Ignite Creation Date:
2024-05-19 @ 5:34 PM
Last Modification Date:
2024-10-26 @ 3:29 PM
Study NCT ID:
NCT06410274
Status:
RECRUITING
Last Update Posted:
2024-05-16
First Post:
2024-05-07
Brief Title:
Ischaemic Lesions in Acute Intracerebral Haemorrhage
Sponsor:
University of Leicester
Organization:
University of Leicester
Study Overview
Official Title:
Ischaemic Lesions in Acute Intracerebral Haemorrhage Pathophysiological Investigation Using Novel Multimodal Cerebral and Systemic Haemodynamic Assessments
Status:
RECRUITING
Status Verified Date:
2024-04
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
CHALLENGE-ICH
Brief Summary:
The aim of this observational study is to determine how and why inadequate brain blood flow occurs after bleeding in patients with intracerebral haemorrhage ICH Treatment for strokes caused by burst blood vessels involves reducing blood pressure BP to stop the bleeding However this reduction in BP may affect blood flow causing blockages in blood vessels within the brain Fast breathing also affects brain blood flow Therefore participants will be asked to undergo a simple brain blood flow assessment using transcranial Doppler TCD within 48 hours upon admission to hospital Patients will then have a follow-up TCD assessment at 4-7 days post-ICH onset in addition to an MRI scan at 7 days This research will help to confirm if blockages after bleeding are caused by reduced blood flow within the brain
Detailed Description:
Stroke is the second-leading cause of death worldwide with high mortality and morbidity rates One stroke type intracerebral haemorrhage ICH refers to spontaneous non-traumatic bleeding within the brain tissue and is the second most common cause of stroke Although ICH can happen at any age it is more common over the age of 70 The most common cause of ICH is hypertension which can cause bursting of cerebral blood vessels resulting in bleeding within the brain National and international guidelines strongly advocate systolic blood pressure BP lowering in ICH as part of bundled care reducing fluctuations in cerebral blood velocity CBv However despite blood pressure BP lowering being deemed clinically safe no reduction in death or disability at 90 days was demonstrated in two landmark large randomised controlled trials Moreover reductions in BP may affect CBv to the whole of the brain inadvertently causing ischaemic stroke blockage of the blood supply
Previous literature has identified that mild-to-moderate ICH stroke severity benefits from early and stable BP lowering but those with excessively systolic high BP 220 mmHg prior to lowering suffer significantly higher rates of neurological deterioration In order to understand the relationship between BP changes and potential clinical benefit in ICH it needs to be determined if there is a global reduction in brain perfusion which is causing ischaemic lesions in the brain following ICH
Prospective studies have shown impairments in dynamic cerebral autoregulation dCA cerebrovascular tone and cerebrovascular resistance in acute ICH Moreover meta-analyses have demonstrated a previously unreported confounder to cerebral autoregulatory function the presence of an acute reduction in spontaneous CO2 tension after ICH potentially reflecting spontaneous hyperventilation measured as partial pressure in arterial blood pCO2 in patients in intensive care and on the ward There is no current explanation for the presence of spontaneous hyperventilation post-ICH However it has been shown that across a range of end-tidal carbon dioxide EtCO2 values cerebral blood flow CBF dCA and other core haemodynamic parameters arterial BP and heart rate have a dose-response relationship
Fast breathing is also known to affect CBv When EtCO2 is low rapid acute cerebral vasoconstriction can occur - risking acute ischaemic injury Therefore in the presence of spontaneous hyperventilation or induced hyperventilation reductions in brain perfusion through vasoconstriction could risk new or worsened ischaemic insults particularly in the presence of BP lowering Whilst the presence of cerebral small vessel disease plays a role in incidence of diffusion-weighted imaging DWI lesions after ICH there have been no mechanistic association studies to date linking key confounding factors BP lowering EtCO2 change dCA and ischaemic lesions
The investigators aim to perform transcranial Doppler TCD to measure CBv in patients with ICH within 48 hours of admission to hospital These patients would then have a follow-up TCD assessment at 4-7 days post-ICH onset in addition to a magnetic resonance imaging MRI scan 7 days Data would be collected and analysed to determine the relationship between cerebral haemodynamics and ischaemic lesions on MRI post-acute ICH
Previous literature has identified that mild-to-moderate ICH stroke severity benefits from early and stable BP lowering but those with excessively systolic high BP 220 mmHg prior to lowering suffer significantly higher rates of neurological deterioration In order to understand the relationship between BP changes and potential clinical benefit in ICH it needs to be determined if there is a global reduction in brain perfusion which is causing ischaemic lesions in the brain following ICH
Prospective studies have shown impairments in dynamic cerebral autoregulation dCA cerebrovascular tone and cerebrovascular resistance in acute ICH Moreover meta-analyses have demonstrated a previously unreported confounder to cerebral autoregulatory function the presence of an acute reduction in spontaneous CO2 tension after ICH potentially reflecting spontaneous hyperventilation measured as partial pressure in arterial blood pCO2 in patients in intensive care and on the ward There is no current explanation for the presence of spontaneous hyperventilation post-ICH However it has been shown that across a range of end-tidal carbon dioxide EtCO2 values cerebral blood flow CBF dCA and other core haemodynamic parameters arterial BP and heart rate have a dose-response relationship
Fast breathing is also known to affect CBv When EtCO2 is low rapid acute cerebral vasoconstriction can occur - risking acute ischaemic injury Therefore in the presence of spontaneous hyperventilation or induced hyperventilation reductions in brain perfusion through vasoconstriction could risk new or worsened ischaemic insults particularly in the presence of BP lowering Whilst the presence of cerebral small vessel disease plays a role in incidence of diffusion-weighted imaging DWI lesions after ICH there have been no mechanistic association studies to date linking key confounding factors BP lowering EtCO2 change dCA and ischaemic lesions
The investigators aim to perform transcranial Doppler TCD to measure CBv in patients with ICH within 48 hours of admission to hospital These patients would then have a follow-up TCD assessment at 4-7 days post-ICH onset in addition to a magnetic resonance imaging MRI scan 7 days Data would be collected and analysed to determine the relationship between cerebral haemodynamics and ischaemic lesions on MRI post-acute ICH
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None