Since Eastcott et al. first reported surgical relief of carotid stenosis in 1954 [1], CEA has become the main treatment strategy for surgical treatment of carotid stenosis [2,3].CEA is effective in preventing stroke, but the high perioperative risk also greatly limits the widespread implementation of CEA.There are many causes of surgery-related stroke, mainly including surgical site thrombosis formation or residual vascular defects [4]. In 1976, Blaisdell et al. found intraoperative digital subtraction angiography (DSA) to reveal residual vascular defects in 26% of patients undergoing CEA [5], and this finding was later confirmed by many researchers using postoperative DSA, ultrasound and CTA [6-9]. Many scholars have studied its possible impact on clinical prognosis, but it is still inconclusive. In this study, we observed the residual vascular defect after CEA by postoperative CTA and explored its impact on clinical prognosis with a follow-up of 4 to 6 months. Jianlin Li, Department of Vascular Surgery, First Affiliated Hospital of Zhengzhou University
Subjects and methods
Patients who underwent CEA between 2011.1.1 and 2012.9.1 (including stenosis ≥50% with clinical symptoms group and severe stenosis ≥70%) were completed CTA within 1 month after surgery and followed up with color ultrasound for 4-6 months. Exclusion included patients with preoperative combination of severe cardiopulmonary disease or large-sided cerebral infarction that could not be objectively evaluated for post-operative complications of CEA. A total of 175 patients (104 men and 71 women) were entered into the study, and the procedure was performed with general anesthesia by endotracheal intubation, all by experienced vascular surgeons. Before carotid artery clamping, systemic heparinization (0.8-1.0 mg/Kg) was performed, the artery was dissected longitudinally along the CCA and ICA, a diverter tube was selectively applied (6 cases, 3.4%), the endothelium was separated from the epithelium by a non-invasive stripper, the CCA endothelial plaque was excised in an exenterative fashion, the ICA endothelial plaque was ingested in a nested fashion, and the endothelial plaque was removed by repeated flushing with heparin saline to carefully remove debris debris and trim the endothelium Endothelial patch fixation was performed if necessary (9 cases, 5.1%), and patch sutures were selectively applied (22 cases, 12.6%). After vascular suturing, the ECA and CCA were opened first with paralleling perfusion of ECA, and finally the ICA was opened to prevent cerebral embolism. Postoperative antiplatelet aggregation and anticoagulation were given.
CTA was performed within 1 month after surgery to evaluate the patency of CCA, ICA and ECA, and to observe and record the residual defects of the vessels. The residual defects included mainly: traces of clamping caused by diverter bundle closure or vascular blocking forceps clamping, endothelial stepping, endothelial lamellae, appendicular thrombus, vascular kinking and anastomotic microfractures (vessel wall outgrowth due to fractures in the anastomosis) [6]. The number of cardiovascular and cerebrovascular events, including: death, ischemic stroke, transient ischemic attack (TIA), retinal infarction, transient dark haze (AF), cerebral hemorrhage, subarachnoid hemorrhage and nonfatal myocardial infarction, were observed and recorded during the postoperative follow-up period of 4 to 6 months. Ultrasound was repeated once a month during postoperative follow-up to evaluate carotid artery patency.
Results
Postoperative CTA of CEA showed the presence of residual defects in 152 cases (86.9%) with a total of 376 defects, including 169 (44.9%) in CCA, 137 (36.4%) in ICA, and 70 (18.7%) in ECA. the defects in CCA were mainly endothelial gradation and residual stenosis, in ICA mainly endothelial gradation, kink and endothelial lamellae, and in ECA mainly endosteal lamellae and residual stenosis. There were 5 (3.0%) CCAs, 12 (8.8%) ICAs, and 33 (47.1%) ECAs causing 30% to 50% stenosis, 3 (1.8%) CCAs, 7 (5.1%) ICAs, and 6 (8.6%) ECAs causing 50% to 60% stenosis, and no ≥60% stenosis. There was no significant correlation between these defects and the surgical operation, and the six patients with a diverter tube had more defects on the CCA, but the difference was not statistically significant, and there were no characteristic traces of clamping with the diverter tube.
Table 1 Defects observed on CTA after CEA surgery.
Defects on CTA
Percentage of reconstructed carotid artery (%)
CCA
ICA
ECA
Endothelial order formation
93 (53.1)
39 (22.3)
6 (3.4)
Endosome sheet
13 (7.4)
26 (14.9)
36 (20.6)
Clamped closed traces
18 (10.3)
0 (0.0)
0 (0.0)
Attachment wall thrombus
7 (4.0)
0 (0.0)
0 (0.0)
Vascular kink
0 (0.0)
42 (24.0)
3 (1.7)
Anastomotic microfracture
4 (2.3)
2 (1.1)
0 (0.0)
Residual stenosis
29 (16.6)
21 (12.0)
19 (10.9)
Other defects
5 (2.9)
7 (4.0)
6 (3.4)
Four cases (2.3%) had cerebrovascular events within 30 days after surgery and there were no fatal cases. Three deaths (one from ischemic stroke and two from other coexisting diseases) and 17 (9.7%) cardiovascular and cerebrovascular events occurred during follow-up, of which 8 (4.6%) had symptoms of ipsilateral cerebral ischemia. There was no significant association between the occurrence of recurrent restenosis (50% to 99%) and residual defect without examination rate residual defect caused by stenosis color ultrasound follow-up.
In images 1-4, the white arrows point to the endocardial formation order; the white arrow-like arrows point to the endocardial sheet; the white arrow head end points to the pinch marks; the white triangle points to the vascular tortuosity; and the white triangle side points to the residual stenosis.
Discussion
In this study, we found that postoperative vascular defects after CEA were widespread in CCA, ICA, and ECA, and almost all (86.9%) CEA patients had residual defects on postoperative CTA. Most of the residual defects were not associated with the occurrence of postoperative cardiovascular and cerebrovascular events and restenosis at follow-up ultrasound. Microscopic malformations and residual defects can be considered as legitimate complications of CEA, and revascularization does not completely restore the vessel. Only the thickened endothelium of the CCA nearest to the atherosclerotic plaque within the operative field can be removed during CEA, and in most patients thickened endothelium remains proximal to the CCA, inevitably forming an endothelial order. The high proportion of residual defects on postoperative CTA suggests that most normal CEAs will leave “traces” of revascularization after surgery, but most of these “traces” do not affect the clinical prognosis without causing restenosis. Only 10 of the CCA and ICA defects resulted in ≥50% stenosis but did not cause cerebral ischemic symptoms. Only ECA defects and observed vascular malformations were correlated in the ultrasound follow-up, and there was no significant correlation between recurrent restenosis (all ≤70%) and residual defects, which may be related to intraoperative resection of the ECA lining without dissection of the ECA, while the mechanism of recurrent restenosis is still not well understood [10]. Most residual defects do not cause stenosis of the lumen do not affect blood flow velocity, so people rarely consider residual defects on CTA after CEA [2,3].
The widespread presence of residual defects and the classification of residual defects described in this study are important for both imaging physicians and clinicians, and the rate of residual defects reported in the study is higher than previous literature reports of 5.3% to 45% [5,7,9], which may be related to the different criteria for developing residual defects and the form of imaging. holder et al. reported a higher rate of residual defects of 91% [11] which is mainly due to its inclusion of small irregularities in the vessel wall that were not included in other studies. In order to avoid the negative impact on clinical CEA due to the reported high percentage of residual defects present, we suggested to divide the stenosis caused by residual defects into two groups with different degrees of stenosis from 30% to 50% and ≥50% to explore the relationship between residual stenosis ≥50% and recurrent restenosis, while there was no association between residual stenosis ≥50% and recurrent restenosis occurrence in this study. Therefore, it is important to determine the “standard” of residual defect on postoperative CTA, for which there is no clear criterion. We expect to follow up the CTA after 1 year to observe those residual defects that persist, to identify the types of residual defects that affect the clinical prognosis, and to explore the possible mechanisms that can guide the surgical approach and clinical intervention. In this study, due to the short follow-up period, the small number of cardiovascular and cerebrovascular events observed during the postoperative follow-up, and the statistical indexes susceptible to individual differences, the impact of residual defects on clinical prognosis is still not very clear.
Conclusion
Residual defects were commonly found on CCA, ICA and ECA by CTA after CEA. However, small defects did not affect the prognosis, and reintervention was considered only when the defects caused severe restenosis. Despite the ionizing radiation involved in performing CTA, early postoperative CTA is important for radiologists and clinicians to understand the type and severity of residual defects.
[1] Eastcott HH, Pickering GW, Rob CG. Reconstruction of internal carotid artery in a patient with intermittent attacks of hemiplegia. Lancet 1954;267( 6846):994-996.
[2] Barnett HJ, Taylor DW, Eliasziw M, et al. Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. north American Symptomatic Carotid Endarterectomy Trial Collaborators. N Engl J Med 1998;339(20):1415-1425.
[3] European Carotid Surgery Trialists’ Collaborative Group. randomised trial of endarterectomy for recently symptomatic carotid stenosis: final results of the MRC European Carotid Surgery Trial (ECST). Lancet 1998;351(9113):1379-1387.
[4] Liapis CD, Paraskevas KI. Role of residual defects following carotid endarterectomy in the occurrence of cerebrovascular symptoms. vasc Endovascular Surg 2006;40(2):119-123.
[5] Blaisdell FW, Lim R Jr, Hall AD. Technical result of carotid endarterectomy. arteriographic assessment. Am J Surg 1967;114(2):239-246.
[6] Carpena JP, Bories J, Chiras J. Post-operative angiographic control. B. Main angiographic appearances after vertebral and internal carotid artery Neuroradiology 1985;27(6):557-566.
[7] Russell D, Bakke SJ, Wiberg J, et al. Patency and flow velocity profiles in the internal carotid artery assessed by digital subtraction angiography and Doppler studies three months following endarterectomy. J Neurol Neurosurg Psychiatry 1986;49(2):183-186.
[8] Pappada G, Guazzoni A, Panzarasa G, et al. Early postoperative angiographic findings after carotid endarterectomy. Acta Neurochir (Wien) 1988;95( 3-4):114-120.
[9] Marro B, Zouaoui A, Koskas F, et al. Computerized tomographic angiography scan following carotid endarterectomy. Ann Vasc Surg 1998;12(5):451-456 .
[10] Gröschel K, Riecker A, Schulz JB, et al. Systematic review of early recurrent stenosis after carotid angioplasty and stenting. Stroke 2005;36(2): 367-373.
[11] Holder J, Binet EF, Flanigan S, et al. Arteriography after carotid endarterectomy. AJR Am J Roentgenol 1981;137(3):483-487.