Background and Purpose:To determine the accuracy of magnetic resonance angiography in assessing patients with cerebrovascular disease, we performed a study comparing the results of conventional cerebral angiography, duplex scanning, and magnetic resonance angiography.Methods: From 42 patients, a total of 25 carotid arteries were evaluated by all three techniques. The studies were independently read and sorted into five categories according to the degree of stenosis: 0-15%, normal; 16-49%, mild; 50-79%, moderate; 80-99%, severe; and totally occluded.Results: Magnetic resonance angiography correlated exactly with conventional angiography in 39 arteries (52%); duplex scanning correlated with conventional angiography in 49 cases (65%). Compared with conventional angiography, both magnetic resonance angiography and duplex scanning tended to overread the degree of stenosis. The most critical errors associated with magnetic resonance angiography were three readings of total occlusion in vessels found to be patent on conventional angiograms.Conclusions: Although magnetic resonance angiography offers great hope of providing high-quality imaging of the carotid artery with no risk and at less cost, data from this study suggest that misreading the degree of stenosis, or misinterpreting a stenosis for an occlusion, could lead to errors in clinical decisions. Guidelines for use of magnetic resonance angiography in a clinical setting are offered. (S • >ke 1992;23:341-346)

A dose-escalation study of the calcium ion entry blocking drug nicardipine was performed using large dose infusions in 67 patients with recent aneurysmal subarachnoid hemorrhage (SAH). A safe, potentially therapeutic dose of the drug was determined. Patients admitted within 7 days of SAH from a documented cerebral aneurysm were entered into the study if no spasm was present on the initial angiogram. Nicardipine was administered as a continuous intravenous infusion throughout the 14-day period after SAH, regardless of the timing of surgery. To determine the safest possible dose, nicardipine was administered at seven dose levels from 0.01 to 0.15 mg/kg/hr. The total daily doses ranged from 27.7 mg to 375.0 mg. A follow-up angiogram was carried out on all 67 patients 7 to 10 days after SAH. Computerized tomography and neurological examinations were used to determine the presence of cerebral infarction. No major adverse effects, unexpected reactions, or permanent sequelae could be attributed to nicardipine. A decline in blood pressure was noted following administration of the drug. This occurred more frequently among patients given the largest dose but did not produce clinical problems or require discontinuation of the drug. Favorable outcomes were noted in 52 patients (78%). Vasospasm was found by arteriography in 31 patients (46%). A dose-related trend was noted: only eight (24%) of 33 patients treated at the highest dose level (approximately 10 mg/hr) developed arteriographic evidence of vasospasm. Symptomatic vasospasm was diagnosed in only two (6%) of 33 patients treated with this dose. Of the 34 patients receiving the lower dose levels, angiographic spasm was observed in 68% and symptomatic vasospasm in 27%. No deaths due to vasospasm occurred. Nicardipine appears to prevent both vasospasm and cerebral ischemia after SAH. A multicenter randomized double-blind trial to test this hypothesis is planned.

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