Relationship Between Changes in the Temporal Dynamics of the Blood-Oxygen-Level-Dependent Signal and Hypoperfusion in Acute Ischemic Stroke

BACKGROUND AND PURPOSE—Changes in the blood-oxygen-level-dependent (BOLD) signal provide a noninvasive measure of blood flow, but a detailed comparison with established perfusion parameters in acute stroke is lacking. We investigated the relationship between BOLD signal temporal delay and dynamic su...

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Published inStroke (1970) Vol. 48; no. 4; pp. 925 - 931
Main Authors Khalil, Ahmed A., Ostwaldt, Ann-Christin, Nierhaus, Till, Ganeshan, Ramanan, Audebert, Heinrich J., Villringer, Kersten, Villringer, Arno, Fiebach, Jochen B.
Format Journal Article
LanguageEnglish
Published United States American Heart Association, Inc 01.04.2017
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ISSN0039-2499
1524-4628
1524-4628
DOI10.1161/STROKEAHA.116.015566

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Summary:BACKGROUND AND PURPOSE—Changes in the blood-oxygen-level-dependent (BOLD) signal provide a noninvasive measure of blood flow, but a detailed comparison with established perfusion parameters in acute stroke is lacking. We investigated the relationship between BOLD signal temporal delay and dynamic susceptibility contrast magnetic resonance imaging (DSC-MRI) in stroke patients. METHODS—In 30 patients with acute (<24 hours) ischemic stroke, we performed Pearson correlation and multiple linear regression between DSC-MRI parameters (time to maximum [Tmax], mean transit time, cerebral blood flow, and cerebral blood volume) and BOLD-based parameters (BOLD delay and coefficient of BOLD variation). Prediction of severe hypoperfusion (Tmax >6 seconds) was assessed using receiver–operator characteristic (ROC) analysis. RESULTS—Correlation was highest between Tmax and BOLD delay (venous sinus reference; time shift range 7; median r=0.60; interquartile range=0.49–0.71). Coefficient of BOLD variation correlated with cerebral blood volume (median r= 0.37; interquartile range=0.24–0.51). Mean R for predicting BOLD delay by DSC-MRI was 0.54 (SD=0.2) and for predicting coefficient of BOLD variation was 0.37 (SD=0.17). BOLD delay (whole-brain reference, time shift range 3) had an area under the curve of 0.76 for predicting severe hypoperfusion (sensitivity=69.2%; specificity=80%), whereas BOLD delay (venous sinus reference, time shift range 3) had an area under the curve of 0.76 (sensitivity=67.3%; specificity=83.5%). CONCLUSIONS—BOLD delay is related to macrovascular delay and microvascular hypoperfusion, can identify severely hypoperfused tissue in acute stroke, and is a promising alternative to gadolinium contrast agent–based perfusion assessment in acute stroke. CLINICAL TRIAL REGISTRATION—URLhttp://www.clinicaltrials.gov. Unique identifierNCT00715533 and NCT02077582.
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ISSN:0039-2499
1524-4628
1524-4628
DOI:10.1161/STROKEAHA.116.015566