Page last updated: 2024-11-01

nicardipine and Brain Edema

nicardipine has been researched along with Brain Edema in 10 studies

Nicardipine: A potent calcium channel blockader with marked vasodilator action. It has antihypertensive properties and is effective in the treatment of angina and coronary spasms without showing cardiodepressant effects. It has also been used in the treatment of asthma and enhances the action of specific antineoplastic agents.
nicardipine : A racemate comprising equimolar amounts of (R)- and (S)-nicardipine. It is a calcium channel blocker which is used to treat hypertension.
2-[benzyl(methyl)amino]ethyl methyl 2,6-dimethyl-4-(3-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate : A dihydropyridine that is 1,4-dihydropyridine substituted by a methyl, {2-[benzyl(methyl)amino]ethoxy}carbonyl, 3-nitrophenyl, methoxycarbonyl and methyl groups at positions 2, 3, 4, 5 and 6, respectively.

Brain Edema: Increased intracellular or extracellular fluid in brain tissue. Cytotoxic brain edema (swelling due to increased intracellular fluid) is indicative of a disturbance in cell metabolism, and is commonly associated with hypoxic or ischemic injuries (see HYPOXIA, BRAIN). An increase in extracellular fluid may be caused by increased brain capillary permeability (vasogenic edema), an osmotic gradient, local blockages in interstitial fluid pathways, or by obstruction of CSF flow (e.g., obstructive HYDROCEPHALUS). (From Childs Nerv Syst 1992 Sep; 8(6):301-6)

Research Excerpts

ExcerptRelevanceReference
"To explore the long-term effects of the calcium antagonist, nicardipine, on cerebral hemodynamics in patients with acute cerebral hemorrhage, we investigated the effects of nicardipine infusion on intracranial pressure (ICP), middle cerebral arterial blood flow velocity (Vmca) , and computed tomographical (CT) findings of bleeding and edema."9.09Continuous nicardipine infusion to control blood pressure after evacuation of acute cerebral hemorrhage. ( Hanaoka, K; Matsukawa, T; Nishiyama, T; Yokoyama, T, 2000)
"Acute cerebral ischemia was produced in rats by injection of arachidonic acid (AA) into the internal carotid artery."7.68Protective effects of benidipine on arachidonic acid-induced acute cerebral ischemia in rats. ( Karasawa, A; Kubo, K; Sano, J; Shirakura, S, 1992)
"To explore the long-term effects of the calcium antagonist, nicardipine, on cerebral hemodynamics in patients with acute cerebral hemorrhage, we investigated the effects of nicardipine infusion on intracranial pressure (ICP), middle cerebral arterial blood flow velocity (Vmca) , and computed tomographical (CT) findings of bleeding and edema."5.09Continuous nicardipine infusion to control blood pressure after evacuation of acute cerebral hemorrhage. ( Hanaoka, K; Matsukawa, T; Nishiyama, T; Yokoyama, T, 2000)
"Acute cerebral ischemia was produced in rats by injection of arachidonic acid (AA) into the internal carotid artery."3.68Protective effects of benidipine on arachidonic acid-induced acute cerebral ischemia in rats. ( Karasawa, A; Kubo, K; Sano, J; Shirakura, S, 1992)
"Moyamoya disease (MMD) and posterior reversible encephalopathy syndrome (PRES) share similar pathophysiological characteristics of endothelial dysfunction and impaired cerebral autoregulation."1.62Posterior reversible encephalopathy syndrome (PRES) in a patient with moyamoya disease: A case report. ( Chou, PS; Teng, CH; Wu, MN; Yang, IH, 2021)

Research

Studies (10)

TimeframeStudies, this research(%)All Research%
pre-19902 (20.00)18.7374
1990's3 (30.00)18.2507
2000's1 (10.00)29.6817
2010's3 (30.00)24.3611
2020's1 (10.00)2.80

Authors

AuthorsStudies
Teng, CH1
Yang, IH1
Wu, MN1
Chou, PS1
Leasure, AC1
Qureshi, AI3
Murthy, SB1
Kamel, H1
Goldstein, JN3
Walsh, KB1
Woo, D1
Shi, FD1
Huttner, HB1
Ziai, WC1
Hanley, DF1
Matouk, CC1
Sansing, LH1
Falcone, GJ1
Sheth, KN1
Palesch, YY2
Martin, R2
Novitzke, J2
Cruz-Flores, S2
Ehtisham, A2
Ezzeddine, MA2
Hussein, HM2
Suri, MF2
Tariq, N2
Kirmani, JF1
Liu, Y1
Lin, SZ1
Chiou, TL1
Chiang, YH1
Song, WS1
Miyazaki, H1
Tanaka, S1
Fujii, Y1
Shimizu, K1
Nagashima, K1
Kamibayashi, M1
Uehara, T1
Okuma, Y1
Nomura, Y1
Nishiyama, T1
Yokoyama, T1
Matsukawa, T1
Hanaoka, K1
Shirakura, S1
Sano, J1
Karasawa, A1
Kubo, K1
Abe, K1
Picard-Claret, M1
Melon, E1
Abhay, KP1
Nguyen, JP1
Gaston, A1

Clinical Trials (2)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Antihypertensive Treatment of Acute Cerebral Hemorrhage (ATACH)-II: A Phase III Randomized Multicenter Clinical Trial of Blood Pressure Reduction for Hypertension in Acute Intracerebral Hemorrhage[NCT01176565]Phase 31,000 participants (Actual)Interventional2011-05-15Terminated (stopped due to Planned interim analysis: no significant outcome differences between groups)
Antihypertensive Treatment in Acute Cerebral Hemorrhage (ATACH)[NCT00415610]Phase 160 participants (Actual)Interventional2005-07-31Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Any Serious Adverse Event Within the 90-day Study Period

The complete count of all subjects who experienced any serious adverse events throughout their participation in the trial was included in this tabulation. Adverse events (AEs) and serious adverse events (SAEs) were assessed by the site investigators for all patients. Potential relatedness to the study treatment was a required reporting element for all adverse events but was not considered in this count. Terminology from the Medical Dictionary for Regulatory Activities (MedDRA) and severity criteria from the Common Terminology Criteria for Adverse Events (CTCAE v. 4.03) were used as a basis for reporting adverse events. Serious adverse events are defined as being fatal, life-threatening, resulting in hospitalization or prolonged hospitalization, resulting in disability or congenital anomaly, or requiring intervention to prevent permanent impairment or damage and were required to be reported promptly. An Independent Oversight Committee (IOC) reviewed and adjudicated adverse event data. (NCT01176565)
Timeframe: From randomization through the 90 day visit (90 ± 14 days per protocol window; up to ± 30 days data is used) or until known death, withdrawal, or loss to follow-up.

InterventionParticipants (Count of Participants)
Standard SBP Reduction Arm100
Intensive SBP Reduction Arm128

Hematoma Expansion (Number of Patients With Hematoma Expansion of 33% or Greater Between the Baseline and 24 +/- 6 Hours Head CTs, as Measured by the Central Reader for Patients With Readable Scans for Both Time Points Submitted by Data Lock.)

Hematoma expansion as determined by serial CT scans: Hematoma expansion was defined as an increase in the volume of intraparenchymal hemorrhage of 33% or greater as measured by a central imaging analyst who was was unaware of the treatment assignments, clinical findings, and time points of image acquisition. The area of the hematoma was delineated by image analysis software with the use of density thresholds on each slice, followed by manual correction. To ensure accuracy and consistency of the readings, images were coded randomly and independently of subject numbers and manual correction was also done without awareness of treatment assignments, clinical findings, or time points of image acquisition. This data point is defined as being present (hematoma expansion of 33% or more was calculated between the baseline scan hematoma volume and the 24 +/- 6 hours hematoma volume measures at data analysis), meaning that hematoma expansion as defined must have occurred or it was not counted. (NCT01176565)
Timeframe: From the baseline head CT to the 24 +/- 6 hours from randomization head CT

InterventionParticipants (Count of Participants)
Standard SBP Reduction Arm104
Intensive SBP Reduction Arm85

Hypotension Within 72 Hours

Hypotension (abnormally low blood pressure) was the most likely adverse event that could be associated with the study treatment, and is the primary basis (risk) on which neurological deterioration or other untoward effects of the study treatment could occur. It is therefore examined as a numerically-measured occurrence in addition to monitoring patients closely for neurological deterioration or other symptoms. Hypotension, when named as an adverse event, was defined as the syndrome of low blood pressure with SBP < 85 mmHg. Instances of hypotension were to be avoided through close monitoring, and administration of fluid bolus for SBP < 110 mmHg. If hypotension did occur, it was to be reversed as quickly as possible through discontinuation of intravenous nicardipine and intravenous fluid administration, which can be accomplished readily in a variety of settings where patients with intracerebral hemorrhage are routinely housed during early hospitalization. (NCT01176565)
Timeframe: From randomization through 72 hours from randomization

InterventionParticipants (Count of Participants)
Standard SBP Reduction Arm3
Intensive SBP Reduction Arm6

Neurological Deterioration Within 24 Hours, Defined by a Decrease of 2 or More Points on the GCS Score or an Increase of 4 or More Points on the NIHSS Score From Baseline, Not Related to Sedation or Hypnotic-agent Use and Sustained for at Least 8 Hours.

Neurologic deterioration was measured using two scales. The Glasgow Coma Scale (GCS) score measures of level of consciousness in eye, motor, and verbal components. At least one point is given in each category. The scale ranges from 3 to 15, with 3 indicating deep unconsciousness and 15 indicating consciousness is not impaired. The National Institutes of Health Stroke Scale (NIHSS) quantifies neurologic deficits in 11 categories. Level of consciousness, horizontal eye movement, visual fields, facial palsy, movement in each limb, sensation, language & speech, and extinction or inattention on one side of the body are tested. Scores range from 0 to 42, with 0 indicating normal function and higher scores indicating greater deficit severity. Neurological status was checked per ICU standards through 24 hours, recommended as hourly GCS and full assessment every 2 hours. NIHSS assessment at baseline and 24 +/- 3 hours was pre-specified. Assessments were added for suspected neurological change. (NCT01176565)
Timeframe: From randomization through the 24-hour treatment period

InterventionParticipants (Count of Participants)
Standard SBP Reduction Arm40
Intensive SBP Reduction Arm55

Treatment-related Serious Adverse Event Within 72 Hours of Randomization

Adverse events (AEs) and serious adverse events (SAEs) were assessed by the site investigators for all patients, including for their potential relatedness to the study treatment. An Independent Oversight Committee (IOC) reviewed and adjudicated all adverse event data. The 72-hours-from-randomization time window was considered the most likely time frame during which treatment-related adverse events or serious adverse events would be observed. Terminology from the Medical Dictionary for Regulatory Activities (MedDRA) and severity criteria from the Common Terminology Criteria for Adverse Events (CTCAE v. 4.03) were used as a basis for reporting adverse events. Serious adverse events are defined as being fatal, life-threatening, resulting in hospitalization or prolonged hospitalization, resulting in disability or congenital anomaly, or requiring intervention to prevent permanent impairment or damage and were required to be reported promptly. (NCT01176565)
Timeframe: From randomization through 72 hours (3 days)

InterventionParticipants (Count of Participants)
Standard SBP Reduction Arm6
Intensive SBP Reduction Arm8

Death or Disability According to Modified Rankin Scale Score at 90 Days (3 Months) From Randomization

The primary outcome was death or disability, defined by modified Rankin scale (mRS) of 4-6 at 90 days following treatment. The modified Rankin Scale score ranges from 0, indicating no symptoms, to 6, indicating death. A score of 4 indicates moderately severe disability including the inability to walk or attend to one's own bodily needs. A score of 5 indicates severe disability; bedridden, incontinent, and requiring constant nursing care. To score a 3 or lower on the mRS, a person must at least be able to walk without the assistance of another person. We chose the mRS because of its high inter-observer reliability, superiority to other indices, and consistency with previous trials in patients with ICH. Reliability was further increased by use of a structured interview template and by requiring mRS assessors to pass a certification test. Persons conducting the 90-day mRS assessment were to be unaware of the treatment arm or clinical course of the patients they assessed. (NCT01176565)
Timeframe: 90 days (± 14 days per protocol window; up to ± 30 days data is used) from randomization

,
InterventionParticipants (Count of Participants)
Death or disability at 90 days (mRS = 4 - 6)Known death at or before 90 days
Intensive SBP Reduction Arm18633
Standard SBP Reduction Arm18134

Quality of Life at 90 Days Using EuroQol (EQ) Measures: EQ-5D (EuroQol Five Dimension), Consisting of Standardized EQ-5D-3L (EuroQol Five Dimension, Three-Level) Questionnaire and EQ VAS (EuroQol Visual Analog Scale) Scores

Standardized scales developed by the EuroQol Research Foundation were used as a secondary outcome measure in addition to the mRS scale score. The EQ-5D is a simple, standardized non-disease-specific instrument for describing and valuating health-related quality of life. The EQ-5D-3L questionnaire consists of 5 questions in 5 different domains and allows for responses from 1 (the best outcome) to 3 (the worst outcome) in each of five categories (mobility, self-care, usual activities, pain/discomfort, and anxiety/depression). Total scores range from 5 to 15, with lower scores indicating better quality of life and a higher score indicating a worse quality of life. A second component of EuroQol outcome measurements is a printed 20 cm visual analogue scale (EQ VAS) that appears somewhat like a thermometer, on which a score from 0 (worst imaginable health state or death) to 100 (best imaginable health state) is marked by the patient (or, when necessary, their proxy) with the scale in view. (NCT01176565)
Timeframe: 90 days (± 14 days per protocol window; up to ± 30 days data is used) from randomization

,
Interventionunits on a scale (Median)
EQ-5D utility scale questionnaireEQ VAS (visual analog scale)
Intensive SBP Reduction Arm0.762.5
Standard SBP Reduction Arm0.770

"Number of Participants With Neurological Deteriorations (Decrease of 2 or More Points on the GCS Score or an Increase of 4 or More Points on the NIHSS Score) During the 24 Hour Treatment,"

Neurological status was monitored quantitatively and independently of other adverse events using two scales. The Glasgow Coma Scale (GCS) score measures level of consciousness in eye, motor, and verbal components. At least one point is given in each category. The scale ranges from 3 to 15, with 3 indicating deep unconsciousness and 15 indicating consciousness is not impaired. The National Institutes of Health Stroke Scale (NIHSS) quantifies neurologic deficits in 11 categories. Level of consciousness, horizontal eye movements, visual fields, facial palsy, movement in each limb, sensation, language and speech, and extinction or inattention on one side of the body are tested. Scores range from 0 to 42; 0 indicates normal function and higher scores indicate greater deficit severity. (NCT00415610)
Timeframe: within the first 72 hours of treatment initiation

Interventionparticipants (Number)
Tier 11
Tier 22
Tier 34

Total Number of Serious Adverse Events Within the Initial 72 Hours From Treatment Per Subject

Serious adverse events were ascertained by site investigators using FDA-defined guidelines, defined as any untoward clinical events having been fatal, life-threatening, resulting in new or prolonged hospitalization, resulting in disability or congenital anomaly, or requiring intervention to prevent permanent impairment or damage. Subjects were followed closely from randomization through 90 days. The initial 72-hour period was chosen as the most meaningful time period for which to examine SAEs likely to be related to the acute safety of the study treatment. (NCT00415610)
Timeframe: from treatment initiation through 72 hours

InterventionParticipants (Count of Participants)
Tier 10
Tier 21
Tier 33

Particpants Who Achieve and Maintain the Systolic Blood Pressure Goals for Each Treatment Tier.

Feasibility of treatment was assessed by whether SBP reduction and maintenance within the respective target range was achieved (treatment success) or not (treatment failure), and secondarily by whether a significant difference between treatment arms was achieved. Treatment failure was defined based on the observed hourly hourly minimum SBP remaining greater than the upper limit of the target range for 2 consecutive hours after initiation of nicardipine infusion. Spontaneous decline of SBP below the lower limit of the specific tier was not considered treatment failure as all such declines were asymptomatic.The lower number in the more intensive treatment groups reflects in part the greater challenge of rapidly lowering systolic blood pressure to a more intensive (lower) range, as a higher number of treatment failures as pre-defined by meeting the SBP range goal within 3 hours of symptom onset in this group predictably occurred. (NCT00415610)
Timeframe: Within 3 hours of symptom onset and sustained through 18-24 hours.

,,
Interventionparticipants (Number)
Meeting Criteria of initial SBP > 170 mmHgNumber treated within 3 hours of symptom onsetTreatment Failure, SBP not in range by 2 hours
Tier 11870
Tier 22050
Tier 32269

Particpants Who Tolerate Rapid Systolic Blood Pressure Reduction and Maintain Treatment Goals

The ability to maintain the Specified Systolic Blood Pressure Range for the 18-24 Hour Period without Neurological Deterioration or Side Effects (NCT00415610)
Timeframe: 3 months

,,
Interventionparticipants (Number)
N with SAE within 72 hoursN with neurologic deterioration within 24 hoursN with symptomatic hematoma expansionN with asymptomatic hematoma expansionN with in-hospital mortalityN with 3-month mortalityN with 1-month favorable outcome, mRS 0-2N missing for 1-month outcome assessmentN with 3-month favorable outcome, mRS 0-2N missing for 3-month outcome assessment
Tier 10106234383
Tier 21212126394
Tier 33443154272

Trials

2 trials available for nicardipine and Brain Edema

ArticleYear
Effect of systolic blood pressure reduction on hematoma expansion, perihematomal edema, and 3-month outcome among patients with intracerebral hemorrhage: results from the antihypertensive treatment of acute cerebral hemorrhage study.
    Archives of neurology, 2010, Volume: 67, Issue:5

    Topics: Adult; Aged; Antihypertensive Agents; Blood Pressure; Brain; Brain Edema; Cerebral Arteries; Dose-Re

2010
Effect of systolic blood pressure reduction on hematoma expansion, perihematomal edema, and 3-month outcome among patients with intracerebral hemorrhage: results from the antihypertensive treatment of acute cerebral hemorrhage study.
    Archives of neurology, 2010, Volume: 67, Issue:5

    Topics: Adult; Aged; Antihypertensive Agents; Blood Pressure; Brain; Brain Edema; Cerebral Arteries; Dose-Re

2010
Effect of systolic blood pressure reduction on hematoma expansion, perihematomal edema, and 3-month outcome among patients with intracerebral hemorrhage: results from the antihypertensive treatment of acute cerebral hemorrhage study.
    Archives of neurology, 2010, Volume: 67, Issue:5

    Topics: Adult; Aged; Antihypertensive Agents; Blood Pressure; Brain; Brain Edema; Cerebral Arteries; Dose-Re

2010
Effect of systolic blood pressure reduction on hematoma expansion, perihematomal edema, and 3-month outcome among patients with intracerebral hemorrhage: results from the antihypertensive treatment of acute cerebral hemorrhage study.
    Archives of neurology, 2010, Volume: 67, Issue:5

    Topics: Adult; Aged; Antihypertensive Agents; Blood Pressure; Brain; Brain Edema; Cerebral Arteries; Dose-Re

2010
Continuous nicardipine infusion to control blood pressure after evacuation of acute cerebral hemorrhage.
    Canadian journal of anaesthesia = Journal canadien d'anesthesie, 2000, Volume: 47, Issue:12

    Topics: Aged; Blood Pressure; Brain Edema; Calcium Channel Blockers; Cerebral Hemorrhage; Cerebrovascular Ci

2000

Other Studies

8 other studies available for nicardipine and Brain Edema

ArticleYear
Posterior reversible encephalopathy syndrome (PRES) in a patient with moyamoya disease: A case report.
    Medicine, 2021, Aug-06, Volume: 100, Issue:31

    Topics: Adult; Antihypertensive Agents; Brain; Brain Edema; Diagnosis, Differential; Humans; Hypertension; M

2021
Intensive Blood Pressure Reduction and Perihematomal Edema Expansion in Deep Intracerebral Hemorrhage.
    Stroke, 2019, Volume: 50, Issue:8

    Topics: Aged; Antihypertensive Agents; Brain Edema; Female; Humans; Intracranial Hemorrhage, Hypertensive; M

2019
Association of serum glucose concentrations during acute hospitalization with hematoma expansion, perihematomal edema, and three month outcome among patients with intracerebral hemorrhage.
    Neurocritical care, 2011, Volume: 15, Issue:3

    Topics: Aged; Aged, 80 and over; Antihypertensive Agents; Blood Glucose; Brain Edema; Cerebral Hemorrhage; D

2011
Combined treatment with nicardipine, phenobarbital, and methylprednisolone ameliorates vasogenic brain edema.
    Acta neurochirurgica. Supplementum, 1994, Volume: 60

    Topics: Animals; Blood Proteins; Blood-Brain Barrier; Brain Edema; Brain Injuries; Drug Therapy, Combination

1994
Neuroprotective effects of a dihydropyridine derivative, 1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarbox ylic acid methyl 6-(5-phenyl-3-pyrazolyloxy)hexyl ester (CV-159), on rat ischemic brain injury.
    Life sciences, 1999, Volume: 64, Issue:10

    Topics: Animals; Body Temperature; Brain Edema; Calcium Channel Blockers; Calcium-Calmodulin-Dependent Prote

1999
Protective effects of benidipine on arachidonic acid-induced acute cerebral ischemia in rats.
    Japanese journal of pharmacology, 1992, Volume: 59, Issue:1

    Topics: Animals; Arachidonic Acid; Benzoquinones; Blood-Brain Barrier; Brain Edema; Brain Ischemia; Calcium

1992
[Effect of nicardipine hydrochloride on ischemic brain edema].
    Neurologia medico-chirurgica, 1987, Volume: 27, Issue:9

    Topics: Animals; Brain Edema; Brain Ischemia; Male; Nicardipine; Rats

1987
[Role of stopping calcium inhibitors in the worsening of postoperative vasospasm during the treatment of intracranial aneurysm].
    Agressologie: revue internationale de physio-biologie et de pharmacologie appliquees aux effets de l'agression, 1989, Volume: 30, Issue:7

    Topics: Adult; Brain Edema; Female; Humans; Intracranial Aneurysm; Ischemic Attack, Transient; Male; Middle

1989