A Phase 2 interventional study of Xenon and air/oxygen in Subarachnoid Hemorrhage, Aneurysmal, Cerebral Injury and Cerebral Ischemia, sponsored by Turku University Hospital. Recruiting at 7 sites in 2 countries. Open to participants aged 18 Years and older. Per ClinicalTrials.gov, last updated 2025-05-01.
Sponsored by Turku University Hospital · Phase 2, Interventional, and Treatment
An investigator-initiated clinical drug study
Main Objective:
To explore neuroprotective properties of xenon in patients after aneurysmal subarachnoid hemorrhage (SAH).
Primary endpoint: Global fractional anisotropy of white matter of diffusion tensor imaging (DTI). Hypothesis: White matter damage is less severe in xenon treated patients, i.e. global fractional anisotropy is significantly higher in the xenon group than in the control group as assessed with the 1st magnetic resonance imaging (MRI).
After confirmation of aSAH and obtaining a signed assent subjects will be randomized to the following groups:
Control group: Standard of Care (SOC) group: Air/oxygen and Normothermia 36.5-37.5°C; Xenon group: Normothermia 36.5-37.5°C +Xenon inhalation in air/oxygen for 24 hours. Brain magnetic resonance imaging techniques will be undertaken to evaluate the effects of the intervention on white and grey matter damage and neuronal loss. Neurological outcome will be evaluated at 3, 12 and 24 months after onset of aSAH symptoms Investigational drug/treatment, dose and mode of administration: 50±2 % end tidal concentration of inhaled xenon in oxygen/air.
Comparative drug(s)/placebo/treatment, dose and mode of administration: Standard of care treatment according to local and international consensus reports.
Duration of treatment: 24 hours
Assessments:
Baseline data Information that characterizes the participant's condition prior to initiation of experimental treatment is obtained as soon as is clinically reasonable. These include participant demographics, medical history, vital signs, oxygen saturation, and concentration of oxygen administered.
Acute data The collected information will contain quantitative and qualitative data of aSAH patients, as recommended by recent recommendations of the working group on subject characteristics, and including all relevant Common Data Elements (CDE) can be applied. Specific definitions, measurements tools, and references regarding each SAH CDE can be found on the weblink here: https://www.commondataelements.ninds.nih.gov/SAH.aspx#tab=Data_Standards.
Assessments of efficacy:
Statistical methods: 1) Basic statistical tests (t-tests, Mann-Whitney, Chi square, etc); 2) Survival analysis methods; 3) An analysis of variance for repeated measurements; 4) A sample size of 100 is estimated on the basis of a recent studies in SAH patients to provide 80% power with a 2-sided α level of 0.05 to detect a mean difference of 0.02 (SD 0.035) in the global fractional anisotropy of white matter between the xenon group and the control group (98). Accordingly, this mean difference is estimated to have a predictive value for DCI and poor neurological outcome (i.e. mRS 3-6).Significance level of 0.05 and an estimation of 95 % confidence intervals will be used in the statistical analyses.
510 studies on the registry are indexed under Subarachnoid Hemorrhage; 128 are open to participants now.
This study's planned enrollment of 160 is above the median of 57 across 264 interventional studies indexed under Subarachnoid Hemorrhage.
Browse Subarachnoid Hemorrhage studies →Turku University Hospital is the lead sponsor of 287 studies on the registry; 67 are open to participants now.
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Go through the criteria one by one — yes, no or not sure — and take the list to your doctor or the study team. Kept in this browser only.
To be considered eligible to participate in this study, a SAH subject must meet the inclusion criteria listed below:
Exclusion Criteria:
An aSAH subject may not be enrolled in the trial if he/she meets any one of the exclusion criteria below:
Underlined terms in the criteria open these too. Explained by clinicaltrials.gg, not part of the registry record. The study team decides who can take part.
Before you join, the study team explains what taking part involves — its purpose, what happens, the risks and possible benefits — and answers your questions, so you can decide freely. Consent is usually recorded on a form (the informed consent form, ICF) signed by you or, where the law allows, by someone legally authorised to decide for you.
You can keep asking questions during the study, you are told of new information that matters, and you can choose to leave at any time.
Judged by the study doctor to matter for your health or for the study. It is a doctor’s decision, so ask the study team if you are unsure whether something counts.
Chronic obstructive pulmonary disease: long-term lung disease that makes it hard to breathe out, including emphysema and chronic bronchitis.
Informed consent
Before you join, the study team explains what taking part involves — its purpose, what happens, the risks and possible benefits — and answers your questions, so you can decide freely. Consent is usually recorded on a form (the informed consent form, ICF) signed by you or, where the law allows, by someone legally authorised to decide for you.
You can keep asking questions during the study, you are told of new information that matters, and you can choose to leave at any time.
Explained by clinicaltrials.gg, not part of the registry record. The study team decides who can take part.
Clinically significant
Judged by the study doctor to matter for your health or for the study. It is a doctor’s decision, so ask the study team if you are unsure whether something counts.
Explained by clinicaltrials.gg, not part of the registry record. The study team decides who can take part.
COPD
Chronic obstructive pulmonary disease: long-term lung disease that makes it hard to breathe out, including emphysema and chronic bronchitis.
Explained by clinicaltrials.gg, not part of the registry record. The study team decides who can take part.
Control arm: air/oxygen with standard of care
Drug: air/oxygen
Xenon arm: xenon inhalation in air/oxygen with standard of care
Drug: Xenon
Fractional anisotropy of the white matter
Global fractional anisotropy of white matter of diffusion tensor imaging (DTI). Hypothesis: White matter damage is less severe in xenon treated patients, i.e. global fractional anisotropy is significantly higher in the xenon group than in the control group as assessed with the 1st MRI.
Time frame: 48-96 hours after start of aSAH symptoms
Fractional anisotropy of white matter at cerebellum and/or at corpus callosum as assessed with the 1st MRI.
Fractional anisotropy of white matter at cerebellum and/or at corpus callosum as assessed with the 1st MRI.
Time frame: 48-96 hours after start of aSAH symptoms
Safety and tolerability of xenon
Safety and tolerability of xenon as assessed with a ratio of adverse events, serious adverse events and suspected unexpected serious adverse reactions (SUSARs) during the follow-up of one year between the xenon group and the control group.
Time frame: during the follow-up of one year
Composite of radiological early brain injury (EBI) and delayed cerebral ischemia (DCI)
Composite of radiological EBI (within 72 hours after start of SAH symptoms) and DCI (Criterion of DCI: 1. a new focal neurological deficit (such as hemiparesis, aphasia, apraxia, hemianopia, or neglect) /decrease in level of consciousness (i.e. decrease of at least 2 points on the Glasgow Coma Scale; either on the total score or on one of its individual components, such as eye, motor on either side, or verbal). This should last for at least 1 hour and not is due to other causes (e.g. hydrocephalus, seizures, metabolic derangement, infection, sedation) and is not apparent immediately after aneurysm occlusion, and cannot be attributed to other causes by means of clinical assessment, CT or MRI scanning of the brain, and appropriate laboratory studies, 2. a new infarct on follow-up imaging (i.e. in any of the following: 2nd MRI, CT, CTA, DSA and perfusion CT) after 4 days post-SAH, or 3. both 1 and 2), and poor outcome at 3-months (good: mRS 0-2; poor: mRS 3-6) at 3-months and at 1 year
Time frame: EBI: within first 72 hours after start of aSAH symptoms; mRS at 3 months and at 1 year and at 2 years after onset of aSAH symptoms
Neurogenic Stress Cardiomyopathy and Stunned Myocardium
Neurogenic Stress Cardiomyopathy and Stunned Myocardium (i.e. myocardial injury caused by sympathetic storm and autonomic dysregulation with hs-troponin elevation, left ventricular dysfunction or ECG changes)
Time frame: follow-up of 1 year
Intracerebral pressure (ICP)
ICP level Duration of therapy for ICP control/monitoring
Time frame: during ICU stay up to 14 days after onset of aSAH symptoms
Intracerebral pressure (ICP)
Need for ICP therapies (hypothermia, decompressive craniotomy)
Time frame: during ICU stay up to 14 days after onset of aSAH symptoms
Intracerebral pressure (ICP)
Duration of therapy for ICP control/monitoring
Time frame: during ICU stay up to 14 days after onset of aSAH symptoms
Plasma catecholamine level
Plasma level of noradrenaline , adrenaline, and dopamine
Time frame: within 3 hours of ICU arrival, at 24h, 48h and 72 h after onset of aSAH symptoms
Selected biomarkers
Selected biomarkers of brain injury: neurofilament light (NF-L), glial fibrillary acidic protein (GFAP), calcium binding protein S100B (S100B), ubiquitin carboxyterminal hydrolase L1 (UCH-L1), total tau, cytokines (tumour necrosis factor alpha, interleukins 6 and 10)
Time frame: within 3 hours of ICU arrival and at 24h, at 48h and at 72h after onset of aSAH symptoms
Development of prognostication models
Development of prognostication models with a selected combination of brain imaging, clinical data, biomarkers and metabolomics by applying artificial intelligence and machine learning for long-term outcome after aSAH
Time frame: long-term outcome at 3 months, at 1 and at 2 years after onset of aSAH symptoms
Development of prognostication models
Development of prognostication models with a selected combination of brain imaging, clinical data, biomarkers and metabolomics by applying artificial intelligence and machine learning for DCI after aSAH
Time frame: between day 4 and 6 weeks after onset of aSAH symtoms
Development of prognostication models
Development of prognostication models with a selected combination of brain imaging, clinical data, biomarkers and metabolomics by applying artificial intelligence and machine learning for vasospasm after aSAH
Time frame: within 21 days after onset of aSAH symptoms
Development of prognostication models
Development of prognostication models with a selected combination of brain imaging, clinical data, biomarkers and metabolomics by applying artificial intelligence and machine learning for EBI after aSAH
Time frame: within 72 hours after onset of aSAH symtoms
Difference of MRI parameters between xenon and control group
Difference of MRI parameters (fractional anisotropy, axial diffucivity, radial diffucivity of diffusion tensor imaging, DTI) between xenon and control group and in predicting risk for EBI
Time frame: within 72 hours after onset of aSAH symptoms
Difference of MRI parameters between xenon and control group
Difference of MRI parameters (fractional anisotropy, axial diffucivity, radial diffucivity of DTI) between xenon and control group and in predicting risk for vasospasm
Time frame: within 21 days after onset of aSAH symptoms
Difference of MRI parameters between xenon and control group
Difference of MRI parameters (fractional anisotropy, axial diffucivity, radial diffucivity of DTI) between xenon and control group and in predicting risk for DCI
Time frame: between day 4 and 6 weeks after onset of aSAH symptoms
Difference of MRI parameters between xenon and control group
Difference of MRI parameters (fractional anisotropy, axial diffucivity, radial diffucivity of DTI) between xenon and control group and in predicting risk for good/poor neurological outcome at 3 moths, at 1 year and at 2 years after onset of aSAH symptoms (mRS 0-2/mRS 3-6).
Time frame: at 3 months, at 1 year and at 2 years after onset of aSAH symptoms
Difference of CTA findings
Difference of CTA ischemic findings between xenon and control group and in predicting risk for EBI
Time frame: within 72 hours after onset of aSAH symptoms
Difference of CTA findings
Difference of ischemic findings in CTA between xenon and control group and in predicting risk for vasospasm
Time frame: within 21 days after onset of aSAH symptoms
Difference of CTA findings
Difference of ischemic findings in CTA between xenon and control group and in predicting risk for DCI
Time frame: between day 4 and 6 weeks after onset of aSAH symptoms
Difference of CTA findings between xenon and control group
Difference of ischemic findings in CTA between xenon and control group and in predicting risk for good/poor neurological outcome at 3 moths, at 1 year and at 2 years after onset of aSAH symptoms (mRS 0-2/mRS 3-6).
Time frame: at 3 months, at 1 year and at 2 years after onset of aSAH symptoms
Difference of DSA findings between xenon and control group
Difference of DSA findings indicating ischemic pattern of perfusion between xenon and control group and in predicting risk for EBI
Time frame: within 72 hours after onset of aSAH symptoms
Difference of DSA findings between xenon and control group
Difference of DSA findings indicating ischemic pattern of perfusion between xenon and control group and in predicting risk for vasospasm
Time frame: within 21 days after onset of aSAH symptoms
Difference of DSA findings between xenon and control group
Difference of DSA findings indicating ischemic pattern of perfusion between xenon and control group and in predicting risk for DCI
Time frame: between day 4 and 6 weeks after onset of aSAH symptoms
Difference of DSA findings between xenon and control group
Difference of DSA findings indicating ischemic pattern of perfusion between xenon and control group and in predicting risk for good/poor neurological outcome at 3 moths, at 1 year and at 2 years after onset of aSAH symptoms (mRS 0-2/mRS 3-6).
Time frame: at 3 months, at 1 year and at 2 years after onset of aSAH symptoms
Activity of microglia cells assessed with PET
It will be explored whether \[11C\](R)-PK11195 can be used to test the hypothesis of neuroprotective effect of xenon and to explore the role of inflammatory process for DCI after SAH. This could be demonstrated by showing less microglial activation in xenon group than in the reference therapy group and in the patients with good outcome, i.e. no DCI; Difference of activity of microglia cells between xenon and control group and in predicting risk for DCI
Time frame: DCI between day 4 and 6 weeks after onset of aSAH symptoms; The 1st PETscan 4 ±1 weeks after onset of aSAH symptoms and the 2nd scan at 3 months after onset of SAH symptoms.
Activity of microglia cells assessed with PET
It will be explored whether \[11C\](R)-PK11195 can be used to test the hypothesis of neuroprotective effect of xenon and to explore the role of inflammatory process for neurological outcome after SAH. This could be demonstrated by showing less microglial activation in xenon group than in the reference therapy group and in the patients with good outcome, i.e. mRS 0-2;
Time frame: The 1st scan at 4 ±1 weeks after and the 2nd scan at 3 months after onset of SAH symptoms. Outcome: at 3 months, at 1 year and at 2 years after onset of aSAH symptoms
Cerebral fluid dynamics
Predictive value of CFD simulations assessed with 3 dimensional DSA within 4 days of ICU arrival in predicting risk for EBI within 72 hours after onset of aSAH symptoms
Time frame: Measures performed within 72 hours of ICU arrival
Cerebral fluid dynamics
Predictive value of CFD simulations assessed with 3 dimensional DSA within 21 days of ICU arrival in predicting risk for neurological outcome at 3 months, at 1 year and at 2 years after SAH (mRS 0-2)
Time frame: Measures performed within 21 days of ICU arrival; outcome at 3 months, at 1 year and at 2 years after onset of aSAH symptoms
Cerebral fluid dynamics
Predictive value of CFD simulations assessed with 3 dimensional DSA within 21 days of ICU arrival in predicting risk for DCI within 6 weeks after onset of aSAH symptoms
Time frame: Measures performed within 21 days of ICU arrival; DCI within 6 weeks after onset of aSAH symptoms
Plan to share: Yes — The data of this study will be available to investigators whose proposed use of the data has been approved by an independent review committee. Individual participant data that underlie the results reported in this Article will be shared (text, tables, figures, and appendices), after de-identification, along with the study protocol. These data will be available 6 months after the Article's pulication and will be available for 12 months from publication. Data can be used for individual participant data meta-analysis. Requests and proposals should be directed to timo.laitio@elisanet.fi. To gain access, data requestors will need to sign a data access agreement.
Supporting information: Study protocol, Statistical analysis plan, Clinical study report
Time frame: data will be available 6 months after the Article's pulication and will be available for 12 months from publication.
Access criteria: Requests and proposals should be directed to timo.laitio@elisanet.fi. To gain access, data requestors will need to sign a data access agreement.
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Studies of the drug tested here: Xenon