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)
Excerpt | Relevance | Reference |
---|---|---|
"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." | 9.09 | Continuous 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." | 7.68 | Protective 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." | 5.09 | Continuous 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." | 3.68 | Protective 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." | 1.62 | Posterior reversible encephalopathy syndrome (PRES) in a patient with moyamoya disease: A case report. ( Chou, PS; Teng, CH; Wu, MN; Yang, IH, 2021) |
Timeframe | Studies, this research(%) | All Research% |
---|---|---|
pre-1990 | 2 (20.00) | 18.7374 |
1990's | 3 (30.00) | 18.2507 |
2000's | 1 (10.00) | 29.6817 |
2010's | 3 (30.00) | 24.3611 |
2020's | 1 (10.00) | 2.80 |
Authors | Studies |
---|---|
Teng, CH | 1 |
Yang, IH | 1 |
Wu, MN | 1 |
Chou, PS | 1 |
Leasure, AC | 1 |
Qureshi, AI | 3 |
Murthy, SB | 1 |
Kamel, H | 1 |
Goldstein, JN | 3 |
Walsh, KB | 1 |
Woo, D | 1 |
Shi, FD | 1 |
Huttner, HB | 1 |
Ziai, WC | 1 |
Hanley, DF | 1 |
Matouk, CC | 1 |
Sansing, LH | 1 |
Falcone, GJ | 1 |
Sheth, KN | 1 |
Palesch, YY | 2 |
Martin, R | 2 |
Novitzke, J | 2 |
Cruz-Flores, S | 2 |
Ehtisham, A | 2 |
Ezzeddine, MA | 2 |
Hussein, HM | 2 |
Suri, MF | 2 |
Tariq, N | 2 |
Kirmani, JF | 1 |
Liu, Y | 1 |
Lin, SZ | 1 |
Chiou, TL | 1 |
Chiang, YH | 1 |
Song, WS | 1 |
Miyazaki, H | 1 |
Tanaka, S | 1 |
Fujii, Y | 1 |
Shimizu, K | 1 |
Nagashima, K | 1 |
Kamibayashi, M | 1 |
Uehara, T | 1 |
Okuma, Y | 1 |
Nomura, Y | 1 |
Nishiyama, T | 1 |
Yokoyama, T | 1 |
Matsukawa, T | 1 |
Hanaoka, K | 1 |
Shirakura, S | 1 |
Sano, J | 1 |
Karasawa, A | 1 |
Kubo, K | 1 |
Abe, K | 1 |
Picard-Claret, M | 1 |
Melon, E | 1 |
Abhay, KP | 1 |
Nguyen, JP | 1 |
Gaston, A | 1 |
Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
---|---|---|---|---|---|---|---|
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 3 | 1,000 participants (Actual) | Interventional | 2011-05-15 | Terminated (stopped due to Planned interim analysis: no significant outcome differences between groups) | ||
Antihypertensive Treatment in Acute Cerebral Hemorrhage (ATACH)[NCT00415610] | Phase 1 | 60 participants (Actual) | Interventional | 2005-07-31 | Completed | ||
[information is prepared from clinicaltrials.gov, extracted Sep-2024] |
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.
Intervention | Participants (Count of Participants) |
---|---|
Standard SBP Reduction Arm | 100 |
Intensive SBP Reduction Arm | 128 |
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
Intervention | Participants (Count of Participants) |
---|---|
Standard SBP Reduction Arm | 104 |
Intensive SBP Reduction Arm | 85 |
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
Intervention | Participants (Count of Participants) |
---|---|
Standard SBP Reduction Arm | 3 |
Intensive SBP Reduction Arm | 6 |
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
Intervention | Participants (Count of Participants) |
---|---|
Standard SBP Reduction Arm | 40 |
Intensive SBP Reduction Arm | 55 |
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)
Intervention | Participants (Count of Participants) |
---|---|
Standard SBP Reduction Arm | 6 |
Intensive SBP Reduction Arm | 8 |
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
Intervention | Participants (Count of Participants) | |
---|---|---|
Death or disability at 90 days (mRS = 4 - 6) | Known death at or before 90 days | |
Intensive SBP Reduction Arm | 186 | 33 |
Standard SBP Reduction Arm | 181 | 34 |
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
Intervention | units on a scale (Median) | |
---|---|---|
EQ-5D utility scale questionnaire | EQ VAS (visual analog scale) | |
Intensive SBP Reduction Arm | 0.7 | 62.5 |
Standard SBP Reduction Arm | 0.7 | 70 |
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
Intervention | participants (Number) |
---|---|
Tier 1 | 1 |
Tier 2 | 2 |
Tier 3 | 4 |
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
Intervention | Participants (Count of Participants) |
---|---|
Tier 1 | 0 |
Tier 2 | 1 |
Tier 3 | 3 |
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.
Intervention | participants (Number) | ||
---|---|---|---|
Meeting Criteria of initial SBP > 170 mmHg | Number treated within 3 hours of symptom onset | Treatment Failure, SBP not in range by 2 hours | |
Tier 1 | 18 | 7 | 0 |
Tier 2 | 20 | 5 | 0 |
Tier 3 | 22 | 6 | 9 |
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
Intervention | participants (Number) | |||||||||
---|---|---|---|---|---|---|---|---|---|---|
N with SAE within 72 hours | N with neurologic deterioration within 24 hours | N with symptomatic hematoma expansion | N with asymptomatic hematoma expansion | N with in-hospital mortality | N with 3-month mortality | N with 1-month favorable outcome, mRS 0-2 | N missing for 1-month outcome assessment | N with 3-month favorable outcome, mRS 0-2 | N missing for 3-month outcome assessment | |
Tier 1 | 0 | 1 | 0 | 6 | 2 | 3 | 4 | 3 | 8 | 3 |
Tier 2 | 1 | 2 | 1 | 2 | 1 | 2 | 6 | 3 | 9 | 4 |
Tier 3 | 3 | 4 | 4 | 3 | 1 | 5 | 4 | 2 | 7 | 2 |
2 trials available for nicardipine and Brain Edema
8 other studies available for nicardipine and Brain Edema
Article | Year |
---|---|
Posterior reversible encephalopathy syndrome (PRES) in a patient with moyamoya disease: A case report.
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.
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.
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.
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.
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.
Topics: Animals; Arachidonic Acid; Benzoquinones; Blood-Brain Barrier; Brain Edema; Brain Ischemia; Calcium | 1992 |
[Effect of nicardipine hydrochloride on ischemic brain edema].
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].
Topics: Adult; Brain Edema; Female; Humans; Intracranial Aneurysm; Ischemic Attack, Transient; Male; Middle | 1989 |