associations between the severity of magnetic resonance perfusion-weighted imaging abnormalities, as assessed by the 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).

Methods: Diffusion-weighted magnetic resonance imaging and perfusion-weighted imaging lesion volumes were determined with the RAPID software program. 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 as well as quartiles. Final infarct volumes were assessed at day 5. Initial infarct growth velocity was calculated as the baseline diffusion-weighted imaging (DWI) lesion volume divided by the delay from symptom onset to baseline magnetic resonance imaging. Total Infarct growth was determined by the difference between final infarct and baseline DWI volumes. Collateral flow was assessed on conventional angiography and dichotomized into good and poor flow. Good functional outcome was defined as modified Rankin Scale ≤2 at 90 days.

Results: Ninety-nine patients were included; baseline DWI, perfusion-weighted imaging, and final infarct volumes increased with HIR quartiles (P<0.01). A high HIR predicted poor collaterals with an area under the curve of 0.73. Initial infarct growth velocity and total infarct growth were greater among patients with a high HIR (P<0.001). After adjustment for age, DWI volume, and reperfusion, a low HIR was associated with good functional outcome: odds ratio=4.4 (95% CI, 1.3-14.3); P=0.014.

Conclusions: HIR can be easily assessed on automatically processed perfusion maps and predicts the rate of collateral flow, infarct growth, and clinical outcome.

Keywords: brain infarction; magnetic resonance imaging; perfusion imaging.

Conflict of interest statement

Disclosures

Dr Albers has equity interest in iSchemaView and has worked as a consultant for Covidien, Codman, and Stryker. Dr Bammer has equity interest in iSchemaView. Dr Zaharchuk receives modest research funding support from GE Healthcare. The other authors report no conflicts.

Figures

Figure 1

Hypoperfusion intensity ratio (HIR) progression between baseline and first follow-up among reperfusers and nonreperfusers. Evolution of the HIR between baseline and follow-up perfusion-weighted magnetic resonance imaging according to the occurrence of an acute reperfusion.

Figure 2

Relationship between hypoperfusion intensity ratio (HIR) quartiles and (A) initial infarct growth velocity (baseline diffusion-weighted magnetic resonance imaging [dMRI] lesion volume/delay from onset to baseline MRI in hours) and (B) final infarct growth (final infarct volume on 5-day fluid attenuated inversion recovery baseline diffusion-weighted imaging volume).

Figure 3

Fifty-year-old patient, baseline National Institutes of Health Stroke Scale was 22, (A) baseline magnetic resonance imaging (MRI) showed a 12-mL diffusion-weighted imaging (DWI; apparent diffusion coefficient [ADC] <600) lesion and (B) a 217-mL perfusion-weighted imaging lesion with an hypoperfusion intensity ratio (HIR) of 0.44. Cerebral angiogram demonstrated a left internal carotid artery occlusion with poor collaterals, and recanalization was not achieved. HIR increased to 0.7 on the follow-up MRI performed 3 hours later (C). The infarct grew to 500 mL at day 5, and the 90-day modified Rankin Scale was 3 (D). FLAIR indicates fluid attenuated inversion recovery; and TMax, time when the residue function reaches its maximum.