HypErpErfUsIon syndroME coMplIcatIng
ExtracranIal carotId artEry stEntIng
Cristian Dina1, Daniela Reisz2, Luminita Banica1, Narcisa Doandes1,
Constantin Luca1, Adina Ionac1, Stefan I. Dragulescu1
Stentarea carotidian\ este utilizat\ tot mai frecvent pentru prevenirea accidentului vascular cerebral produs de leziuni severe ale segmentului extracranian al
arterei carotide. Sindromul de hiperperfuzie cerebral\ este o complica]ie rar\ dar poten]ial devastatoare a revasculariz\rii carotidiene [i poate surveni att dup\
endarterectomia carotidian\, ct [i dup\ stentare. Prezent\m cazul unui pacient cu stenoz\ carotidian\ sever\ care a dezvoltat un sindrom de hiperperfuzie
cerebral\ asociat cu hemoragie intracerebral\ dup\ o procedur\ de stentare carotidian\. Sunt prezentate datele postprocedurale, ct [i monitorizarea clinic\ [i
angiografic\ a pacientului la 12 luni.
Cuvinte cheie: sindrom de hiperperfuzie, stentare carotidian\, hemoragie intracerebral\
Carotid artery stenting (CAS) is increasingly used for the prevention of stroke generated by severe obstructive lesions of the extracranial carotid artery.
Hyperperfusion syndrome (HPS) is a rare but potentially devastating complication of carotid revascularization that can occur after carotid endarterectomy (CEA)
or CAS. We report the case of a patient with high grade carotid stenosis who developed HPS with intracerebral hemorrhage (ICH) post CAS. Post procedural,
and 12 month clinical and angiographic follow-up data are presented.
Key Words: hyperperfusion syndrome, carotid artery stenting, intracerebral hemorrhage
IntrodUctIon casE rEport
Severe extracranial carotid artery disease is treated We report the case of a 56 years old male patient
by arterial revascularization. Surgical endarterectomy who was referred to our department with severe
or endovascular stenting can be complicated by stenosis of the left carotid artery bifurcation. The
hyperperfusion syndrome (HPS) in 0.3 to 5% of patient was a treated hypertensive with statin-
cases.1,2 The complication occurs hours to days after controlled hypercholesterolemia and had a history of
a successful procedure despite immediate excellent multiple endovascular interventions. He was diagnosed
angiographic results. The presentation is variable and with severe coronary artery disease and underwent a
includes atypical migrainous phenomena, confusion, coronary endovascular procedure (stenting of the left
focal deficit, seizure, intracerebral hemorrhage. anterior descending artery) in 2002.
Cerebral CT reveals focal edema or hemorrhage, Two years later the patient was asymptomatic
which, when present, alters the prognosis. Mortality however follow-up examination detected a right
rates above 50% have been reported.3 lateral cervical bruit. Carotid ultrasound evaluation
was performed. Peak systolic velocities measured over
both carotid arteries suggested severe 70-99% ostial
Institute of Cardiovascular Medicine, 2 Department of Neurology, Victor stenosis of the right internal carotid and a 50-70%
Babes University of Medicine and Pharmacy, Timisoara, Romania
stenosis of the left internal carotid. The patient had
Correspondence to: no history of neurological symptoms or cerebral
Dr.Cristian Dina, Department of Invasive Cardiology, Institute of Cardiovascular vascular acute event. Carotid angiography confirmed
Medicine, 13A G. Adam Str., 300310 Timisoara, Romania, Tel: +40723532966, the presence and severity of bilateral obstructive
extracranial carotid disease. Based on lesion severity
the decision was made to treat only the right carotid
Received for publication: Mar. 16, 2006. Revised: Sep 12, 2006. artery.
176 TMJ 2006, Vol. 56, No. 2-3
After signing the informed consent the patient adequate intravascular volume. Blood pressure was
underwent endovascular angioplasty and stenting of controlled at about 140/80 mmHg.
the right common carotid bifurcation with a good
procedural result and uneventful post-procedural
evolution. Forty-eight hours after stenting the patient
was doing well and was discharged. The daily drug
regimen recommended at discharge included 75 mg
of aspirin, 75 mg of clopidogrel, 8 mg of perindopril,
12.5 mg of hydrochlorothiazide, 10 mg of felodipin
and 40 mg of simvastatin. Follow-up visits were
scheduled every three months and there was very good
compliance to antiplatelet, blood pressure lowering
and lipid lowering therapy.
One year after right carotid stenting doppler
examination diagnosed significant progression of the
left carotid lesion. The patient underwent a new carotid
angiography procedure that revealed very good patency
of the right carotid stent, (Fig. 1) with no restenosis,
but severe stenosis of the proximal segment of the left
internal carotid artery. (Fig. 2)
Figure 2. Severe lesion of the proximal segment of the left internal
The patient was taken to the Catheterization Lab.
An 8F sheath was inserted in the right femoral artery
and an intravenous heparin bolus of 5,000 units was
administered. An 8F Judkins Right guiding catheter was
positioned into the ostia of the right common carotid
artery. The lesion was crossed with a 6 mm cerebral
protection device (CPD) that was deployed in the right
internal carotid artery distal to the lesion. To prevent
bradycardia 1 mg of i.v. atropine was administered and
the lesion was then predilated using a 3 mm diameter
coronary balloon catheter. We stented the target
arterial segment with a 8 mm diameter, 40 mm long
self-expandable carotid stent and postdilated the stent
with a 5.5 mm diameter balloon catheter. There was a
15% residual stenosis that was considered acceptable
and the CPD was retrieved and inspected for debris.
(Fig. 3) Procedural time (filter deployment to filter
Figure 1. Angiographic image of the right carotid stent one year after
implantation; the stent is patent with minimal intimal hyperplasia. removal time) was 12 minutes. We performed the final
angiogram that revealed patency of the extracranial
The patient was scheduled for another endo- carotid artery and of its intracerebral branches and no
vascular carotid revascularization intervention. He evidence of spasm, dissection or thrombus.
was already on long-term aspirin, and clopidogrel was Severe hypotension occurred following stent
added three days prior to intervention. Intravenous postdilatation. Repeated boluses of ephedrine and
saline was administered over 24 hours to maintain intravenous dopamine were used to stabilize systolic
Cristian Dina et al 177
blood pressure at 120-140mmHg. The patient was pressure was normal. The onset signs suggested
then transferred from the Cath Lab to the Coronary intracranial hypertension but this could not have been
Care Unit. caused by the small hemorrhage detected on cerebral
CT image. The location of the small hyperdense image
was unusual for a primary intracerebral hemorrhage as
was the rapid improvement that followed.
Clinical status showed significant improvement
over the next hours with progressive remission of
neurological dysfunction. Next morning there was
almost complete recovery with only slight right
hemiparesis persisting. The patient was transferred
back to the Cardiology Department. Because of the
patient’s favorable evolution and of the very high risk
of stent thrombosis associated with antiplatelet drugs
discontinuation we decided to continue the combined
aspirine-clopidogrel therapy. After another 48 hours
there was complete resolution of symptoms and the
patient was discharged.
One month later cerebral CT imaging showed
complete resolution of the left frontal hematoma.
Follow-up was performed every three month. At
twelve month the patient was readmitted for a
complete evaluation. He was asymptomatic, there was
good control of his blood pressure and his plasma
cholesterol and triglycerides were within therapeutic
range. Echocardiography findings were unremarkable
and the stress test showed no signs of myocardial
Figure 3. Final result of left CAS; there is a 15% residual stenosis with no ischemia. Neurological status was normal. Carotid
angiographic evidence of dissection or thrombus. angiography documented very good patency of both
carotid stents with no signs of restenosis.
Postprocedural examination performed in the
CCU was unremarkable. Femoral arterial introducer dIscUssIon
was retrieved and hemostasis was achieved with a
compressive bandage. The ECG and blood pressure CAS is increasingly used for the treatment of
were monitored. Except for the procedural heparin carotid disease. It is less invasive than CEA, it offers
dose no additional dose was administered. excellent results in terms of acute and late patency
Four hours later patient status was altered by of the treated artery and it was proved to be at least
severe headaches and vomiting. He rapidly developed as safe and effective as surgery in stroke prevention.4
confusion, right hemiparesis and motor aphasia. Like CEA, CAS is associated with rare but significant
The ECG was normal, the blood pressure was complications.
120/70mmHg. The symptoms were suggestive of a One potentially lethal complication is the HPS, first
HPS complicating the revascularization procedure. The described by Sundt in 1981 after CEA and more recently
patient was immediately transferred to the Neurology observed during CAS.5 It occurs hours to days after the
Department of The County Hospital. procedure. It was initially believed to be caused by the
Initial neurological examination doccumented failure of normal cerebral autoregulation secondary to
pure motor right hemiparesis of medium intensity, long-standing changes in perfusion pressure but now
pyramidal signs, motor aphasia, and confusional it seems more likely that microembolic showers are the
status. CT imaging revealed a 1 cm diameter cortico- real cause of a true HPS.
subcortical left frontal hematoma. The ECG was Risk factors for HPS include critical carotid
normal and the blood pressure was stable. artery stenosis, critical or occlusive contralateral
Intraparenchymal hemorrhage secondary to carotid disease, decreased cerebral vascular
anticoagulant therapy was excluded. The blood reserve, periprocedural uncontrolled hypertension,
178 TMJ 2006, Vol. 56, No. 2-3
unprotected CAS, aggressive use of anticoagulants, recovery over the next 72 hours. After discharge the
use of IIb-IIIa inhibitors.6,7 Mortality rate is up to 80% evolution was very good. Within the next year there
in cases associated with ICH.8 was no neurological event and both stented segments
In our case the HPS occurred in atypical conditions. were patent.
No identifiable risk factor for this complication was
present. There was adequate periprocedural control conclUsIon
of blood pressure. The contralateral carotid lesion was
treated one year prior to the actual procedure and the Despite adequate case selection, optimal
stent was patent providing very good blood flow to the preprocedural patient preparation and good
brain. There was no aggressive use of antithrombotics. interventional technique CAS is not a risk-free
Seventy-five mg of aspirine and 75 mg of clopidogrel intervention. HPS can complicate CAS. It is an
were administered daily. Procedural heparin was unpredictable event and even good control of risk
restricted to an i.v. bolus of 5,000 units and there factors cannot always prevent it. Careful monitoring
was no additional dose of aspirin administered after of the patient in the first 24 hour after the procedure
the procedure. IIb-IIIa inhibitors were not an issue. is paramount for the rapid diagnosis of this condition.
There is no sound evidence of benefit with their use Although the mortality rates are high for patients with
during carotid interventions and we do not use them.9 associated HPS and ICH, full recovery is possible and
We always perform carotid stenting using cerebral is associated with good long-term outcome.
protection and this case was no exception. The short
procedural time makes cerebral embolization of rEfErEncEs
device related thrombus unlikely. Internal carotid
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Cristian Dina et al 179