Hyperintense acute reperfusion marker associated with hemorrhagic transformation in the WAKE-UP trial.

Hyperintense acute reperfusion marker (HARM) is an indicator of early disruption of the blood-brain-barrier. Our aim was to investigate the incidence of HARM in patients with a diffusion weighted imaging (DWI) - fluid attenuated inversion recovery (FLAIR) mismatch and determine the association between this marker and hemorrhagic complications as well as clinical outcome. We included patients from the Efficacy and Safety of MRI-Based Thrombolysis in Wake-Up Stroke (WAKE-UP) trial who underwent baseline perfusion weighted imaging (PWI). HARM was defined as a hyperintense signal in the cerebrospinal fluid space on FLAIR imaging at 24 h after baseline imaging. We compared baseline characteristics in patients with and without HARM and investigated the association between HARM and any hemorrhagic transformation (HT) and parenchymal hematoma (PH) in a multivariate logistic regression. We also explored HARM as an independent predictor of poor outcome, defined as a modified Rankin Scale of 3-6 at 90 days. HARM was present in 14 of 223 (6%) patients with a DWI-FLAIR mismatch and baseline characteristics were similar in patients with vs without HARM. HARM showed an independent relationship with any HT (OR 6.67; 95%CI 1.72-26.58) and any PH (OR 6.92; 95%CI 1.34-29.49). The rate of HARM was similar in patients with good and poor outcome (5%, p = 0.90). In the WAKE-UP trial, the incidence of HARM was only 6% at 24 h. An association was present between HARM and hemorrhagic complications, but no relationship with functional outcome was observed.

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© European Stroke Organisation 2021.

Déclaration de conflit d'intérêts

Declaration of conflicting interests: The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: GT received Consulting fees from Acandis, grant support and lecture fees from Bayer, lecture fees from Boehringer Ingelheim, Bristol-Myers Squibb/Pfizer, and Daiichi Sankyo, and consulting fees and lecture fees from Stryker. CG received funding from German Research Council (DFG), European Union, Federal Ministry of Education and Research (BMBF), German Statutory Pension Insurance Scheme (RV Nord), National Innovation Fond, Wegener Foundation, and Schilling Foundation; he received honoraria as speaker or consultant from Abbott, Amgen, Bayer Vital, Bristol-Myers-Squibb, Boehringer Ingelheim, Sanofi Aventis, and Prediction Biosciences. JF reports consulting and advisory board fees from BioClinica, Cerevast, Artemida, Brainomix, Biogen, BMS, and EISAI, outside the submitted work. KM has participated in advisory boards for Bayer, Boehringer-Ingelheim and Daiichi-Sankyo; and receives research support from Boehringer-Ingelheim for the ATTEST-2 trial. ME reports grant support from Bayer, and fees paid to the Charité from Bayer, Boehringer Ingelheim, Bristol-Myers Squibb, Pfizer, Daiichi Sankyo, Amgen, GlaxoSmithKline, Sanofi, Covidien, Novartis, all outside the submitted work.