4.5 Article

Hyperintense Vessels on FLAIR: Hemodynamic Correlates and Response to Thrombolysis

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AMERICAN JOURNAL OF NEURORADIOLOGY
卷 36, 期 8, 页码 1426-1430

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AMER SOC NEURORADIOLOGY
DOI: 10.3174/ajnr.A4320

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资金

  1. Federal Ministry of Education and Research via the grant Center for Stroke Research Berlin [01 EO 0801]
  2. Volkswagen Foundation
  3. EU (EUSTROKE, ARISE)
  4. German Research Foundation (NeuroCure) [SFB-TR 43]

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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.

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