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Original research
Distribution of symptomatic cerebral vasospasm following subarachnoid hemorrhage assessed using cone-beam CT angiography
  1. Davide Simonato1,
  2. Robin Jacob Borchert2,3,
  3. Fabrice Vallee4,5,
  4. Jona Joachim4,5,
  5. Vittorio Civelli6,
  6. Luca Cancian7,
  7. Emmanuel Houdart6,
  8. Marc-Antoine Labeyrie4,6
  1. 1Neuroradiology, Oxford University Hospitals NHS Foundation Trust, Oxford, UK
  2. 2Clinical Neurosciences, University of Cambridge, Cambridge, UK
  3. 3Neurology, Lister Hospital, Stevenage, UK
  4. 4INSERM U942, PARIS, France
  5. 5Intensive Care Unit Department, Groupe Hospitalier Saint-Louis Lariboisiere et Fernand-Widal, Paris, France
  6. 6Neuroradiology, GH Lariboisiere Fernand-Widal, Paris, France
  7. 7Radiology, Azienda ULSS 6 Euganea, Padova, Italy
  1. Correspondence to Dr Marc-Antoine Labeyrie, Neuroradiology, Groupe hospitalier Lariboisiere Fernand-Widal, Paris 75010, France; marc-antoine.labeyrie{at}aphp.fr

Abstract

Background and purpose Cone-beam CT angiography (CB-CTA) provides a three-dimensional spatial resolution which is, so far, unmatched in clinical practice compared with other conventional techniques such as two-dimensional digital subtracted angiography. We aimed to assess the distribution of symptomatic cerebral vasospasm following aneurysmal subarachnoid hemorrhage (aSAH) using CB-CTA.

Methods 30 consecutive patients with aSAH undergoing vasospasm percutaneous balloon angioplasty (PBA) were recruited and underwent CB-CTA in this single-center prospective cohort series. Intracranial arteries were systematically analyzed by two independent observers from the large trunks to the distal cortical branches and perforators using a high-resolution reconstruction protocol. Intermediate and severe cerebral vasospasm was defined as 30–50% and >50% narrowing in the diameter of the vessel, respectively.

Results 35 arterial cervical artery territories were analyzed, of which 80% were associated with clinical or radiological signs of delayed cerebral ischemia. The median spatial resolution was 150 µm (range 100–250 µm). Intermediate or severe vasospasm was observed in the proximal (86%, 95% CI 74% to 97%), middle (89%, 95% CI 78% to 99%), and distal (60%, 95% CI 44% to 76%) segments of the large trunks, as well as the cortical branches (11%, 95% CI 1% to 22%). No vasospasm was observed in basal ganglia or cortical perforators, or in arteries smaller than 900 µm. Vasospasm was more severe in middle or distal segments compared with proximal segments in 43% (95% CI 26% to 59%) of cases.

Conclusions Our study demonstrated that symptomatic cerebral vasospasm following aSAH did not involve arteries smaller than 900 µm, and frequently predominated in middle or distal segments. These results offer new insights into the potential management options for vasospasm using PBA.

  • subarachnoid
  • hemorrhage
  • angiography
  • technology
  • angioplasty

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

  • Twitter @robinborchert

  • Contributors All authors made substantive intellectual contributions to the development of this research. DS, RJB, MAL contributed to the study conception and development, data collection and data interpretation, and critical revision of the manuscript. FV, VC, LC, EH undertook critical revision of the manuscript. LC, MAL, EH approved the final version of this manuscript. MAL attests that all listed authors meet authorship criteria and that no others meeting the criteria have been omitted. MAL is the guarantor.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • 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.

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