Subarachnoid Hemorrhage, AneurysmalCASAHNCT03987139
Cerebral Autoregulation in Patients With Aneurysmal SubArachnoid Haemorrhage
A study testing Hypertension, Hyper- and hypoxia and Hyper- and hypocapnia in people with Subarachnoid Hemorrhage, Aneurysmal, run by Copenhagen University Hospital, Rigshospitalet at 1 site in Denmark.
Trial summary
The purpose is, in patients with aneurysmal subarachnoid haemorrhage in the early phase after ictus, to examine the following: 1. The effect of spontaneous and induced changes on the brain's static and dynamic autoregulation calculated by transcranial Doppler (TCD), ICP and MAP (primary purposes) and ICP and PbtO2; 2. Read more about this study
- Who is it for?
- Ages 18 years and olderHealthy volunteers can take part
- Conditions the study is for
- Subarachnoid Hemorrhage, Aneurysmal
- What is being tested?
- Hypertension, Hyper- and hypoxia and Hyper- and hypocapnia
- Type of treatment
- Injection or infusion
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 45 participants
- Where
- 1 siteDenmark
- Study dates
- 15 Jun 2019to 1 Mar 2022
- Phase
- Interventional
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 years and older
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Who may be able to join
- Admittance to neurointensive care unit, Rigshospitalet
- Age ≥ 18 years old
- Aneurysmal subarachnoid haemorrhage
- Clinical indication for placement of an external ventricular drain
- Measurements can be done within 3 days of ictus
- Closest relatives understand written and spoken danish
Show all 13Show fewer
- Age ≥ 18 years old;
- Understands written and spoken danish
- Oral and written consent
- No medication expect hay fever medications
- Alcohol consumption within the limits from the danish health care board
- Healthy without previous or current cerebrovascular diseases
- Insonation is possible from the middle cerebral artery
Who cannot join
- No aneurysm identified
- Conservative og failed treatment of aneurysm
- Pupils dilated and do not react to light
- Incarceration before inclusion
- Expected death within 48 hours
- Acute or chronic diseases associated with impaired autoregulation
- Severe chronic lung failure with a PaCO2 > 6.5 kPa or PaO2 < 8 kPa.
Trial locations and contacts
1 site in 1 country.
Denmark1 site
Department of Neuroanaesthesiology
Copenhagen, Capital Region, 2200
About this study
The purpose is, in patients with aneurysmal subarachnoid haemorrhage in the early phase after ictus, to examine the following:
- The effect of spontaneous and induced changes on the brain's static and dynamic autoregulation calculated by transcranial Doppler (TCD), ICP and MAP (primary purposes) and ICP and PbtO2;
- The effect of mild hyper- and hypocapnia as well as of mild hyper- and hypoxia on the brain's static and dynamic autoregulation, ICP and PbtO2;
- The relationship between brain autoregulation, mild hyper- and hypocapnia, as well as of mild hyper- and hypoxia and metabolism in microdialysate on the one hand and the occurrence of DCI during hospitalization and poor neurological outcome one year after ictus on the other.
Read the detailed description
Spontaneous aneurysm subarachnoid hemorrhage (SAH) occurs annually in approximately 400 people in Denmark. SAH is most commonly seen in younger (median age 56 years) and women (71%), have a high mortality (21-44%) and result in a poor neurological outcome in about 50% of patients. Due to the relatively young patient population and high mortality and morbidity, SAH in the population causes the same number of lost working years as blood clots in the brain.
The occurrence of complications like hydrocephalus and re-bleeding can be minimized by rapid external ventricular drainage and aneurysm closure, and so-called delayed cerebral ischaemia (DCI) is currently considered to be the most frequent serious complication of SAH. DCI occurs in 20-30% of patients, most often within the first 14 days, is characterized by a reduction in consciousness or focal neurological deficit lasting at least one hour without any other underlying cause and is associated with a significantly increased risk of a poor outcome. The cause and treatment of DCI is controversial, and the previous hypothesis of vasospasm as the sole contributor is currently supplemented by a broader focus on several other mechanisms, including the brain's blood supply and its regulation.
The brain's blood supply (CBF) is kept relatively constant in healthy by changing cardiac diameter and thus the cerebrovascular resistance (CVR) during changes in brain perfusion pressure (CPP, measured as mean arterial pressure (MAP) minus intracranial pressure (ICP)) within certain limits. This mechanism is known as cerebral autoregulation. Outside these limits, respectively. decreases and increases CBF, with the consequent risk of hypoperfusion/ischemia and hyperperfusion/vasogenic edema with prolonged changes.
Weakened autoregulation, i.e. that CBF varies passively with CPP also within the normal autoregulation limits, is described in e.g. traumatic brain injury (TBI), ischemic stroke, acute liver failure and meningitis, with complete or partial restoration of autoregulation by hyperventilation (mild hypocapnia). SAH also describes impaired autoregulation with varying association with disease severity, DCI and outcome. It is not known whether mild hypocapnia restores autoregulation in patients with SAH, whereas animal experimental studies suggest this.
Reduced intracerebral oxygenation (PbtO2) is associated with a worse outcome after SAH. Cerebral microdialysis measures the concentration of certain metabolites in the brain and can provide an insight into whether metabolic activity is affected by oxygen deficiency, and so-called anaerobic combustion occurs. Microdialysis measurements with elevated lactate concentration, which is a metabolic product, among other things. Anaerobic combustion appears to occur prior to clinical signs of DCI, as well as during the DCI episodes, decreasing PbtO2. It is possible that these findings could be due to a condition of impaired autoregulation and too low perfusion pressure to meet brain metabolic needs, but this has not previously been elucidated. It is also unknown if it is possible to improve brain metabolism by increasing the brain's perfusion pressure.
The purpose of this study is therefore to investigate brain autoregulation in patients with SAH.
- Conditions
- Subarachnoid Hemorrhage, Aneurysmal
- Being tested
- Hypertension, Hyper- and hypoxia, Hyper- and hypocapnia
- Keywords
- cerebral autoregulation
- Medical subject headings
- Subarachnoid Hemorrhage
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
HypertensionOther
Hypertension is induced by an infusion of noradrenaline within acceptable limits Baseline recording (10 minutes) is performed. MAP gradually increases in steps of 5-10 mmHg during ongoing TCD. When the desired maximum MAP is reached, measurement is made at steady state (10 minutes).
Noradrenaline infusion is stopped. When MAP is stabilized, new baseline is measured for 10 minutes.
Hyper- and hypoxiaOther
The mechanical ventilator is adjusted to mild hypoxia, normoxia and mild hyperoxia. Measurements are made for 10 minutes at normoxia and after steady state is reached, respectively. hyperoxia and hypoxia. Oxygenation is controlled by arterial blood gas before and during steady state.
Hyper- and hypocapniaOther
The mechanical ventilator is adjusted to a delta PaCO2 on the ventilator for both hypocapnia and hypercapnia. Measurements are made for 10 minutes at normocapnia and after steady state is reached, respectively. hyper- and hypocapnia.
| Study group | Role | What they receive |
|---|---|---|
| All patients | Other | Patients included in the study. Receives: Other: Hypertension; Other: Hyper- and hypoxia; Other: Hyper- and hypocapnia |
What is being measured
The primary outcome is the main question the study is designed to answer.
Middle cerebral artery flow velocity (MCAv) + induced hypertension
Measuring MCAv after induced hypertension
Measured: within 5 days after ictus, for 10 minutes after steady state
Secondary outcomes (6)
Intracranial pressure (ICP) + induced hypertension
Measuring changes in ICP after induced hypertension
Measured: within 5 days after ictus
Partial brain tissue oxygenation (PbtO2) + induced hypertension
Measuring changes in ICP after induced hypertension
Measured: within 5 days after ictus
Intracranial pressure (ICP) + hyper- and hypocapnia
Measuring during induction of hyper- and hypocapnia
Measured: within 5 days after ictus, for 10 minutes after steady state
Partial brain tissue oxygenation (PbtO2) + hyper- and hypocapnia
Measuring during induction of hyper- and hypocapnia
Measured: within 5 days after ictus, for 10 minutes after steady state
Intracranial pressure (ICP) + hyper- and hypoxia
Measuring during induction of hyper- and hypoxia
Measured: within 5 days after ictus, for 10 minutes after steady state
Partial brain tissue oxygenation (PbtO2) + hyper- and hypoxia
Measuring during induction of hyper- and hypoxia
Measured: within 5 days after ictus, for 10 minutes after steady state
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted14 Jun 2019
- Study start15 Jun 2019
- Primary completion1 Oct 2021
- Study completion1 Mar 2022 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (23)Papers the sponsor has linked to this study.
- Other trials for Subarachnoid Hemorrhage, AneurysmalStudies of the same condition, open and under way.
- More trials run by Copenhagen University Hospital, RigshospitaletThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase N/A
- Primary purpose
- Basic science
- Allocation
- Not applicable
- Intervention model
- Sequential
- Model description
- Intervention is performed once in both patients (after the aneurysm is closed and max. 5 days after ictus) and controls. The procedure consists of the following sessions: 1. Induced hypertension; as well 2. (Only in mechanically ventilated patients) either 1. Mild hyper- and hypocapnia or 2. Mild hyper- and hypoxia. In session 2 (hyper- / hypoxia or hyper- / hypocapnia), patients are randomized to order the interventions.
- Masking
- None (open label)
- Enrolment
- 45 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Copenhagen University Hospital, Rigshospitalet
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Markus Harboe Olsen, Copenhagen University Hospital, Rigshospitalet
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT03987139
- Sponsor's protocol ID
- H-19017185
- Acronym
- CASAH
- Status last verified
- Oct 2021
- First submitted
- 11 Jun 2019
- Last updated
- 29 Oct 2021
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- Yes: Data from each individual participant will be available after publication of planned manuscripts, with a valid reason, and after signing a data processing agreement.
Publications
Kurian MA, Li Y, Zhen J, Meyer E, Hai N, Christen HJ, Hoffmann GF, Jardine P, von Moers A, Mordekar SR, O'Callaghan F, Wassmer E, Wraige E, Dietrich C, Lewis T, Hyland K, Heales S Jr, Sanger T, Gissen P, Assmann BE, Reith ME, Maher ER. Clinical and molecular characterisation of hereditary dopamine transporter deficiency syndrome: an observational cohort and experimental study. Lancet Neurol. 2011 Jan;10(1):54-62. doi: 10.1016/S1474-4422(10)70269-6. Epub 2010 Nov 25.
PubMed 21112253Olsen MH, Orre M, Leisner ACW, Rasmussen R, Bache S, Welling KL, Eskesen V, Moller K. Delayed cerebral ischaemia in patients with aneurysmal subarachnoid haemorrhage: Functional outcome and long-term mortality. Acta Anaesthesiol Scand. 2019 Oct;63(9):1191-1199. doi: 10.1111/aas.13412. Epub 2019 Jun 7.
PubMed 31173342van Gijn J, Kerr RS, Rinkel GJ. Subarachnoid haemorrhage. Lancet. 2007 Jan 27;369(9558):306-18. doi: 10.1016/S0140-6736(07)60153-6.
PubMed 17258671Brathwaite S, Macdonald RL. Current management of delayed cerebral ischemia: update from results of recent clinical trials. Transl Stroke Res. 2014 Apr;5(2):207-26. doi: 10.1007/s12975-013-0316-8. Epub 2013 Dec 13.
PubMed 24338266Schmidt JM, Wartenberg KE, Fernandez A, Claassen J, Rincon F, Ostapkovich ND, Badjatia N, Parra A, Connolly ES, Mayer SA. Frequency and clinical impact of asymptomatic cerebral infarction due to vasospasm after subarachnoid hemorrhage. J Neurosurg. 2008 Dec;109(6):1052-9. doi: 10.3171/JNS.2008.109.12.1052.
PubMed 19035719Dankbaar JW, Slooter AJ, Rinkel GJ, Schaaf IC. Effect of different components of triple-H therapy on cerebral perfusion in patients with aneurysmal subarachnoid haemorrhage: a systematic review. Crit Care. 2010;14(1):R23. doi: 10.1186/cc8886. Epub 2010 Feb 22.
PubMed 20175912Roos YB, de Haan RJ, Beenen LF, Groen RJ, Albrecht KW, Vermeulen M. Complications and outcome in patients with aneurysmal subarachnoid haemorrhage: a prospective hospital based cohort study in the Netherlands. J Neurol Neurosurg Psychiatry. 2000 Mar;68(3):337-41. doi: 10.1136/jnnp.68.3.337.
PubMed 10675216Dorhout Mees SM, Kerr RS, Rinkel GJ, Algra A, Molyneux AJ. Occurrence and impact of delayed cerebral ischemia after coiling and after clipping in the International Subarachnoid Aneurysm Trial (ISAT). J Neurol. 2012 Apr;259(4):679-83. doi: 10.1007/s00415-011-6243-2. Epub 2011 Sep 24.
PubMed 21947244Budohoski KP, Czosnyka M, Kirkpatrick PJ, Smielewski P, Steiner LA, Pickard JD. Clinical relevance of cerebral autoregulation following subarachnoid haemorrhage. Nat Rev Neurol. 2013 Mar;9(3):152-63. doi: 10.1038/nrneurol.2013.11. Epub 2013 Feb 19.
PubMed 23419369Macdonald RL. Delayed neurological deterioration after subarachnoid haemorrhage. Nat Rev Neurol. 2014 Jan;10(1):44-58. doi: 10.1038/nrneurol.2013.246. Epub 2013 Dec 10.
PubMed 24323051LASSEN NA. Cerebral blood flow and oxygen consumption in man. Physiol Rev. 1959 Apr;39(2):183-238. doi: 10.1152/physrev.1959.39.2.183. No abstract available.
PubMed 13645234Berg, R.M.G., Pedersen, M., Møller, K.: Static cerebral blood flow autoregulation in humans. Curr. Hypertens. Rev. 5, 140-157 (2009).
Czosnyka M, Smielewski P, Piechnik S, Steiner LA, Pickard JD. Cerebral autoregulation following head injury. J Neurosurg. 2001 Nov;95(5):756-63. doi: 10.3171/jns.2001.95.5.0756.
PubMed 11702864Eames PJ, Blake MJ, Dawson SL, Panerai RB, Potter JF. Dynamic cerebral autoregulation and beat to beat blood pressure control are impaired in acute ischaemic stroke. J Neurol Neurosurg Psychiatry. 2002 Apr;72(4):467-72. doi: 10.1136/jnnp.72.4.467.
PubMed 11909905Strauss G, Hansen BA, Knudsen GM, Larsen FS. Hyperventilation restores cerebral blood flow autoregulation in patients with acute liver failure. J Hepatol. 1998 Feb;28(2):199-203. doi: 10.1016/0168-8278(88)80006-0.
PubMed 9514532
Study at a glance
From the registry record, last updated by the sponsor on 29 Oct 2021. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Cerebral Autoregulation in Patients With Aneurysmal SubArachnoid Haemorrhage
- ClinicalTrials.gov ID
- NCT03987139
- Acronym / sponsor ID
- CASAH / H-19017185
- Conditions
- Subarachnoid Hemorrhage, Aneurysmal
- Keywords
- cerebral autoregulation
- Study type
- Interventional
- Recruitment status
- Unknown status
- Enrolment
- 45 participants (estimated)
- Lead sponsor
- Copenhagen University Hospital, RigshospitaletUniversity, hospital or other
- Study start
- 15 Jun 2019 (actual)
- Primary completion
- 1 Oct 2021 (actual)
- Study completion
- 1 Mar 2022 (estimated)
- First posted
- 14 Jun 2019 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
The purpose is, in patients with aneurysmal subarachnoid haemorrhage in the early phase after ictus, to examine the following:
- The effect of spontaneous and induced changes on the brain's static and dynamic autoregulation calculated by transcranial Doppler (TCD), ICP and MAP (primary purposes) and ICP and PbtO2;
- The effect of mild hyper- and hypocapnia as well as of mild hyper- and hypoxia on the brain's static and dynamic autoregulation, ICP and PbtO2;
- The relationship between brain autoregulation, mild hyper- and hypocapnia, as well as of mild hyper- and hypoxia and metabolism in microdialysate on the one hand and the occurrence of DCI during hospitalization and poor neurological outcome one year after ictus on the other.
Detailed description
Spontaneous aneurysm subarachnoid hemorrhage (SAH) occurs annually in approximately 400 people in Denmark. SAH is most commonly seen in younger (median age 56 years) and women (71%), have a high mortality (21-44%) and result in a poor neurological outcome in about 50% of patients. Due to the relatively young patient population and high mortality and morbidity, SAH in the population causes the same number of lost working years as blood clots in the brain.
The occurrence of complications like hydrocephalus and re-bleeding can be minimized by rapid external ventricular drainage and aneurysm closure, and so-called delayed cerebral ischaemia (DCI) is currently considered to be the most frequent serious complication of SAH. DCI occurs in 20-30% of patients, most often within the first 14 days, is characterized by a reduction in consciousness or focal neurological deficit lasting at least one hour without any other underlying cause and is associated with a significantly increased risk of a poor outcome. The cause and treatment of DCI is controversial, and the previous hypothesis of vasospasm as the sole contributor is currently supplemented by a broader focus on several other mechanisms, including the brain's blood supply and its regulation.
The brain's blood supply (CBF) is kept relatively constant in healthy by changing cardiac diameter and thus the cerebrovascular resistance (CVR) during changes in brain perfusion pressure (CPP, measured as mean arterial pressure (MAP) minus intracranial pressure (ICP)) within certain limits. This mechanism is known as cerebral autoregulation. Outside these limits, respectively. decreases and increases CBF, with the consequent risk of hypoperfusion/ischemia and hyperperfusion/vasogenic edema with prolonged changes.
Weakened autoregulation, i.e. that CBF varies passively with CPP also within the normal autoregulation limits, is described in e.g. traumatic brain injury (TBI), ischemic stroke, acute liver failure and meningitis, with complete or partial restoration of autoregulation by hyperventilation (mild hypocapnia). SAH also describes impaired autoregulation with varying association with disease severity, DCI and outcome. It is not known whether mild hypocapnia restores autoregulation in patients with SAH, whereas animal experimental studies suggest this.
Reduced intracerebral oxygenation (PbtO2) is associated with a worse outcome after SAH. Cerebral microdialysis measures the concentration of certain metabolites in the brain and can provide an insight into whether metabolic activity is affected by oxygen deficiency, and so-called anaerobic combustion occurs. Microdialysis measurements with elevated lactate concentration, which is a metabolic product, among other things. Anaerobic combustion appears to occur prior to clinical signs of DCI, as well as during the DCI episodes, decreasing PbtO2. It is possible that these findings could be due to a condition of impaired autoregulation and too low perfusion pressure to meet brain metabolic needs, but this has not previously been elucidated. It is also unknown if it is possible to improve brain metabolism by increasing the brain's perfusion pressure.
The purpose of this study is therefore to investigate brain autoregulation in patients with SAH.
Study design
- Primary purpose
- Basic science
- Allocation
- Not applicable
- Intervention model
- Sequential
- Masking
- None (open label)
- Number of arms
- 1
- Model description
- Intervention is performed once in both patients (after the aneurysm is closed and max. 5 days after ictus) and controls. The procedure consists of the following sessions: 1. Induced hypertension; as well 2. (Only in mechanically ventilated patients) either 1. Mild hyper- and hypocapnia or 2. Mild hyper- and hypoxia. In session 2 (hyper- / hypoxia or hyper- / hypocapnia), patients are randomized to order the interventions.
| Arm | Type | Receives |
|---|---|---|
| All patients | Other | Other: Hypertension, Other: Hyper- and hypoxia, Other: Hyper- and hypocapniaPatients included in the study. |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (13 listed)
- Admittance to neurointensive care unit, Rigshospitalet
- Age ≥ 18 years old
- Aneurysmal subarachnoid haemorrhage
- Clinical indication for placement of an external ventricular drain
- Measurements can be done within 3 days of ictus
Key exclusion criteria (7 listed)
- No aneurysm identified
- Conservative og failed treatment of aneurysm
- Pupils dilated and do not react to light
- Incarceration before inclusion
- Expected death within 48 hours
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| HypertensionHypertension is induced by an infusion of noradrenaline within acceptable limits Baseline recording (10 minutes) is performed. MAP gradually increases in steps of 5-10 mmHg during ongoing TCD. When the desired maximum MAP is reached, measurement is made at steady state (10 minutes). Noradrenaline infusion is stopped. When MAP is stabilized, new baseline is measured for 10 minutes. | Other | All patients |
| Hyper- and hypoxiaThe mechanical ventilator is adjusted to mild hypoxia, normoxia and mild hyperoxia. Measurements are made for 10 minutes at normoxia and after steady state is reached, respectively. hyperoxia and hypoxia. Oxygenation is controlled by arterial blood gas before and during steady state. | Other | All patients |
| Hyper- and hypocapniaThe mechanical ventilator is adjusted to a delta PaCO2 on the ventilator for both hypocapnia and hypercapnia. Measurements are made for 10 minutes at normocapnia and after steady state is reached, respectively. hyper- and hypocapnia. | Other | All patients |
Primary outcome
Middle cerebral artery flow velocity (MCAv) + induced hypertension
Time frame: within 5 days after ictus, for 10 minutes after steady state
Measuring MCAv after induced hypertension
6 secondary outcomes
Intracranial pressure (ICP) + induced hypertension
Time frame: within 5 days after ictus
Partial brain tissue oxygenation (PbtO2) + induced hypertension
Time frame: within 5 days after ictus
Intracranial pressure (ICP) + hyper- and hypocapnia
Time frame: within 5 days after ictus, for 10 minutes after steady state
Partial brain tissue oxygenation (PbtO2) + hyper- and hypocapnia
Time frame: within 5 days after ictus, for 10 minutes after steady state
Intracranial pressure (ICP) + hyper- and hypoxia
Time frame: within 5 days after ictus, for 10 minutes after steady state
Partial brain tissue oxygenation (PbtO2) + hyper- and hypoxia
Time frame: within 5 days after ictus, for 10 minutes after steady state
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 29 Oct 2021.
- Background: PubMed 21112253Kurian MA, Li Y, Zhen J, Meyer E, Hai N, Christen HJ, Hoffmann GF, Jardine P, von Moers A, Mordekar SR, O'Callaghan F, Wassmer E, Wraige E, Dietrich C, Lewis T, Hyland K, Heales S Jr, Sanger T, Gissen P, Assmann BE, Reith ME, Maher ER. Clinical and molecular characterisation of hereditary dopamine transporter deficiency syndrome: an observational cohort and experimental study. Lancet Neurol. 2011 Jan;10(1):54-62. doi: 10.1016/S1474-4422(10)70269-6. Epub 2010 Nov 25.
- Background: PubMed 31173342Olsen MH, Orre M, Leisner ACW, Rasmussen R, Bache S, Welling KL, Eskesen V, Moller K. Delayed cerebral ischaemia in patients with aneurysmal subarachnoid haemorrhage: Functional outcome and long-term mortality. Acta Anaesthesiol Scand. 2019 Oct;63(9):1191-1199. doi: 10.1111/aas.13412. Epub 2019 Jun 7.
- Background: PubMed 17258671van Gijn J, Kerr RS, Rinkel GJ. Subarachnoid haemorrhage. Lancet. 2007 Jan 27;369(9558):306-18. doi: 10.1016/S0140-6736(07)60153-6.
- Background: PubMed 24338266Brathwaite S, Macdonald RL. Current management of delayed cerebral ischemia: update from results of recent clinical trials. Transl Stroke Res. 2014 Apr;5(2):207-26. doi: 10.1007/s12975-013-0316-8. Epub 2013 Dec 13.
- Background: PubMed 19035719Schmidt JM, Wartenberg KE, Fernandez A, Claassen J, Rincon F, Ostapkovich ND, Badjatia N, Parra A, Connolly ES, Mayer SA. Frequency and clinical impact of asymptomatic cerebral infarction due to vasospasm after subarachnoid hemorrhage. J Neurosurg. 2008 Dec;109(6):1052-9. doi: 10.3171/JNS.2008.109.12.1052.
- Background: PubMed 20175912Dankbaar JW, Slooter AJ, Rinkel GJ, Schaaf IC. Effect of different components of triple-H therapy on cerebral perfusion in patients with aneurysmal subarachnoid haemorrhage: a systematic review. Crit Care. 2010;14(1):R23. doi: 10.1186/cc8886. Epub 2010 Feb 22.
- Background: PubMed 10675216Roos YB, de Haan RJ, Beenen LF, Groen RJ, Albrecht KW, Vermeulen M. Complications and outcome in patients with aneurysmal subarachnoid haemorrhage: a prospective hospital based cohort study in the Netherlands. J Neurol Neurosurg Psychiatry. 2000 Mar;68(3):337-41. doi: 10.1136/jnnp.68.3.337.
- Background: PubMed 21947244Dorhout Mees SM, Kerr RS, Rinkel GJ, Algra A, Molyneux AJ. Occurrence and impact of delayed cerebral ischemia after coiling and after clipping in the International Subarachnoid Aneurysm Trial (ISAT). J Neurol. 2012 Apr;259(4):679-83. doi: 10.1007/s00415-011-6243-2. Epub 2011 Sep 24.
- Background: PubMed 23419369Budohoski KP, Czosnyka M, Kirkpatrick PJ, Smielewski P, Steiner LA, Pickard JD. Clinical relevance of cerebral autoregulation following subarachnoid haemorrhage. Nat Rev Neurol. 2013 Mar;9(3):152-63. doi: 10.1038/nrneurol.2013.11. Epub 2013 Feb 19.
- Background: PubMed 24323051Macdonald RL. Delayed neurological deterioration after subarachnoid haemorrhage. Nat Rev Neurol. 2014 Jan;10(1):44-58. doi: 10.1038/nrneurol.2013.246. Epub 2013 Dec 10.
- Background: PubMed 13645234LASSEN NA. Cerebral blood flow and oxygen consumption in man. Physiol Rev. 1959 Apr;39(2):183-238. doi: 10.1152/physrev.1959.39.2.183. No abstract available.
- BackgroundBerg, R.M.G., Pedersen, M., Møller, K.: Static cerebral blood flow autoregulation in humans. Curr. Hypertens. Rev. 5, 140-157 (2009).
- Individual participant dataSharing planned: Yes. Data from each individual participant will be available after publication of planned manuscripts, with a valid reason, and after signing a data processing agreement.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
The record lists no contact. Use the official record to reach the sponsor.
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing Hypertension, Hyper- and hypoxia and Hyper- and hypocapnia in people with Subarachnoid Hemorrhage, Aneurysmal, run by Copenhagen University Hospital, Rigshospitalet at 1 site in Denmark.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 13 inclusion and 7 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: status not confirmed, as of the sponsor's last update on 29 Oct 2021. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Denmark. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Middle cerebral artery flow velocity (MCAv) + induced hypertension (time frame: within 5 days after ictus, for 10 minutes after steady state). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT03987139, which also lists 23 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 29 Oct 2021.