Determinants of the distribution and severity of hypoperfusion in patients with ischemic stroke

Background: In acute cerebral ischemia, two variables characterize the extent of hypoperfusion: the volume of hypoperfused tissue and the intensity of hypoperfusion within these regions. We evaluated the determinants of the intensity of hypoperfusion within oligemic regions among patients who were eligible for recanalization therapy for acute ischemic stroke. Methods: We analyzed data, including pretreatment diffusion-weighted imaging (DWI) and perfusion-weighted imaging, on 119 patients with acute middle cerebral artery infarctions. The intensity of hypoperfusion within oligemic regions was characterized by the hypoperfusion intensity ratio (HIR), defined as the volume of tissue with severe hypoperfusion (Tmax ≥8 seconds) divided by the volume of tissue with any hypoperfusion (Tmax ≥2 seconds). Based on the DWI data, we divided the patients into four stroke phenotypes: large cortical, small (<1 cm diameter) cortical, border-zone, and deep pattern. Results: The mean (SD) volume of severe hypoperfusion was 54.6 (52.5) mL, and that of any hypoperfusion was 140.8 (81.3) mL. The HIR ranged widely, from 0.002 to 0.974, with a median of 0.35 (interquartile range 0.13–0.60). The volume of any hypoperfusion did not predict the intensity of hypoperfusion within the affected region (r = 0.10, p = 0.284). Angiographic collateral flow grade was associated with HIRs (p value for trend = 0.019) and differed among DWI lesion patterns. In multivariate analysis, diastolic pressure on admission (odds ratio 0.959, 95% CI 0.922–0.998) and DWI pattern of deep infarcts (odds ratio 18.004 compared with large cortical pattern, 95% CI 1.855–173.807) were independently associated with a low HIR. Conclusions: The intensity of hypoperfusion within an oligemic field is largely independent of the size of the oligemia region. Predictors of lesser intensity of hypoperfusion are lower diastolic blood pressure and presence of a deep diffusion-weighted imaging lesion pattern. GLOSSARY: AIF = arterial input function; DWI = diffusion-weighted imaging; HDL = high-density lipoprotein; HIR = hypoperfusion intensity ratio; ICA = internal carotid artery; IQR = interquartile range; LDL = low-density lipoprotein; MCA = middle cerebral artery; MR = magnetic resonance; MRA = magnetic resonance angiography; NIHSS = NIH Stroke Scale; OR = odds ratio; PWI = perfusion-weighted imaging.

[1]  F Viñuela,et al.  Impact of collateral flow on tissue fate in acute ischaemic stroke , 2007, Journal of Neurology, Neurosurgery, and Psychiatry.

[2]  A. Alexandrov,et al.  Association of Pretreatment Blood Pressure With Tissue Plasminogen Activator-Induced Arterial Recanalization in Acute Ischemic Stroke , 2007, Stroke.

[3]  Scott Hamilton,et al.  Magnetic resonance imaging profiles predict clinical response to early reperfusion: The diffusion and perfusion imaging evaluation for understanding stroke evolution (DEFUSE) study , 2006, Annals of neurology.

[4]  Werner Hacke,et al.  MRI versus CT-based thrombolysis treatment within and beyond the 3 h time window after stroke onset: a cohort study , 2006, The Lancet Neurology.

[5]  Steven Warach,et al.  Dose Escalation of Desmoteplase for Acute Ischemic Stroke (DEDAS): Evidence of Safety and Efficacy 3 to 9 Hours After Stroke Onset , 2006, Stroke.

[6]  O. Bang,et al.  Internal and Cortical Border-Zone Infarction: Clinical and Diffusion-Weighted Imaging Features , 2006, Stroke.

[7]  A. Weaver,et al.  Initial emergency department blood pressure as predictor of survival after acute ischemic stroke , 2005, Neurology.

[8]  P. Lee,et al.  Specific DWI lesion patterns predict prognosis after acute ischaemic stroke within the MCA territory , 2005, Journal of Neurology, Neurosurgery & Psychiatry.

[9]  G. Christoforidis,et al.  Angiographic assessment of pial collaterals as a prognostic indicator following intra-arterial thrombolysis for acute ischemic stroke. , 2005, AJNR. American journal of neuroradiology.

[10]  P. Barber,et al.  Refining the Perfusion—Diffusion Mismatch Hypothesis , 2005, Stroke.

[11]  À. Rovira,et al.  Safety and Efficacy of Intravenous Tissue Plasminogen Activator Stroke Treatment in the 3- to 6-Hour Window Using Multimodal Transcranial Doppler/MRI Selection Protocol , 2005, Stroke.

[12]  G. Donnan,et al.  Selection of thrombolytic therapy beyond 3 h using magnetic resonance imaging , 2005, Current opinion in neurology.

[13]  S. Warach,et al.  Magnetic Resonance Imaging Criteria for Thrombolysis in Acute Cerebral Infarct , 2005, Stroke.

[14]  G. Schroth,et al.  Blood Pressure and Vessel Recanalization in the First Hours After Ischemic Stroke , 2005, Stroke.

[15]  S. Warach,et al.  The Desmoteplase in Acute Ischemic Stroke Trial (DIAS): A Phase II MRI-Based 9-Hour Window Acute Stroke Thrombolysis Trial With Intravenous Desmoteplase , 2005, Stroke.

[16]  Lynn A Smaha,et al.  The American Heart Association Get With The Guidelines program. , 2004, American heart journal.

[17]  Nancy J Fischbein,et al.  Regional Angiographic Grading System for Collateral Flow: Correlation With Cerebral Infarction in Patients With Middle Cerebral Artery Occlusion , 2004, Stroke.

[18]  J. Alger,et al.  Beyond Mismatch: Evolving Paradigms in Imaging the Ischemic Penumbra With Multimodal Magnetic Resonance Imaging , 2003, Stroke.

[19]  R. Higashida,et al.  Trial Design and Reporting Standards for Intra-Arterial Cerebral Thrombolysis for Acute Ischemic Stroke , 2003, Stroke.

[20]  Jeffry R Alger,et al.  Perfusion-Weighted Magnetic Resonance Imaging Thresholds Identifying Core, Irreversibly Infarcted Tissue , 2003, Stroke.

[21]  G. Donnan,et al.  Neuroimaging, the ischaemic penumbra, and selection of patients for acute stroke therapy , 2002, The Lancet Neurology.

[22]  H. Naritomi,et al.  Microembolic signals and diffusion-weighted MR imaging abnormalities in acute ischemic stroke. , 2001, AJNR. American journal of neuroradiology.

[23]  J. Alger,et al.  Impact on stroke subtype diagnosis of early diffusion-weighted magnetic resonance imaging and magnetic resonance angiography. , 2000, Stroke.

[24]  G. Schlaug,et al.  Multiple acute stroke syndrome , 2000, Neurology.

[25]  J. Wales Hypergonadotropic Hypogonadism in a 3-Yea r-Old Girl with Blepharophimosis, Ptosis, and Epicanthus inversus Syndrome , 1998, Hormone Research in Paediatrics.

[26]  J. Bogousslavsky,et al.  Large infarcts in the middle cerebral artery territory Etiology and outcome patterns , 1998, Neurology.

[27]  B. Rosen,et al.  High resolution measurement of cerebral blood flow using intravascular tracer bolus passages. Part I: Mathematical approach and statistical analysis , 1996, Magnetic resonance in medicine.

[28]  C. Yutani,et al.  Atheromatous embolism in the brain , 1994, Neurology.

[29]  L. Caplan Brain embolism, revisited , 1993, Neurology.

[30]  N M Branston,et al.  Cortical Evoked Potential and Extracellular K+ and H+ at Critical Levels of Brain Ischemia , 1977, Stroke.