Effect of nimodipine (Bay e 9736) on postischaemic cerebrovascular reactivity, as revealed by measuring regional cerebral blood flow (rCBF)

Gelmers, H. J.

doi:10.1007/bf01728883

Cited by 65 publications

(17 citation statements)

References 15 publications

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“…However, as early as 1982, the first results of clinical studies on the effect of nimodipine on cerebral blood flow in stroke patients were reported. 49 On the basis of the hypothesis of the calciumdependent final common pathway in cell death and his previous experiments, an author started a "single-blind" pilot study, which showed that treatment with nimodipine was promising. 50 In 1988, the same author reported the results of a placebo-controlled, double-blind, randomized clinical trial.…”

Section: Discussionmentioning

confidence: 99%

Nimodipine in Animal Model Experiments of Focal Cerebral Ischemia

Horn

Haan

Vermeulen

et al. 2001

Stroke

200

139

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Background and Purpose-Based on the results of animal experiments, clinical trials were performed with nimodipine, which did not demonstrate a beneficial effect on outcome after stroke. The aim of this study was to determine whether the evidence from animal experiments with nimodipine supported the use of nimodipine in clinical trials. Methods-We performed a systematic review of animal experiments with nimodipine in focal cerebral ischemia. Studies were identified by searching Medline and Embase. We assessed whether these studies showed a beneficial effect of active treatment. In-depth analyses were performed on infarct size and amount of edema, and subgroup analyses were performed on the length of the time window to the initiation of treatment and the methodological quality of the studies. Results-Of 225 identified articles, 20 studies were included. The methodological quality of the studies was poor. Of the included studies, 50% were in favor of nimodipine. In-depth analyses showed statistically significant effects in favor of treatment (10 studies). No influence of the length of time to the initiation of treatment or of the methodological quality on the results was found. Conclusions-We conclude that the results of this review did not show convincing evidence to substantiate the decision to perform trials with nimodipine in large numbers of patients. There were no differences between the results of the animal experiments and clinical studies. Surprisingly, we found that animal experiments and clinical studies ran simultaneously.

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Section: Discussionmentioning

confidence: 99%

Nimodipine in Animal Model Experiments of Focal Cerebral Ischemia

Horn

Haan

Vermeulen

et al. 2001

Stroke

200

139

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“…Interference with the collat eral blood supply has probably resulted in transformation of reversible ischaemia to infarction. These haemody namic effects of the drug were unexpected because im provement of cerebral blood flow in the ischaemic area has been observed following treatment with nimodipine [24,25). Furthermore, hypotension was not a major con cern in clinical trials on patients with subarachnoid haem orrhage [8,9], although these patients were certainly younger and less affected by concomitant cardiovascular problems.…”

Section: Discussionmentioning

confidence: 99%

Intravenous Nimodipine West European Stroke Trial (INWEST) of Nimodipine in the Treatment of Acute Ischaemic Stroke

MacMahon²,

et al. 1994

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A randomised, double-blind, placebo-controlled trial of intravenous nimodipine was conducted in 295 patients with acute ischaemic stroke. Nimodipine was given as an intravenous infusion of 1 or 2 mg/h for 5 days followed by an oral dose of 120 mg daily for a total treatment period of 21 days. Patients with a clinical diagnosis of ischaemic stroke in the carotid artery territory within 24 h entered the study at 34 centres, involving 11 European countries: 100 were randomly assigned to placebo, 101 to nimodipine with an initial intravenous dose of 1 mg/h and 94 patients to an initial dose of 2 mg/h. The trial, initially aiming at a patient inclusion of 600, was terminated because of concerns arising from safety monitoring. Primary efficacy variables were neurological outcome according to the Orgogozo scale and functional outcome according to the Barthel scale at day 21. There were apparent differences between the groups in neurological and functional outcome with a better outcome in the placebo group. The differences between the placebo group and the 2-mg/h group were statistically significant (p = 0.0005 for the Orgogozo scale and p = 0.0033 for the Barthel scale). The differences were even more pronounced at the final follow-up at 24 weeks (p = 0.0001 and p = 0.0002, respectively). There were no statistically significant differences in mortality between the groups. There were statistically significant differences between the groups regarding the effect of the first few days of intravenous treatment on systolic and diastolic blood pressure with the most pronounced reduction in the 2-mg/h nimodipine treatment group at day 2 (p = 0.0001). An explorative analysis indicated a correlation between diastolic blood pressure reduction in the nimodipine-treated groups and unfavourable neurological outcome (p = 0.0005). A potential neuroprotective effect of nimodipine by preventing calcium overload in ischaemic neurons may thus have been outweighed by detrimental haemodynamic effects in the ischaemic area.

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“…A second explanation is the presence of a late cerebral steal phenomenon in which there is an increase in CBF in unaffected brain regions, shunting perfusion away from ischemic vasoparalyzed regions. 20 It would, however, be unusual for this to be preceded by significant reperfusion or an inverse steal phenomenon. Nonnutritional reperfusion, or luxury perfusion, is therefore a more tenable explanation.…”

Section: Discussionmentioning

confidence: 99%

“…There have been no published studies evaluating nimodipine after stroke using HMPAO SPECT. A small number of studies have used either 133 Xe SPECT 20,21 or positron emission tomography (PET), 22,23 but none of these included outcome studies.…”

mentioning

confidence: 99%

Nimodipine and Perfusion Changes After Stroke

Infeld

Davis

Donnan

et al. 1999

Stroke

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Background and Purpose —Meta-analysis of previous trials of oral nimodipine in acute stroke has suggested a benefit when commenced within 12 hours of onset. We sought to study the effect of oral nimodipine on reperfusion after acute stroke and the relation between reperfusion and outcome. Methods —Fifty patients with acute middle cerebral artery territory cortical infarction were blindly randomized within 12 hours of onset to either oral nimodipine (30 mg every 6 hours) or placebo. Treatment was continued for 2 weeks. Cerebral blood flow was assessed with the use of 99m Tc–hexamethylpropyleneamine oxime single-photon emission CT before therapy, 24 hours later, and at 3 months. Hypoperfusion was measured by a validated volumetric technique. Neurological impairment and functional outcome were assessed with the Canadian Neurological Scale and Barthel Index, respectively. Tissue loss was measured with CT at 3 months. Four patients were excluded from analysis for technical reasons. Results —Twenty-three patients received nimodipine, and 23 received placebo. In the nimodipine group, there was early reperfusion that was not maintained at outcome ( P =0.01). In the placebo group, mean infarct hypoperfusion volumes showed no overall change. Nonnutritional reperfusion in nimodipine-treated patients was associated with adverse neurological ( P =0.05) and functional outcome ( P =0.06). There was, however, no difference in clinical outcome between the 2 groups. Conclusions —Oral nimodipine administered within 12 hours enhanced acute reperfusion, but this was largely nonnutritional. Larger studies using a shorter treatment delay are required to evaluate the clinical efficacy of nimodipine in acute ischemic stroke.

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Effect of nimodipine (Bay e 9736) on postischaemic cerebrovascular reactivity, as revealed by measuring regional cerebral blood flow (rCBF)

Cited by 65 publications

References 15 publications

Nimodipine in Animal Model Experiments of Focal Cerebral Ischemia

Nimodipine in Animal Model Experiments of Focal Cerebral Ischemia

Intravenous Nimodipine West European Stroke Trial (INWEST) of Nimodipine in the Treatment of Acute Ischaemic Stroke

Nimodipine and Perfusion Changes After Stroke

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