RESUMO
No multicenter randomized clinical trial has been conducted worldwide to date on indications, types of surgery and their comparison with conservative treatment in patients with PI BSA. OBJECTIVE: Of the study is to improve the results of surgical treatment in patients with pathological tortuosity of the internal carotid artery. MATERIAL AND METHODS: The study included 119 patients (41 (34%) men and 78 (66%) women) with PI ICA aged 34 to 71 years (average age 53.2±7.5 years) divided into 2 groups. 64 patients (54%) of group I underwent BSA resection with lower mouth and 55 patients (46%) of group II underwent BSA prosthetics. Depending on the degree of neurological disorders, patients were distributed according to the classification of A.V. Pokrovsky. RESULTS: In the early postoperative period, TIA was noted in one patient, and transient lesions of the cranial nerves were observed in 5 patients. During 5 years of follow-up, none of the patients developed TIA, IS or other vascular events. In the early surgical period, there were no significant differences in effectiveness between the groups of patients. In the long-term period (5 years after surgery), a higher frequency of asymptomatic patients was noted in group I. CONCLUSION: Resection and replacement of a pathologically tortuous internal carotid artery (ICA) is a safe and effective surgical treatment. A multicenter randomized trial should be conducted to compare the effectiveness of surgical treatment of PI ICA with a conservative approach to effectively treat patients.
Assuntos
Artéria Carótida Interna , Tratamento Conservador , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Artéria Carótida Interna/diagnóstico por imagem , Artéria Carótida Interna/cirurgia , Face , Boca , Período Pós-OperatórioRESUMO
OBJECTIVE: To evaluate the results of surgical treatment of internal carotid artery kinking following fibromuscular dysplasia. MATERIAL AND METHODS: There were 32 patients who underwent surgical treatment of internal carotid artery kinking following fibromuscular dysplasia. Structural changes of carotid artery wall were analyzed using immunohistochemical survey. Considering destructive changes revealed, we divided all patients into 2 groups in order to assess long-term postoperative outcomes: 1 - ICA resection followed by anastomosis in end-to-end fashion; 2 - ICA replacement. Postoperative analysis included incidence of stroke, thrombosis and deformities of anastomosis zone, regression of cerebrovascular insufficiency. RESULTS: The main «phenotype¼ of arterial wall in patients with ICA kinking following fibromuscular dysplasia is a large number of smooth muscle cells releasing matrix matelloproteinases-2 and -9 and low level of their tissue inhibitor type 1. Postoperative deformities are more common within a year after surgery. Maximum incidence is observed after 12 months. Both ICA resection and replacement are followed by similar incidence of deformity later. No severe deformities were diagnosed. Resection of ICA kinking on the background of fibromuscular dysplasia is followed by comparable results with ICA replacement regarding the incidence stroke, thrombosis and regression of cerebrovascular insufficiency. CONCLUSION: Despite degradation of extracellular matrix, destruction of elastic fibers and their fragmentation, no significant deformities are observed in long-term postoperative period in patients with ICA kinking and fibromuscular dysplasia.
Assuntos
Doenças das Artérias Carótidas , Artéria Carótida Interna/cirurgia , Constrição Patológica/cirurgia , Displasia Fibromuscular , Doenças das Artérias Carótidas/etiologia , Doenças das Artérias Carótidas/metabolismo , Doenças das Artérias Carótidas/cirurgia , Artéria Carótida Interna/metabolismo , Constrição Patológica/etiologia , Constrição Patológica/metabolismo , Displasia Fibromuscular/complicações , Displasia Fibromuscular/metabolismo , Humanos , Metaloproteinases da Matriz Secretadas/metabolismo , Inibidores Teciduais de Metaloproteinases/metabolismoRESUMO
AIM: To assess an efficacy of carotid arteries reconstruction in patients with internal carotid artery stenosis combined with tortuosity. MATERIAL AND METHODS: 86 patients with ICA tortuosity and stenosis were enrolled. All patients were divided into groups depending on type of surgery: group I - open carotid endarterectomy (CEA) followed by obligatory repair with synthetic patch (31 (36%) patients); group II - eversion CEA with ICA resection, redressation and reimplantation into own ostium (35 (40.7%) patients); group III - ICA replacement (20 (23.3%) patients). Synthetic prosthesis and autovein were used in 13 (65%) and 7 (35%) patients respectively. The study included patients with ICA stenosis ≥60% (any type of plaque) and any degree of cerebrovascular insufficiency or ICA stenosis <60% (plaque type I-III) with CVI grade II-IV combined with S- or C-tortuosity, bend or loop with blood flow velocity over 110 cm/s and its turbulence. Only 6 (7.0%) out of 86 patients had no clinical signs of CVI/previous stroke. Asymptomatic/symptomatic patients ratio was following in all groups: group I - 12 (38.7%)/19 (61.3%); group II - 29 (82.9%)/6 (17.1%); group III - 10 (50%)/10 (50%). RESULTS: Within 6-month follow-up 22 (70.9%) out of 31 patients were asymptomatic in group I, 30 (85.7%) (p=0.9475) out of 35 - in group II, 9 (45%) (p=0.9511) out of 20 patients - in group III and 1 (5%) patient developed thrombosis of the reconstruction zone followed by ischemic stroke. After 12 months following patients were asymptomatic: 22 (70.9%) in group I, 30 (85.7%) (p=0.9475) in group II and 9 (45%) patients (p=0.9511) in group III. After 1 year 4 (33.3%) out of 12 patients with CVI grade IV had partial regression of focal neurological symptoms. CONCLUSION: Surgery for ICA tortuosity combined with stenosis confirmed its efficacy and safety for both asymptomatic and symptomatic patients. Significantly better results were observed in eversion CEA compared with conventional procedure and ICA replacement.
Assuntos
Artéria Carótida Interna , Estenose das Carótidas , Endarterectomia das Carótidas , Complicações Pós-Operatórias/diagnóstico , Acidente Vascular Cerebral/prevenção & controle , Assistência ao Convalescente , Velocidade do Fluxo Sanguíneo , Artéria Carótida Interna/diagnóstico por imagem , Artéria Carótida Interna/patologia , Artéria Carótida Interna/cirurgia , Estenose das Carótidas/complicações , Estenose das Carótidas/diagnóstico , Estenose das Carótidas/cirurgia , Transtornos Cerebrovasculares/etiologia , Transtornos Cerebrovasculares/prevenção & controle , Endarterectomia das Carótidas/efeitos adversos , Endarterectomia das Carótidas/métodos , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Avaliação de Processos e Resultados em Cuidados de Saúde , Acidente Vascular Cerebral/etiologia , Avaliação de Sintomas , Resultado do Tratamento , Ultrassonografia Doppler Dupla/métodosRESUMO
UNLABELLED: The principal morphological sign of fibromuscular dysplasia in pathological tortuosity (PT) of the internal carotid artery (ICA) is the fragmentation of elastic fibers that are degraded by matrix metalloproteinases 2 and 9 (MMP-2, MMP-9). Nevertheless, the role of MMPs and their inhibitors in the pathogenesis of ICA PT remains completely unexplored. AIM: to investigate the expression of elastin-degrading MMPs and their inhibitors in the wall of the ICA in PT by immunohistochemistry and confocal laser scanning microscopy. METHODS: Immunohistochemical examination was made using antibodies to MMP-2, MMP-9 and their tissue inhibitors TIMP-1 and TIMP-2. MMP-9 and TIMP-1 levels were determined by confocal laser scanning microscopy. RESULTS: Immunohistochemical examination revealed a statistically significant predominance of high concentrations of MMP-2 and MMP-9 and a low level of their inhibitor TIMP-1 in ICA PT, while simultaneous obvious accumulation of both markers was most often identified in the control group (p<0.05). Analysis of MMP-2/TIMP-2 and MMP-9/TIMP-2 ratios showed the prevalence of the simultaneously high expression of both proteins in ICA PT and in the control group too. The similar data were also obtained by confocal microscopy: the control group showed elevated MMP-9 and TIMP-1 expressions and the ICA PT control displayed a high proteinase and low inhibitor levels (p<0.05). CONCLUSION: Elastic fiber fragmentation in ICA PT is due to imbalance between MMPs and their inhibitors; namely, the prevalence of MMP-2 and MMP-9 over their inhibitor TIMP-1, which leads to the degradation of extracellular matrix components, primarily elastin.
Assuntos
Artéria Carótida Interna/patologia , Metaloproteinase 2 da Matriz/metabolismo , Metaloproteinase 9 da Matriz/metabolismo , Inibidor Tecidual de Metaloproteinase-1/metabolismo , Inibidor Tecidual de Metaloproteinase-2/metabolismo , Malformações Vasculares/patologia , Adulto , Idoso , Artéria Carótida Interna/anormalidades , Artéria Carótida Interna/metabolismo , Estudos de Casos e Controles , Tecido Elástico/metabolismo , Tecido Elástico/patologia , Matriz Extracelular/metabolismo , Feminino , Humanos , Masculino , Metaloproteinase 2 da Matriz/genética , Metaloproteinase 9 da Matriz/genética , Pessoa de Meia-Idade , Inibidor Tecidual de Metaloproteinase-1/genética , Inibidor Tecidual de Metaloproteinase-2/genética , Malformações Vasculares/metabolismoRESUMO
OBJECTIVE: to study a change in the content of main components of the internal carotid artery (ICA) wall in pathological tortuosity (PT) resulting from fibromuscular dysplasia, using immunohistochemistry and confocal laser scanning microscopy. MATERIAL AND METHODS: Immunohistochemical (IHC) analysis using antibodies to elastin, collagen types I and III, and smooth muscle actin was made. The levels of elastin and matrix metalloproteinase 9 (MMP-9) were determined by confocal laser scanning microscopy. The relative area of expression and the area of co-location of these markers were measured. RESULTS: IHC examination of the expression of elastin revealed that the patients with PT of ICA had its higher content than the controls, but they were observed to have fiber fragmentation. Comparison of collagen types I and III expressions showed no significant differences between the groups. The found significantly lower smooth muscle actin expression in the patients with PT of ICA than in the controls was suggestive of the decreased levels of smooth muscle cells. Confocal microscopy analysis showed high elastin and low MMP-9 expressions in the control group and, on the contrary, low elastin and high proteinase levels in the PT group (Ñ<0.05). CONCLUSION: One of the causes of PT is impairment in vascular elastic properties due to the destruction of elastic fibers and to their fragmentation, as well as to the decreased count of smooth muscle cells, which in turn causes enhanced MMP-9 activity and tissue matrix degradation.