Nicardipine Prolonged-Release Implants for Preventing Cerebral Vasospasm After Subarachnoid Hemorrhage: Effect and Outcome in the First 100 Patients

Krischek, Boris; Kasuya, Hidetoshi; Onda, Hideaki; Hori, Tomokatsu

doi:10.2176/nmc.47.389

Cited by 31 publications

(11 citation statements)

References 26 publications

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“…110 Approximately 236 addi tional patients have been treated in openlabel studies in Japan. 111 Targeting microthromboembolism Metaanalysis of seven randomized clinical trials of antiplatelet drugs in a total of 1,385 patients found trends towards reduction in poor outcome (RR 0.79, 95% CI 0.62-1.01) but also towards increased intra cranial haemor rhage (RR 1.36, 95% CI 0.59-3.12). 112 Further trials are needed to determine whether these drugs are efficacious in this indication.…”

Section: Clinical Trialsmentioning

confidence: 99%

Delayed neurological deterioration after subarachnoid haemorrhage

2013

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Subarachnoid haemorrhage (SAH) causes early brain injury (EBI) that is mediated by effects of transient cerebral ischaemia during bleeding plus effects of the subarachnoid blood. Secondary effects of SAH include increased intracranial pressure, destruction of brain tissue by intracerebral haemorrhage, brain shift, and herniation, all of which contribute to pathology. Many patients survive these phenomena, but deteriorate days later from delayed cerebral ischaemia (DCI), which causes poor outcome or death in up to 30% of patients with SAH. DCI is thought to be caused by the combined effects of angiographic vasospasm, arteriolar constriction and thrombosis, cortical spreading ischaemia, and processes triggered by EBI. Treatment for DCI includes prophylactic administration of nimodipine, and current neurointensive care. Prompt recognition of DCI and immediate treatment by means of induced hypertension and balloon or pharmacological angioplasty are considered important by many physicians, although the evidence to support such approaches is limited. This Review summarizes the pathophysiology of DCI after SAH and discusses established treatments for this condition. Novel strategies--including drugs such as statins, sodium nitrite, albumin, dantrolene, cilostazol, and intracranial delivery of nimodipine or magnesium--are also discussed.

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Section: Clinical Trialsmentioning

confidence: 99%

Delayed neurological deterioration after subarachnoid haemorrhage

2013

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“…Of these, nicardipine is a second-generation dihydropyridine-type calcium channel blocker that has vasodilator properties with a unique cerebrovascular profile. It is administered routinely via continuous intravenous [13] or IA infusion [14,15], or as prolonged-release implants [16,17,18]. However, as conceded in the current guidelines, the primary limitation of IA vasodilator therapy is its short duration of benefit [19].…”

Section: Introductionmentioning

confidence: 99%

Temporal evolution of vasospasm and clinical outcome after intra-arterial vasodilator therapy in patients with aneurysmal subarachnoid hemorrhage

et al. 2017

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Intra-arterial (IA) vasodilator therapy is one of the recommended treatments to minimize the impact of aneurysmal subarachnoid hemorrhage-induced cerebral vasospasm refractory to standard management. However, its usefulness and efficacy is not well established. We evaluated the effect IA vasodilator therapy on middle cerebral artery blood flow and on discharge outcome. We reviewed records for 115 adults admitted to Neurointensive Care Unit to test whether there was a difference in clinical outcome (discharge mRS) in those who received IA infusions. In a subset of 19 patients (33 vessels) treated using IA therapy, we tested whether therapy was effective in reversing the trends in blood flow. All measures of MCA blood flow increased from day -2 to -1 before infusion (maximum Peak Systolic Velocity (PSV) 232.2±9.4 to 262.4±12.5 cm/s [p = 0.02]; average PSV 202.1±8.5 to 229.9±10.9 [p = 0.02]; highest Mean Flow Velocity (MFV) 154.3±8.3 to 172.9±10.5 [p = 0.10]; average MFV 125.5±6.3 to 147.8±9.5 cm/s, [p = 0.02]) but not post-infusion (maximum PSV 261.2±14.6 cm/s [p = .89]; average PSV 223.4±11.4 [p = 0.56]; highest MFV 182.9±12.4 cm/s [p = 0.38]; average MFV 153.0±10.2 cm/s [p = 0.54]). After IA therapy, flow velocities were consistently reduced (day X infusion interaction p<0.01 for all measures). However, discharge mRS was higher in IA infusion group, even after adjusting for sex, age, and admission grades. Thus, while IA vasodilator therapy was effective in reversing the vasospasm-mediated deterioration in blood flow, clinical outcomes in the treated group were worse than the untreated group. There is need for a prospective randomized controlled trial to avoid potential confounding effect of selection bias.

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“…Although this was neither a controlled, nor a blinded, investigation its findings were complemented by a summary of the first 100 patients treated with NPRIs, 8 where NPRI placement completely prevented vasospasm in vessels adjacent to the pellet, but not in more remote regions. Findings of a multicentre cooperative study on NPRIs in Tokyo was then able to confirm these findings yet again in 136 patients, where the rates of angiographic vasospasm (24.6 %), cerebral infarction (12.4 %) and DIND (8.2 %) were found to be decreased significantly.…”

Section: Summary Of Previous Investigationsmentioning

confidence: 99%

Nicardipine Prolonged-release Implants - A Potential Tool for the Prevention of Cerebral Vasospasm?

Schubert¹,

Seiz²,

Thomé³

2011

European Neurological Review

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Despite considerable effort, no effective prophylactic treatment for cerebral vasospasm after subarachnoid haemorrhage (SAH) has been identified thus far. Treatment approaches have included the application of intravenous and therefore systemic vasodilatory drugs, which in turn have been found to be associated with significant side effects while at the same time exerting only limited efficacy. Consequently, a more local application, namely the intrathecal delivery of nicardipine prolonged-release implants (NPRI) has been developed. After surgical clipping of the causative aneurysm, these implants may be positioned adjacent to the proximal vasculature most at risk for developing delayed vasospasm. Several studies were able to show a dramatic reduction in both the incidence and severity of angiographic vasospasm, which in turn reduces the development of cerebral infarction and delayed ischaemic neurological deficits. While efficacy appears to be dose dependent, a reduction of angiographic vasospasm incidence from 70 % to less than 10 % has been observed, paralleled by an improvement of functional outcome. However, when applied intraventricularly after coiling of the offending aneurysm, effects were less pronounced. At this time, NPRIs seem to represent a very promising treatment option for the prevention of cerebral vasospasm after SAH, and larger studies will be needed to further supplement previous findings.

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Nicardipine Prolonged-Release Implants for Preventing Cerebral Vasospasm After Subarachnoid Hemorrhage: Effect and Outcome in the First 100 Patients

Cited by 31 publications

References 26 publications

Delayed neurological deterioration after subarachnoid haemorrhage

Delayed neurological deterioration after subarachnoid haemorrhage

Temporal evolution of vasospasm and clinical outcome after intra-arterial vasodilator therapy in patients with aneurysmal subarachnoid hemorrhage

Nicardipine Prolonged-release Implants - A Potential Tool for the Prevention of Cerebral Vasospasm?

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