Cerebral Flow and Perfusion Reserve Capacity in Hemodynamic Carotid Transient Ischemic Attacks Due to Innominate 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 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 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 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 (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 (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 —5 —3 0 0 —2 34F 0 8 0 6 5 0 1 patient did not present such a coexistent lesion. In a large A—3L0 —5—1 —1 —4—5 2 —2 series of 324 patients with subclavian steal phenomenon, 4FP 0 7 2 2 5 7 —1 —3 Hennerici et at. (4) reported only six patients with hemi A5L —5 —12—5 —6 —12—4 —7 —12 spheric symptoms due to innominate obstruction without —4P 6 14 7 7 15 5 9 15 A3L 1 —3 —3 —5 —4 —2 —1 2 carotid disease. The most common neurologic symptoms —1PC 0 5 4 6 5 4 2 —1 are related to vertebrobasilarinsufficiency (3,4,22,24,25). A1L —2 —1—1 3 —11 3 —2 —10 Hemiparesis, hemihypesthesia or monoparesisare rareand 00 3 2 2 —2 14 —1 3 13 usually explained by coexistent extra- or intracranialca A0L 6 —12 0 1 —10 0 —2 —8 0Interhemisphenc5 15 0 0 13 0 3 9 rotid artery occlusive disease (2,4,26) which was absent in our case. The neurological deficit, Doppler ultrasonogra phy and SPECT results were compatible with a focal isch +48 differences(%)calculatedineach ROlontheOM withacetazolamidemm,OM+ 60 mmand OM+ 72 mmsliceswithout(basal)and emia in the rightMCA territory.Despite a subclaviansteal, testing before (AZI)and after (AZ2)PCTA:PF = pre the blood flow in the basilararterywas normal. Moreover, frontal,F = frontal,FP = frontoparletal,P = parletal,P0 = parieto the absence of associated vertebrobasilar symptoms cx ocapital,0 = ocdpltal. cludes the likelihood of vertebrobasilarinsufficiencyto cx plain the pure motor deficit. Lacunar syndrome is unlikely in the absence of hypertension, diabetes mellitus or angio graphic findings of atherosclerotic disease of the basilar artery. The absence of floating thrombus and the repetitive ‘J.lAsin the same territory make a mechanism of emboli are given in Table 2. The other slices did not show any originatingfrom the innominate stenosis unlikely. The si significant interhemispheric differences for the three multaneous occurence ofTIAs and hypotensive lipothymia SPECT examinations. SPECT performed30 days afterthe is consistent with transient carotid hemodynamic insuffi last attack showed a mild but nonsignificant hypoperfusion ciency. Angiography, Doppler ultrasonography and SPECT

. in the right cortical frontoparietal area (Fig. 2A). On the with acetazolamide test showed reduced CBF in the right second SPECT examination, the acetazolamide test in carotid system. Grosset et at. (27) reported one patient in duced a CBF increase in the left cortical regions and en whom SPECF showed similarreduced hemisphericperfu hanced a more marked cortical hypoperfusion in the right sion ipsilateral to innominate occlusion. In our patient, only frontoparietal and parieto-occipital regions (Fig. 2B). SPECT with acetazolamide test showed hypoperfusion re Three days after angioplasty, SPECT with acetazolamide flectingan exhausted cerebrovascular reserve capacity in the test showed no significant asymmetry between either hemi rightMCAterritory.Indeed,the markedCBF increaseinthe sphere and was considered normal (Fig. 2C). left cortical regions without response in the right MCA

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1270 The Journal of NuclearMedicine•Vol.36 •No. 7 •July 1995 territoryenhanced the interhemisphericdifference with a 6. Grosveld WJHM, Lawson JA, Eikelboom BC, v.D. Windt JM, Ackerstaff right relative hypoperfusion. Acetazolamide stimulation of RGA.Clinicalandhemodynamicsignificanceof innominatearterylesions evaluatedby ultrasonographyand digitalangiography.Stroke1988;19:958— fers a simple and reliable method for assessing the cerebro 962. vascular reserve capacity in occlusive extracranial diseases 7. RautenbergW, HennericiM. Pulsed Doppler assessmentof innominate (17-21).Thesignificantrestrictionofcompensatoryvasodi artery obstructivediseases. 1988;19:1514—1520. 8. KlingelhoferJ, Conrad B, Benecke R, Frank B. TranscranialDoppler latationmakes the CBF directly dependenton blood pres ultrasonographyof the carotid.basilarcollateralcirculationin subclavian sure. In our patient, blood pressure monitoring revealed sev steal. Stroke 1989;19:1036—1043. era! periods of nocturnal and postprandial hypotension. We 9. Aaslid R. Transcranial Doppler ultrasound. New York, Springer Wien: 1986:57. hypothesize that some episodes of more severe hypotension 10. Franceschi C. L' investigation vasculaire par ultrasonographie Doppler. associated with tight innominate artery stenosis could be Paris:Masson;1979:35. responsible for worsening of pre-existing hemoclynamic in 11. Laloux P, Doat M, Brichant Ch, Cauwe F, JamartJ, Dc Coster P. Clinical sufficiency. Failure of autoregulation causing local hemi usefulness of@Fc-HMPAO SPECT imagingto map the ischemic lesion in acute stroke: a re.evaluation. Ce,@bmvasc DLc1994;4:280-286. spheric ischemia in the presence of a drop in systemic blood 12. PodrekaI, Suess E, GoldenbergG, et al. Initialexperiencewith ‘@“Fc pressure in regions of already disturbed circulation has been HMPAObrain SPECF.JNucl Med 1987;1657-1666. stressed by Hennenci et al. to explain hemispheric events 13. MorettiJL,Defer0, CinottiL,etat.Luxuryparfusionwith @Tc-HMPAO and‘@I-IMPSPECFimagingduringthe subacutephaseof stroke.EurI without coincidentalcarotidobstruction(4). NuciMed 1990;16:17-22. After PCTA, the flow velocities in the right extracranial 14. SteinlingM, MazingueA, KassiotisPh,GaudetY, FialdesP, DuhamelA, carotid and subclavian artery increased enough to DuboisP, VergnesR. La HMPAO @Fccommeindicateurdu debit san restore normal CBF and vascular reserve capacity in the gumcérébrallocal:étudequantilIéecomparéea la méthodepar inhalation au xénon-133.Ann Radiol 1988;31:229—238. MCA territory, which resulted in cessation of ischemic 15. Giubilei F, Lenzi GL, Di P1cmV, et al. Predictive value of brain perfusion attacks. This is also supported by the slight decrease of SPECFinacuteischemicstroke.Stroke1990;21:895-900. velocities in the left carotid arteries and MCA which likely 16. Hanson5K, GrortaJC, RhoadesH, Iran HD, LamkiLM, BarronBJ, Taylor WJ. Value of SPECF in acute stroke therapeutic trials. Stmke supplied the right MCA through collaterals before angio 1993;24:1322—1329. plasty. Similar restoration of blood flow has also been well 17. KassiotisP, SteinlingM. I.e debitsanguincérébrallocalCtsa réactivitéa documented by Doppler and SPEC!' studies after carotid l'acétazolamidedansles accidentsischémiquestransitomis.Etudede 20cas par tomographiegamma.RevNeurol (Pwis) 1987;12:806—813. artery endarterectomy (28). 18. PiepgrasA, SchmiedekP. LeinsingerG, HaberlRL,KirschCM,Einhhupl Thus, in patients with innominate artery stenosis with KM. A simple test to assesscerebrovascularreservecapacity using trans. out coexistent carotid occlusive lesion, HMPAO-SPECF cranialDopplersonographyand acetazolamide.Stmke 1990;21:1306-1311. 19. 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