Redo carotid endarterectomy
Sachinder Singh Hans, Alexander D Shepard, Mitchell R Weaver, Paul G Bove, Graham W Long in Endovascular and Open Vascular Reconstruction, 2017
Very early on, recurrent carotid stenosis (RCS) is usually due to technical problems with the initial repair. Restenosis that develops within the first 24 months is most likely due to intimal hyperplasia. After 24 months, RCS is usually due to recurrent atherosclerosis. Restenosis may be asymptomatic or symptomatic. When patients are referred for RCS requiring intervention, it is the responsibility of the surgeon to determine the best treatment modality. Factors that enter the equation include: plaque morphology; anticipated neck “hostility;” level of the recurrent lesion; and the patient’s overall health and anticipated life expectancy. Finally, the open and endovascular operative skill sets of the treating surgeon need to be weighed when determining the best approach. The author does not have adequate information from his own experience to determine whether stenting is appropriate for the treatment of RCS. However, the good long-term results for RCEA have led him to recommend this treatment for most of his patients.6
Complications of stenting for occlusive disease of aortic arch branches
Sachinder Singh Hans, Mark F. Conrad in Vascular and Endovascular Complications, 2021
Early reports of endovascular repair showed that the primary patency was inferior to open surgical repair, and long-term studies are rare. In a recent report of 411 patients with long-term follow-up, restenosis occurred in 15% of patients, and most of these presented with symptom recurrence. The primary patency in this cohort was 92% at 1 year and 82.6% at 5 years, and patients with innominate interventions were more likely to present with recurrent stenosis.30 Follow-up after intervention usually consists of a clinic visit and noninvasive imaging at 6 weeks and then yearly thereafter. Most patients who developed restenosis experienced a return of symptoms as well. If a change is noted on noninvasive imaging, the anatomy can be further defined with axial imaging via a CTA or MRA. If a patient has restenosis but remains asymptomatic, they should be treated with medical therapy and monitoring with serial imaging. However, symptomatic patients should undergo re-intervention. Repeat intervention is usually endovascular, and open repair is rarely required. Indeed, in the previously noted study, the secondary patency at 5 years was 96%.30
Chronic Total Occlusions: New Therapeutic Approaches
Richard R Heuser, Giancarlo Biamino in Peripheral Vascular Stenting, 1999
Scheinert et al13 published results from a large series of patients that underwent excimer laser assisted revascularization of chronic SFA occlusions. With a total number of 318 patients (411 limbs or lesions, mean occlusion length 19.4 ± 6.0 cm) being treated with excimer laser assisted angioplasty, the primary success rate for revascularization was 83.2% (342/411 cases). A secondary attempt was performed in 44 cases, including using the retrograde popliteal approach in 39 cases. The total technical success rate was 90.5% (372/411 cases). Relevant interventional complications were acute reocclusion (1.0%), perforation (2.2%), and embolization/distal thrombosis (3.9%). Restenosis was detected in more than 50% of the cases; however, using secondary interventions, the majority of the reobstructions were treatable on an outpatient basis. As a result, the clinical benefit was maintained in 75.1% of the patients after 1 year.
A fully coupled framework for in silico investigation of in-stent restenosis
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2019
Shibo Li, Long Lei, Ying Hu, Yanfang Zhang, Shijia Zhao, Jianwei Zhang
From biological perspectives, various studies have shown that restenosis is caused by neointimal hyperplasia (Dussaillant et al. 1995; Shah 2003; Kleinedler et al. 2012), which is characterized by the proliferation and migration of vascular smooth muscle cells (VSMCs) in the tunica intima of the artery wall. This process is illustrated in Figure 1. The restenosis process starts with tissue damage and inflammation resulted from stent implantation or angioplasty procedure, followed by extracellular matrix (ECM) degradation and VSMC phenotype switches (Thyberg et al. 1997), which would result in neointimal formation. Moreover, increasing evidences have shown that the proliferation, migration and apoptosis behaviors of VSMCs are regulated by matrix-degrading metalloproteinases (MMPs) (Zempo et al. 1996; Newby 2006). Despite the complexity of the biological processes, mathematical models for computational purposes have been built for various problems (Garzón-Alvarado et al. 2012; Prokharau et al. 2014; Boyle et al. 2011).
Morphology and histology of silent and symptom-causing atherosclerotic carotid plaques – Rationale and design of the Helsinki Carotid Endarterectomy Study 2 (the HeCES2)
Published in Annals of Medicine, 2018
Krista Nuotio, Petra Ijäs, Hanna M. Heikkilä, Suvi M. Koskinen, Jani Saksi, Pirkka Vikatmaa, Pia Sorto, Laura Mäkitie, Henrietta Eriksson, Sonja Kasari, Heli Silvennoinen, Leena Valanne, Mikko I. Mäyränpää, Petri T. Kovanen, Lauri Soinne, Perttu J. Lindsberg
By the initiation of our study, the study patients have also consented to the follow-up of their health and medical data throughout the study. Information on recurrent cerebrovascular symptoms (TIA, stroke), cardiac events (myocardial infarctions, unstable angina, occurrence of atrial fibrillation) and other thromboembolic diseases will be retrieved from the National Care Register for Health Care up until 10 years from the recruitment. Deaths and the causes of death are collected from the Finnish public authority Statistics Finland. Study patients will be contacted no later than 10 years after their CEA, at which time they will be interviewed. A Doppler ultrasound examination will be performed in order to detect possible restenosis. Clinical records on general health, vascular events, medication and blood pressure will be revisited. Blood samples will be obtained as well.
Pinellia ternata attenuates carotid artery intimal hyperplasia and increases endothelial progenitor cell activity via the PI3K/Akt signalling pathway in wire-injured rats
Published in Pharmaceutical Biology, 2020
Hai-Ke Lu, Yan Huang, Xiao-Yu Liang, Ying-Yi Dai, Xin-Tong Liu
Within 6 months of wire angioplasty and stenting, approximately 15–40% of treated patients present with clinically significant renarrowing of the arteries causing vasospasm, thrombosis and intimal hyperplasia (Swanson et al. 2003). Although the use of stents reduces the incidence of restenosis after angioplasty, intimal hyperplasia, as the main mechanism of poststent restenosis, causes restenosis to remain a substantial clinical problem (Bhardwaj et al. 2005). The roles of VEGFs in intimal hyperplasia and atherogenesis are still unclear. Some studies have reported that certain members of the VEGF family can reduce intimal hyperplasia, while others accelerate restenosis and atherosclerosis (Cooney et al. 2007). In a rabbit model, Bhardwaj et al. (2005) found that efficient adventitial production of VEGF-A and VEGF-D could cause thickening of the inner layer of the artery. Our study found that VEGF expression levels were decreased in intimal hyperplasia model rats, that PT treatment upregulated VEGF expression, and that the PI3K/Akt pathway inhibitor LY294002 reduced VEGF expression. These results show that VEGF reduces intimal hyperplasi.
Related Knowledge Centers
- Angina
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- Stenosis
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- Blood Vessel
- Artery
- Atherosclerosis
- Percutaneous Coronary Intervention