BACKGROUND: Intra-arterial (IA) nicardipine is often used to treat cerebral vasospasm associated with subarachnoid hemorrhage (SAH). While hypotension has been noted to be a dose-limiting side effect of intravenous infusions, this has seldom been reported for IA administration. METHODS: We reviewed a consecutive series of patients who received IA nicardipine for SAH-associated vasospasm. Nicardipine was titrated to angiographic response, with blood pressure and intracranial pressure monitoring. We analyzed data using Wilcoxon signed rank, Student's t-test, Spearman's correlation, and χ(2) statistics as appropriate. A P value <0.05 was considered significant. RESULTS: Thirty patients underwent 50 procedures in which nicardipine was the sole chemical vasodilator (median dose, 15 mg). Median mean arterial pressures (MAP) decreased from 118 to 100 mmHg (P < 0.001), with an intra-operative low of 80 mmHg. Both intra-operative and post-operative decreases in MAP were directly related to nicardipine dose (r (s) = 0.352, P = 0.022 and r (s) = 0.308, P = 0.047, respectively). Hypotension (MAP < 70 mmHg) occurred in 22%, and 44% required initiation of or increases in vasopressor therapy. After the first treatment, 11 of 16 patients treated with vasodilator therapy alone, and 5 of 14 patients who underwent additional balloon angioplasty (68.8 vs. 35.7%, P = 0.141), required further endovascular treatments due to recurrent vasospasm on subsequent days. CONCLUSIONS: Intra-arterial nicardipine is associated with significant intra-operative blood pressure lowering, an increased requirement for intra-operative vasopressor therapy, and a tendency toward re-treatment when used as initial monotherapy for vasospasm.
BACKGROUND: Intra-arterial (IA) nicardipine is often used to treat cerebral vasospasm associated with subarachnoid hemorrhage (SAH). While hypotension has been noted to be a dose-limiting side effect of intravenous infusions, this has seldom been reported for IA administration. METHODS: We reviewed a consecutive series of patients who received IA nicardipine for SAH-associated vasospasm. Nicardipine was titrated to angiographic response, with blood pressure and intracranial pressure monitoring. We analyzed data using Wilcoxon signed rank, Student's t-test, Spearman's correlation, and χ(2) statistics as appropriate. A P value <0.05 was considered significant. RESULTS: Thirty patients underwent 50 procedures in which nicardipine was the sole chemical vasodilator (median dose, 15 mg). Median mean arterial pressures (MAP) decreased from 118 to 100 mmHg (P < 0.001), with an intra-operative low of 80 mmHg. Both intra-operative and post-operative decreases in MAP were directly related to nicardipine dose (r (s) = 0.352, P = 0.022 and r (s) = 0.308, P = 0.047, respectively). Hypotension (MAP < 70 mmHg) occurred in 22%, and 44% required initiation of or increases in vasopressor therapy. After the first treatment, 11 of 16 patients treated with vasodilator therapy alone, and 5 of 14 patients who underwent additional balloon angioplasty (68.8 vs. 35.7%, P = 0.141), required further endovascular treatments due to recurrent vasospasm on subsequent days. CONCLUSIONS: Intra-arterial nicardipine is associated with significant intra-operative blood pressure lowering, an increased requirement for intra-operative vasopressor therapy, and a tendency toward re-treatment when used as initial monotherapy for vasospasm.
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