Cerebral Blood Flow and Perfusion Reserve Capacity in Hemodynamic Carotid Transient Ischemic Attacks Due to Innominate Artery Stenosis
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Cerebral Blood Flow and Perfusion Reserve Capacity in Hemodynamic Carotid Transient Ischemic Attacks Due to Innominate Artery Stenosis Patrice Laloux, Fabienne Richelle, Hubert Meurice and Patrick Dc Coster University ofLouvain School ofMedicine and Depanmentc ofNeurolo@ and Nuclear Medicine, Mont-Godinne University Hospita!@Yvoir, Belgium CASE REPORT Ischemia in the carotid artery territorydue to atherosclerotic A 43-yr-oldmanwitha historyof alcoholandtobaccoaddic stenosis of the innominateartery is rare. We report a case in tions developed acute lipothymiaand weakness in the left upper whichtranscranialDopplerultrasonography(TCD)and SPECT andlowerlimblastingfor5 min.He didnot complainof head withacetazolamidechallengeprovedthe hemOdynamiCmech achesandhadno alterationof consciousnessordisorientationin anism.ThepatientpresentedwiththreehypotenalveTL4@sinthe time and space. The attack occured 1 hr after lunch. On admis nghtmiddlecerebralarteryterritory.Angiographyshowed a tight sion, neurologicaland neuropsychologicalexaminations were innominateartery stenosis and subdavisn steal but no coedst normal. General examination revealed a right cervical bruit. antcarotidorvertebrobasilarlesion.SPECTshowed disturbed Bloodpressurewas 110170mmHgon the left. Informationabout regionalbloodflowinthe middlecerebralarteryteffitoryalong radial and brachial pulseswas unavailable at this time. Laboratozy withan exhaustedperfusionreservecapacity.Afterangioplasty, tests disclosed an increased rate of LDL cholesterol (170 mg/dl). flowvelocitieswere normaland the perfusionreservewas re Brain CT with contrast was normal. Electrocardiogram(ECG), stored. SPECT should be used to select patientsat risksuscep ambulatory24-hrECG and transthoracic/transesophagealecho tibleto benefitfromangioplasty. cardiographywere normal.CeiViCaIDopplerultrasoundwas like KeyWords: innominatearterystenosis;transientischemicat wise normal. The patient was then discharged without any treat tack;single-photonemissioncomputedtomography;ultrasound ment. Fivemonthslater,thepatientsufferedtwoadditionaltransient J Nuci Md 1995; 36:1268—1271 attacks of left brachiocruralparesis and lipothymialasting for 3 and5 min, respectively, without anyothersymptoms. The attacks were not precipitated by exercise, change of head position or sudden rising from a seated position. The first attack occurred theroscieroticocclusion or stenosis of the innominate whenthepatientwas atrest1hrafterbreakfastandthesecond2 artery is rare. In the Joint Study of Extracranial Arterial hr afterlunch.He was admittedto our department4 wk later. Neurologicaland neuropsychologicalexaminationswere normal. Occlusions (1), frequencies were 0.6% and 4.2%, respec Generalexaminationshowedno rightradialandbrachialpulses tively. These lesions may be asymptomatic or cause isch without ischemic syndrome in the upper limb. A bruit was heard emic syndrome in the right upper limb, vertebrobasilar in the rightsupraclavicularfossa. Blood pressurewas 120/80 system and, less frequently, in the carotid arteiy territory mmHg on the left. Blood pressure monitoring revealed several in the absence of coexistent carotid disease (2—4).Al episodesofnocturnalandpostprandialhypotensiondownto 80/50 though embolic originhas been reportedin some cases (5), mmHg. Fundoscopic examination was normal. Laboratory tests the mechanism of neurologic deficit is commonly hemody disclosed a high rate of LDL cholesterol (167 mg/dl). Brain CF namic (6,7). We report a patient in whom SPECT images was normal. After angiographic demonstration of a tight stenosis with acetazolamide challenge and transcranialDoppler ul of the innominateartery,percutaneoustransluminalangioplasty trasonography(TCD) supported the hypothesis of transient (PCFA) was successfully performed 6 days after admission with carotid hemodynamic insufficiency. Percutaneous translu outcomplication.Transientischemicattacksdidnotrecurovera follow-upperiodof 12mo. minal angioplasty of the innominate artery improved cere bralperfusion. METhODS Doppler Ultrasonography ReceivedJuL8, 1994;revisionaccepted Nov.1, 1994. Forcorrespondencecr reprintscon@ P. Laloux@MD,Depab@ientofNeurol Cervical and TCD ultrasonographywere performedwith an ogy,Mont-GodinneUniversityHospital,B-5530Yvoir,Belgium. EME TC2000 transcranial ultrasound system with a 2-MHz probe 1268 TheJournalof NuclearMedicine•Vol.36 •No. 7 •July1995 (Uberlingen,Germany).The systolicvelocitieswere recorded A accordingtostandardtechniquesforextracranialinternalcarotid, B subclavian, vertebrobasilar and intracranial vessels (8,9) and compared with normal values (9,10). For the ophthalmic and vertebralarteries, the patient served as his own controlbecause the velocities are dependent on the insonation angle and the re corded segment of the artery. Brachial artery compression and release tests could not be obtained to seek a flow reversal of the vertebral artery recorded. Hypotensive provocative tests were not carriedout for ethical reasons. SPECT Evaluation of Cerebral PerfUsiOn Regionalcerebralbloodflow(rCBF)was measuredby brain SPEC!'afterthe intravenousinjectionof 20 mCi (740 MBq) @Tc-HMPAOunderrestingconditionswitheyesopenin a dim, quietroom.Acquisitionwascarriedout10—30mmafterinjection of thetracerwitha single-headrotatinggammacamera(General Electric, Milwaukee, WI) and a standard low-energy, high-reso lutioncollimatorusing64projectionsof 30sec each.Thematrix rIGURE 1. @cangiogramshowsatightsteno&sc@einnom@ sizewas 64 x 64pixels(pixelsize6 mm).The raw datawere first nate artery(A@and Itspartialremovalafterangiopissty(B). compressed to permitreconstructionofeight consecutive parallel axial slices every 12 mm parallel to and above the orbitomeatal line. By contrast, flow velocities were increased in the left MCA Filteredbackprojectionwith linearlizationwas performedfor and vertebral artery (VA) (Table 1). The flow in the right data reconstruction using a Shepp-Loganfilter (with Hanning VA was anterogradeand so reduced that precise calcula window)which is a modifiedversion of the ramp filter.Because tion of flow velocity was impossible. Two days after an attenuation is only mild in the cerebral cortical areas studied, gioplasty, flow velocities, though remainingabnormal, in correctionof scatter and attenuationwas not used. Furthermore, creased in the right subclavian artery and ICA and were the semiquantitative analysis used in this study makes ratios of normal in the CCA, MCA, OA and VA. Moreover, the counts not affected by such a method. Visual and semiquantitative analysiswere performed.FourteensymmetricalROIs (3 x 3 velocities increased in the basilar artery and decreased pixels) were automaticallylocated on the cortical ribbon, four in within the normal range in the left CCA, ICA, MCA and the anterior,middle, and posteriorhemisphericareas and one in VA. Therefore, angioplasty restored normal intracranial each cerebellar hemispherewith a computerizedprogramdevel flow (Table 1). o_ inourlaboratory(11).Thus,theROIscoveredtheprefron All data for the ROIs on the OM + 48 mm, OM +60mm tal, frontal,frontoparietal,parietal,parieto-occipitalandoccipital andOM + 72 mm slices before and afterPCTA in the right regions.Becauseofthe poorspatialresolutionofthe device,ROIs symptomatic and left asymptomatic cerebral hemisphere were not placedin subcorticalregions.In eachROI,the differ ences in total count were expressed as a percentageof the values fromthe symmetricalROl in the contralateralhemisphere(12— TABLE 1 16). Interhemispheric difference (IHD) of at least 10% was con Doppler Ultrasonography Data before and after PCTA sidered to be significant (1Z13,16). To assess cerebrovascular (cn@sec)NormalBeforeAfterArtery reservecapacity,acetazolamide(1g)was givenintravenously10 mm before the SPEC!' examination in accordance with the DepthS@cveloolty methodused in previousstudies(17—21).Stimulationswere per (mm)valuesPCTAPCTA formedbefore (All) and after (AZ2)angioplasty. R 70-90355018518070—1003680706089±23314590605294±23559552140 L RESULTS R Cerebral arterial angiography demonstrated a tight ste L R nosis of the innominate artery without floating thrombus as LICA well as a retrogradeflow in the rightvertebral artery and R slow flow in the right internal carotid artery (Fig. 1A). LMCA There was no extracranialor intracranialcarotid or verte R 20 35 brobasilaratheroscleroticdisease. AfterPCFA, the innomi L OA 3870—9070220909664±137010050100 A VA nate artery's tight stenosis was removed, but the residual L VA lumen was estimated to be narrowed by one-third (Fig. BA 1B). Cervical Doppler ultrasound and TCD demonstrated re PCTA = percutaneous transluminal angloplasty CCA = common duced flow velocities in the right subclavian artery, com carotid artery; ICA = Internal carotid artery@MCA = middle cerebral mon carotid artery (CCA), internal carotid artery (ICA), artery OA = ophthalmicarter@VA = vertebral artery@BA = baadar middle cerebral artery (MCA) and ophthalmic artery (OA). art@y. CBFand PerfusionReserveinTransientIschemicAttacks•Lalouxat at. I269 TABLE 2 DISCUSSION InterhemisphericDifferencesin the RightSymptomaticand LeftAsymptomaticCerebral Hemispheres Innominatearterystenotic lesions are commonly athero sclerotic and predominate in the initial third of the artery cmAOl OM + 48 cmOM + 60 cmOM + 72 (2). Although all series of patients with innominate artery Side BasalAZIAZ2BasalAZ1AZ2BasalAZ1AZ2 atherostenosis have mentioned a high frequency of coinci dental carotid and vertebral artery disease (1,4,22,23), our PF R—3L 1 —6 0