Intra-Arterial Nicardipine Infusion Improves CT
Perfusion–Measured Cerebral Blood Flow in
Patients with Subarachnoid Hemorrhage–Induced
BACKGROUND AND PURPOSE: Our aim was to determine the effects of intra-arterial (IA) nicardipine
infusion on the cerebral hemodynamics of patients with aneurysmal subarachnoid hemorrhage
(aSAH)–induced vasospasm by using first-pass quantitative cine CT perfusion (CTP).
MATERIALS AND METHODS: Six patients post-aSAH with clinical and transcranial Doppler findings
suggestive of vasospasm were evaluated by CT angiography and CTP immediately before angiography
for possible vasospasm treatment. CTP was repeated immediately following IA nicardipine infusion.
Maps of mean transit time (MTT), cerebral blood volume (CBV), and cerebral blood flow (CBF) were
constructed and analyzed in a blinded manner. Corresponding regions of interest on these maps from
the bilateral middle cerebral artery territories and, when appropriate, the bilateral anterior or posterior
cerebral artery territories, were selected from the pre- and posttreatment scans. Normalized values
were compared by repeated measures analysis of variance.
RESULTS: Angiographic vasospasm was confirmed in all patients. In 5 of the 6 patients, both CBF and
MTT improved significantly in affected regions in response to nicardipine therapy (mean increase in
CBF, 41 ? 43%; range, ?9%–162%, P ? .0004; mean decrease in MTT, 26 ? 24%; range, 0%–70%,
P ? .0002). In 1 patient, we were unable to quantify improvement in flow parameters due to
section-selection differences between the pre- and posttreatment examinations.
CONCLUSIONS: IA nicardipine improves CBF and MTT in ischemic regions in patients with aSAH-
induced vasospasm. Our data provide a tissue-level complement to the favorable effects of IA
nicardipine reported on prior angiographic studies. CTP may provide a surrogate marker for monitoring
the success of treatment strategies in patients with aSAH-induced vasospasm.
deed, the presence of cerebral vasospasm has been associated
with a 1.5 to threefold increase in mortality during the first 2
patients with aSAH die from vasospasm.1,2According to the
Cooperative Aneurysm Study, 70% of the patients who
present with aSAH develop vasospasm, with symptomatic
brain ischemia or infarcts occurring in 36% of all patients.3
the management of patients with aSAH is the prevention, de-
tection, and treatment of vasospasm. The most commonly
used approaches include oral nimodipine; induced hyperten-
sion, hemodilution, and hyperdynamic (triple-H) therapy;
and endovascular techniques, including intra-arterial (IA) in-
elayed cerebral ischemia represents one of the leading
causes of morbidity and mortality in patients with aneu-
gioplasty (PTA), or a combination of the 2.
Given its short duration of action and several potential
complications, papaverine has been largely replaced by other
dene IV),6or nimodipine7as the drug of choice for IA vaso-
the primary endovascular vasospasm treatment at our hospi-
tal. Nicardipine is known to affect positively both angio-
graphic (increasing vessel diameter) and clinical vasospasms.6
The degree to which nicardipine actually augments tissue-
level perfusion, however, has not, to our knowledge, been
evaluation of patients with clinically significant aSAH-in-
duced vasospasm has been previously demonstrated.8-11The
IA nicardipine infusion on the cerebral hemodynamics of pa-
tients with aSAH-induced vasospasm as measured by first-
esis that CTP may be a useful tool in the quantification of the
future clinical trials.
Materials and Methods
aSAH between September 2002 and June 2004. Approval was ob-
tained from the institutional review board at our institution to con-
Received March 28, 2008; accepted after revision July 11.
From the Endovascular Neurosurgery/Interventional Neuroradiology Section, Departments
of Radiology and Neurosurgery (R.G.N., J.A.H., J.D.R., J.C.P.); Neurocritical Care and
Vascular Neurology Section, Department of Neurology (R.G.N., G.A.R.); Diagnostic Neuro-
radiology Section, Department of Radiology (M.H.L., L.R., R.G.G., E.F.H.); Vascular Neuro-
surgery Section, Department of Neurosurgery (C.S.O.), Massachusetts General Hospital,
Harvard Medical School, Boston, Mass.
Paper previously presented in part at: Annual Meeting of the American Society of
Neuroradiology, June 5–11, 2004; Seattle, Wash.
Please address correspondence to Raul G. Nogueira, MD, Department of Interventional
Neuroradiology and Endovascular Neurosurgery, Massachusetts General Hospital, 55 Fruit
St, GRB-2-241, Boston, MA, 02114; e-mail: RNOGUEIRA@PARTNERS.ORG
Nogueira ? AJNR 30 ? Jan 2009 ? www.ajnr.org