Saphenous vein bypass: An alternative to internal carotid reconstruction

Saphenous vein bypass: An alternative to internal carotid reconstruction

Eur J VascEndovascSurg 12, 26-30 (1996) Saphenous Vein Bypass: An Alternative to Internal Carotid Reconstruction* A. Branchereau, P. Pietri, P. E. Ma...

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Eur J VascEndovascSurg 12, 26-30 (1996)

Saphenous Vein Bypass: An Alternative to Internal Carotid Reconstruction* A. Branchereau, P. Pietri, P. E. Magnan and E. Rosset Service de Chirurgie Vasculaire, Hdpital Sainte-Marguerite, Marseille, France Objective: Venous grafting is rarely employed for carotid reconstruction; the aim of this retrospective study was to assess its value as an alternative to endarterectomy. Material: Between January 1980 and June 1990, we performed 212 carotid artery venous bypasses (CVB) on 208 patients. Twenty-nine patients were asymptomatic, 60 had non-hemispheric symptoms and 119 focal symptoms. The indication for surgery was stenosis in 185 cases, kinking in 18 and aneurysms in nine. The main criteria to use CVB were length of the lesion in 86 cases, extent of atherosclerosis in 75, dysplasia in 12, intraoperative failure of endarterectomy in 21, aneurysms in seven and long-term restenosis or occlusion in 12. Results: There were 11 deaths, three strokes and nine transient ischaemic attacks. Angiographic control showed one occlusion giving an immediate patency rate of 99.5%. Mean follow-up was 104.3 + 46.1 months with 15 patients lost to follow-up. Eighty patients died; life expectancy was 52.4 + 7.5 at 10 years. Including occlusions and restenosis as failures, the secondary patency rate was 96.4 +_ 3.7 at 10 years. The annual stroke rate was 1.3% and the neurologic event-freepopulation 87 +_ 2.4% at 10 years. Conclusion: CVB is a valuable alternative to endarterectomy for reconstruction of the carotid artery. The indications are extensive atherosclerosis involving the common carotid artery, intraoperative anatomic failure of endarterectomy, and longterm restenosis. Key Words: Internal carotid artery; Surgical reconstruction; Venous graft; Venous bypass.

Introduction The principal problem in carotid artery reconstruction is to reduce the risk of postoperative neurologic complications. The first cause of these postoperative events is thromboembolic complications which are technical in origin. 1-4 Achieving anatomic perfection of surgical reconstruction must be the main goal of this surgery. Thromboendarterectomy (TE) with or without patch is of course, the "gold standard" technique. Nevertheless, depending on the type of lesion, it may be inappropriate in certain cases. Internal carotid reconstruction by a saphenous vein by-pass (CVB), widely used in France by Cormier since the early 1970s~-9 is rarely performed elsewhere. The aim of the present study was to review our experience with this technique between 1980 and 1990,

*Presented at the 9th annual meeting of the European Societyfor Vascular Surgery,Antwerp, Belgium(September/October 1995).

to present the short and long-term results and to discuss its indications.

Patients and Methods Between January 1980 and June 1990, we performed 212 CVB on 208 patients, four of them having a twostage bilateral reconstruction. Seventy of them had a reconstruction of the other carotid artery by another procedure: 67 classic TE, two eversion TE, and one PTFE by-pass. During the same period of time, 700 TE were performed on 630 patients. The population included 152 males and 56 females aged from 35 to 88 with a mean of 67.1 _+ 8.3 years. The associated risk factors are given in Table 1. Twenty-nine patients were asymptomatic, 60 presented with non-hemispheric symptoms and 119 with focal ischaemia : motor or sensory deficit 79, amaurosis 14, motor or sensory deficit associated with nonhemispheric symptoms 19, and motor deficit associated with amaurosis four. At the time of surgery, 34

1078-5884/96/050026 +05 $12.00/0 © 1996W. B. Saunders CompanyLtd.

Carotid Bypass Table 4. Indications for CVB

Table 1. Risk factors

Arterial hypertension Coronary disease Non-ischaemic cardiopathy Lower limb arterial disease Respiratory insufficiency Renal insufficiency Diabetes mellitus Hypercholesterolemia Tobacco abuse

Number patients

%

99 52 12 51 19 4 30 32 89

47.6 25 5.8 24.5 9.1 1.9 14.4 15.4 42.8

out of the 119 patients with focal ischaemia h a d a m i l d deficit. Two out of the 60 patients w i t h non hemispheric s y m p t o m s h a d a m i l d deficit in the vertebrobasilar territory. The internal carotid lesions in these patients a n d corrected b y CVB are s h o w n in Table 2. There w e r e nine a n e u r y s m s : six atherosclerotic, two dysplasic a n d one d e v e l o p e d on a v e n o u s patch. N i n e t y patients h a d a significant lesion on the other carotid artery (Table 3). The reason for p e r f o r m i n g CVB w a s a l w a y s dictated b y pre a n d intraoperative findings which were classified into five g r o u p s (Table 4). All patients were o p e r a t e d u n d e r general anaesthesia m a i n t a i n i n g a n o r m o t e n s i v e and n o r m o c a p n i c status w i t h o u t a n y cerebral monitoring. A shunt w a s u s e d in six cases (2.8%) : the decision for shunting w a s m a d e p r e o p e r a t i v e l y on the angiographic findings s h o w i n g controlateral internal carotid occlusion associated with obstructive lesions of the vertebral arteries. In 34 cases, CVB w a s associated with an arteri o t o m y a n d an e n d a r t e r e c t o m y of the external a n d c o m m o n carotid arteries in order to relieve a severe stenosis of the external carotid artery. An instrumental dilatation of the distal internal carotid artery w a s Table 2. Arterial lesions corrected by CVB

Stenosis

0-29% 30-69% 70~89% a90%

55 35 70 25 18 9

Tortuosities* Aneurysms

*In cases of stenosis plus tortuosity, only the stenosis was considered.

Group 1 Group 2

Group 3 Group 4

Group 5

Tortuosities Diffusion of artherosclerosis proximal 21 distal 25 proximal+ distal 29 Intraoperative failure Postoperative mid or long-term failure restenosis 10* PTFE failure 1 Specificlesions dysplasia 12"* aneurysms 7

86 75

21 11

19

*One associated with an aneurysm developed on a venous patch. **One responsible of an aneurysm.

p e r f o r m e d in seven cases to correct a dysplasic lesion. A c o m b i n e d reconstruction of another artery to the h e a d w a s p e r f o r m e d in 21 patients : 18 of which w e r e s i m u l t a n e o u s (ipsilateral subclavian artery in 2 a n d vertebral artery in 16 cases) a n d three times as a twostaged p r o c e d u r e to reconstruct three contralateral vertebral arteries. In one patient, a neurosurgical p r o c e d u r e was p e r f o r m e d s i m u l t a n e o u s l y to correct an a n e u r y s m of the anterior c o m m u n i c a t i n g artery. Three patients s i m u l t a n e o u s l y u n d e r w e n t CVB comb i n e d with an arterial p r o c e d u r e in another territory : one a b d o m i n a l aortic a n e u r y s m repair, one aortobifem o r a l bypass, and one femoral artery a n e u r y s m repair.

Results Short-term results These were collected on the 30th p o s t o p e r a t i v e d a y or on discharge w h e n hospital stay exceeded 30 days. We o b s e r v e d 11 deaths ; their causes are reported in Table 5. Two of the m y o c a r d i a l infarctions occurred d u r i n g the third a n d fourth postoperative weeks, the patients h a v i n g been discharged. The t w o m u l t i o r g a n failures occurred after c o m b i n e d surgery : in one case, after a t h o r a c o a b d o m i n a l aortic a n e u r y s m repair p e r f o r m e d 1 w e e k after the carotid reconstruction and in the other Table 5. Causes of early postoperative mortality

Table 3. Contralateral carotid arterial lesions

Dysplasia Senosis <50% Stenosis a50% Occlusion

27

Number

%

6 34 38 12

2.9 16.3 18.3 5.8

Myocardial infarction Pulmonary embolism Multiorgan failure Pulmonary infection Stroke Total

3 1 2 1 4 11

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case, after a simultaneous correction of carotid stenosis and infrarenal aortic aneurysm. The four strokes were ipsilateral and in close relationship with the carotid reconstruction. Their causes were as follows : one postoperative occlusion of the CVB, one intraoperative thrombosis of the middle cerebral arter)5 one postoperative cerebral haemorrage and one cerebral ischaemia during cross-clamping. Twelve patients developed non-fatal neurologic complications : nine transient ischaemic attacks (TIA), and three strokes with mild (2) or severe (1) sequelae. An angiogram was performed in these 12 patients : 11 grafts were patent and one was occluded. The total mortality plus stroke rate was 14 cases (11 deaths, 3 non-fatal strokes) representing 6.6% of cases and 6.7% of patients. The postoperative patency of the grafts was assessed by Duplex scan or angiography in all except six cases who presented with lethal complications, (all general in origin). We observed two occlusions as previously mentioned : one was responsible for a lethal stroke and the other for an amaurosis. The patency rate was 99.03%.

Long-term results These were collected between January and April 1995. Fifteen patients were lost to follow-up : nine after their discharge and six during follow-up. One hundred and eighty-two patients were followed from 45-176 months (mean 104.3 + 46.1 months). The pate ncy of the CVB was assessed by Duplex-scan and angiography when there was a doubt in the quality of reconstruction. Four late occlusions were observed : one in the 21st month causing hemiplegia, one in the 34th month causing hemianopsia, one in the 39th month which was asymptomatic and one in the 62nd month causing hemiplegia. A restenosis was observed in five cases respectively diagnosed in months 5, 25, 27, 47, and 91. Three were asymptomatic, one responsible for a TIA and one for a stroke. Three were successfully treated by surgery : two new venous grafts and one angioplasty of the distal anastomosis. An aneurysm developed in one case on the body of the venous graft, diagnosed during follow-up and successfully treated by PTFE interposition. We considered the following as anatomic failure: late occlusions, restenosis and aneurysm. According to the lifetable method, primary patency at 5 and 10 years was respectively 95.4 + 3.15% and 92.3 + 4.5% and secondary patency at 5 and 10 years was respectively 96.4 _+ 2.4% and 94.5 + 3.7% (Fig. 1). Thirty-two neurologic events, (17 TIA and 15 Eur J Vasc Endovasc Surg Vol 12, July 1996

100 90-

g,

80 Primary patency: 95.4 -+ 3.2 % at 5 years 92.3 ± 4.5 % at lO years

70 60 I

f

0

176"170 177t171 L I 1 2

156 158 I 3

143 146 I 4

117 119 I 5 Years

95 96 I 6

84 85 I 7

73 74 I 8

59 60 I 9

50 51 I 10

* Reconstructions at risk (primary patency) t Reconstructions at risk (secondary patency) Fig, 1. Primary and secondary cumulative patency of CVB. All anatomic events (restenosis, aneurysm) were considered as occlusions. ( - - ) primary patency; ( - - - ) secondary pateney.

strokes), were observed during follow-up : 30 were hemispheric or ocular (ipsi or contralateral) and two were non-focal. Using the life-table method and taking the immediate post-operative complications into account, the stroke-free population at 5 and 10 years was respectively 89.9 + 4.3% and 87.2 + 5.1%. The annual stroke rate was 1.3% (Fig. 2). Eighty deaths occurred after the 30th postoperative day ; their causes are shown in Table 6. The cumulative life expectancy at 5 and 10 years was respectively 69 +_ 6.4% and 52.4 + 7.5% (Fig. 3).

100 90 v

& d)

r

80 70

89.9 ± 4.3 % at 5 years 87.2 ± 5.1% at 10 years

60 50 171" 165 154 b I __1 1 2 3

143 ] 4

116 92 81 I ~__1 5 6 7 Years

70 58 I 1 ~ 8 9

50 10

* Patients at risk Fig. 2. Cumulative stroke-free population after carotid reconstruction by CVB.

Carotid Bypass

Table 6. Causes of

long-term mortality

Ischaemic cardiopathy Other cardiopathy Total cardiopathy Cancers Infradural haematoma Stroke Total neurologicevents Other arterial disease Sudden death Multiorgan failure Pulmonary embolism Renal failure Intestinal bleeding Suicide Unknown Total

14 16 30 24 8 3 5 3 1 1 1 1 3 80

Discussion In this series the indications for CVB were always based on either pre or intraoperative anatomic data. The first reason for choosing CVB was tortuosity with or without stenosis (group i in Table 4). The classic TE in this situation does not relieve tortuosity. 1° Moreover in case of kinking, there m a y be a postoperative stenosis at the upper limit of the endarterectomy w h e n the atheromatous process ends at the level of the kinking. 1~ In this situation, the alternative techniques are CVB or eversion endarterectomy with reimplantation. Group 2 is characterised by distal extension of the atheromatous process. When atherosclerosis extends distally, one solution is to attach the distal atheroma b y an overpass suture. This solution, we have used elsewhere, looks unsatisfactory first because it leaves a residual atheromatous lesion and second because it m a y be one cause of restenosis. Another solution is to perform an eversion in order to

i

100 90 80 70 I 60 50 4O 3O 2O lO

69.0 ± 6.4 % at 5 years 52.4 ± 7.5%at 10 years

177" 171 159 15o 123 95 I

1

2

3

4

I

5 6 Years

86

76

I~

1

7

8

63

51

9

10

I

* Patients at risk Fig. 3. Life-expectancyof the population operated by CVB.

29

extend the endarterectomy as far as necessary] 2 The CVB in this situation represents a simple and safe solution. More frequentl)~ atherosclerosis extends into the proximal common carotid artery (50 cases in this series, Table 4). In this situation, TE m a y require a very long open endarterectomy otherwise some plaque m a y be neglected with the possibility of embolisation or dissection. 5'8 CVB originating from a healthy area is always possible at the limit of the thoracic outlet and is, in our opinion, the best solution. Group 3 is composed of TE intraoperative anatomic failures assessed visually or by intraoperative angiography. Group 4 includes mid or long-term carotid restenosis : CVB presents two advantages : first to avoid the previous operative site, and second to correct the lesion by a different procedure without another endarterectomy. 13 The indications for group 5 need not be discussed here. The stroke plus death rate observed in this popluation was higher than the standards presently accepted. ~4 Considering the 11 deaths, two of them were caused by multiorgan failure secondary to aortic surgery. In these two cases, carotid reconstruction was prophylactic and death was unrelated. Considering the non-fatal strokes, two of them resulted in mild sequelae and one was disabling. Thus, if we consider only the related-to-carotid-surgery deaths plus disabling strokes, the number of events was 10, resulting in a rate of 4.7% of cases and 4.8% of patients. Moreover, this series was carried out for 10 years. We have demonstrated and published elsewhere that the results obtained in carotid reconstruction had dramatically improved between the beginning of the 1980s and the beginning of the 1990s. 15 As previously described by m a n y authors, longterm mortality was quite high with roughly half of the population dead at 10 years. The principal causes of death in our series, like in other series, 16"17 were cardiovascular disease and cancer. If we consider the neurologic events, sudden deaths and renal insufficiency in the group of cardiovascular disease it represents 48 out of the 80 deaths observed (Table 6). These data stress the potential benefit of an aggressive approach to cardiovascular disease. The annual stroke rate of 1.3% is lower than reported in the literature for a non-operated population presenting with carotid artery disease. 1 4 •1 8 - 2 0 These data show the prophylactic role of carotid surgery n o w clearly demonstrated b y multicenter trials. 1s-z° The methodology of this study did not make it possible to compare the anatomic results of this technique with endarterectomy. Nevertheless, the long-term anatomic results (5 restenosis plus 5 occlusions at 10 years) are at least Eur J Vasc Endovasc Surg Vol 12, July 1996

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A. Branchereau et aL

equal to those reported in the literature after endarterectomy.13'21'22 In conclusion, CVB is an alternative technique for reconstruction of the internal carotid artery. Compared with classic TE, our immediate and long-term anatomic results were equal or better. In the case of atherosclerotic lesions, the best indications for this technique are proximal extension of atheroma, intraoperative failure of endarterectomy and restenosis, Another possible indication is when there is severe tortuosity.

References 1 TOWNE JB, BERNHARD VI~. Neurologic deficit following carotid endarterectomy. Surg GynecoI Obstet 1982; 154: 849-852. 2 STEED CL, PEITZMAN AB, GRUNDYBL, WEBSTERMW. Causes of stroke in carotid endarterectomy. Surgery 1982; 92: 634-641. 3 ROSENTHALD, ZEICHNER~WD, LAMISPZ, STANTONPE. Neurologic deficit after carotid endarterectomy : pathogenesis and management. Surgery 1983; 94: 776-780. 4 BRANCHEREAU A, ONDO N'DoNG F, BORDEAUX J, SAMBUC R. Complications neurologiques de la chirurgie carotidienne : m6canismes et facteurs pr6dictifs. Ann Chir Vasc 1986; 1: 79-85. 5 CORMIERJM, LAGNEAUP, JANNEAUD. 103 revascularisations de la carotide interne par greffe veineuse. J Chir 1978; 115: 7-12. 6 CORMIERJM, LAUR/ANC, GIGOUF, FRANCESCHIC, LuIzY 17. Greffe veineuse contre thrombo-endart6riectomie carotidienne, f Mat Vase 1982; 7: 25-31. 7 CORMrCR JM, R~cco JB. Carotid graft for cerebro-vascular insufficiency. In : Bergan JJ, Yao JST, eds. Cerebrovascular Insufficiency. New York: Grnne & Stratton, 1983; 275-284. 8 CORMIER JM, CHAPELIER A. Greffe veineuse carotidienne. In : Kieffer E, Natali J, eds. Aspects techniques de la chirurgie carotidienne Paris: AERCV, 1987; 183-198. 9 COrU'~ERJM, CHAPELIERA. R6sultats tardifs de la revascularisation par greffe veineuse des st6noses ath6roscl6reuses de la carotide interne. In : Kieffer E, Bousser MG, eds. Indications et rdsultats de la chirurgie carotidienne. Paris: AERCV, 1988; 101-115. 10 THEVENET A. Chirurgie des 16sions non ath6romateuses car-

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otidiennes. In : Kieffer E, Natali J, eds. Aspects techniques de la chirurgie carotidienne. Paris: AERCV, 1987; 219-239. 11 BRANCHEREAUA, ONDO N'DoNG F, SCOTTI L. M6canismes des complications neurologiques post-op6ratoires en chirurgie carotidienne. In : Kieffer E, Natali J, eds. Aspects techniques de la chirurgie carotidienne. Paris: AERCV, 1987; 317-331. 12 KIENYRl HIRSCHD, SEILLERC, THIRANOSJC, PETITH. Does carotid eversion endarterectomy and reimplantation reduce the risk of restenosis? Ann Vasc Surg 1993; 7: 407-413. 13 KmNY R, MANTZ F~ KURTZTh et al. Les rest6noses carotidiennes apr6s endart6riectomie. In : Kieffer E, Bousser MG, eds. Indications et r~sultats de la chirurgie carotidienne. Paris : AERCV, 1988: 77-100. 14 MooRE WS, MOHRJP, NAJAFI H/ROBERTSON J% STONEYRJ, TOOLE JF. Carotid endarterectomy : Practice guidelines. J Vasc Surg 1992; 15: 469-479. 15 MAGNAN PC, CAUS T, BRANCHEREAU A, ROSSET E, PRIMA F. R6sultats a 10 ans des restaurations chirurgieales de l'art6re carotide interne. Ann Vasc Surg 1993; 7: 521-529. 16 BERNSTEINEF, HUMBER PB, COLLINS GM, DILLEY RB, DEVIN JB, STUART SH. Life expectancy and late stroke following carotid endarterectomy. Ann Surg 1983; 198: 80-86. 17 KIEFFEREz KOSKAS• BAHNINIAet al. R6sultats cliniques tardifs de la chh:urgie carotidienne. In : Kieffer E, Bousser MG, eds. Indications et r~sultats de la chirurgie carotidienne. Paris: AERCV, 1988; 51-66. 18 NORTH AMERICANSYMPTOMATICCAROTID ENDARTERECTOMYTRIAL COLLABORATORS. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl ] Med 1991; 325: 445-453. 19 EUROPEAN CAROTID SURGERY TRIALIST'S COLLABORATIVE GROUP. MRC European carotid surgery trial : interim results for symptomatic patients with severe (70-99%) or with mild (0-29%) carotid stenosis. Lancet 1991; 337: 1235-1243. 20 EXECUTIVECOMMITTEEFOR THE ASYMPTOMATICCAROTID ATHEROSCLEROSIS STUDy. Endarterectomy for asymptomatic carotid artery stenosis. JAMA 1995; 273: 1421-1428. 21 PIERCE GE, LLIOPOULOSJL, HOLCOMB MA, RIEDER CFI HERMRECK AS, THOMAS JH. Incidence of recurrent stenosis after carotid endarterectomy determined by digital subtraction angiography. Am ] Surg 1984; 148: 848-854. 22 SANDERSCA, HOENEVELDH, EIKELBOOMBC, LUDVaGJW, VERMEULEN FE, ALKERSTAFFRG. Residual lesions and early recurrent stenosis after carotid endarterectomy. J Vasc Surg 1987; 5: 731-737.

Accepted 28 November 1995