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New Remote Cerebral Microbleeds on T2-Weighted Echo Planar MRI After Intravenous Thrombolysis for Acute Ischemic Stroke. | LitMetric

AI Article Synopsis

  • The study examines the association between intravenous administration of recombinant tissue plasminogen activator (rtPA) for acute ischemic stroke (AIS) and the formation of cerebral microbleeds (CMBs) following treatment.
  • Researchers conducted MRI scans on 59 AIS patients before and after receiving rtPA to assess the appearance of new CMBs and their relationship with hemorrhagic transformation.
  • Findings revealed that about 30% of patients developed new CMBs post-treatment, with pre-existing CMBs significantly increasing the risk of new ones, but the initial load of CMBs did not predict hemorrhagic transformation.

Article Abstract

Background: The main and well-defined complication of intravenous administration of recombinant tissue plasminogen activator (tPA) in patients with acute ischemic stroke (AIS) is symptomatic intracranial hemorrhage (sICH). However, rtPA might also be connected with the formation of cerebral microbleeds (CMBs), located remotely from the ischemic lesions, that may remain clinically silent. This association might be important because the load of CMBs has been associated with cognitive impairment. We investigated whether administration of rtPA in AIS results in the appearance of new CMBs and if the initial load of CMBs is associated with hemorrhagic transformation.

Methods: A total of fifty-nine consecutive patients with AIS treated with rtPA underwent MRI including T2-weighted Echo Planar Imaging (T2-EPI) shortly before and 7-9 days after rtPA administration. We calculated the load of new CMBs located outside the MR diffusion restriction area in the follow-up imaging and assessed hemorrhagic transformation with ECASS-II scoring.

Results: A total of forty-nine patients were included for the final analysis. On initial T2-EPI-GRE, 37 baseline microbleeds (CMBs) were observed in 14 patients (28.6%). On follow-up T2-EPI-GRE amount of CMBs increased to a total number of 103. New CMBs were found in 5 (14.3%) of 35 patients without and in 9 (64.3%) of 14 with any baseline CMBs. Multiple logistic regression analysis indicated that presence of baseline CMBs (risk ratio [RR] 5.95, 95% CI 2.69-13.20, < 0.001) and lower platelets level (risk ratio [RR] 0.992, 95% CI 0.986-0.998, = 0.007) were independently associated with new CMBs. The baseline load of CMBs was not associated with the risk of hemorrhagic transformation.

Conclusion: In this study, new CMBs were found in nearly 30% of patients with AIS on the 7-9 days after rtPA treatment. Baseline CMBs correlated with a higher risk of new CMBs appearing after the rtPA treatment, independently of other factors. At the same time, in our sample, baseline CMBs did not correlate with an increased risk of hemorrhagic transformation. Since the associations between the CMBs load and cognitive impairment have already been proved, further studies are warranted to investigate possible associations between the thrombolytic treatment of patients with AIS, mainly those with baseline CMBs, and the risk of earlier cognitive decline.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8886895PMC
http://dx.doi.org/10.3389/fneur.2021.744701DOI Listing

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