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Original research
Intracranial non-occlusive intraluminal thrombus may indicate underlying etiology of large vessel occlusion in patients undergoing endovascular therapy
  1. Seong Hwa Jang1,
  2. Hyungjong Park1,
  3. Joonsang Yoo1,2,
  4. Jeong-Ho Hong1,
  5. Jin Soo Lee3,
  6. Seong-Joon Lee3,
  7. Yong-Won Kim4,
  8. Ji Man Hong3,
  9. Jin Wook Choi5,
  10. Dong-Hun Kang6,
  11. Yong-Sun Kim7,
  12. Yang-Ha Hwang4,
  13. Sung-Il Sohn1
  1. 1 Department of Neurology, Keimyung University School of Medicine, Daegu, Republic of Korea
  2. 2 Department of Neurology, Yonsei University College of Medicine, Yonging Severance Hospital, Yongin, Republic of Korea
  3. 3 Department of Neurology, School of Medicine Ajou University, Suwon, Republic of Korea
  4. 4 Department of Neurology, School of Medicine, Kyungpook National University, Daegu, Republic of Korea
  5. 5 Department of Radiology, School of Medicine, Ajou University, Suwon, Republic of Korea
  6. 6 Department of Neurosurgery, School of Medicine, Kyungpook National University, Daegu, Republic of Korea
  7. 7 Department of Radiology, School of Medicine, Kyungpook National University, Daegu, Republic of Korea
  1. Correspondence to Dr Hyungjong Park, Department of Neurology, Keimyung University School of Medicine, Daegu, Republic of Korea; hjpark209042{at}gmail.com; Sung-Il Sohn, Department of Neurology, Keimyung University School of Medicine, Daegu, Republic of Korea; sungil.sohn{at}gmail.com

Abstract

Background The underlying etiology of intracranial non-occlusive intraluminal thrombus (iNOT) remains unknown. This study aimed to investigate whether the presence of iNOT can indicate the underlying etiology of large vessel occlusion (LVO) in patients undergoing endovascular therapy (EVT).

Methods Among patients who underwent EVT at three comprehensive stroke centers, we included those with intracranial LVO in the anterior circulation. The presence of iNOT was determined by pretreatment DSA. We investigated the association between iNOT and intracranial atherosclerotic stenosis (ICAS) related LVO.

Results Of 546 patients, 44 (8.1%) had iNOT. Patients with iNOT were younger, had less hypertension, atrial fibrillation, and a history of antiplatelet use. In addition, the involvement of the M1 segment of the middle cerebral artery (MCA) was more frequent. However, they had a lower National Institutes of Health Stroke Scale (NIHSS) score on admission and longer onset to recanalization time compared with patients with no iNOT. In a logistic regression model adjusting for age, sex, atrial fibrillation, smoking, prior antiplatelet and anticoagulant use, intravenous tissue plasminogen activator, NIHSS on admission, number of technical trials, intraprocedural re-occlusion, and the location of LVO (p<0.10 in the univariate analysis), the presence of iNOT was significantly associated with ICAS related LVO (adjusted OR 3.04; 95% CI 1.33 to 6.90; p=0.007).

Conclusions The presence of iNOT may reflect an underlying ICAS related LVO in patients undergoing EVT.

  • atherosclerosis
  • stroke
  • thrombectomy

Data availability statement

Data are available upon reasonable request.

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Data availability statement

Data are available upon reasonable request.

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Footnotes

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  • Correction notice Since this article was first published online, the author affiliations have been updated and ORCID IDs has been listed for more authors.

  • Contributors SHJ: study design, data collection, data analysis, data interpretation, preparation of manuscript review, and editing. HP: study design, data collection, data analysis, data interpretation, preparation of manuscript review, and editing. JY: data collection, imaging analysis, review, and editing. J-HH, JSL, S-JL, Y-WK, JMH, JWC, D-HK, Y-SK, Y-HH, and S-IS: data collection, review, and editing.

  • Funding This work was supported by a National Research Foundation of Korea grant funded by the Korean government (MSIT) (18 No 2020R1G1A007100).

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.