Milrinone for the Treatment of Cerebral Vasospasm After Aneurysmal

Subarachnoid Hemorrhage
Amanda Tarabini Fraticelli, Bernard P. Cholley, Marie-Reine Losser, Jean-Pierre
Saint Maurice and Didier Payen
Stroke 2008;39;893-898; originally published online Jan 31, 2008;
DOI: 10.1161/STROKEAHA.107.492447
Stroke is published by the American Heart Association. 7272 Greenville Avenue, Dallas, TX 72514
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 Milrinone for the Treatment of Cerebral Vasospasm After
Aneurysmal Subarachnoid Hemorrhage
Amanda Tarabini Fraticelli, MD; Bernard P. Cholley, MD, PhD; Marie-Reine Losser, MD, PhD;
Jean-Pierre Saint Maurice, MD; Didier Payen, MD, PhD

Background and Purpose—Attempts to reverse cerebral vasospasm (CVS) after aneurysmal subarachnoid hemorrhage
(aSAH) rely on a limited number of treatments. Calcium channel blockers have proven a benefit but their vasodilating
effect on spastic cerebral arteries is relatively modest. Milrinone, a phosphodiesterase inhibitor, combines vasodilating
and inotropic properties, but limited data exist to support its use for the treatment of CVS. We assessed the efficacy and
tolerance of milrinone in patients with CVS secondary to aSAH.
Methods—Twenty-two consecutive patients with angiographically-proven CVS (arterial diameter reduction ⬎40%) have
been studied. Intraarterial milrinone was infused in the cerebral territory(ies) involved and followed by continuous
intravenous infusion until Day 14 after initial bleeding. We evaluated angiographic reversal of CVS, hemodynamic
tolerance, and neurological outcome 1 year after aSAH.
Results—Thirty-four selective intraarterial infusions of milrinone were required to treat 72 vasospastic territories.
Intraarterial milrinone resulted in 53⫾37% increase in arterial diameter (P⬍.0001). Milrinone infusion resulted in
moderately increased heart rate, but systemic arterial pressure remained unchanged. Five patients (23%) had
angiographically-proven vasospasm recurrence within 48 hours after the procedure. Two of them were successfully
reversed after another intraarterial infusion of milrinone. The remaining 3 underwent mechanical angioplasty. Two
patients (9%) died in ICU, and 2 were lost to follow-up. All other patients had very good neurological outcome
(modified Rankin scale: 0.8⫾1.0; Barthel index: 100 [95–100]).
Conclusion—This study suggests that milrinone is effective and safe for reversal of CVS after aSAH and should be tested
in a large randomized trial. (Stroke. 2008;39:893-898.)
Key Words: angioplasty and stenting 䡲 outcome 䡲 subarachnoid hemorrhage 䡲 vasospasm
䡲 phosphodiesterase inhibitors

C erebral vasospasm (CVS) is present in up to 70% of

patients suffering from aneurysmal subarachnoid hem-
orrhage (aSAH) and is symptomatic in nearly half of cases
with subsequent increased morbidity, mortality, and cost of
care.1 Up to now, there is no satisfactory therapy to prevent
this complication. Various cerebral protectants have been
tested in patients with aSAH, but only calcium channel
blockers have demonstrated a beneficial effect on outcome,
especially oral nimodipine.2,3
Attempts to reverse CVS rely on a limited number of
treatments. “Triple H” (hypervolemia, hypertension, hemodi-
lution) never demonstrated any benefit in outcome and is
associated with numerous side effects. Intraluminal balloon
angioplasty (also called mechanical angioplasty) has been
introduced in the late 80’s.4,5 Although very effective on
angiographically proven CVS, this technique is associated
with a high risk of arterial damage such as wall rupture or
dissection.6,7 Chemical angioplasty, consisting in intraarterial
infusion of vasodilators at the time of cerebral arteriography,
is a less aggressive procedure. Papaverine was used first, but
this agent has only transient efficacy and is sometimes
responsible for serious adverse events.8 –10 Intraarterial cal-
cium channel blockers have also been tested, but only
nonrandomized studies support their efficacy.11–14 Inhibitors
of the phosphodiesterase III isoenzyme have vasodilating
properties combined with inotropic effects and are currently
used for heart failure treatment. Few investigators have tested
intraarterial infusion of these agents to treat CVS secondary
to aSAH in experimental models (Khajavi, 1997)15 and in
selected patients (Arakawa, 2001).16 Their results indicated a
good efficacy, which prompted us to perform a pilot trial in
patients with CVS secondary to aSAH despite maximum

Received April 28, 2007; July 23, 2007; accepted August 2, 2007.
From Département d’Anesthésie-Réanimation-SMUR (A.T.F., B.P.C., M.R.L., D.P.) and Service de Neuroradiologie Interventionnelle (J.-P.S.M.),
Assistance Publique Hôpitaux de Paris, Hôpital Lariboisière, Université Paris, Diderot, France.
Current affiliation for B.P.C.: AP-HP, Hôpital Européen Georges Pompidou, Service d’Anesthésie-Réanimation; Université Paris René Descartes.
Current affiliation for M.-R.L.: AP-HP, Hôpital Saint Louis, Université Paris 7 Diderot.
Correspondence to Dr Didier Payen, MD, PhD, Département d’Anesthésie-Réanimation-SMUR, Hôpital Lariboisière; 2 rue Ambroise Paré; 75475
Paris cedex 10, France. E-mail dpayen1234@aol.com
© 2008 American Heart Association, Inc.
Stroke is available at http://stroke.ahajournals.org DOI: 10.1161/STROKEAHA.107.492447

Downloaded from stroke.ahajournals.org893

at McGill University on January 27, 2011
894 Stroke March 2008
conventional treatment. The goal of this prospective study
was to assess the efficacy and tolerance of intraarterial
milrinone, followed by a prolonged intravenous infusion, in
patients with CVS after aSAH.
Methods
Patients
Twenty-two consecutive patients suffering from aSAH with
angiographically-proven CVS have been prospectively studied from
February 2002 to April 2004 after approval of the local Ethics
Committee. All patients underwent endovascular treatment of their
cerebral arterial aneurysm under general anesthesia within 24 hours
after admission. The following standard protocol of care was applied
to all patients on admission: oral Nimodipine (360 mg/d) was given
orally or in the gastric tube if patients remained ventilated; analgesic
treatment consisted in IV paracetamol (4 g/d) and IV or subcutane-
ous opioids (fentanyl or morphine sulfate, respectively); antiepileptic
treatment (valproate acid 2g/d) if required. In addition, patients
received fluids: normal saline 30 to 40 mL/kg/d and gelatin 10
mL/kg/d. When mean arterial pressure (MAP) was less than
90 mm Hg, norepinephrine infusion was started using incremental
doses until the 90 mm Hg threshold was reached. In 7 patients who
had external ventricular drainage to treat hydrocephalus, cerebral
perfusion pressure (CPP) was directly monitored and the end point of
resuscitation was to maintain CPP above 75 mm Hg.
The early detection of cerebral vasospasm was based on repeated
neurological examination in intensive care unit and on body temper-
ature monitoring. Routine transcranial Doppler velocimetry of cere-
bral arteries was performed at least daily, or more if required. CVS
was suspected when patients exhibited neurological alteration, hy-
perthermia, or suggestive Doppler changes,17 either separately or in
combination. The diagnosis of CVS was confirmed by a new
cerebral angiography, performed using the exact same incidence as
that used for admission angiography. CVS was defined as a reduc-
tion in vessel diameter greater than 40% with respect to admission
diameter. The magnitude of reduction was used to grade the severity
of CVS as moderate (40% to 60%) or severe (ⱖ60%).
Cerebral Arterial Dilatation Procedure
Patients who developed CVS despite the standard preventive treat-
ment were eligible for active arterial dilatation therapy using
milrinone, occasionally associated with mechanical angioplasty.
Patients themselves, or next of kin when neurological status was
altered, were informed of the procedure. Patients with CVS were
treated openly with the following method: (1) Intraarterial milrinone
was infused (8 mg over 30 minutes) in the main artery dedicated to
the vasospastic territory (internal carotid, dominant vertebral artery).
Infusion could be repeated once in the same territory if an incomplete
reversal was observed. Intraarterial milrinone infusion could also be
repeated in a different territory in situation of extensive vasopasm,
with a maximum milrinone dose of 24 mg. An independent radiol-
ogist assessed the efficacy of intraarterial infusion by measuring
angiographic enlargement of the vessel diameter. (2) Mechanical
angioplasty was performed only if vasospasm persisted after 2
intraarterial milrinone challenges, or if severe CVS occurred before
Day 5 (suggesting a high risk of recurrence). (3) All patients received
a prolonged continuous intravenous infusion of milrinone. If well
tolerated, the dose was progressively incremented from 0.5 ␮g/kg/
min to 1.5 ␮g/kg/min (i.e.: twice the regimen recommended for heart
failure patients) to maintain relatively high plasma concentrations of
the drug after intraarterial infusion. This dose incrementation was
stopped when tachycardia (HR ⬎100 bpm) or blood pressure
reduction (⬎20%) occurred. Intravenous milrinone infusion was
maintained during the entire “high risk” period, i.e.: up to Day 14
after the initial bleeding. When CVS recurrence was suspected, a
new angiogram was performed and the procedure could be repeated.
Patients remained in ICU until Day 14 and were then transferred to
the ward in the absence of other ICU complication.
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Parameters collected included the following clinical data and
radiological findings: Age, gender, SAPSII score, World Federation
of Neuro Surgeons (WFNS) score (⫽clinical severity of aSAH),
Fisher score (⫽CT scan severity of aSAH), radiological character-
istics of intracranial aneurysm on admission angiogram (location,
number, and size) angiographic characteristics of CVS (severity,
arterial territories involved); delay between CVS detection and initial
hemorrhage, arterial diameter variation after intraarterial milrinone
infusion, number of CVS recurrences, number of mechanical angio-
plasties, clinical tolerance of intraarterial and IV milrinone infusion
(systemic arterial pressure, heart rate, peripheral oxygen saturation,
and end-tidal CO2 in ventilated patients), and occurrence of hypo-
kalemia. In addition, long-term neurological outcome was assessed
12 to 18 months after aSAH by telephone interview using modified
Rankin score18 (0 to 6 points) and Barthel index19 (0 to 100 points).
Data Analysis
The vasodilating response to intraarterial milrinone infusion was
assessed by referring to premilrinone arterial diameter, and was also
compared between the different arterial territories: anterior cerebral
artery (ACA), middle cerebral artery (MCA), internal carotid artery
(ICA), and basilar artery (BA).
Statistical Analysis
Data were expressed as mean⫾SD, or as median [extremes] when
distribution was not normal. Data were analyzed using Student t test,
signed rank test, or 2-way ANOVA as appropriate.
Results
Twenty-two patients were studied over a 2-year period, from
February 2002 to April 2004. Demographic data, WFNS
score, Fisher score, and number and location of intracranial
aneurysm on initial angiography are presented in Table 1. The
day of occurrence of CVS after initial hemorrhage, number of
arterial territories involved in each patient, and the severity of
vasospasm are described in Table 2. Seventy-two vasospastic
territories were treated using the procedure described above,
requiring a total of 34 selective intraarterial infusions of
milrinone (mean dose⫽12⫾6 mg). The anatomic distribution
of vasospastic vessels was: internal carotid artery (n⫽25);
middle cerebral artery (n⫽21); anterior cerebral artery
(n⫽19); and basilar artery (n⫽7). Intraarterial milrinone
infusion resulted in a 53⫾37% overall increase in vessel
diameter (P⬍0.0001; Figure). There was a greater vessel
diameter increase after milrinone when vasospasm was “se-
vere” with respect to “moderate”: 73⫾23% versus 40⫾46%,
respectively, P⫽0.0001. The response to milrinone did not
differ among the different territories (ANOVA, P⫽0.6).
Hemodynamic Tolerance
Two patients received norepinephrine infusion (0.3⫾0.05
␮g/kg/min) to maintain mean arterial pressure (or cerebral
perfusion pressure) within the predefined range. Intraarterial
milrinone infusion resulted in increased heart rate (75⫾14
versus 89⫾21 beats per min, P⫽0.002), but systolic (SBP)
and diastolic (DBP) blood pressures did not change signifi-
cantly (SBP: 135⫾30 versus 131⫾29 mm Hg, NS; DBP:
65⫾14 versus 63⫾14 mm Hg, NS). End-tidal CO2 was
monitored in a subgroup of 11 mechanically ventilated patients
and remained unchanged (32⫾4 versus 32⫾4 mm Hg, NS).
Intraarterial milrinone infusion did not alter peripheral arte-
rial oxygen saturation (99⫾1% versus 99⫾1%, NS). The
average dose of intravenous milrinone was 1⫾0.55 ␮g/kg/
 Tarabini Fraticelli et al Milrinone for Vasopasm After Subarachnoid Hemorrhage 895

Table 1. Patients Characteristics

Patient No. Age Gender SAPS2 WFNS Fisher Aneurysms, n Aneurysm Location
1 59 F 37 4 4 1 BA apex
2 53 M 24 2 4 1 Left MCA
3 40 F 15 4 4 1 Azygos ACA
4 53 F 20 3 4 1 Right MCA
5 38 M 8 1 2 2 AcoA, Left opht art
6 53 M 24 1 2 1 Left MCA
7 48 F 27 3 3 1 BA apex
8 37 M 10 1 3 1 Left MCA
9 31 M 8 1 1 1 AcoA
10 53 F 45 4 4 2 AcoA, Internal carotid
11 42 F 28 4 4 1 AcoA
12 30 F 8 1 3 1 Right PcoA
13 72 F 33 1 2 1 AcoA
14 31 F 8 1 3 1 Left MCA
15 39 F 8 1 2 1 Right PcoA
16 51 F 21 1 3 1 Left ACA
17 39 M 8 1 3 1 AcoA
18 35 F 8 1 3 2 Right opht art, Ant choroid
19 61 F 23 4 4 1 Left PcoA
20 49 F 36 4 4 2 AcoA, Right opht art
21 34 M 42 3 4 1 Left PcoA
22 37 F 25 1 4 0 /
Mean⫾SD 45⫾11 21⫾12 2⫾1 3⫾1 1⫾0
BA apex indicates apex of basilar artery; MCA, middle cerebral artery; ACA, anterior cerebral artery; AcoA, anterior communicating
artery; PcoA, posterior communicating artery; opht art, ophtalmic artery; choroid, choroid artery.

min, for a duration of 7⫾3 days, and this infusion was well
tolerated. After IV milrinone introduction 2 more patients
required IV norepinephrine (0.25⫾0.04 ␮g/kg/min) during
less than 24 hours. Heart rate increased after IV milrinone
infusion, with higher minimum and maximum values over 24
hours: 66⫾8 versus 72⫾11 bpm, P⫽0.03, and 81⫾10 versus
90⫾12 bpm, P⫽0.003, respectively. Five patients had a low
serum potassium (ⱕ3.5 mEq/L) while receiving IV
milrinone.
CVS Recurrence
Twelve patients of 22 had a control angiography between the
first and the fourth day after intraarterial milrinone for
suspicion of CVS recurrence. Five patients (23%) had
angiographically-proven CVS recurrence, which occurred
within 48 hours after the procedure. Two CVS recurrences
were successfully reversed after another intraarterial infusion
of milrinone. The remaining 3 patients underwent mechanical
angioplasty.
Mechanical Angioplasty
In our series, a total of 8 patients underwent mechanical
angioplasty. As mentioned above, 3 patients had this proce-
dure to treat CVS recurrence whereas 5 patients had it
initially, when CVS was first recognized. For those 5 patients,
mechanical angioplasty was associated to intraarterial milri-
none because the vasospasm persisted after 2 intraarterial
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milrinone challenges, or because severity and precocity
(before Day 5) suggested a high risk of recurrence.
Outcome
Only 2 patients died in ICU (9%) as a consequence of
extensive cerebral ischemia associated with intracranial hy-
pertension. We calculated outcome scores 12 to 18 months
after aSAH. Two patients were lost to follow-up; the remain-
ing 18 patients had a modified Rankin score of 0.8⫾1.0, and
a Barthel index of 100 [95–100] (median [extremes]). Nine
patients (41%) were able to resume all their anterior activi-
ties, including their professional life. For the 9 other patients
disability was minimal and mainly related to memory deficits
and speech disorders, which did not limit their autonomy.
These patients were all able to care for themselves, and 4
were able to drive an automobile and practice sports. There
was no outcome difference, neither for modified Rankin score
nor for Barthel index (P⫽0.28 and P⫽0.60, respectively),
when comparing patients who underwent mechanical angio-
plasty and those who did not.
Discussion
The present study suggests that an arterial dilatation proce-
dure based on a combination of intraarterial milrinone infu-
sion followed by intravenous administration (up to Day 14
after initial bleeding) can be effective and safe for cerebral
vasospasm (CVS) treatment. A third of our patients also
896 Stroke March 2008

Table 2. Characteristics of Cerebral Vasospasm (CVS) patients experiencing aSAH develop neurological impair-
Patient Day of Territories, Moderate CVS, Severe CVS,
ment, and up to 70% have angiographically-proven vaso-
No. CVS n n n spasm within the first week.1 The poor prognosis associated
with CVS after aSAH has prompted the search for therapeutic
1 5 6 0 6
strategies aiming at reversing arterial vasoconstriction and
2 4 2 1 1
avoid, or limit, subsequent cerebral ischemia.
3 8 1 1 0 Mechanical angioplasty is very effective to reverse CVS,
4 10 4 2 2 but this procedure can generate physical damage to intracra-
5 6 1 0 1 nial arteries and may worsen CVS per se.6,7 Moreover, the use
6 8 3 1 2 of this technique is limited by the localization of CVS,
7 8 2 2 0 because smaller distal arteries are not accessible to angio-
8 5 6 2 4 plasty. Therefore, this technique should be complementary
9 4 1 0 1
with chemical angioplasty. In the present study, mechanical
angioplasty was performed in selected patients with early (i.e.
10 9 1 0 1
high risk of recurrence) or recurrent CVS limited to the
11 4 8 3 5
terminal segment of carotid siphon, M1 segment of MCA,
12 9 5 4 1 intracranial vertebral arteries, and basilar artery. In our
13 10 3 2 1 experience, the benefit/risk ratio may be favorable in this
14 7 2 1 1 subgroup of patients.
15 5 4 4 0 Intraarterial infusion of vasodilators (or “chemical” angio-
16 9 1 0 1 plasty) is therefore an important alternative for CVS treat-
17 8 6 6 0 ment, and different pharmacologic agents have been tested
including papaverine and calcium channel antagonists. In-
18 8 2 1 1
traarterial papaverine was the first drug to be tested and has
19 15 6 6 0
been widely used in patients with symptomatic CVS, but no
20 4 1 1 0
outcome improvement could be demonstrated in comparison
21 7 1 1 0 to standard medical treatment.9 Moreover, papaverine is
22 10 6 6 0 associated with serious neurotoxic side effects including:
Mean⫾SD 7⫾3 3⫾2 2⫾2 1⫾2 severe brain stem depression, increased intracranial pressure,
mydriasis, neurological deficits, seizures, and coma,10 possi-
bly related to precipitation of papaverin hydrochloride crys-
required a mechanical angioplasty in addition to milrinone tals.8 Various calcium channel blockers have also been
infusion to treat their CVS. In our cohort, mortality was only administered as intraarterial infusion. Intraarterial verapamil
9% and patients who survived had very mild disability scores was found to increase vessel diameter, and the authors
at one year after aneurysmal subarachnoid hemorrhage. suggested that it could also improve immediate clinical
Subarachnoid hemorrhage secondary to intracranial aneu- status.11 Nicardipine and nimodipine have also been shown to
rysm rupture occurs with a worldwide incidence of 10.5 new reverse CVS after intraarterial infusion.12 Subsequent imme-
cases per 100 000 persons-year.20 According to recent publi- diate clinical improvement was documented in 76% of
cations, half of patients who sustain aSAH die, one third of patients receiving intraarterial nimodipine, and a similar
survivors need lifelong care, and only 20% to 35% attain a proportion had favorable outcome at 6 months.13 Some of
good recovery.20,21 One of the major causes of disabilities and these preliminary trials showed encouraging results, but
death after aSAH is cerebral ischemia secondary to cerebral randomized and adequately powered studies are still war-
vasospasm. Despite recommended treatment, one third of ranted to demonstrate the impact of intraarterial infusion of

Figure. Cerebral vasospasm of left internal

carotid and branches; effect of intraarterial
milrinone injection. Representative exam-
ple of a CVS involving left internal carotid
artery and branches (arrows) before (A)
and after (B) intraarterial milrinone infusion.
The severity of vasospasm was moderate
for ICA and MCA, whereas it was consid-
ered severe for ACA. Arrowhead indicates
ACA aneurysm treated by endovascular
procedure.

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 Tarabini Fraticelli et al Milrinone for Vasopasm After Subarachnoid Hemorrhage
calcium channel blockers on CVS, and its impact on out-
come. Phosphodiesterase III inhibitors combine vasodilating
and inotropic properties, resulting from the increase in cAMP
in the cytosol of vascular smooth muscle cells and cardio-
myocytes. Among these agents, milrinone is widely used to
treat patients with acute heart failure. The combination of
potent vasodilatation with reinforcement of inotropy is also
very attractive to treat aSAH. Milrinone has similar systemic
hemodynamic effects as the beta-agonist dobutamine in
patients with altered left ventricular function after aSAH.22
The potential role of increased cardiac output in improving
cerebral tissue perfusion independently of mean arterial
pressure has been suggested by several authors.23,24 The first
and unique clinical study using intraarterial milrinone showed
angiographic effectiveness to reverse CVS in patients with
aSAH.16 In this study, intraarterial milrinone was also fol-
lowed by an intravenous infusion for up to 2 weeks after
initial bleeding. Another recent study by the same authors
reported their initial experience with cisternal irrigation using
lactated Ringer’s solution containing urokinase and milrinone
in 12 aSAH patients with WFNS grade 4 or 5.25 The authors
reported good results in these patients presenting very severe
aSAH: few CVS and only 1 new permanent ischemic deficit
related to CVS. The patients also had better outcome than
historical controls receiving the same treatment except for
cisternal irrigation.
Our findings confirmed the preliminary observations by
Arakawa et al,16 demonstrating a significant enlargement in
diameter of vasospastic intracranial arteries. This effect was
independent from location of CVS. The vessel diameter
enlargement was more pronounced in severe than in moderate
CVS. Because CVS remains a threat during approximately 2
weeks after initial bleeding, milrinone infusion was main-
tained intravenously until Day 14 after the onset of aSAH.
Intraarterial infusion was very well tolerated and no serious
adverse reaction was observed on standard hemodynamic and
gas exchange parameters. In 2 patients receiving intravenous
milrinone and sedation, mean arterial pressure dropped below
the predefined threshold (90 mm Hg). This hypotension was
corrected using norepinephrine infusion during less than 24
hours. The increase in heart rate was moderate and never
required milrinone discontinuation. Hypokalemia is known to
occur in subjects treated with phosphodiesterase inhibitors,
but only 5 patients required potassium supplementation to
maintain a normal kalemia. Overall, milrinone was effective
to reverse CVS and well tolerated during both intraarterial
and intravenous infusions in our cohort of patients.
The observed outcome in this population of consecutive
patients was surprisingly good. A 9% in-hospital mortality
was far less than the 40% mortality reported for similar
patients in recent reviews.20,21 However, other authors have
already reported a low mortality rate in similar patients,26,27
but Rabinstein A et al observed 52% of permanent deficits
attributable to CVS in survivors in a series of aSAH patients
of comparable severity (WFNS IV or V: 35%; WFNS I, II,
and III: 65%) treated with intraarterial papaverine or angio-
plasty. In our series, among patients discharged from the
hospital, 2 were lost to follow-up, but none of the 18
remaining was severely disabled 1 year after aSAH. Nine of
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897
them attained full recovery and returned to their professional
life, whereas 9 had minimal neurological impairment (mainly
speech disorders and memory deficits), which did not limit
their autonomy. In a systematic review of mortality and
functional outcome, Hop et al reported that 10% to 20% of
patients remain severely disabled after aSAH,28 whereas
Suarez et al estimate that almost one third of survivors need
lifelong care.20 The proportion of patients with good neuro-
logical outcome in the present series is at least 81%, clearly
more than 35%, the figure that is usually accepted.
Limitations of the Study
This pilot study was performed to test the efficacy of
milrinone to reverse CVS in patients with aSAH and to
evaluate its tolerance. We did not obtain systematic cardiac
output measurements in these patients and were therefore
unable to quantify the effects of milrinone on hemodynamic
targets such as cardiac output and systemic vascular resis-
tance. The lack of control group does not allow to conclude
on the impact of milrinone in the observed favorable out-
come. However, the angiographically-proven reversal of
CVS after intraarterial milrinone infusion suggests a positive
role of this agent in preventing CVS-related brain ischemia.
To summarize, intraarterial milrinone infusion was found
to be safe and very effective to reverse CVS secondary to
aSAH. Milrinone should be compared randomly and blindly
to another vasodilator such as nimodipidine to evaluate which
drug is the best for chemical angioplasty in aSAH patients.
Sources of Funding
This work was supported in part by the “Plan quadriennal 2003–
2007” Université Paris7 Diderot, EA 322.
Disclosures
None.
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