Editor’s Choice
Editor’s Comment
The authors evaluated 62 consecutive patients with ischemic stroke with proven vessel occlusion with MRI before and within 24 hours of treatment and defined a hypoperfusion intensity ratio (volume with severe/mild hypoperfusion [time-to-maximum ≥ 8 seconds / time-to-maximum ≥ 2 seconds]). Patients with extensive hyperintense vessels on FLAIR (>4 sections) had higher NIHSS scores, larger baseline lesion volumes, higher rates of perfusion-diffusion mismatch, and more severe hypoperfusion intensity ratio.
Abstract
![MR imaging (left-to-right: acute FLAIR, acute DWI, acute Tmax, dichotomized Tmax, follow-up DWI) of patients with middle cerebral artery occlusions (M1). Patient A (82 years of age; baseline NIHSS score, 13; baseline lesion volume, 1.4 mL; HIR, 0.031; recanalization to Thrombolysis in Myocardial Infarction 2 following treatment; absolute infarct growth, 3.3 mL) had FLAIR hyperintense vessels on 3 sections (FHV ≤ 4; not visible on the depicted section) and patient B (76 years of age; baseline NIHSS score, 23; baseline lesion volume, 63.8 mL; HIR, 0.53; no recanalization following treatment [Thrombolysis in Myocardial Infarction, 0]; absolute infarct growth, 80.2 mL) had FHV on 8 sections (arrows; FHV > 4).](http://www.ajnrblog.org/wp-content/uploads/ec-kufner.jpg)
Background and Purpose
Hyperintense vessels on baseline FLAIR MR imaging of patients with ischemic stroke have been linked to leptomeningeal collateralization, yet the ability of these to maintain viable ischemic tissue remains unclear. We investigated whether hyperintense vessels on FLAIR are associated with the severity of hypoperfusion and response to thrombolysis in patients treated with intravenous tissue-plasminogen activator.
Materials and Methods
Consecutive patients with ischemic stroke with an MR imaging before and within 24 hours of treatment, with proved vessel occlusion and available time-to-maximum maps were included (n = 62). The severity of hypoperfusion was characterized on the basis of the hypoperfusion intensity ratio (volume with severe/mild hypoperfusion [time-to-maximum ≥ 8 seconds / time-to-maximum ≥ 2 seconds]). The hypoperfusion intensity ratio was dichotomized at the median to differentiate moderate (hypoperfusion intensity ratio ≤ 0.447) and severe (hypoperfusion intensity ratio > 0.447) hypoperfusion. Good outcome was defined as a modified Rankin Scale score of ≤2.
Results
Hyperintense vessels on FLAIR were identified in 54 patients (87%). Patients with extensive hyperintense vessels on FLAIR (>4 sections) had higher NIHSS scores, larger baseline lesion volumes, higher rates of perfusion-diffusion mismatch, and more severe hypoperfusion (hypoperfusion intensity ratio). In stepwise backward multivariate regression analysis for the dichotomized hypoperfusion intensity ratio (including stroke etiology, age, perfusion deficit, baseline lesion volume, smoking, and extent of hyperintense vessels on FLAIR), extensive hyperintense vessels on FLAIR were independently associated with severe hypoperfusion (OR, 6.8; 95% CI, 1.1–42.7;P = .04). The hypoperfusion intensity ratio was an independent predictor of a worse functional outcome at 3 months poststroke (OR, 0.2; 95% CI, 0.5–0.6; P < .01).
Conclusions
Hyperintense vessels on FLAIR are associated with larger perfusion deficits, larger infarct growth, and more severe hypoperfusion, suggesting that hyperintense vessels on FLAIR most likely indicate severe ischemia as a result of insufficient collateralization.
Read this article: http://www.ajnr.org/content/36/8/1426.full
