- ICH GCP
- US Clinical Trials Registry
- Clinical Trial NCT03000283
Conivaptan for the Reduction of Cerebral Edema in Intracerebral Hemorrhage- A Safety and Tolerability Study
The goal of this study is to preliminarily determine/estimate feasibility and whether frequent and early conivaptan use, at a dose currently determined to be safe (i.e., 40mg/day), is safe and well-tolerated in patients with cerebral edema from intracerebral hemorrhage (ICH) and pressure (ICP). A further goal is to preliminarily estimate whether conivaptan at this same dose can reduce cerebral edema (CE) in these same patients. This study is also an essential first step in understanding the role of conivaptan in CE management.
Hypothesis: The frequent and early use of conivaptan at 40mg/day will be safe and well-tolerated, and also reduce cerebral edema, in patients with intracerebral hemorrhage and pressure.
Study Overview
Status
Intervention / Treatment
Detailed Description
This is a single-center, open-label, safety and tolerability study. Based on findings in the literature from both animal research and clinical observations with ICH (intracerebral hemorrhage) associated with TBI (traumatic brain injury), this study will begin to look at the safety, tolerability, as well as potential effectiveness, of conivaptan to reduce CE (cerebral edema) in patients with non-traumatic ICH.
The seven patients in this study will receive 40mg/day of the study medication conivaptan. In this early phase study, our focus will be to assess the safety and tolerability of this medication. The available clinical data on conivaptan in the neurocritical care population suggest the potential harm is negligible. Data in TBI patients demonstrate conivaptan is safe and well tolerated using a single dose (20mg) to increase Na+ in a controlled fashion to reduce ICP. Previous work has demonstrated the safety and tolerability of conivaptan, in doses ranging from 20-80mg/day, in the neurocritical care population. Conivaptan has been demonstrated to be safe and effective in lowering ICP, and increasing serum sodium, in the neurocritical care population. Also noted have been improvements in cerebral perfusion pressure (CPP) and stable blood pressure, and a prolonged reduction in ICP. Finally, the method of intermittent bolus dosing of conivaptan is equally effective in raising and maintaining serum sodium in the neurocritical care population as continuous infusion, with potentially less risk of adverse reactions including phlebitis.
Conivaptan, a non-selective Arginine-Vasopressin (AVP) V1A/V2 antagonist that reduces aquaporin 4 production and promotes aquaresis, is approved for the treatment of euvolemic and hypervolemic hyponatremia. The exact cause of the observed reduction in ICP with conivaptan is uncertain. However, the mechanism most likely represents a combination of an acute pure aquaresis, removing free water from brain tissue, and a sustained down regulation of aquaporin 4 to abate/slow development of CE. The V2 antagonism of conivaptan promotes free water loss, and the V1 antagonism may improve cerebral blood flow (CBF) and reduce blood brain barrier permeability. Notably, serum sodium tends to correlate inversely with both ICP and CE. The early use of conivaptan could potentially be used clinically to reduce CE by these means.
It is with this in mind, the research team feels justified in pursuing this study with the hopes that the data obtained will lead to potential good and removal of harm in future patients with this devastating disease. Given the enormous costs of ICH, problems with current therapies, and variability in treatment, there is an urgent need to identify a therapy that has a better safety and effectiveness profile compared to the currently used agents. This study will use a dose (40mg/day) currently approved. Further, given that the primary purpose of the use of this medication in this study is not to correct hyponatremia, an investigational new drug (IND) application to the FDA was submitted, and the study was determined exempt.
Our central hypothesis is that through reductions in aquaporin-4 (AQP4) expression, the early use of conivaptan will reduce CE while also being safe to the patient. Our long term goal is to show that early use of conivaptan in ICH will reduce CE. If this reduction is possible, we hypothesize improved outcome and reducing the need for rescue therapies, ICU length of stay, and overall treatment cost will follow. However, more data is needed to evaluate the dosing and amount of drug. With respect to conivaptan's efficacy in correction of hyponatremia, a direct dose-response relationship exists. Further, this effect was more noted at milder degrees of hyponatremia.
Study Type
Enrollment (Actual)
Phase
- Phase 1
Contacts and Locations
Study Locations
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-
Minnesota
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Saint Paul, Minnesota, United States, 55102
- United Hospital
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Participation Criteria
Eligibility Criteria
Ages Eligible for Study
Accepts Healthy Volunteers
Genders Eligible for Study
Description
Inclusion Criteria:
- Age >18 years old and < 80 years.
- Diagnosis of primary ICH > 20 cc in volume.
- Enrollment within 48 hours from initial symptoms.
- Signed informed consent from the patient or obtained via their legally authorized representative (if the patient is not able to sign the informed consent themselves). The patient's decisional capacity to either provide or refuse consent will be determined using the Glasgow Coma Scale (GCS), which is being assessed at baseline and at 24 hours (+/-6hrs) after enrollment. A potential study participant with a GCS > 14 will be asked to provide their own initial study consent. A GCS ≤ 14 would indicate the need to pursue consent via legally authorized representative.
Exclusion Criteria:
- Current need for renal replacement therapy (RRT).
- Glomerular filtration rate (GFR) of <30 mL/minute at time of admission.
- Participation in another study for ICH or intraventricular hemorrhage.
- ICH related to infection, thrombolysis, subarachnoid hemorrhage, trauma or tumor.
- Presence of HIV or active fungal infection that is known based on information in the electronic medical record (EMR).
- Continued use of digoxin or amlodipine (as recommended by the manufacturer due to cytochrome P450 3A4 "CYP3A" inhibition).
- Active hepatic failure as defined by aspartate aminotransferase (AST) >160 units/L and/or alanine transaminase (ALT) >180 units/L, or total bilirubin levels greater than four times normal levels (>4.8mg/dL).
- Serum Na+> 145 mmol/L (admission labs or any time prior to recruitment/enrollment).
- Unable to receive conivaptan based on contraindications indicated by the manufacturer.
- Pregnant or lactating females.
- Not expected to survive within 48 hours of admission, or a presumed diagnosis of brain death.
Study Plan
How is the study designed?
Design Details
- Primary Purpose: Treatment
- Allocation: N/A
- Interventional Model: Single Group Assignment
- Masking: None (Open Label)
Arms and Interventions
Participant Group / Arm |
Intervention / Treatment |
---|---|
Experimental: Conivaptan Treatment Group
All seven patients in this arm will receive conivaptan as described in Interventions.
|
Patients will receive 20mg IV of the study drug every 12 hours equaling 40mg/day over 2 days (4 doses total), in addition to the standardized ICH management targets using the PI's version of standardized ICH management targets.Usual standard of care can include sedation and analgesia as needed, elevation of the head of the bed, mannitol and/or saline as needed to reduce ICP, and temperature control with antipyretics such as acetaminophen. The conivaptan bolus (20mg), which is premixed with 100ml of 5% dextrose in water, is infused (peripherally) over 30 minutes, most commonly through an already placed central line.
Other Names:
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What is the study measuring?
Primary Outcome Measures
Outcome Measure |
Measure Description |
Time Frame |
---|---|---|
Patient Tolerance of Conivaptan
Time Frame: Baseline to 168 hours post-enrollment
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The number of participants with abnormal seizure activity and/or abnormal lab values and/or increase in infection rate and/or any drug-related adverse events.
|
Baseline to 168 hours post-enrollment
|
Secondary Outcome Measures
Outcome Measure |
Measure Description |
Time Frame |
---|---|---|
In-hospital Mortality
Time Frame: Enrollment through hospital discharge, up to 3 weeks
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All-cause deaths during hospitalization
|
Enrollment through hospital discharge, up to 3 weeks
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Change in Cerebral Edema
Time Frame: Baseline to 168 hours post-enrollment
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Changes in cerebral edema (CE) as measured on CT.
Goal is a -5 to -10% change in CE over time.
Change will be measured both as absolute change in volume, calculated as the final volume minus the baseline volume measure and converted to a percentage of the baseline volume measure.
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Baseline to 168 hours post-enrollment
|
Cost
Time Frame: Enrollment through hospital discharge, up to 3 weeks
|
Cost as measured by length of stay in the neuro ICU.
|
Enrollment through hospital discharge, up to 3 weeks
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Cost
Time Frame: Baseline to 168 hours post-enrollment
|
Cost as measured by:
|
Baseline to 168 hours post-enrollment
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Modified Rankin Scale (mRS) Score
Time Frame: At discharge from ICU and from hospital, up to 3 weeks
|
Modified Rankin Scale (0 to 6) at discharge from the hospital.
A score of 0 indicates no disability and a score of 6 indicates the patient died.
Functional independence is defined as a score of 2 or less.
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At discharge from ICU and from hospital, up to 3 weeks
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Collaborators and Investigators
Sponsor
Investigators
- Principal Investigator: Jesse J Corry, MD, Allina Health
Publications and helpful links
General Publications
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- Marik PE, Rivera R. Therapeutic effect of conivaptan bolus dosing in hyponatremic neurosurgical patients. Pharmacotherapy. 2013 Jan;33(1):51-5. doi: 10.1002/phar.1169.
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- Murphy T, Dhar R, Diringer M. Conivaptan bolus dosing for the correction of hyponatremia in the neurointensive care unit. Neurocrit Care. 2009;11(1):14-9. doi: 10.1007/s12028-008-9179-3. Epub 2009 Jan 4.
- Naidech AM, Paparello J, Liebling SM, Bassin SL, Levasseur K, Alberts MJ, Bernstein RA, Muro K. Use of Conivaptan (Vaprisol) for hyponatremic neuro-ICU patients. Neurocrit Care. 2010 Aug;13(1):57-61. doi: 10.1007/s12028-010-9379-5. Erratum In: Neurocrit Care. 2011 Aug;15(1):210. Leibling, Storm M [corrected to Liebling, Storm M].
- Nathan BR. Cerebral correlates of hyponatremia. Neurocrit Care. 2007;6(1):72-8. doi: 10.1385/NCC:6:1:72.
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- Rosenberg GA, Scremin O, Estrada E, Kyner WT. Arginine vasopressin V1-antagonist and atrial natriuretic peptide reduce hemorrhagic brain edema in rats. Stroke. 1992 Dec;23(12):1767-73; discussion 1773-4. doi: 10.1161/01.str.23.12.1767. Erratum In: Stroke 1993 Jun;24(6):913.
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Study record dates
Study Major Dates
Study Start (Actual)
Primary Completion (Actual)
Study Completion (Actual)
Study Registration Dates
First Submitted
First Submitted That Met QC Criteria
First Posted (Estimate)
Study Record Updates
Last Update Posted (Actual)
Last Update Submitted That Met QC Criteria
Last Verified
More Information
Terms related to this study
Keywords
Additional Relevant MeSH Terms
- Pathologic Processes
- Cardiovascular Diseases
- Vascular Diseases
- Cerebrovascular Disorders
- Brain Diseases
- Central Nervous System Diseases
- Nervous System Diseases
- Intracranial Hemorrhages
- Hemorrhage
- Edema
- Cerebral Hemorrhage
- Brain Edema
- Physiological Effects of Drugs
- Molecular Mechanisms of Pharmacological Action
- Natriuretic Agents
- Antidiuretic Hormone Receptor Antagonists
- Conivaptan
Other Study ID Numbers
- NSJC-1601
Plan for Individual participant data (IPD)
Plan to Share Individual Participant Data (IPD)?
Drug and device information, study documents
Studies a U.S. FDA-regulated drug product
Studies a U.S. FDA-regulated device product
product manufactured in and exported from the U.S.
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