Reperfusion of very low cerebral blood volume lesion predicts parenchymal hematoma after endovascular therapy.
- Mishra NK From the Stanford Stroke Center, Department of Neurology and Neurological Sciences, Stanford University, Palo Alto, CA (N.K.M., S.C., M.S., M.M., S.K., C.W.C., G.W.A., M.G.L.); Department of Experimental Neurology, KU Leuven, Leuven, Belgium (A.W.); Department of Medicine and Neurology, Royal Melbourne Hospital, University of Melbourne, Victoria, Australia (B.C.V.C.); Stroke Center, Department of Neurology, Neurocenter (EOC) of Southern Switzerland, Lugano, Switzerland (C.W.C.); and Department of Radiology, Stanford University Medical Center, CA (R.B., M.P.M.).
- Christensen S From the Stanford Stroke Center, Department of Neurology and Neurological Sciences, Stanford University, Palo Alto, CA (N.K.M., S.C., M.S., M.M., S.K., C.W.C., G.W.A., M.G.L.); Department of Experimental Neurology, KU Leuven, Leuven, Belgium (A.W.); Department of Medicine and Neurology, Royal Melbourne Hospital, University of Melbourne, Victoria, Australia (B.C.V.C.); Stroke Center, Department of Neurology, Neurocenter (EOC) of Southern Switzerland, Lugano, Switzerland (C.W.C.); and Department of Radiology, Stanford University Medical Center, CA (R.B., M.P.M.).
- Wouters A From the Stanford Stroke Center, Department of Neurology and Neurological Sciences, Stanford University, Palo Alto, CA (N.K.M., S.C., M.S., M.M., S.K., C.W.C., G.W.A., M.G.L.); Department of Experimental Neurology, KU Leuven, Leuven, Belgium (A.W.); Department of Medicine and Neurology, Royal Melbourne Hospital, University of Melbourne, Victoria, Australia (B.C.V.C.); Stroke Center, Department of Neurology, Neurocenter (EOC) of Southern Switzerland, Lugano, Switzerland (C.W.C.); and Department of Radiology, Stanford University Medical Center, CA (R.B., M.P.M.).
- Campbell BC From the Stanford Stroke Center, Department of Neurology and Neurological Sciences, Stanford University, Palo Alto, CA (N.K.M., S.C., M.S., M.M., S.K., C.W.C., G.W.A., M.G.L.); Department of Experimental Neurology, KU Leuven, Leuven, Belgium (A.W.); Department of Medicine and Neurology, Royal Melbourne Hospital, University of Melbourne, Victoria, Australia (B.C.V.C.); Stroke Center, Department of Neurology, Neurocenter (EOC) of Southern Switzerland, Lugano, Switzerland (C.W.C.); and Department of Radiology, Stanford University Medical Center, CA (R.B., M.P.M.).
- Straka M From the Stanford Stroke Center, Department of Neurology and Neurological Sciences, Stanford University, Palo Alto, CA (N.K.M., S.C., M.S., M.M., S.K., C.W.C., G.W.A., M.G.L.); Department of Experimental Neurology, KU Leuven, Leuven, Belgium (A.W.); Department of Medicine and Neurology, Royal Melbourne Hospital, University of Melbourne, Victoria, Australia (B.C.V.C.); Stroke Center, Department of Neurology, Neurocenter (EOC) of Southern Switzerland, Lugano, Switzerland (C.W.C.); and Department of Radiology, Stanford University Medical Center, CA (R.B., M.P.M.).
- Mlynash M From the Stanford Stroke Center, Department of Neurology and Neurological Sciences, Stanford University, Palo Alto, CA (N.K.M., S.C., M.S., M.M., S.K., C.W.C., G.W.A., M.G.L.); Department of Experimental Neurology, KU Leuven, Leuven, Belgium (A.W.); Department of Medicine and Neurology, Royal Melbourne Hospital, University of Melbourne, Victoria, Australia (B.C.V.C.); Stroke Center, Department of Neurology, Neurocenter (EOC) of Southern Switzerland, Lugano, Switzerland (C.W.C.); and Department of Radiology, Stanford University Medical Center, CA (R.B., M.P.M.).
- Kemp S From the Stanford Stroke Center, Department of Neurology and Neurological Sciences, Stanford University, Palo Alto, CA (N.K.M., S.C., M.S., M.M., S.K., C.W.C., G.W.A., M.G.L.); Department of Experimental Neurology, KU Leuven, Leuven, Belgium (A.W.); Department of Medicine and Neurology, Royal Melbourne Hospital, University of Melbourne, Victoria, Australia (B.C.V.C.); Stroke Center, Department of Neurology, Neurocenter (EOC) of Southern Switzerland, Lugano, Switzerland (C.W.C.); and Department of Radiology, Stanford University Medical Center, CA (R.B., M.P.M.).
- Cereda CW From the Stanford Stroke Center, Department of Neurology and Neurological Sciences, Stanford University, Palo Alto, CA (N.K.M., S.C., M.S., M.M., S.K., C.W.C., G.W.A., M.G.L.); Department of Experimental Neurology, KU Leuven, Leuven, Belgium (A.W.); Department of Medicine and Neurology, Royal Melbourne Hospital, University of Melbourne, Victoria, Australia (B.C.V.C.); Stroke Center, Department of Neurology, Neurocenter (EOC) of Southern Switzerland, Lugano, Switzerland (C.W.C.); and Department of Radiology, Stanford University Medical Center, CA (R.B., M.P.M.).
- Bammer R From the Stanford Stroke Center, Department of Neurology and Neurological Sciences, Stanford University, Palo Alto, CA (N.K.M., S.C., M.S., M.M., S.K., C.W.C., G.W.A., M.G.L.); Department of Experimental Neurology, KU Leuven, Leuven, Belgium (A.W.); Department of Medicine and Neurology, Royal Melbourne Hospital, University of Melbourne, Victoria, Australia (B.C.V.C.); Stroke Center, Department of Neurology, Neurocenter (EOC) of Southern Switzerland, Lugano, Switzerland (C.W.C.); and Department of Radiology, Stanford University Medical Center, CA (R.B., M.P.M.).
- Marks MP From the Stanford Stroke Center, Department of Neurology and Neurological Sciences, Stanford University, Palo Alto, CA (N.K.M., S.C., M.S., M.M., S.K., C.W.C., G.W.A., M.G.L.); Department of Experimental Neurology, KU Leuven, Leuven, Belgium (A.W.); Department of Medicine and Neurology, Royal Melbourne Hospital, University of Melbourne, Victoria, Australia (B.C.V.C.); Stroke Center, Department of Neurology, Neurocenter (EOC) of Southern Switzerland, Lugano, Switzerland (C.W.C.); and Department of Radiology, Stanford University Medical Center, CA (R.B., M.P.M.).
- Albers GW From the Stanford Stroke Center, Department of Neurology and Neurological Sciences, Stanford University, Palo Alto, CA (N.K.M., S.C., M.S., M.M., S.K., C.W.C., G.W.A., M.G.L.); Department of Experimental Neurology, KU Leuven, Leuven, Belgium (A.W.); Department of Medicine and Neurology, Royal Melbourne Hospital, University of Melbourne, Victoria, Australia (B.C.V.C.); Stroke Center, Department of Neurology, Neurocenter (EOC) of Southern Switzerland, Lugano, Switzerland (C.W.C.); and Department of Radiology, Stanford University Medical Center, CA (R.B., M.P.M.).
- Lansberg MG From the Stanford Stroke Center, Department of Neurology and Neurological Sciences, Stanford University, Palo Alto, CA (N.K.M., S.C., M.S., M.M., S.K., C.W.C., G.W.A., M.G.L.); Department of Experimental Neurology, KU Leuven, Leuven, Belgium (A.W.); Department of Medicine and Neurology, Royal Melbourne Hospital, University of Melbourne, Victoria, Australia (B.C.V.C.); Stroke Center, Department of Neurology, Neurocenter (EOC) of Southern Switzerland, Lugano, Switzerland (C.W.C.); and Department of Radiology, Stanford University Medical Center, CA (R.B., M.P.M.). lansberg@stanford.edu.
- 2015-04-02
Published in:
- Stroke. - 2015
cerebral
hemorrhage
magnetic resonance imaging
perfusion imaging
stroke
Aged
Aged, 80 and over
Brain Ischemia
Cerebral Hemorrhage
Cerebrovascular Circulation
Endovascular Procedures
Female
Fibrinolytic Agents
Humans
Hypovolemia
Magnetic Resonance Imaging
Male
Middle Aged
Prospective Studies
Reperfusion
Risk Assessment
Stroke
Tissue Plasminogen Activator
Treatment Outcome
English
BACKGROUND AND PURPOSE
Ischemic stroke patients with regional very low cerebral blood volume (VLCBV) on baseline imaging have increased risk of parenchymal hemorrhage (PH) after intravenous alteplase-induced reperfusion. We developed a method for automated detection of VLCBV and examined whether patients with reperfused-VLCBV are at increased risk of PH after endovascular reperfusion therapy.
METHODS
Receiver operating characteristic analysis was performed to optimize a relative CBV threshold associated with PH in patients from the Diffusion and Perfusion Imaging Evaluation for Understanding Stroke Evolution 2 (DEFUSE 2) study. Regional reperfused-VLCBV was defined as regions with low relative CBV on baseline imaging that demonstrated normal perfusion (Tmax <6 s) on coregistered early follow-up magnetic resonance imaging. The association between VLCBV, regional reperfused-VLCBV and PH was assessed in univariate and multivariate analyses.
RESULTS
In 91 patients, the greatest area under the curve for predicting PH occurred at an relative CBV threshold of <0.42 (area under the curve, 0.77). At this threshold, VLCBV lesion volume ≥3.55 mL optimally predicted PH with 94% sensitivity and 63% specificity. Reperfused-VLCBV lesion volume was more specific (0.74) and equally sensitive (0.94). In total, 18 patients developed PH, of whom 17 presented with VLCBV (39% versus 2%; P=0.001), all of them had regional reperfusion (47% versus 0%; P=0.01), and 71% received intravenous alteplase. VLCBV lesion (odds ratio, 33) and bridging with intravenous alteplase (odds ratio, 3.8) were independently associated with PH. In a separate model, reperfused-VLCBV remained the single independent predictor of PH (odds ratio, 53).
CONCLUSIONS
These results suggest that VLCBV can be used for risk stratification of patients scheduled to undergo endovascular therapy in trials and routine clinical practice.
Ischemic stroke patients with regional very low cerebral blood volume (VLCBV) on baseline imaging have increased risk of parenchymal hemorrhage (PH) after intravenous alteplase-induced reperfusion. We developed a method for automated detection of VLCBV and examined whether patients with reperfused-VLCBV are at increased risk of PH after endovascular reperfusion therapy.
METHODS
Receiver operating characteristic analysis was performed to optimize a relative CBV threshold associated with PH in patients from the Diffusion and Perfusion Imaging Evaluation for Understanding Stroke Evolution 2 (DEFUSE 2) study. Regional reperfused-VLCBV was defined as regions with low relative CBV on baseline imaging that demonstrated normal perfusion (Tmax <6 s) on coregistered early follow-up magnetic resonance imaging. The association between VLCBV, regional reperfused-VLCBV and PH was assessed in univariate and multivariate analyses.
RESULTS
In 91 patients, the greatest area under the curve for predicting PH occurred at an relative CBV threshold of <0.42 (area under the curve, 0.77). At this threshold, VLCBV lesion volume ≥3.55 mL optimally predicted PH with 94% sensitivity and 63% specificity. Reperfused-VLCBV lesion volume was more specific (0.74) and equally sensitive (0.94). In total, 18 patients developed PH, of whom 17 presented with VLCBV (39% versus 2%; P=0.001), all of them had regional reperfusion (47% versus 0%; P=0.01), and 71% received intravenous alteplase. VLCBV lesion (odds ratio, 33) and bridging with intravenous alteplase (odds ratio, 3.8) were independently associated with PH. In a separate model, reperfused-VLCBV remained the single independent predictor of PH (odds ratio, 53).
CONCLUSIONS
These results suggest that VLCBV can be used for risk stratification of patients scheduled to undergo endovascular therapy in trials and routine clinical practice.
- Language
-
- English
- Open access status
- green
- Identifiers
-
- DOI 10.1161/STROKEAHA.114.008171
- PMID 25828235
- Persistent URL
- https://sonar.ch/global/documents/279191
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