972

The Rationale For Patch-Graft Angioplasty After CarotidEndarterectomy: Early and Long-Term Follow-Up

GIOVANNI P. DERIU, M.D. , ENZO BALLOTTA, M . D . , LUIGI BONAVINA, M.D.

FRANCO GREGO, M . D . , SIMONETTA ALVINO, M.D. , LORENZA FRANCESCHI, M.D. ,

GIORGIO MENEGHETTI, M.D. ,* AND ALDO SAIA, M.D.*

SUMMARY A prospective study was undertaken in March 1980, at the Vascular Surgery Department ofthe Padua University, Medical School, to establish whether patch graft angioplasty is useful in preventingrestenosls after carotid endarterectomy (CE). Seventy-four patients underwent 86 CE (bilateral in 12 cases)for atherosclerotic disease involving the carotid bifurcation. Thirty-eight (51.4%) patients presented TIA'sor non hemispheric symptoms of cerebrovascular insufficiency; 30 (40.5%) were asymptomatic and 6(8.1 %) had partial nonprogressing or fixed strokes. All operations were performed under general anesthe-sia, with pharmacologic hypertension and systemic heparinization; in all cases, continuous EEG monitor-ing and 'stump pressure' measurement were employed. The operation was performed without a temporaryintraluminal shunt in the patients showing tolerance to carotid clamping. The protection of the shunt wasrequired only in patients with EEG monitoring changes (17). All carotid arteriotomies were extended intothe internal carotid artery to overpass the end of the endarterectomy. Overpass was also used in theproximal edge of the arterlotomy, in the common carotid artery. The distal intima was never fixed withstitches and the arteriotomy was routinely closed with a PTFE patch graft angioplasty. Early results ofcerebral protection were excellent. No patient presented permanent or transient postoperative neurologicalproblems and no patient died in the postoperative period for causes related to the operation. This issubstantiated by results we achieved during the period 1970-1979 in 192 patients, when all carotid endar-terectomies were routinely performed without a shunt, with figures of 2.5% of postoperative stroke and1.5% of mortality.

Longterm follow-up (from 6 to 36 months) was completed in 51 patients (60 operations). All patients wereclinically evaluated and tested for patency of the endarterectomized vessel and the contralateral carotidartery by means of c.w. Dopplersonography and, occasionally, by Duplex scanning. Patency of the endarter-ectomized carotid artery with absence of hemodynamically significant lesions was well detected in all cases.There were 4 late deaths unrelated to cerebrovascular insufficiency. Two patients showed a neurologicdeficit. They were investigated with carotidography: both presented intracranial lesions. The absence ofcarotid restenosis, documented with noninvasive cerebrovascular testing, confirms that the closure withpatching effectively delays and prevents this complication by means of a mechanism related to the compen-sation of the volumetrical increase either of the new atherosclerotic plaque or neointimal hyperplasia. Theauthors believe that-direct closure of the vessel is the primary cause of recurrent stenosis and thereforerecommend routine patch graft angioplasty after carotid endarterectomy.

Stroke Vol 15, No 6, 1984

CAROTID ENDARTERECTOMY (CE) is an effec-tive and relatively safe procedure for the treatment ofatherosclerotic disease involving carotid bifurcation.In the period immediately after operation during carot-id clamping, either technical errors (such as residualintimal flap, suture stenosis or shunt-induced trauma)or the temporary interruption of blood flow, may occa-sionally cause transient and permanent neurologicaldeficits or fatal strokes.

Although an intraluminal shunt (IS) may be usedroutinely,1"3 many find it an awkward method to ensureadequate cerebral perfusion during carotid crossclamping. Moreover, this procedure gives a higherpercentage of cerebral strokes for purely technical rea-sons (intimal dissection, embolism, poor blood flow,traumatization and shunt flexion).

Therefore, there is a tendency toward selectiveplacement of an IS in patients who cannot tolerate

From the Department of Vascular Surgery,* and the Institute ofNeurological Clinic, University of Padua, School of Medicine, Padua,Italy.

Address correspondence to: Prof. Giovanni P. Deriu, Chief, Depart-ment of Vascular Surgery, University of Padua, Via Giustiniani, 235100 Padova, Italy.

Received December 3, 1983; revision #1 accepted July 27, 1984.

carotid clamping.4 We have selected patients based onthe following: continuous intraoperative EEG monitor-ing and 'stump pressure' measurement. However, re-stenosis of the endarterectomized segment constitutesa late complication of the CE.5"19 Most, but not all, ofthese recurrent lesions have no clinical significance.This report describes our surgical experience with theperformance of the CE routinely closed with patchingto delay and prevent recurrent carotid stenosis.

Material and Methods

From March 1980 to July 1983 at the Department ofVascular Surgery of Padua University, MedicalSchool, 74 patients underwent 86 CE (bilateral in 12cases) for atherosclerotic disease involving carotidbifurcation with the routine use of continuous intra-operative EEG monitoring and stump pressuremeasurement.

The decision for surgery in each case was based onthe parameters summarized in table 1, which explainsthe factors indicating the need for CE. The preoper-ative symptoms in 74 patients were as follows: TIAs ornonhemispheric symptoms (38 cases); fixed or partialnonprogressing strokes (6) and 30 cases of asymptom-

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PATCH-GRAFT ANGIOPLASTY AFTER CAROTID ENDARTERECTOMY/Denu et al 973

TABLE 1 Indications and Contraindications for Carotid Endar-terectomy

A) Indications:

1) Transient ischemic attacks (TTA's) or other symptoms of ce-rebrovascular insufficiency (stenosis greater than 75% andless than 75%);

2) Asymptomatic patients (stenosis > 75%);

3) Asymptomatic patients (stenosis < 75% with angiographicfeature of ulcerated plaque);

4) Asymptomatic patients (stenosis > 50% and complete occlu-sion of contralateral carotid artery);

5) Asymptomatic patients (bilateral stenoses > 50%).

B) Contraindications:

1) Technical reasons: complete occlusion of internal carotid ar-tery;

2) Acute stroke;

3) Chronic stroke with fixed severe neurological deficit;

4) Biological age;

5) Severe psychic impairment.

atic patients. There were 61 males, aged from 40 to 77years (mean age: 62) and 13 females, aged from 42 to78 (mean age: 56).

All patients underwent preoperative arteriography(bilateral carotid arteripgrams with serial films of thehead and neck showing intracranial and extracranialvessels in both anteroposterior and lateral planes andangiography of the aortic arch, in the presence of clini-cal findings of insufficiency of the supraaortic trunks).They were studied with EEG and bidirectional con-tinuous-wave (C.W.) Doppler ultrasound device, theday before the operation. C.C.T. (computerized cere-bral topography) was performed in alj cases with clini-cal findings of previous cerebral infarction or partialnonprogressing stroke. In 10 cases CCT was per-formed pre and postoperatively in order to find anyabnormalities due to carotid clamping.

All the operations were performed by the seniorauthor (GPD) and under genera) anesthesia (neurolept-anajgesia) which does not interfere with EEG interpre-tation; inhalant anesthetics were never employed.

The EEGs were recorded on 8 channel SiemensElema® electroencephalograph and performed duringsurgery.

Needle electrodes were placed over frontal-temporaland occipital regions, according to the international 0 -20 system, in bipolar derivation. The systemic bloodpressure was continuously recorded by a pressuretransducer attached to a catheter in the radial artery,and one channel was used to monitor the EKG.

When necessary, two different kinds of shunt wereused: a T-sh,aped carotid shunt and, during the lastperiod of the series, a T-balloon shunt.

Ten days after the operation, all patients were exam-ined by C.W. Dopple'rsonography. Follow-up studieswere performed on all patients.

Information concerning the occurrence of new neu-rological symptoms during the years of follow-up andthe patency of the endarterectqmized vessel were ob-

tained by means of clinical examination, of C.W.Dopplersonography20 (fig. 1) and, occasionally bymeans of Duplex scanning with spectral analysis. Allthe operated patients in which a new neurologicalsymptomatology appeared underwent a new carotido-graphy.

Operative TechniqueThe carotid bifurcation is dissected without block-

ing or cutting the carotid body. Immediately beforeclamping, the systemic blood pressure is increased to180-200 mm Hg with metaraminol and systemic hep-arinization is always used. After carotid crossclamp-ing, the stump pressure is always measured below thestenosis, at the level of the internal carotid artery. Thearteriotomy from the common carotid artery is ex-tended into the internal carotid artery beyond the distaledge of the plaque, so that its upper end is clearlyvisualized and the distal intima easily controlled.

CE is performed using a standard vascular surgerytechnique with particujar attention to removal of theentire plaque and avoidance of intimal flaps.21 Thearteriotomy closure technique for the following rea-sons always includes a PTFE (Gore-tex®) patch graftangioplasty21 " with continuous over-and-over 5-0polypropylene monofilament (PROLENE) suture: 1)the suture is easier (prevention of immediate technicalerrors); 2) the suture is facilitated when an IS is insert-ed; it is interesting to note that the IS constitutes anobvious obstacle in the performance of the distal sutureline when the arteriotomy is extended into the internalartery and it does not end at the bulb, especially if theinternal carotid artery diameter is small; 3) early re-stenosis at the suture line can be avoided if edges of thearteriotomy are indented; 4) arterial lumen is enlarged,thus preventing recurrent stenosis due either to myoin-timal hyperplasia or new atherosclerotic plaque or,finally, scar retraction of the suture line.

Overpass criterion can avoid a new stenosis at thedistal edge of the arteriotomy. Therefore, closure with-out patching leads to an incidence of recurrent carotidstenosis in cases in which the arteriotomy ends at thebulb. The percentage would be higher if one employedthe personal technique to prolong the arteriotomy be-yond the distal edge of the plaque, in order to assuredistal intima control. The overpass is routinely em-ployed proximally, at the level of the common carotidartery. Distal intima is never fixed with interrupted orrunning sutures.

ResultsIn 69 CEs, normal intraoperative EEG monitoring

allowed the performance of the operation without pro-tection of an IS. EEG abnormalities during carotidcrossclamping appeared in 17 cases. In these patients atemporary IS was inserted selectively. Three of thesepatients had EEGs consistent with ischemia despite astump pressure greater than 50 mm Hg (table 2). In 16patients EEG changes appeared within 20 and 60 sec-onds after clamping; in 1 patient after 20 minutes.

EEG criteria for placing an IS were as follows: 1)

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974 STROKE VOL 15, No 6, NOVEMBER-DECEMBER 1984

>O»TOPE««TI v t

* * * . PROXt M AL

INTERNAL

CAROTIDARTERY

FIGURE 1. Pre and postoperative continu-ous-wave Doppler ultrasound device. At thelevel of the proximal internal carotid artery,preoperative c.w. Dopplersonography (left)shows a "turbulence" consistent with hemo-dynamicalfy significant stenosis. The turbu-lence disappears after carotid endarterectomywhen normal blood flow is restored (right).

generalized bilateral slow-wave activity (5 cases); 2)ipsilateral slow-wave activity (9 cases); 3) ipsilateralslow-wave activity with suppression of fast-wave ac-tivity (3). Contralateral slow-wave activity never oc-curred. All 17 patients reverted to baseline after shuntinsertion. In 1 patient the EEG abnormalities (bilateralslow-wave activity) appeared after the placement ofthe needle electrodes and indicated a need to replacethe head. EEG changes immediately disappeared.

Lesions of the contralateral internal carotid arterywere present in 55 (74%) patients; in the patients bi-laterally operated, the first operated side was consid-ered normal. All 17 patients requiring IS protectionpresented contralateral internal carotid artery lesions(table 3).

None of the 74 patients, whether operated with se-lective use of the IS (17) or without shunt (57) devel-oped transient or permanent neurological deficits. Nopatient died in the postoperative period for causes re-lated to the operation.

TABLE 2 Total Series (86 carotid endartercctomies): EEG Moni-toring and Stump Pressure Values

Stump pressure> 50 mm Hg

Stump pressure< 50 mm Hg

Normal EEG

Ischemic EEG

693*

These data can be compared to case-control patients(192) who had undergone CE (204) performed by thesame author from 1970 to 1979. In these patients CEwas routinely carried out without IS protection and thearteriotomy was closed with patching,23 with figures of2.5% of neurological deficits and 1.5% of earlymortality.

In the immediate postoperative period, all patientswere reassessed with EEG and C.W. Dopplersonog-raphy: in all cases the success of the operation wasamply tested. Longterm follow-up (from 6 to 36months) was done in 51 patients (60 CE). All patientsof this series were questioned with regard to any post-operative symptoms. Eight patients were unwilling toattend for review, but their general practitioner statedthat they did not suffer with any postoperative neuro-

TABLE 3 Contralateral Internal Carotid Artery Degree of Steno-sis Compared with Intraluminal Shunt Necessity

Degree of stenosisby arteriography (%) No. patients IS use

*Only in these patients the IS was selectively inserted.

Thrombosis> 90

75-90

50-75

10-50

0

14

*

10

10

17

19

9

1

1ff

10

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PATCH-GRAFT ANGIOPLASTY AFTER CAROTID ENDARTERECTOMY/D«nu et al 975

FIGURE 2. Left, internal carotid artery Duplex scanning 36 months after endarterectomy and,right, corresponding control arteriography. Duplex scanning (A is the internal carotid arterycovered by the patch, B the end of the patch and C the distal internal carotid artery) shows thepatency of the vessel and the absence of restenosis; angiography confirms this datum.

logical symptoms; two patients had moved from thearea but also remained well. Since the absence of post-operative symptoms is no guarantee of vessel patency,all patients were also evaluated for patency of the en-darterectomized carotid and the contralateral artery bymeans of C.W. Dopplersonography.9 M Duplex scan-ning was occasionally employed.

All patients in whom neurological symptoms ap-peared or in whom there was evidence of contralateralunoperated carotid artery progressive disease under-went a new carotid angiogram.

There were 4 late deaths. Causes were as follows:myocardial infarcion (2); intestinal infarction (1) andcerebral hemorrhage (1). Two years after operation,one patient suffered a transient ischemic episode ipsi-lateral to endarterectomized carotid. C.W. Doppler-sonography tested the complete patency of the vesseloperated. A new carotidography confirmed this databut it also revealed a carotid siphon stenosis and thecomplete occlusion of several intracranial vessels. Oneyear after CE, another patient suffered a minor strokeinvolving the cerebral hemisphere ipsilateral to theendarterectomized vessel. C.W. Dopplersonographyand the control angiogram confirmed the patency ofthe carotid artery operated. This patient presented aconcomitant carotid siphon stenosis with lumen reduc-tion of about 70%. None of remaining patients dis-played temporary or prolonged neurological problemsand all symptomatic patients showed complete remis-sion of symptoms.

Patency of the endarterectomized carotid artery withabsence of hemodynamically significant lesions waswell detected in all cases (fig. 2). No pseudoaneurysmdeveloped; and no patch infection occurred.

DiscussionThe risk of cerebral stroke following carotid cross-

clamping is always present during carotid endarterec-tomy. Continuous intraoperative EEG monitoringidentified those patients who could not tolerate carotidclamping because of an inadequate collateral cerebralperfusion. In this group alone the protection of anindwelling shunt is required. The selective use of thisprocedure has eliminated the possibility of permanentneurological deficits in a very high percentage of pa-tients undergoing CE, limiting the potential appear-ance of complications to the small group in whichshunt protection is required.

Sundt* showed that four groups of EEG changes canbe identified related to different times of ischemia ca-pable of producing irreversible cerebral lesions (4-5minutes; 8-10 minutes; 15-16 minutes and, finally,20-22 minutes).

It is evident that not all patients with EEG changeswould have suffered cerebral stroke or neurologicaldeficits if IS had not been inserted. In fact, in most

*ln discussion at XHIth World Congress of the International Union ofAngiology; Rochester, Minnesota, U.S.A. Sept. 1983.

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976 STROKE VOL 15, No 6, NOVEMBER-DECEMBER 1984

patients the cerebral blood flow following carotid en-darterectomy had been restored in sufficient time forpreventing cerebral lesions due to ischemia after carot-id clamping. The remaining patients with EEGchanges consistent with cerebral ischemia, would havepresented neurological problems during and after sur-gery. It would be hypothetical to -prognosticate theresults of eliminating a shunt, or the duration of theprocedure and clamping. The shunt was inserted in allpatients with EEG changes, to minimize the possibilityof risk of cerebral infarctioh.

The success of this method is corroborated by com-parison with those results achieved during the periodfrom 1970 to 1979, when all CEs were routinely per-formed without IS protection, relying on CE and rapidpatch procedure (12-15 minutes of carotid cross-clamping, in the first series vs. 30-45 minutes in thelatter series).21-23

On the grounds of excellent results achieved in thelatter series, confirming the findings of other authors,we can say that this method is effective and draw thefollowing conclusions: 1) On the basis of EEG abnor-malities requiring IS protection, carotid cross clamp-ing could cause cerebral stroke or neurological deficitsin a percentage of 17 patients; 2) EEG changes normal-ly appear immediately after clamping, but the possibil-ity that this occurs also after 20 minutes must be kept inmind and it is the reason for continuous EEG monitor-ing; 3) In a very high percentage of cases, EEGchanges consistent with cerebral ischemia appear inthe presence of occlusion of the opposite carotid artery;4) Stump pressure alone is not reliable in 100% ofcases, as demonstrated by personal observation ofthree patients with stump pressure greater than 50 mmHg despite EEG abnormalities suggesting cerebralischemia4; 5) Prejudice against CE in asymptomaticpatients is unjustified in view of harmlessness of theoperation. Therefore, regardless of very tight carotidartery stenosis, the indication for surgery is also justi-fied in hemodyhamically significant lesions. An exam-ple is lesions with a degree of lurnen stenosis of about75%. In fact, because the natural anatomical history ofcarotid lesions is complete occlusion in spite of clinicalfindings which characterize it (from asymptomaticthrombosis to complete stroke), the indication for sur-gery is valid since contralateral internal carotid arteryis also involved in 80%24 " and potentially in 100% ofcases. Therefore, during increasing stenosis on oneside, the situation will be different depending uponwhether the opposite carotid is occltided because ofatherosclerotic disease, or patent, due to previous en-darterectomy. In the present series, the contralateralunoperated carotid artery showed a progression of thedisease in two cases: one asymptomatic complete oc-clusion and one progression of the stenosis.

The possibility of recurrent carotid stenosis has beendocumented by several authors,5"19 although theincidence varies from 0.6 to 19 percent, dependingupon the method employed for the postoperative fol-low-up. Restenosis is probably more common thanrecognized because it may remain undetected until

neurological symptoms develop and until prompt clini-cal investigation.

Technical factors have been suggested by some au-thors as a major cause of postoperative carotid steno-sis. Vascular clamp injury, incomplete removal ofplaques, intimal flaps, suturing faults — all may con-tribute to the formation of stenotic lesions which, inthe majority of cases, are localized at the carotid bulb,but which also are located at, or just beyond, the proxi-mal or distal suture line. Further, it is possible thatsome proximal or distal recurrences are secondary toatherogenesis provoked by intimal damage caused byvascular clamps. In this regard, it is important to em-phasize how there is not only one standard techniquefor CE, but this surgical procedure is performed inmany different technical ways, depending upon thedetails reported in table 4.

No author has attached any importance to the pres-ence or absence of an enlarging patch graft. Stoney andString5 report that in all 29 patients of their series theoriginal arteriotomy had been closed without patching.Cossman and Callow* noted that of the nine arteriesthat became restenotic, eight had been closed withoutpatching at the original operation. A pseudoaneurysmalong with restenosis developed in a patient whosearteriotomy had been closed with a vein patch graft atthe original operation. In the Hertzer's series,7 16 of1252 patients undergoing CE presented a recurrentstenosis; in these patients primary closure had beenperformed without patching. Cossman and his associ-

TABLE 4. Carotid Endarterectomy Procedure: the SurgicalTechnique is Performed in Many Different Ways, Depending uponthe Combination of the Following Technical Details

1) Arteriotomy prolonged into theinternal carotid artery

2) Proximal overpass

3) Distal overpass

4) Distal intima fixed with stitches

5) Direct closure of arteriotomy

6) Routine patch graft (vein or PTFE)angioplasty

7) Dissection plane of the plaque:

8) "Peeling" (removal of medialfragments)

Yes*

No

. Subintimal*• Intramedial*" Subadventitial*" Change of planes*

Yes*

No

•Personal surgical technique of carotid endarterectomy.

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PATCH-GRAFT ANGIOPLASTY AFTER CAROTID ENDARTERECTOMY/Denu et al 977

ates8 present a series of 16 arteries in 14 patients withrecurrent stenosis: primary closure of the internal ca-rotid artery had been performed without patch graftangioplasty. In the Terpstra's experience," 11 of 159endarterectomized carotid arteries presented a late re-stenosis; in this series, patch graft angioplasty neverbut once had been employed. Clagett and his associ-ates12 have reported there was no significant differencein the incidence of hypertension, diabetes mellitus,

FIGURE 3. This histologic specimen concerns a patient, 62years old, who underwent a left CE and PTFE patching for avery tight stenosis, in January 1978. After 1 week, the samepatient underwent afemoropopliteal bypass for a femoropopli-teal complete occlusion with gangrena at the 1st, 2nd and 3rdtoes. He felt very well until February 1, 1982, when he wasadmitted to the Medicine Clinic of the University of Padua formassive myocardial infarction. On the following day he died.At autopsy, the operated carotid artery was excised. The exter-nal surface was dissected to expose the patch. The commoncarotid artery (c.c.a.) was then opened longitudinally with theincision line running along the posterior wall, opposite to thepatch (arrows) and was comprehensive of the internal carotidartery. The external carotid artery was then opened from theostium. Macroscopic examination showed a very bright surfaceof contiguous arterial tract corresponding to the endarterec-tomized tract and to the patch. This segment had not undergonesurgical manipulation, except for a small tract of commonartery in which traumatism due to autoptic technique remotionwas evident (•). The vessel was patent and there was nostenosis.

coronary artery disease, other vascular operations orfamily history for atherosclerosis in patients with re-current stenosis compared to control patients. The re-port, however, underestimates the importance of theuse of the patch graft angioplasty. Zierler et al10 alone,make a superficial mention of the problem of patching,but they conclude that, unfortunately, the number andtype of patch angioplasties used is too small to provideany definitive answers. Nevertheless, they maintainthat the questions raised by their study indicate theneed for further investigation. Since the associationbetween direct closure and recurrence is very strong,these authors are not aware that patching appears to bethe most important reason for prevention of recurrentstenosis. For reasons of organization, in the first seriesof 192 patients surgically treated from 1970 to 1979, aprospective study had not been made. Only in 40 pa-tients was follow-up study possible. None of thesepatients tested with C.W. Dopplerultrasound present-ed recurrent stenosis.

FIGURE 4. Low magnification of the histo-logic specimen. The endarterectomized arteri-al surface and patch graft (arrow) have beencovered by cellular fibrous tissue. This wascovered by an intimal "neoendothelium"(Van Gieson for elastic fibers, X 12)

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978 STROKE VOL 15, No 6, NOVEMBER-DECEMBER 1984

FIGURE 5. A higher magnification photo of the intimal

'neoendothelium'. (hematoxylin-eosin, x 160)

Although our series of 74 patients is not large, incontrast with others, the absence of carotid restenosis,documented with noninvasive cerebrovascular test-ing,9- M confirms that this procedure effectively delaysand prevents this complication. The reliability of C.W.Dopplerultrasound in demonstrating a recurrent steno-sis is the same as that concerning studies for assess-ment of carotid artery disease.9-20 In fact, the naturalhistory of patch graft is the same as endarterectomizedcarotid artery. The patch is covered by sparsely cellu-lar fibrous tissue that may interact with platelets andcoagulation factors to induce a proliferative response,especially in the arterial wall; finally the surface iscovered by a reendothelial cell proliferation. This isconfirmed by the original autoptic specimen of thefigures 3, 4, and 5 which was microscopically exam-ined.

Therefore, in our opinion, excluding the above-mentioned technical factors, the advantage of patchingto prevent the decreasing of lumen is possible bymeans of two mechanisms: 1) Patch graft enlarges the

lumen at the level of possible increase of the myointi-mal fibroplasia or new atherosclerotic plaque, whetherit occurs on the endarterectomized segment or beyondthe distal edge of the plaque where intima is intact(overpass) (fig. 6); 2) By enlarging the lumen, thepatch may influence the development of intimal le-sions;26 27 it could serve as a source of cells for a rapidreendothelialization of the endarterectomized segmentand so might decrease the incidence of proliferativelesions in the endarterectomized wall.

On the basis of our experience, we believe the directclosure of the endarterectomized carotid artery is theprimary cause of recurrent stenosis and we recommendthe routine patch graft angioplasty after CE to preventa possible recurrence.

AcknowledgmentThe Authors gratefully acknowledge Prof. Gaetano Thiene, Associ-

ate Professor of Cardiovascular Pathology of the University of Padua,Medical School, for his assistance in preparing histologic material, andMr. Paolo Crepaldi, scientific photographer.

7.

ReferencesJavid H, Julian OC, Dye WS et al: Seventeen-year experience withroutine shunting in carotid artery surgery. World J Surg 3: 167,1979Hertzer NR, Beven EG, Greenstreet RL, Humphries AW: Internalcarotid back pressure, intraoperative shunting, ulcerated atheromaand the incidence of stroke during carotid endarterectomy. Surgery83: 3, 306, 1978Baker WH, Domer DB, Barnes RW: Carotid endarterectomy: Is anindwelling shunt necessary? Surgery 82: 321, 1977Kelly JJ, Callow AD, O'Donnell TF, et al: Failure of carotid stumppressures. (Its incidence as a predictor for a temporary shunt duringcarotid endarterectomy). Arch Surg 114: 1361, 1979Stoney RJ, String ST; Recurrent carotid stenosis. Surgery 80: 6,705, 1976Cossman D, Callow AD, Matsumoto G: Early restenosis aftercarotid endarterectomy. Arch Surg 113: 275, 1978Hertzer NR, Martinez BD, Beven EG: Recurrent stenosis aftercarotid endarterectomy. Surg Gynec Obstet 149: 360, 1979

8. Cossman DV, Treiman RL, Foran RF, Levin PM, Cohen JL:Surgical approach to recurrent carotid stenosis. Am J Surg 140:209, 1980

DIRBCT CLOSURE PATCH GRAFT ANOIOPLASTY

• ' • ? • • •

tHiH. LUHftt

FIGURE 6. Diagram shows how patch graft angioplasty following carotid endarterectomy inhibits restenosis.

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9. Aukland A, Huriow RA, Hamer JD: Carotid artery occlusion fol-lowing endartercctomy: evaluation by spectral analysis of Dopplerultrasound signals. Brit J Surg 69: 45, 1982

10. Zierler RE, Bandylc DF, Thiele BL, Strandness E: Carotid arterystenosis following endartercctomy. Arch Surg 117: 1408, 1982

11. Van den Akker PJ, van Schilfggarde R, Terpstra JL: Operative andlate results of surgery for obstructive carotid artery disease. InProgress in Stroke Research 2; Chapter 46,465-479, Pitman Press,1983

12. Clagett GP, Rich NM, Mcdonald PT et al: Etiologic factors forrecurrent carotid artery stenosis. Surgery 93: 2, 313, 1983

13. Kremen JE, Gee W, Kaupp HA et al: Restenosis or occlusion aftercarotid endarterectomy: A survey with ocular pneumoplethysmog-raphy. Arch Surg 114: 608, 1979

14. French BN, Rewcastle NB: Recurrent stenosis at the site of carotidendarterectomy. Stroke 8: 597, 1977

15. Turnipseed WD, Bcrkoff HA, Crummy A: A Postoperative occlu-sion after carotid endarterectomy. Arch Surg 115: 573, 1980

16. Callow AD: Recurrent stenosis after carotid endarterectomy. ArchSurg 117: 1082, 1982

17. Kartchner MM: Non-invasive data from postoperative carotid sur-gery patients. Presented at "San Diego Symposium on Non-inva-sive Diagnostic Technique in Vascular Disease," September, 1979

18. Shanik DG, Colgan MP, Kingston V: Stenosis following carotidendarterectomy. In Progress in Stroke Research 2; Chapter 49:492-498, Pitman Press, London, 1983

19. Sundt TM Jr, Sandok BA, Whisnant JP: Carotid endarterectomy:Complications and preoperative assessment of risk. Mayo ClinProc50: 301, 1975

20. Keller H, Meier W, Yonekawa Y, Kumpe D: Noninvasive angiog-raphy for the diagnosis of carotid artery disease using Dopplerultrasound (Carotid artery Doppler). Stroke 7: 4, 354, 1976

21. Deriu GP, Ballotta E, Battaglia L et al: II monitoraggio EEGcontinuo per la prevenzione deH'ischemia cerebrale durante clam-paggio carotideo. Min Chirur 37: 19, 1551, 1982

22. Deriu GP, Ballotta E, Alvino S et al: The PTFE graft angioplastyafter endartercctomy. Personal experience and longterm follow-up.Vase Surgery 18: 1, 37, 1984

23. Deriu GP: Endarterectomia della carotide senza shunt. Acta ChirItal XXVII: 1,37, 1971

24. Javid H, Ostermiller WE, Hengensh JW et al: Natural history ofcarotid bifurcation atheroma. Surgery 67: 1, 80, 1970

25. Thompson JE: The development of carotid artery surgery. ArchSurg 107: 643, 1973

26. Imparato AM, Bracco A, Kim GE et al: Intimal and neointimalfibrous proliferation causing failure of arterial reconstructions.Surgery 72: 1007, 1972

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G P Deriu, E Ballotta, L Bonavina, F Grego, S Alvino, L Franceschi, G Meneghetti and A Saiafollow-up.

The rationale for patch-graft angioplasty after carotid endarterectomy: early and long-term

Print ISSN: 0039-2499. Online ISSN: 1524-4628 Copyright © 1984 American Heart Association, Inc. All rights reserved.

is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Stroke doi: 10.1161/01.STR.15.6.972

1984;15:972-979Stroke. 

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