HypErpErfUsIon syndroME coMplIcatIng ExtracranIal carotId artEry

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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 att dup\
endarterectomia carotidian\, ct [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, ct [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
Fax: +40256207491
                                                                                     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
                                                                         carotid artery.

                                                                              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
                                                             1. Ascher E, Markevich N, Schutzer RW, et al. Cerebral hyperperfusion
artery showed no evidence of spasm at the place of                  syndrome after carotid endarterectomy: predictive factors and
CPD deployment and there was no local intraarterial                 hemodynamic changes. J Vasc Surg 2003;37:769-77.
                                                             2. Meyers PM, Higashida RT, Phatouros CC, et al. Cerebral hyperperfusion
administration of vasodilators. Moreover, the patient
                                                                    syndrome after percutaneous transluminal stenting of the
had a previous uncomplicated contralateral carotid                  craniocervical arteries. Neurosurgery. 2000;47:335-43.
revascularization procedure, suggesting good cerebral        3. Willis HW, David VC, Alik F, et al. Hyperperfusion syndrome after
                                                                    carotid endarterectomy. Ann Vasc Surg 2005;19:479-86.
vascular reserve.
                                                             4. Yadav JS, Wholey MH, Kuntz RE, et al. Protected carotid-artery
      There was no accident or complication during                  stenting versus endarterectomy in high-risk patients. N Engl J Med
angioplasty of the left carotid artery, the final                   2004;351:1493-501.
angiographic result was very good and the patient was        5. Sundt TM, Sharbrough FW, Piepgras DG, et al. Correlation of
                                                                    cerebral blood flow and electroencephalographic changes during
asymptomatic. Four hours later he developed severe                  endarterectomy with results of surgery and hemodynamics of
deterioration and based on the neurological findings                cerebral ischemia. Mayo Clin Proc 1981;56:533-43.
and cerebral CT images an HPS with associated ICH            6. Henderson RD, Phan TG, Piepgras DG, et al. Mechanisms of
                                                                    intracerebral hemorrhage after carotid endarterectomy. J Neurosurg
was diagnosed. Despite the use of a filter-type CPD                 2001;95:964-9.
it is possible that small embolic particles embolized        7. Ogasawara K, Yukawa H, Kobayashi M, et al. Prediction and monitoring
through the 100μ pores of the filter membrane. Post                 of cerebral hyperperfusion after carotid endarterectomy by using
                                                                    single-photon emission computerized tomography scanning. J
CAS diffusion-weighted MR imaging demonstrated                      Neurosurg 2003;99(3):504-10.
that CPD are not fully protective, embolization              8. Piepgras DG, Morgan MK, Sundt TM Jr., et al. Intracerebral hemorrhage
do occur and produce new small lesions.10 These                     after carotid endarterectomy. J Neurosurg. 1988;68:532-6.
                                                             9. Qureshi Al, Saad M, Zaidat OO, et al. Intracerebral hemorrhages
microembolic events are asymptomatic in most of the                 associated with neurointerventional procedures using a combination
cases. On rare occasions they can initiate a HPS, and it            of antithrombotic agents including abciximab. Stroke 2002;33:1916-9.
is likely that this happened in our patient.                 10. Du Mesnil De Rochemont R, Schneider S, Yan B, et al. Diffusion-
                                                                    weighted MR imaging lesions after filter-protected stenting of
      Although ICH associated to HPS carries a high                 high-grade symptomatic carotid artery stenosis. Am J Neuroradiol
mortality risk, the patiend had a fast and complete                 2006;27(6)1321-5.

                                                                                                             Cristian Dina et al   179

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