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The natural history of early recurrent carotid artery stenosis
The Natural History of Early Recurrent Carotid Artery Stenosis CPT Chatt A. Johnson, MD, MC, COL David F. J. Tollefson, MD, MC, LTC Stephen B. Olsen, MD, MC, COL Charles A. Andersen, MD, MC, Jennifer McKee-Johnson, PhD, Tacoma, Washington
BACKGROUND: Early recurrent carotid stenosis, defined as greater than 50% stenosis within 2 years of a carotid endarterectomy (CEA), occurs in 4% to 19% of patients. These lesions are secondary to myointimal hyperplasia (MH). The natural history of these lesions has been examined prospectively, but the appropriate management of these lesions has not been clearly defined. The vascular surgery service at Madigan Army Medical Center (MAMC) has prospectively collected a cohort of patients with recurrent highgrade carotid stenoses following CEA to determine their natural history and define the ideal therapeutic approach for those lesions. METHODS: Patients undergoing CEA between January 1, 1993, and January 1, 1997, at a single tertiary care institution were followed prospectively with postoperative carotid duplexes at 3-month intervals for the first year and then every 6 months for a year and then annually thereafter. Data were collected regarding patient demographics, type of carotid closure, neurologic morbidity, and death. These results were compared with accepted rates in the literature. Discrete variables were tested for significance by chi-square analysis and Fisher’s exact test. A P value less than or equal to 0.05 was considered significant. RESULTS: One hundred and seventy-four (174) patients with 181 operative sites were evaluated. Fourteen patients with 17 sites (9%) had recurrent stenosis. Twelve patients with 14 sites (7%) had stenoses of 50% to 79%. All were asymptomatic. Two patients with 3 sites (2%) had stenoses greater than 80%. Two sites were managed operatively because of neurologic symptoms or preocclusive nature and one remains asymptomatic and stable on serial duplex imaging. All lesions were present at 6 months and those in the 50% to 79% category did not progress in follow-up. Recurrent carotid stenosis occurred to a significantly higher degree in
From the Vascular Surgery Service, Madigan Army Medical Center, Tacoma, Washington. Requests for reprints should be addressed to CPT Chatt A. Johnson, MD, MC, General Surgery Service, Madigan Army Medical Center, Tacoma, Washington 98431. Presented at the 85th Annual Meeting of the North Pacific Surgical Association, Tacoma, Washington, November 13–14, 1998.
© 1999 by Excerpta Medica, Inc. All rights reserved.
women (women 11 of 60 18.3% versus men 6 of 114 5.3%; P 5 0.25), primary closure versus patch angioplasty (primary 6 of 22 27.3% versus patch 11 of 159 6.9%; P 5 0.01), and dacron versus polytetrafluoroethylene (PTFE) patch angioplasty (dacron 7 of 36 19.4% versus PTFE 2 of 100 2.0%; P 5 0.02). CONCLUSION: Early recurrent stenosis (50% to 79%) is a benign lesion. Patch angioplasty is preferred over primary closure. Dacron patches had a significantly higher rate of recurrent stenosis when compared with PTFE patches. Women undergoing CEA are more prone to recurrent stenosis. Postoperative duplex at 3 and 6 months will identify recurrent carotid stenosis (given a normal duplex prior to discharge following CEA). Moderate high-grade (50% to 79%) stenoses are benign. High-grade (80% to 99%) stenoses require individual management. Am J Surg. 1999;177:433– 436. © 1999 by Excerpta Medica, Inc.
T
he ability of carotid endarterectomy (CEA) to ameliorate the risk of stroke ipsilateral to a high-grade carotid stenosis has been defined recently in both the symptomatic and asymptomatic patient by the North American Symptomatic Carotid Endarterectomy Trial (NASCET) and Asymptomatic Carotid Atherosclerosis Study (ACAS), respectively.1,2 However, the therapeutic role of carotid endarterectomy in recurrent carotid stenosis is less clearly defined.3,4 This is especially true in early recurrent carotid stenosis, a greater than 50% diameter reduction occurring in less than 2 years, when the etiology is felt to be due to myointimal hyperplasia.5,6 The purpose of this study was to determine the natural history of early recurrent carotid artery stenosis.
PATIENTS AND METHODS From January 1993 to January 1997, the Vascular Surgery Service studied 174 patients who underwent carotid endarterectomy (181 total operative sites) at Madigan Army Medical Center. All patients were followed up in a prospective carotid surveillance protocol. Duplex imaging was performed during or immediately postoperatively, then in most cases, every 3 months for the first year postoperatively, then every 6 months for a year and then at yearly intervals. Criteria for determination of percent stenosis of the studied carotid artery has been previously defined (Table). All duplex analyses were performed in an accredited vascular laboratory (ICAVL) by one of two registered vascular technologists (RVT) using colorflow duplex scanning (ATL HDI 3000 with ESP and ATL Ultramark 9, 0002-9610/99/$–see front matter PII S0002-9610(99)00076-8
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TABLE Madigan Army Medical Center Duplex Criteria* for Carotid Stenosis 1% to 15% 16% to 49%
50% to 69% 70% to 79% 80% to 99%
No spectral broadening, peak systolic , 125 cm/sec Spectral broadening systolic deceleration only, peak systolic , 125 cm/sec Spectral broadening t/o systole, peak systolic . 125 cm/sec, ICA/CCA,4 Spectral broadening t/o systole, peak systolic . 125 cm/sec, ICA/CCA.4 End diastole . 140 cm/sec
* Based on the Moneta et al (7) modification of the Unviersity of Washington criteria for carotid stenosis. ICA/CCA 5 internal carotid artery peak systolic velocity/common carotid artery peak systolic velocity; t/o 5 throughout.
HDI with ESP). Degree of recurrent stenosis, demographics, type of operative closures (patch versus no patch), neurologic morbidity, and mortality were collected for all patients. Recurrent carotid stenoses were classified into 50% to 69% stenosis, 70% to 79% stenosis, and 80% to 99% stenosis (Table). All procedures were performed under general anesthesia. Intraluminal shunting and patching upon closure of the carotid artery were at the discretion of the surgeon. CEA was performed using standard vascular techniques. Systemic heparin was given, and intraoperative analysis of all repairs was performed. Early in our experience, arteriography or spectral analysis was used to interrogate the carotid artery. Currently, all CEAs are assessed by intraoperative colorflow duplex. Any defect noted was corrected during the initial operation. Low molecular weight dextran was given intraoperatively and postoperatively at the discretion of the surgeon. All patients received aspirin postoperatively unless contraindicated. Discrete variables were tested for significance by chisquare analysis and Fisher’s exact test. A P value less than or equal to 0.05 was considered significant.
RESULTS One hundred and seventy-four (174) patients with 181 operative sites were evaluated. The perioperative ipsilateral stroke rate (within 30 days) was 1.7% (3 of 181). There were no perioperative deaths. Two patients died remote to CEA, 1 of respiratory failure and 1 of myocardial failure. Four (2.3%) patients had cranial nerve injury. There were 114 (66%) men and 60 (34%) women in the study group. Operative closure of the carotid was with patch angioplasty in 159 (88%) and primary closure in 22 (12%). Patch closure consisted of saphenous vein (23, 14%), dacron (36, 23%), and polytetrafluoroethylene (PTFE; 100, 63%). There were no strokes during the 2 years following CEA. Seventeen (17 of 181, 9%) carotids were identified during follow-up to have recurrent stenosis. Eleven (11) were in the 50% to 69% range and 3 were 70% to 79%. These 14 stenoses were present by the 6-month evaluation, and no lesion progressed during the 2-year follow-up. All lesions remained asymptomatic. Three CEA sites in 2 patients had greater than 80% recurrent stenosis. One patient with 434
Figure. Incidence of early recurent carotid artery stenosis by patch angioplasty type. Dacron patch angioplasty was associated with a statistically higher rate of recurrent stenosis compared with polytetrafluoroethylene patch but not with vein patch closure (P 5 0.02).
high-grade stenosis at 3 months was asymptomatic. However, prior to the 6-month evaluation the patient had an ipsilateral transient ischemic attack, prompting CEA that was performed uneventfully. Two CEA sites in 1 patient (left and right sides) were identified at the 6-month evaluation to be 80% to 99% stenosed. Both lesions were asymptomatic. One site showed regression over the next 6 months. The other side progressed even further to a preocclusive stenosis, 90% plus by arteriography, by the 9-month follow-up and although asymptomatic, underwent an uneventful CEA. Pathology was consistent in both operative cases with myointimal hyperplasia. Regression of early recurrent stenoses was suggested by duplex evaluation. Duplex velocities decreased in 6 (35%), remained stable in 10 (59%), and progressed in only one (6%) site. Primary repair of the carotid endarterectomy site was associated with a significantly higher rate of recurrent stenosis (P 5 0.01). Six of 22 (27.3%) primary repair sites and 11 of 159 (6.9%) patch angioplasties had recurrent carotid stenoses. The incidence of recurrent carotid stenosis with each type of patch angioplasty closure is outlined in the Figure. Dacron patch angioplasty was associated with a statistically significant higher recurrent carotid stenosis rate compared with PTFE patch closure (P 5 0.02). Women had a significantly higher rate of recurrent stenosis. Eleven of 60 (18.3%) women had recurrent stenosis whereas only 6 of 114 (5.3%) men did (P 5 0.025). Distribution of recurrent stenosis in women by type of carotid repair was as follows: primary repair, 2 of 6 (33%); dacron patch, 5 of 17 (29%); PTFE, 2 of 30 (7%); and vein patch, 2 of 7 (29%). The incidence of recurrent stenosis was significantly higher (P 5 0.01) in dacron patch angioplasty versus PTFE patch closure. The distribution of re-
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current carotid stenosis in men based on type of carotid repair was as follows: primary repair, 4 of 16 (25%); dacron patch, 2 of 19 (11%); PTFE, 0 of 70 (0.0%); and vein, 0 of 16 (0.0%). The incidence of recurrent carotid stenosis in comparison with patch angioplasty technique in men never reached statistical significance for any method.
COMMENTS Carotid endarterectomy prevents stroke in individuals with primary high-grade carotid stenoses.1,2 This was supported by our experience with a perioperative stroke rate of 1.7% with no strokes postoperatively for the 2 years following. The role of CEA in stroke prevention for recurrent carotid stenosis is less clear. This is especially the case in early recurrent carotid stenosis occurring within the first 2 years after CEA.3,6,8 The reported incidence of recurrent carotid stenosis following carotid endarterectomy ranges from 1% to 36%.9 –11 Early recurrent carotid stenosis, occurring within 2 years after CEA is reported to occur in 4% to 19%.5,11–14 Our reported incidence of 9% is consistent with these reports. Although the natural history of primary carotid stenosis is clearly defined, that of recurrent early carotid stenosis is not. Early recurrent carotid stenosis following CEA, as described by Stoney and String,10 has been felt to be due to myointimal hyperplasia rather than atherosclerosis. Myointimal hyperplasia, grossly firm and homogenous, has a high collagen and smooth muscle content. It is not prone to ulcerate or calcify.3,10,15–17 These lesions have also been reported to remodel with a decrease in the severity of stenosis with time.5,12,18 We have found this to be the case in our series in over one third of our patients. These lesions do not ulcerate or suffer intraplaque hemorrhage. These characteristics are thought to cause less turbulence at the lesion site and minimize the potential for embolism. This may explain why the reported clinical behavior of early recurrent carotid stenosis is more benign.3,5,13,19 Indeed, in our patients with recurrent carotid stenoses of 50% to 69% and 70% to 79%, all were asymptomatic. All moderate recurrent stenoses were present by 6 months and remained stable or regressed thereafter. Although recurrent stenoses that were high grade were a small number, they posed the greatest therapeutic challenge. One patient’s site developed symptoms and clearly required reintervention. In the other two sites, one progressed and one regressed but both remained asymptomatic. Concerns of eventual carotid thrombosis prompted operative intervention in the lesion that progressed to a preocclusive nature. Carotid thrombosis has been shown to be a morbid event by Carballo et al .11 In their series, 2 of 3 patients with high-grade recurrent stenosis thrombosed and suffered severe stroke. There were some markers of recurrent carotid stenosis that were clearly identified. Sites that were closed primarily were at a distinctly higher risk of recurrent carotid stenosis, with over a threefold risk of recurrent stenosis. While patch angioplasty repair of a CEA decreased the risk of recurrent carotid stenosis, not all patch angioplasty closure techniques were equivalent. Dacron patching resulted in greater than twofold increased risk of recurrent stenosis in comparison with PTFE patch angioplasty. Because the operations were done by different surgeons, this difference in
recurrent stenosis between patch angioplasty types may be secondary to the operating surgeon. Women also had a threefold greater risk over men of recurrent carotid stenosis. The recurrent lesions in women were increased in all types of repairs when compared with types of repair in men, reflecting a true increased propensity for recurrent stenosis. Dacron patch angioplasty showed a propensity for higher recurrent stenosis in comparison with PTFE. Although recurrent stenosis was higher with dacron versus vein patch angioplasty, this did not reach statistical significance. When patching technique was broken down for male and female patients, the difference between dacron and PTFE was only statistically significant for women, although there was a trend toward significance in men. Whether that is due to the dacron patch technique or to the propensity for recurrent carotid stenosis in women after CEA will require further evaluation.
CONCLUSION Early recurrent carotid stenosis following carotid endarterectomy is an uncommon occurrence with an incidence of 9%. The histopathology of these lesions is consistent with myointimal hyperplasia. Patch angioplasty should be performed for all initial carotid endarterectomies to reduce the risk of recurrent carotid stenosis. This is recommended especially in women. The types of patching techniques need to be further investigated, but our data suggest that dacron patching may not be as ideal in comparison with PTFE. Clinically, the stenoses occur early in the postoperative course, most being evident by 6 months. These lesions tend to remain stable or regress thereafter. Moderate recurrent carotid stenoses tend to be asymptomatic, and no operative intervention is needed. High-grade stenoses (80% to 99%) must be handled on a case-by-case basis. Reoperative intervention would be reasonable for symptomatic or preocclusive lesions.
REFERENCES 1. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade stenosis. NEJM. 1991;325:445– 453. 2. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid artery stenosis. JAMA. 1995;273:1421–1428. 3. Lattimer CR, Burnand KG. Recurrent carotid stenosis after carotid endarterectomy. Br J Surg. 1997;84:1206 –1219. 4. Toursardissian B, Rubin BG, Sicard GA. Recurrent carotid artery stenosis. J Am Coll Surg. 1997;184:93–98. 5. Zierler RE, Bandyk DF, Thiele BL, Strandness DE. Carotid artery stenosis following endarterectomy. Arch Surg. 1982;117: 1408 –1412. 6. Nicholls SC, Phillips DJ, Bergelin RO, et al. Carotid endarterectomy: relationship of outcome to early restenosis. J Vasc Surg., 1985;2:375–381. 7. Moneta GL, Edwards JM, Papanicolaou G, et al. Screening for asymptomatic internal carotid artery stenosis: duplex criteria for discriminating 60% to 99% stenosis. J Vasc Surg. 1995;21:989 –984. 8. Healy DA, Zierler RE, Nicholls SC, et al. Long-term follow-up and clinical outcome of carotid restenosis. J Vasc Surg. 1989;10: 662– 668. 9. Norrving B, Nilsson B, Olsson JE. Progression of carotid disease after carotid endarterectomy: a doppler ultrasound study. Ann Neurol. 1982;12:548 –552.
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10. Stoney RJ, String ST. Recurrent carotid stenosis. Surgery. 1976;80:705–710. 11. Carballo RE, Towne JB, Seabrook GR, et al. An outcome analysis of carotid endarterectomy: the incidence and natural history of recurrent stenosis. J Vasc Surg. 1996;23:749 –754. 12. Thomas M, Otis SM, Rush M, et al. Recurrent carotid artery stenosis following endarterectomy. Ann Surg. 1984;200:74 –79. 13. Baker WH, Hayes AC, Mahler D, Littooy FN. Durability of carotid endarterectomy. Surgery. 1983;94:112–115. 14. Bernstein EF, Torem S, Dilley RB. Does carotid restenosis predict an increased risk of late symptoms, stroke, or death? Ann Surg. 1990;212:629 – 636. 15. Gagne PJ, Riles TS, Jacobowitz GR, et al. Long-term follow-up
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of patients undergoing reoperation for recurrent carotid artery disease. J Vasc Surg. 1993;18:991–1001. 16. Das MB, Hertzer NR, Ratliff NB, et al. Recurrent carotid stenosis. Ann Surg. 1985;202:28 –35. 17. Callow AD. Recurrent stenosis after carotid endarterectomy. Arch Surg. 1982;117:1082–1085. 18. Sanders EACM, Hoenveld H, Eikelboom BC, et al. Residual lesions and early recurrent stenosis after carotid endarterectomy. A serial follow-up study with duplex scanning and intravenous digital subtraction angiography. J Vasc Surg. 1987;5:731–737. 19. Washburn WK, Mackey WC, Belkin M, O’Donnell TF. Late stroke after carotid endarterectomy: the role of recurrent stenosis. J Vasc Surg. 1992;15:1032–1037.
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BACKGROUND: Early recurrent carotid stenosis, defined as greater than 50% stenosis within 2 years of a carotid endarterectomy (CEA), occurs in 4% to 19% of patients. These lesions are secondary to myointimal hyperplasia (MH). The natural history of these lesions has been examined prospectively, but the appropriate management of these lesions has not been clearly defined. The vascular surgery service at Madigan Army Medical Center (MAMC) has prospectively collected a cohort of patients with recurrent highgrade carotid stenoses following CEA to determine their natural history and define the ideal therapeutic approach for those lesions. METHODS: Patients undergoing CEA between January 1, 1993, and January 1, 1997, at a single tertiary care institution were followed prospectively with postoperative carotid duplexes at 3-month intervals for the first year and then every 6 months for a year and then annually thereafter. Data were collected regarding patient demographics, type of carotid closure, neurologic morbidity, and death. These results were compared with accepted rates in the literature. Discrete variables were tested for significance by chi-square analysis and Fisher’s exact test. A P value less than or equal to 0.05 was considered significant. RESULTS: One hundred and seventy-four (174) patients with 181 operative sites were evaluated. Fourteen patients with 17 sites (9%) had recurrent stenosis. Twelve patients with 14 sites (7%) had stenoses of 50% to 79%. All were asymptomatic. Two patients with 3 sites (2%) had stenoses greater than 80%. Two sites were managed operatively because of neurologic symptoms or preocclusive nature and one remains asymptomatic and stable on serial duplex imaging. All lesions were present at 6 months and those in the 50% to 79% category did not progress in follow-up. Recurrent carotid stenosis occurred to a significantly higher degree in
From the Vascular Surgery Service, Madigan Army Medical Center, Tacoma, Washington. Requests for reprints should be addressed to CPT Chatt A. Johnson, MD, MC, General Surgery Service, Madigan Army Medical Center, Tacoma, Washington 98431. Presented at the 85th Annual Meeting of the North Pacific Surgical Association, Tacoma, Washington, November 13–14, 1998.
© 1999 by Excerpta Medica, Inc. All rights reserved.
women (women 11 of 60 18.3% versus men 6 of 114 5.3%; P 5 0.25), primary closure versus patch angioplasty (primary 6 of 22 27.3% versus patch 11 of 159 6.9%; P 5 0.01), and dacron versus polytetrafluoroethylene (PTFE) patch angioplasty (dacron 7 of 36 19.4% versus PTFE 2 of 100 2.0%; P 5 0.02). CONCLUSION: Early recurrent stenosis (50% to 79%) is a benign lesion. Patch angioplasty is preferred over primary closure. Dacron patches had a significantly higher rate of recurrent stenosis when compared with PTFE patches. Women undergoing CEA are more prone to recurrent stenosis. Postoperative duplex at 3 and 6 months will identify recurrent carotid stenosis (given a normal duplex prior to discharge following CEA). Moderate high-grade (50% to 79%) stenoses are benign. High-grade (80% to 99%) stenoses require individual management. Am J Surg. 1999;177:433– 436. © 1999 by Excerpta Medica, Inc.
T
he ability of carotid endarterectomy (CEA) to ameliorate the risk of stroke ipsilateral to a high-grade carotid stenosis has been defined recently in both the symptomatic and asymptomatic patient by the North American Symptomatic Carotid Endarterectomy Trial (NASCET) and Asymptomatic Carotid Atherosclerosis Study (ACAS), respectively.1,2 However, the therapeutic role of carotid endarterectomy in recurrent carotid stenosis is less clearly defined.3,4 This is especially true in early recurrent carotid stenosis, a greater than 50% diameter reduction occurring in less than 2 years, when the etiology is felt to be due to myointimal hyperplasia.5,6 The purpose of this study was to determine the natural history of early recurrent carotid artery stenosis.
PATIENTS AND METHODS From January 1993 to January 1997, the Vascular Surgery Service studied 174 patients who underwent carotid endarterectomy (181 total operative sites) at Madigan Army Medical Center. All patients were followed up in a prospective carotid surveillance protocol. Duplex imaging was performed during or immediately postoperatively, then in most cases, every 3 months for the first year postoperatively, then every 6 months for a year and then at yearly intervals. Criteria for determination of percent stenosis of the studied carotid artery has been previously defined (Table). All duplex analyses were performed in an accredited vascular laboratory (ICAVL) by one of two registered vascular technologists (RVT) using colorflow duplex scanning (ATL HDI 3000 with ESP and ATL Ultramark 9, 0002-9610/99/$–see front matter PII S0002-9610(99)00076-8
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TABLE Madigan Army Medical Center Duplex Criteria* for Carotid Stenosis 1% to 15% 16% to 49%
50% to 69% 70% to 79% 80% to 99%
No spectral broadening, peak systolic , 125 cm/sec Spectral broadening systolic deceleration only, peak systolic , 125 cm/sec Spectral broadening t/o systole, peak systolic . 125 cm/sec, ICA/CCA,4 Spectral broadening t/o systole, peak systolic . 125 cm/sec, ICA/CCA.4 End diastole . 140 cm/sec
* Based on the Moneta et al (7) modification of the Unviersity of Washington criteria for carotid stenosis. ICA/CCA 5 internal carotid artery peak systolic velocity/common carotid artery peak systolic velocity; t/o 5 throughout.
HDI with ESP). Degree of recurrent stenosis, demographics, type of operative closures (patch versus no patch), neurologic morbidity, and mortality were collected for all patients. Recurrent carotid stenoses were classified into 50% to 69% stenosis, 70% to 79% stenosis, and 80% to 99% stenosis (Table). All procedures were performed under general anesthesia. Intraluminal shunting and patching upon closure of the carotid artery were at the discretion of the surgeon. CEA was performed using standard vascular techniques. Systemic heparin was given, and intraoperative analysis of all repairs was performed. Early in our experience, arteriography or spectral analysis was used to interrogate the carotid artery. Currently, all CEAs are assessed by intraoperative colorflow duplex. Any defect noted was corrected during the initial operation. Low molecular weight dextran was given intraoperatively and postoperatively at the discretion of the surgeon. All patients received aspirin postoperatively unless contraindicated. Discrete variables were tested for significance by chisquare analysis and Fisher’s exact test. A P value less than or equal to 0.05 was considered significant.
RESULTS One hundred and seventy-four (174) patients with 181 operative sites were evaluated. The perioperative ipsilateral stroke rate (within 30 days) was 1.7% (3 of 181). There were no perioperative deaths. Two patients died remote to CEA, 1 of respiratory failure and 1 of myocardial failure. Four (2.3%) patients had cranial nerve injury. There were 114 (66%) men and 60 (34%) women in the study group. Operative closure of the carotid was with patch angioplasty in 159 (88%) and primary closure in 22 (12%). Patch closure consisted of saphenous vein (23, 14%), dacron (36, 23%), and polytetrafluoroethylene (PTFE; 100, 63%). There were no strokes during the 2 years following CEA. Seventeen (17 of 181, 9%) carotids were identified during follow-up to have recurrent stenosis. Eleven (11) were in the 50% to 69% range and 3 were 70% to 79%. These 14 stenoses were present by the 6-month evaluation, and no lesion progressed during the 2-year follow-up. All lesions remained asymptomatic. Three CEA sites in 2 patients had greater than 80% recurrent stenosis. One patient with 434
Figure. Incidence of early recurent carotid artery stenosis by patch angioplasty type. Dacron patch angioplasty was associated with a statistically higher rate of recurrent stenosis compared with polytetrafluoroethylene patch but not with vein patch closure (P 5 0.02).
high-grade stenosis at 3 months was asymptomatic. However, prior to the 6-month evaluation the patient had an ipsilateral transient ischemic attack, prompting CEA that was performed uneventfully. Two CEA sites in 1 patient (left and right sides) were identified at the 6-month evaluation to be 80% to 99% stenosed. Both lesions were asymptomatic. One site showed regression over the next 6 months. The other side progressed even further to a preocclusive stenosis, 90% plus by arteriography, by the 9-month follow-up and although asymptomatic, underwent an uneventful CEA. Pathology was consistent in both operative cases with myointimal hyperplasia. Regression of early recurrent stenoses was suggested by duplex evaluation. Duplex velocities decreased in 6 (35%), remained stable in 10 (59%), and progressed in only one (6%) site. Primary repair of the carotid endarterectomy site was associated with a significantly higher rate of recurrent stenosis (P 5 0.01). Six of 22 (27.3%) primary repair sites and 11 of 159 (6.9%) patch angioplasties had recurrent carotid stenoses. The incidence of recurrent carotid stenosis with each type of patch angioplasty closure is outlined in the Figure. Dacron patch angioplasty was associated with a statistically significant higher recurrent carotid stenosis rate compared with PTFE patch closure (P 5 0.02). Women had a significantly higher rate of recurrent stenosis. Eleven of 60 (18.3%) women had recurrent stenosis whereas only 6 of 114 (5.3%) men did (P 5 0.025). Distribution of recurrent stenosis in women by type of carotid repair was as follows: primary repair, 2 of 6 (33%); dacron patch, 5 of 17 (29%); PTFE, 2 of 30 (7%); and vein patch, 2 of 7 (29%). The incidence of recurrent stenosis was significantly higher (P 5 0.01) in dacron patch angioplasty versus PTFE patch closure. The distribution of re-
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current carotid stenosis in men based on type of carotid repair was as follows: primary repair, 4 of 16 (25%); dacron patch, 2 of 19 (11%); PTFE, 0 of 70 (0.0%); and vein, 0 of 16 (0.0%). The incidence of recurrent carotid stenosis in comparison with patch angioplasty technique in men never reached statistical significance for any method.
COMMENTS Carotid endarterectomy prevents stroke in individuals with primary high-grade carotid stenoses.1,2 This was supported by our experience with a perioperative stroke rate of 1.7% with no strokes postoperatively for the 2 years following. The role of CEA in stroke prevention for recurrent carotid stenosis is less clear. This is especially the case in early recurrent carotid stenosis occurring within the first 2 years after CEA.3,6,8 The reported incidence of recurrent carotid stenosis following carotid endarterectomy ranges from 1% to 36%.9 –11 Early recurrent carotid stenosis, occurring within 2 years after CEA is reported to occur in 4% to 19%.5,11–14 Our reported incidence of 9% is consistent with these reports. Although the natural history of primary carotid stenosis is clearly defined, that of recurrent early carotid stenosis is not. Early recurrent carotid stenosis following CEA, as described by Stoney and String,10 has been felt to be due to myointimal hyperplasia rather than atherosclerosis. Myointimal hyperplasia, grossly firm and homogenous, has a high collagen and smooth muscle content. It is not prone to ulcerate or calcify.3,10,15–17 These lesions have also been reported to remodel with a decrease in the severity of stenosis with time.5,12,18 We have found this to be the case in our series in over one third of our patients. These lesions do not ulcerate or suffer intraplaque hemorrhage. These characteristics are thought to cause less turbulence at the lesion site and minimize the potential for embolism. This may explain why the reported clinical behavior of early recurrent carotid stenosis is more benign.3,5,13,19 Indeed, in our patients with recurrent carotid stenoses of 50% to 69% and 70% to 79%, all were asymptomatic. All moderate recurrent stenoses were present by 6 months and remained stable or regressed thereafter. Although recurrent stenoses that were high grade were a small number, they posed the greatest therapeutic challenge. One patient’s site developed symptoms and clearly required reintervention. In the other two sites, one progressed and one regressed but both remained asymptomatic. Concerns of eventual carotid thrombosis prompted operative intervention in the lesion that progressed to a preocclusive nature. Carotid thrombosis has been shown to be a morbid event by Carballo et al .11 In their series, 2 of 3 patients with high-grade recurrent stenosis thrombosed and suffered severe stroke. There were some markers of recurrent carotid stenosis that were clearly identified. Sites that were closed primarily were at a distinctly higher risk of recurrent carotid stenosis, with over a threefold risk of recurrent stenosis. While patch angioplasty repair of a CEA decreased the risk of recurrent carotid stenosis, not all patch angioplasty closure techniques were equivalent. Dacron patching resulted in greater than twofold increased risk of recurrent stenosis in comparison with PTFE patch angioplasty. Because the operations were done by different surgeons, this difference in
recurrent stenosis between patch angioplasty types may be secondary to the operating surgeon. Women also had a threefold greater risk over men of recurrent carotid stenosis. The recurrent lesions in women were increased in all types of repairs when compared with types of repair in men, reflecting a true increased propensity for recurrent stenosis. Dacron patch angioplasty showed a propensity for higher recurrent stenosis in comparison with PTFE. Although recurrent stenosis was higher with dacron versus vein patch angioplasty, this did not reach statistical significance. When patching technique was broken down for male and female patients, the difference between dacron and PTFE was only statistically significant for women, although there was a trend toward significance in men. Whether that is due to the dacron patch technique or to the propensity for recurrent carotid stenosis in women after CEA will require further evaluation.
CONCLUSION Early recurrent carotid stenosis following carotid endarterectomy is an uncommon occurrence with an incidence of 9%. The histopathology of these lesions is consistent with myointimal hyperplasia. Patch angioplasty should be performed for all initial carotid endarterectomies to reduce the risk of recurrent carotid stenosis. This is recommended especially in women. The types of patching techniques need to be further investigated, but our data suggest that dacron patching may not be as ideal in comparison with PTFE. Clinically, the stenoses occur early in the postoperative course, most being evident by 6 months. These lesions tend to remain stable or regress thereafter. Moderate recurrent carotid stenoses tend to be asymptomatic, and no operative intervention is needed. High-grade stenoses (80% to 99%) must be handled on a case-by-case basis. Reoperative intervention would be reasonable for symptomatic or preocclusive lesions.
REFERENCES 1. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade stenosis. NEJM. 1991;325:445– 453. 2. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid artery stenosis. JAMA. 1995;273:1421–1428. 3. Lattimer CR, Burnand KG. Recurrent carotid stenosis after carotid endarterectomy. Br J Surg. 1997;84:1206 –1219. 4. Toursardissian B, Rubin BG, Sicard GA. Recurrent carotid artery stenosis. J Am Coll Surg. 1997;184:93–98. 5. Zierler RE, Bandyk DF, Thiele BL, Strandness DE. Carotid artery stenosis following endarterectomy. Arch Surg. 1982;117: 1408 –1412. 6. Nicholls SC, Phillips DJ, Bergelin RO, et al. Carotid endarterectomy: relationship of outcome to early restenosis. J Vasc Surg., 1985;2:375–381. 7. Moneta GL, Edwards JM, Papanicolaou G, et al. Screening for asymptomatic internal carotid artery stenosis: duplex criteria for discriminating 60% to 99% stenosis. J Vasc Surg. 1995;21:989 –984. 8. Healy DA, Zierler RE, Nicholls SC, et al. Long-term follow-up and clinical outcome of carotid restenosis. J Vasc Surg. 1989;10: 662– 668. 9. Norrving B, Nilsson B, Olsson JE. Progression of carotid disease after carotid endarterectomy: a doppler ultrasound study. Ann Neurol. 1982;12:548 –552.
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THE AMERICAN JOURNAL OF SURGERY® VOLUME 177 MAY 1999