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Title: Nicardipine Helps Restore Cerebral Oxygenation in Hypertensive Crisis Without Deleterious Effects: Presented at ISC
 "Nicardipine Helps Restore Cerebral Oxygenation in Hypertensive Crisis Without Deleterious Effects: Presented at ISC"


By Paula Moyer ORLANDO, FL -- February 27, 2006 -- Intravenous nicardipine is an effective way of restoring cerebral oxygenation without deleterious effects in patients who have been treated for hypertensive crisis, according to investigators who presented their findings here February 17[th at the 31st International Stroke Conference (ISC).

"There was no reduction in oxygen delivery to the brain despite a reduction in the required fraction of inspired oxygen [FiO2] and cerebral perfusion pressure [CPP]," said principal investigator Pradeep K. Narotam, MD. "In ischemic patients, an 81% improvement in cerebral oxygenation was reported." Dr. Narotam is an assistant professor of neurosurgery at Creighton University Medical Center in Omaha, Nebraska.

The investigators were concerned about the effect of treatment-induced sudden hypotension on cerebral oxygenation in patients who present in acute hypertension and the poor neurologic outcome associated with cerebral oxygen deficiency. They were interested in whether intravenous nicardipine would be neuroprotective because physicians are already using it to reverse vasospasm in such patients.

Therefore, they designed a single-arm, prospective study to evaluate the effects of nicardipine on patients in acute hypertension who were undergoing brain tissue oxygen monitoring. The investigators recruited 30 patients who had 62 hypertensive episodes. In addition to FiO2 and CPP, they also assessed blood pressure, brain tissue oxygen (PbtO2) intracranial pressure (ICP), central venous pressure (CVP), and mean arterial pressure (MAP). The investigators assessed these parameters before the nicardipine and 4 and 8 hours after treatment. The investigators defined cerebral hypo-oxygenation as a brain tissue oxygen of less than 20 mmHg. They measured brain tissue oxygen with a parenchymal bolt inserted with a twist drill.

Treatment with nicardipine was associated with a 19-point reduction in MAP at 4 hours, at which time a 21% reduction in mean CPP was documented. The investigators noted that brain tissue oxygen was 26.7 mmHg pre-infusion and 27.37 at four hours.

Among these patients, 11 patients who had 13 events had low oxygen delivery. Patients with hypo-oxygenation were more likely to have higher systolic blood pressure (P < .025), MAP (P = .04), and brain tissue oxygenation (P = .000); such patients also required higher FiO2 to support oxygen delivery (P = .02). At 4 and 8 hours, the brain tissue oxygen significantly improved (P = .002 and P = .005, respectively), even though the MAP and CPP had decreased (P = .0000072 and P = .0009, respectively).

These findings led investigators to conclude that nicardipine is an effective treatment of acute hypertension without a harmful effect on brain tissue oxygenation.


[Presentation title: Impact of IV Nicardipine on Cerebral Oxygenation in Neurologic Disorders Requiring IV Antihypertensive Therapy. Abstract P313]






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