The article describes a computer modeling technique that allows predicting the development of restenosis of the internal carotid artery after carotid endarterectomy (CEE). A clinical case has been demonstrated that proves the effectiveness of the developed method. It is indicated that for the correct formation of the geometric model, data from multispiral computed tomography with angiography of the patient after CEE with a layer thickness of 0.6 mm and a current of 355 mA are required. To build a flow model, data of color duplex scanning in three sections are required: 1. In the proximal section of the common carotid artery (3 cm proximal to the bifurcation); 2. In the section of the external carotid artery, 2 cm distal to the carotid sinus; 3. In the section of the internal carotid artery, 2 cm distal to the carotid sinus. The result of computer calculations using specialized software (Sim Vascular, Python, Open Foam) is a mathematical model of blood flow in a vessel. It is an array of calculated data describing the speed and other characteristics of the flow at each point of the artery. Based on the analysis of RRT and TAWSS indicators, a computer model of bifurcation is formed, which makes it possible to predict areas of increased risk of restenosis development. Thus, the developed technique is able to identify a cohort of patients after CEE, subjected to a high probability of loss of the vessel lumen. Such an opportunity will provide a more precise supervision of these patients in the postoperative period with the aim of early diagnosis of restenosis and timely prevention of the development of adverse cardiovascular events.
<p>This review investigates the various methods used for carotid endarterectomy (CEE). These methods are presented, and allow us to analyse effective revascularisation with extended damage to the internal carotid artery. The data of studies comparing the results of eversion and classical carotid endarterectomy with plasty of the reconstruction zone with a patch made of diepoxy-treated pericardium are presented. Special attention is paid to emergency carotid endarterectomy and carotid endarterectomy in the acute period of ischemic stroke. The important and main aspects of the glomus-saving species of CEE are also demonstrated. The main complications behind operations, and causes of restenosis in long-term follow-up periods are also duly noted. Similarly, suggestions to eliminate these issues are also proposed. This review comprehensively covers the state of the art of carotid endarterectomy and dissects current techniques and methods in the area.</p><p>Received 16 July 2020. Revised 24 August 2020. Accepted 25 August 2020.</p><p><strong>Conflict of interest:</strong> Authors declare no conflicts of interest.</p><p><strong>Funding:</strong> The study did not have sponsorship.</p><p><strong>Author contributions</strong><br />Conception and study design: G.G. Khubulava<br />Drafting the article: A.N. Kazantsev<br />Critical revision of the article: A.A. Erofeev, V.N. Kravchuk, K.P. Chernykh<br />Final approval of the version to be published: G.G. Khubulava, A.N. Kazantsev, A.A. Erofeev, V.N. Kravchuk, K.P. Chernykh</p>
Objective: to analyze the in-hospital and long-term outcomes of classical carotid endarterectomy (CEE) in extended atherosclerotic lesions in comparison with the outcomes of this operation in local atherosclerotic plaque (AP). Materials and Methods. This study, which lasted from January 2010 to December 2020, included 148 patients with extended AP and hemodynamically significant internal carotid artery (ICA) stenosis. The term “extended” was understood as a hemodynamically significant lesion ≥ 5 cm long. These patients made up Group 1. Group 2 was formed over the same period of time from 632 patients with hemodynamically significant stenosis <5 cm long. In both cohorts, CEE with repair of the reconstruction zone with a diepoxide-treated xenopericardial patch was performed. Long-term follow-up was 71.4 ± 45.6 months. Results. The groups were comparable in terms of frequency of in-hospital complications: death (group 1: 0.67%, n = 1; group 2: 0.5%, n = 3; p = 0.74; OR = 1.42; 95% Cl 0.14-13.6), myocardial infarction (MI) (group 1: 0.67%, n = 1; group 2: 0.5%, n = 3; p = 0.74; OR = 1.42; 95% CI 0.14-13.6), ischemic stroke (group 1: 0%; group 2: 0.5%, n = 3; p = 0.91; OR = 0.6; 95% CI 0.03-11.8), combined endpoint (death + MI + stroke) (group 1: 1.35%, n = 2; group 2: 1.4%, n = 9; p = 0.74; OR = 0.94; 95% CI 0.2-4.43). The groups were also comparable in terms of frequency of long-term complications: death (group 1: 2.0%, n = 3; group 2: 2.05%, n = 13; p = 0.76; OR = 0.98; 95% CI 0.27-3.5), MI (group 1: 2.7%, n = 4; group 2: 2.4%, n = 15; p = 0.95; OR = 1.14; 95% CI 0.37-3.49), ischemic stroke (group 1: 5.4%, n = 8; group 2: 5.2%, n = 33; p = 0.9; OR = 1.03; 95% CI 0.46-2.29), ICA occlusion and restenosis (group 1: 12.8%, n = 19; group 2: 13.3%, n = 84; p = 0.99; OR = 0.96; 95% CI 0.56-1.63), combined endpoint (death + MI + stroke) (group 1: 10.1%, n = 15; group 2: 9.6%, n = 61; p = 0.98; OR = 1.05; 95% CI 0.58-1.91). Analysis of survival graphs revealed no significant intergroup differences for all types of complications (lethal outcome: p = 0.56; MI: p = 0.73; stroke/mini-stroke: p = 0.89; ICA restenosis/occlusion: p = 0.82; combined end point: p = 0.71). Their increase was uniform in both groups. However, more than half of all ICA restenoses and occlusions were visualized in the first 6 months after CEE. Conclusion. Implantation of a long patch (≥ 5 cm) is not characterized by increased incidence of restenosis and all adverse cardiovascular events during in-hospital and long-term follow-up.
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