The evolving surgical management of recurrent carotid stenosis

The evolving surgical management of recurrent carotid stenosis Gerald S. Treiman, MD, Judith M. Jenkins, R N , MSN, William H. Edwards, Sr., MD, William Barlow, Phi), William H. Edwards, Jr., MD, R a y m o n d S. Martin III, MD, and Joseph L. Mulherin, Jr., M D , Nashville, Tenn., Los Angeles, Calif., and Seattle, Wash. The traditional approach to recurrent carotid stenosis has been repeat endarterectomy or patch angioplasty. Concern with the durability of repeat carotid endarterectomy has resulted in our use of carotid resection with autogenous graft interposition. This study was designed to determine the outcome and efficacy of carotid resection compared with repeat carotid endarterectomy in the management of recurrent carotid stenosis. From 1974 to

1991, 162 operations (repeat carotid endarterectomy 105, carotid resection 57) were performed for recurrent carotid stenosis. Indication for operation was hemispheric symptoms in 63% of patients, nonlateralizing symptoms in 25%, asymptomatic stenosis in 7%, and previous stroke in 5%. Ninety-one percent of patients had stenosis greater than 90% on arteriography. The perioperative stroke rate for carotid resection was 3.5%, with a subsequent rate of 0.0064 strokes per year. For repeat carotid endarterectomy, the perioperative stroke rate was 1.9% with a subsequent rate of 0.011 strokes per year. Graft patency after carotid resection was 93% (mean follow-up, 35 months). Four patients treated with carotid resection had graft thrombosis, and two of the four remained asymptomatic. After repeat carotid endarterectomy, one patient had carotid thrombosis, and recurrent stenosis greater than 50% developed in 23 patients (mean follow-up, 64 months). Twenty patients treated with repeat carotid endarterectomy underwent an additional operation for further symptomatic recurrent carotid stenosis. We conclude carotid resection is a safe and effective alternative to repeat carotid endartereetomy for patients undergoing operation for recurrent carotid stenosis. (J VASC SURG 1992;16:354-63.)

Carotid endarterectomy (CEA) is the most common major vascular procedure performed in the United States. Recurrent carotid artery stenosis develops in approximately 10% to 25% of patients after CEA, and symptomatic recurrent carotid artery stenosis occurs in 3% to 5%. I"2The natural history of recurrent carotid artery stenosis has not been clearly defined, however, and the optimal management remains controversial. Studies attempting to determine if patients with recurrent carotid artery stenosis are at increased risk of stroke have yielded conflicting results, s'7 Reported operative morbidity and mortality rates have varied from 0% to 10%, s,r and the annual stroke rate after carotid reoperation is unFrom the Department of Surgery, Section of Surgical Sciences, Vanderbilt UniversityMedical Center and the Department of Surgery, St. Thomas Hospital, Nashville. Presented at the Sixteenth Annum Meeting of the Southern Association for Vascular Surgery, St. Thomas, Virgin Islands, Jan. 22-25, 1992. Reprint requests: WilliamH. Edwards, Sr., MD, Suite 705, 4230 Harding Rd., Nashville,TN 37205. 24/6/37939 354

known. This uncertainty has prompted a variety of recommendations for the treatment of recurrent carotid artery stenosis. The traditional approach has been to reserve operation for patients with symptomatic recurrent carotid artery stenosis and for asymptomatic patients with high-grade stenosis. The standard operative procedure has been repeat CEA with patch closure or patch angioplasty alone. Further symptoms or recurrent recurrent carotid artery stenosis (secondary recurrent carotid artery stenosis) will develop in some patients after operative repair of recurrent carotid artery stenosis. Consequently, in recent years we have used carotid resection with autogenous vein graft interposition in the treatment of patients with recurrent carotid artery stenosis, attempting to prevent further stenosis, symptoms, and subsequent stroke. In 1987 we reported our initial experience with carotid resection and suggested that carotid resection may be a safe and durable alternative to multiple CEAs. 8 The present review was undertaken to determine the risks and long-term benefit of carotid resection compared with

Volume 16 Number 3 September 1992

repeat CEA in the treatment of recurrent carotid artery stenosis, and to better define the indications for carotid resection in the treatment of patients undergoing operation for recurrent carotid stenosis. PATIENTS IN THE STUDY A N D METHODS The records of patients undergoing operation for recurrent carotid artery stenosis at Saint Thomas Hospital from 1974 to 1991 were reviewed. All patients underwent arteriography to cortfirm the diagnosis of recurrent carotid artery stenosis and determine the degree of stenosis. Recurrent carotid artery stenosis was defined as more than 50% reduction in the diameter of the carotid artery at the point of maximal stenosis compared with the diameter of the normal artery'. After operation, patients were examined at 1- to &month intervals for the first year and semiannually thereafter. All patients undergoing carotid resection had follow-up duplex examination with use of the Ultramark 9 H D I (Advanced Technology Laboratories, Bothel, Wash.). For patients treated with repeat CEA, follow-up duplex studies were obtained on all symptomatic patients and most patients operated on since 1987. Patients who had greater than 50% stenosis on duplex scanning or patients with recurrent symptoms underwent arteriography. Our operative technique has been previously described and has not undergone major changes during the study period, s All operations were performed by the authors (W.H.E., J.L.M.) on a single surgical service. Since 1986, aspirin (325 nag twice daily) and dipyridamole (25 mg three times a day) were given routinely during the perioperative and postoperative periods. Patients not on aspirin therapy before operation received low molecular weight dextran (dextran 40) at 50 ml per hour in the intraoperative period and for 24 hours after operation. Demographic variables, risk factors, and operafive procedures were statistically analyzed by use of a Cox regression model of time to stroke or recurrent symptomatic stenosis (symptomatic second~'y recurrent carotid artery stenosis). In compa:fing the incidence of stroke after carotid resection or repeat CEA, Cox regression analysis was used because of varying lengths of follow-up between the two procedures. The Kaplan-Meier product limit method was used to create life-table plots. For purposes of analysis, patients undergoing staged or multiple procedures were considered an individual patient for each operation.

Evolving surgical management of recurrent carotid stenosis 355

RESULTS

From 1974 to 1991, 162 patients (81 men, 81 women) underwent operation for recurrent carotid artery stenosis (Table I). One hundred forty-seven of these patients had their initial CEA performed by the authors at Saint Thomas Hospital. The patients ranged in age from 35 to 84 years (mean, 65 years). One hundred forty-eight patients (91%) had stenosis greater than 70%, and 14 patients (9%) had stenosis between 50% and 70% on arteriography. One hundred ten patients (68%) had hypertension, 30 (19%) had chronic obstructive pulmonary disease (COPD), and 22 (14%) had diabetes meUitus. One hundred thirty-nine patients (89%) smoked cigarettes, and almost all continued to smoke after carotid reoperation. Twenty-four patients (15%) were on medication for hyperhpidemia. Ninety-five patients (58%) had symptomatic coronary artery disease° Forty-five patients had contralateral carotid stenosis greater than 70%, and 14 patients had contralateral carotid occlusion. Indications for operation were transient ischemic attack (TIA) or arnaurosis fugax in 102 patients, nonlateralizing symptoms (ataxia, vertigo, dizziness, visual disturbances other than amaurosis fugax) in 41, completed stroke with partial functional recovery in 8, and asymptomatic stenosis in 11 (Table II). All 11 asymptomatic patients had stenosis greater than 70%, and two had stenosis greater than 90%. Fifty-seven patients had carotid resection with autogenous graft replacement (Figs. 1 and 2). The greater saphenous vein was used in 54 patients, the basilic vein in 1, and the lesser saphenous vein in 1. One patient did not have an adequate vein, so a short segment of the superficial femoral artery was used for carotid reconstruction, with polytetrafluoroethylene used to restore lower extremity perfusion. Twenty of the 57 patients had two previous ipsilateral procedures, five patients had three, and one patient had four. The interval between the previous CEA and resection was less than 2 years in 10 patients, 2 to 5 years in 15, 5 to 10 years in 28, and more than 10 years in four (mean, 5 years) (Fig. 3). One hundred five patients were treated with repeat CEA and patch closure. Five of these patients had patch angioplasty alone. Patch material was Dacron in 102 patients and vein in three. One hundred patients had undergone one previous CEA, and five had undergone two previous procedures. The interval between the previous CEA and repeat CEA was less than 2 years in 23 patients, 2 to 5 years in 33, 5 to 10 in 34, and more than 10 in 15 (mean, 5 years) (Table III).

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Table I. Demographics

Patients Age (mean) Sex (M : F) Risk factors Hypertension COPD Diabetes ASHD

Total

Carotid resection

Repeat CEA

162 65 81 : 81

57 64 28 : 29

105 65 53 : 52

110 30 22 35

40 11 5 60

70 19 17 95

ASHD, Atherosclerotic heart disease.

Table II. Indication for operation Patients Hemispheric symptoms Nonlateralizing symptoms Stroke-partial recovery Asymptomatic stenosis

102 41 8 ll

(63%) (25%) (5%) (7%)

CAROTID RESECTION Two (3.5%) of the 57 patients treated with carotid resection had a perioperative stroke. One stroke occurred 4 hours after operation, and at reoperation the vein graft was patent. The patient had gradual return of neurologic function with a mild residual deficit. The other stroke occurred 24 hours after resection. At reoperation carotid thrombosis was found requiring vein graft removal and replacement with a new saphenous vein graft. Despite patency of the new graft, the patient had minimal functional improvement. The only postoperative death occurred 10 days after resection from acute myocardial infarction. The combined perioperative stroke and death rate was 5.3% (3 patients). The remaining 54 patients were monitored from 3 to 99 months (mean, 35 months). Complete follow-up to present was available on all 54 patients. Thirteen patients died of non-stroke-related causes. Thirty-nine of the 41 patients who were alive at the completion of follow-up were asymptomatic, one had recurrent TIAs, and one had an ipsilateral stroke 2 months after resection. Arteriography demonstrated graft thrombosis, and his neurologic deficit gradually improved. Aneurysmal dilation of the vein graft developed in one patient 7 years after carotid resection. The vein was resected and replaced with a new graft without complications. With use of lifetable analysis, the stroke rate after carotid resection was 6.41 strokes/1000 person-years (0.0064 strokes per year) (Fig. 4). All patients undergoing carotid resection had

duplex imaging to study graft patency. Noninvasive studies of the 54 arteries identified three graft occlusions at 2 months, 5 months, and 4 years, respectively, and two of these patients were asymptomatic. The other patient had the only follow-up stroke. The overall graft patency was 93%. On duplex examination, stenosis was less than 50% in 46 grafts. One patient had 60% stenosis found 18 months after resection, and four patients had greater than 70% stenosis identified at 1 month, 6 months, 8 months, and 2 years, respectively. With use of life-table analysis, the rate of graft occlusion was 31.8/1000 graft-years, with a graft stenosis rate (stenosis > 70%) of 57.2/1000 graft-years. REPEAT CAROTID ENDARTERECTOMY One hundred five patients were treated with repeat CEA. Two patients (1.9%) had a perioperative stroke (Table III). One stroke occurred 7 days after operation, and the patient eventually died of strokerelated complications. The other stroke occurred 3 weeks after repeat CEA, and the patient survived with gradual return of neurologic function. In both patients arteriography after the stroke demonstrated a patent carotid artery without residual stenosis. The remaining 103 patients were monitored from 2 to 149 months after repeat CEA (mean, 64 months). Thirty-four patients died of non-strokerelated causes, although one of the 34 patients had a nonfatal stroke. Seventy patients were alive at the completion of follow-up; 45 were asymptomatic, 21 had recurrent hemispheric symptoms, and four patients had a stroke. The five follow-up strokes after repeat CEA occurred at 5 weeks, 2 months, 4 months, 57 months, and 58 months, respectively. One stroke involved the occipital lobe, and arteriography demonstrated a patent carotid artery without recurrent stenosis. The other four strokes were in the ipsilateral middle cerebral artery circulation. Three of the four patients were asymptomatic before stroke, and one had amaurosis fugax. All four patients underwent arteriography after the stroke. One patient had a thrombosed internal carotid artery (ICA), and three patients had a patent carotid artery with recurrent stenosis. Two patients had good functional recovery after rehabilitation, and two patients had a persistent severe deficit. With use of life-table analysis, the annual stroke rate was 10.7 strokes/1000 person-years (0.011 strokes per year) (Fig. 4). Twenty of the 105 patients undergoing repeat CEA underwent an additional procedure for symptomatic secondary recurrent ca-

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Evolving surgical management of recurrent carotid stenosis 357

Fig. 1. Arteriogram of a patient after carotid resection and nonreversed saphenous vein graft interposition.

rotid artery stenosis (Fig. 5). Sixteen of the 20 patients had TIAs, one had amaurosis fugax, and three had nonlateralizing symptoms. The interval from repeat CEA to subsequent reoperation was less than 2 years in five patients, 2 to 5 years in 11, and greater than 5 years in four. Fifty-four of the I05 patients treated with repeat CEA had follow-up duplex examination or arteriography. Follow-up studies found that secondary recurrent stenosis from 50% to 70% developed in seven patients at 18,24,48,60,85,99, and 109 months, respectively. Secondary recurrent carotid artery stenosis greater than 70% developed in 16 from 7

months to 9 years after repeat CEA. One patient had carotid occlusion identified 5 years after operation. The incidence of carotid occlusion was 4.1 occlusions/1000 person-years, and the restenosis rate (time to stenosis greater than 70%) was 47.3/1000 patient-years. All patients undergoing reoperation for secondary recurrent carotid artery stenosis had greater than 70% stenosis on arteriography in addition to recurrent hemispheric symptoms. Four of the 162 patients (2.4%) in this study had transient cranial nerve deficits, three with hoarseness and one with hypoglossal nerve palsy. Two of the four patients underwent repeat CEA and two were

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Fig. 2. Photograph of saphenous vein graft after carotid resection.

0-1

2

3

4

5 6 Years

7

8

9

10 10+

Fig. 3. Interval from previous CEA to reoperation. treated with carotid resection. No patient had a cranial nerve deficit that persisted beyond 3 months. A wound hematoma that required reoperation developed in one patient. Each of the independent variables was statistically analyzed to determine its relationship with stroke (Table IV). Patients with a longer interval between

CEA and the development of recurrent carotid artery stenosis, patients with diabetes, and women were more likely to have a stroke, but none of these relationships reached statistical significance. Patients treated with repeat CEA had similar risk factors as patients treated with carotid resection. There was no statistically significant difference in age,

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Evolving surgical management of recurrent carotid stcnosis 3 5 9

i00

......

I~- . . . . . . . . . . . . . . . .

"k . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

75 Patients

Stroke Free 50 ' - -

(%) - -

Carotid

.....

Re-endarterectomy

Resection

(CR) (RCEA)

I

!

0!

20

2, 40

i 60

I

I

80 100 Time (months)

i' 120

_ 140

160

Fig. 4. Life-table plot of effect of repeat CEA or carotid resection on incidence of stroke. Table III. Outcome All patients Asymptomatic Recurrent hemispheric symptoms Stroke Total

Carotid resection

Repeat CEA

125 (77%) 27 (17%)

49 (86%) 5 (9%)

76 (72%) 22 (21%)

10 (6%)

3 (5%)

7 (6%)

57 (100%)

105 (100%)

162 (100%)

sex (p = 1.00), hypertension (p = 0.73), diabetes (p = 0.23), COPD (do = 0.84), or coronary artery disease (p = 0.62) between the two groups. The incidence of contralateral stenosis (repeat CEA 24% vs carotid resection 16%), previous stroke (repeat CEA 5.3% vs carotid resection 4.7%), and hemispheric symptoms (repeat CEA 73% vs carotid resection 57%) was similar for patients undergoing each procedure. Patients treated with carotid resection had more previous ipsilateral carotid operations. No statistically significant difference occurred in the stroke rate for patients treated with carotid resection or repeat CEA (p = 0.996). The gross and histologic features of the recurrent disease varied with the interval to recurrent carotid artery stenosis. Patients admitted within 12 to 18 months had neointimal fibromuscular hyperplasia (myointimal hyperplasia) involving the endarterectomized artery. These lesions tended to be white, rubbery, and more adherent to the outer media and adventitia. Recurrent atherosclerosis was the predominant finding in patients admitted more than 24 months after CEA (Fig. 6). These plaques were hard

Table IV. Relationship of independent variables with stroke Variable

p ealue

Interval from CEA to operation Diabetes Sex (male vs female) COPD ASHD Age Patch closure Hemispheric symptoms Hypertension Treatment (carotid resection vs repeat CEA)

0.102 0.134 0.234 0.493 0.688 0.740 0.858 0.882

0.906 0.996

and frequently ulcerated. This usually involved the endarterectomized area, but 15 patients had recurrence in the distal ICA and 18 in the pro~mal common carotid artery. DISCUSSION Several techniques have been advocated for the operative treatment of recurrent carotid artery stenosis depending on the patholo~ - and the number of previous procedures. The traditional approach has been repeat CEA with patch closure, 9 although others have treated myointimal hyperplasia with patch closure alone. 1°,7 Carotid bifurcation advancement has been used, but on comparison with primary closure and vein patch angioplasty this technique demonstrated no significant difference in rate of restenosis} 1,12 In our experience, repeat CEA with patch angioplasty was assodated with a I9% (20 of 105 patients) incidence of recurrent symptomatic stenosis of greater than 70%. We have increasingly

)'ournal of VASCULAR SURGERY

360 Treiman et al.

10o 75 L~ ...........

t

Patients Stroke & RCEA 50 Free

(%)

25 ~

00

- -

Carotid Resection (CR)

.....

Re-endarterectomy

20

40

(RCEA)

60

80 100 Time (months)

120

140

160

Fig. 5. Life-table plot of effect of repeat CEA or carotid resection on incidence of stroke or symptomatic secondary recurrent carotid artery stenosis. used carotid resection in the treatment of these patients, attempting to decrease the incidence of symptomatic secondary recurrent carotid artery stenosis and the risk of subsequent stroke. A consideration of pathologic and hemodynamic findings in recurrent disease has provided theoretic support for carotid replacement. The development of intimal plaques at the carotid bifurcation may reflect flow disturbances and turbulence at the origins of the ICA and external carotid artery. Removal of the area of turbulence may minimize recurrent plaque formation. Recurrent plaque or thrombus can damage the arterial wall, resulting in increased thrombogenicity in the area of recurrent disease.la The vein intima may be less thrombogenic than the endarterectomized arterial segment, a conclusion supported by the superiority of vein bypass to endarterectomy in other arterial segments. In addition, repeat CEA may be difficult because clear tissue planes are not present. The presence of thrombus, calcification, scarring, or thinning of the arterial wall from multiple previous procedures may prohibit satisfactory endarterectomy.14 Finally, some patients have an abnormal response to vessel injury and are prone to develop recurrent severe myointimal hyperplasia. Greater than 70% recurrent carotid artery stenosis developed in 18 patients in our experience within 24 months of repeat CEA, and in four patients this occurred after successive operations. Carotid resection provides the best treatment for these patients. In most reports on the treatment of recurrent carotid artery stenosis, carotid resection has been

used when repeat CEA is technically difficult or when secondary recurrent carotid artery stenosis is present. Consequently, experience with carotid resection has been limited, is In the six largest series on recurrent carotid artery stenosis, a total of 14 patients were treated with carotid resection. 3,s,9,1saS,16 In these reports saphenous vein was used in eight patients, Dacron in three, hypogastric artery in two, and bovine artery in one. No operative or follow-up strokes were reported in this group of patients. These anecdotal reports do not allow for determination of the durability of carotid resection or for comparison of the safety and effectiveness of carotid resection with repeat CEA. Perioperative stroke and death rates have usually been higher after recurrent carotid operation compared with initial CEA. Bernstein et al.s in summarizing thc results of six surgical series involving 284 patients operated on for recurrent disease, noted the operative death rate varied from 0% to 3.1% (average, 1.4%), with a stroke rate of 0% to 10.4% (average, 3 . 9 % ) . 5"7"9,1a,16,17 In our initial experience with 106 operations for recurrent carotid artery stenosis, we found the combined operative stroke and death rate was 0.8%. 8 In the present series four perioperative strokes (2.4%) and one death from myocardial infarction (0.6%) occurred. We found no statistically significant difference in the rate of perioperative morbidity and mortality between patients treated with repeat CEA or carotid resection. The operative stroke rate for patients undergoing carotid resection was 3.5% compared with 1.9% for patients treated with repeat CEA

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Evolving surgical management of recurrent carotid stenosis 361

Fig. 6. Photograph of resected carotid artery demonstrating recurrent atherosderofic disease at the carotid bifurcation. (p = 0.99). Both procedures require dissection and mobilization of the common carotid artery and ICA, and the incidence of cranial nerve injuries was comparable. Overall, only two (3.5%) patients treated with carotid resection and two (1.9%) undergoing repeat CEA had transient hoarseness or hypoglossal nerve palsy. On long-term follow-up with use of life-table analysis, both carotid resection and repeat CEA were associated with a low incidence of ipsilateral stroke (6.41/1000 person-years vs 10.7/1000 personyears). Recurrent symptomatic stenosis was more likely to develop in patients treated with repeat CEA than in patients undergoing carotid resection. However, follow-up was longer on patients undergoing repeat CEA than on patients treated with carotid resection (mean, 64 months vs 35 months). The increased incidence of symptomatic recurrent carotid artery stenosis may therefore reflect longer follow-up rather than the operation performed. Although carotid resection may prove to be more effective in preventing tim_her symptomatic recurrent carotid artery stenosis, longer follow-up is necessary to determine if the incidence of symptomatic recurrent carotid artery stenosis will be less after carotid resection and whether this will ultimately result in a lower incidence of stroke. Carotid resection has proved to be a durable procedure, with a low incidence of subsequent recurrent stenosis. Our greatest concern has been graft thrombosis, but this occurred in only four patients, one on the first postoperative day. Two of

the fore- patients remained asymptomatic. We believe autogenous grafts are less thrombogenic than prosthetic grafts, and have used autogenous grafts whenever possible. In one patient, this required use of a short segment of the superficial femoral artery for carotid reconstruction, with polytetrafluoroethylene used to restore lower extremity perfusion. Our previous studies found that antiplatelet agents inhibit carotid thrombosis, 18 and we use such agents routinely. Our present operative approach depends on the number of previous ipsilateral carotid operations, the interval since the last procedure, and the appearance of the carotid artery at operation. For patients with primary recurrent carotid artery stenosis, our standard treatment is repeat CEA if a satisfactory endarterectomy can be performed. We found carotid resection is safe and effective in these patients, however, and are using resection more frequently. We use carotid resection preferentially for patients with primary recurrent carotid artery stenosis when repeat CEA is technically difficult or when a clean endarterectomized artery can not be obtained because of scarring or thinning of the arterial -wall. Patients with secondary recurrent carotid artery stenosis are treated with carotid resection unless the artery is suitable for repeat endarterectomy and autogenous graft is not available for carotid replacement. In our experience, both carotid resection and repeat CEA are associated with few perioperative complications and a low incidence of subsequent

362

Treiman et al.

stroke (less than i % per year). L o n g e r follow-up will be required to determine if patients treated with carotid resection will have a lower incidence o f s y m p t o m a t i c recurrent carotid artery stenosis and w h e t h e r this will lower the incidence o f subsequent stroke. Nevertheless, carotid resection is p r o v i n g to be a safe and effective alternative w h e n repeat C E A is technically difficult, contraindicated, or has resulted in secondary recurrent carotid artery stenosis. REFERENCES

1. ColganMP, Kingston V, Shanik G. Stenosis following carotid endatterectomy-its implication in management of asymptomatic carotid stenosis. Arch Surg 1984;119:1033-5. 2. Matzos MA, Shamma AR, Rossi N, et aL Is duplex follow-up cost-effectivein the first year after carotid endarterectomy? Am J Surg 1988;156:91-5. 3. Cossman D, Callow AD, Stein A, Matsumoto. Early restenosis after carotid endarterectomy. Arch Surg 1978;113: 275-8. 4. Nicholls SC, Phillips DJ, Bergelin RO, Sttandness DE Jr. Carotid endarterectomy: relationship of outcome to early restenosis. J VAsc SURG 1985;2:375-81. 5. Bernstein EF, Torem S, Dilley B. Does carotid restenosis predict an increased risk of late symptoms, stroke or death? Ann Surg 1990;212:629-36. 6. Clagett GP, Rich NM, McDonald PT, et al. Etiologic factors for recurrent carotid artery stenosis. Surgery 1988;93: 313-8. 7. Zbomikova V, Elfsttom J, Lassvik C, lohansson I, Olson JE, Bjomlert U. Restenosis and occlusion after carotid surgery assessed by duplex scanning and digital subtraction angiography. Stroke 1986;17:1137-42.

Journal of VASCULAR SURGERY

8. Edwards Wt-I Jr, Edwards WH, Mulherin JL Jr, Martin KS III. Recurrent carotid artery stenosis: resection with autogenous vein replacement. Ann Surg 1989;209:662-8. 9. Bardett FF, Rapp JH, Goldstone J, Ehrenfeld WK, Stoney RJ. Recurrent carotid stenosis: operative strategy and late results. J VASCSURG 1987;5:452-6. 10. Cossman DV, Treiman RL, Foran RF, Levin PM, Cohen JL. Surgical approach to recurrent carotid stenosis. Am J Surg 1980;140:209-11. 11. Rosenman J, Edwards WS, RobiUard D, Geary G. Carotid arterial bifiarcation advancement. Surg Gynecol Obstet 1984; 209:662-8. 12. Curley S, Edwards WS, Jacob TP. Recurrent carotid stenosis after autologous tissue patching. J VASCSUV,G 1987;6:350-3. 13. Piepgras DG, Marsh WR, Mussman LA, Sundt TM Jr, Fode NC. Recurrent carotid stenosis: results and complications of 57 operations. Ann Surg 1986;203:205-13. 14. Clagett GP, Robinowitz M, Youkey JR, et al. Morphogenesis and clinicopathologic characteristics of recurrent carotid disease. J VASCSUV,G 1986;3:10-23. 15. Hertzer NR, Martinez BD, Beven EG. Recurrent stenosis after carotid endarterectomy. Surg Gynecol Obstet 1988;149: 360-4. 16. Kazmers A, Zierler RE, Huang TW, Pulliam CW, Radke HM. Reoperative carotid surgery. Am 1 Surg 1988;156:34652. 17. Das MB, Hertzer NR, Ratliff NB, O'Hara PJ, Beven EG. Recurrent carotid stenosis: a five-year series of 65 reoperations. Ann Surg 1985;202:28-35. 18. Edwards WH, Edwards WH Jr, Mulherin JL, Jenkins JM. The role of antiplatelet drugs in carotid reconstructive surgery. Ann Surg 1985;210:765-70. Submitted Jan. 27, 1992; accepted March 16, 1992.

DISCUSSION

Dr. J. Timothy Fulenwider (Gainesville, Ga.). Dr. Treirnan, we appreciate you bringing this fortunately unusual but very interesting and important topic to our attention, and we commend you and your authors for your very favorable results with this complex problem. Certainly this represents one of the largest series reported in the literature with over 100 patients, and I believe that this reflects the fact that these patients are monitored with a very rigorous compulsiveness and that these are truly recurrent defects and not persistence of incorrectly or inappropriately treated CEAs. We are all aware that the arterial injury that is created by the CEA does initiate a very dynamic healing process of indeterminate length. Most of our information comes from the experimental model and early on the phase of healing is that of a proliferative response that seems to be intensified by both hypercholesterolemia and hypertension. This response also occurs in the human setting, but our data that we know about the healing of CEA sites in hmnans are

sparse. Most data come from pathology specimens, from autopsy data, and from late postoperative specimens at repeat CEA. I noticed in your series that you had a very favorably low incidence of cranial nerve palsies after your repeat operations, certainly less than 3%. This is sixfold to sevenfold less than that as recorded in the literature and certainly far less than recorded in my own personal experience. Are these data not difficult to extract from the progress notes? It is found that if you look at these patients prospectively, the incidence of cranial nerve neurapraxia after repeat operations is at least 25% to 30%. H o w many of these primary endarterectomies were followed by a patch arterioplasty of one type or another? Also, it is of some concern to me that when you perform the repeat CEA and patch closure that your incidence of late neurologic advanced ischemic brain infarctions was somewhat higher than that reported in the literature and at least higher than that of other colleagues