Exploring the value of the double source CT angiography in diagnosing in-stent restenosis in lower limb artery
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Objectives This paper is aimed to explore the value of double source CT angiography (DS-CTA) for diagnosing in-stent restenosis in lower limb artery. Methods From January 2016 to October 2018, all patients with stent in lower limb artery in our hospital were investigated by both DS-CTA and digital subtraction angiography. We measured the minimum lumen diameter and the diameter of the proximal normal vessels under each stent placement. The in-stent restenosis is defined as restenosis when the lumen area decreased by more than 50%. Digital subtraction angiography was performed within 1 week after DS-CT scan. Relationship between DS-CTA and digital subtraction angiography for diagnosing in-stent restenosis in lower limb artery was analyzed. The sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of DS-CTA for diagnosis of in-stent restenosis were analyzed with digital subtraction angiography as the reference standard. A total of 68 stents were placed in 51 patients. Among these patients, 27 cases were diagnosed as in-stent restenosis, presenting as endovascular contrast agent bias or crescent filling defect with the lumen area reducing over 50%, 6 cases of which had no significant in-stent restenosis by digital subtraction angiography analysis. Furthermore, 12 cases were occlusion, in which there was no high density contrast agent in stents; the remaining 41 stents were unobstructed and the contrast agent was filled well, 8 cases of which had significant in-stent restenosis by digital subtraction angiography analysis. In addition, four stents were deformed or distorted. Statistical analysis demonstrated the concentrations of DS-CTA and digital subtraction angiography in diagnosing in-stent restenosis for lower limb artery were closely related, and the sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of DS-CTA were 72.4%, 84.6%, 77.8%, 80.5%, and 79.4%, respectively. Conclusion DS-CTA has a potential reliability for diagnosis of in-stent restenosis in lower limb artery, which may be further improved to be used for clinical interventional treatment of vascular diseases.1. Defining the Clinical Problem 2. Pathophysiology of Restenosis 3. Clinical Presentations and Noninvasive Assessment of Restenosis 4. Clinical, Biochemical, Angiographic and Intravascular Ultrasound Predictors of Restenosis 5. Importance of Physiological Assessment Pre- and Post Intervention 6. The Role of Intravascular Ultrasound in Prevention and Treatment of Restenosis 7. Pharmacological Approaches to Prevent Restenosis 8. Drug-coated Stent for Restenosis 9. Gene Transfer for Coronary Restenosis 10. Stenting to Prevent Restenosis 11. Debulk/Stenting 12. Management of In-stent Restenosis 13. Management of Restenosis through Radiation Therapy 14. Radiation for Restenosis 15. Radioisotope Stents 16. Restenosis in the Peripheral Vasculature
Intravascular Ultrasound
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Objective:To evaluate the advantages of transradial artery coronary angiography.Method:Transradial artery coronary angiography was performed in 64 cases.Result:4 of 64 cases had radial artery angiography including 3 cases relieved with nitroglycerin injection and 1 case treated with transfemoral artery coronary angiography.Conclusion:Transradial artery coronary angiography should be recommended with less local complications and higher success rate.
Conventional angiography
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In summary, this discussion has dealt with the current state of restenosis occurring after coronary angioplasty. I have developed the theory that the lesion responsible for cases of restenosis is largely a proliferative lesion composed of activated and proliferating vascular smooth muscle cells. When this uncontrolled process continues it will finally obliterate the lumen, between three and six months after the dilatation. The restenosis process is predicted or at least more likely to occur in patients to have certain risk factors. These risk factors don't appear to be related to the patient per se but instead to the lesion and some procedural factors. Lesions that are proximal, particularly in the left anterior descending and vein grafts are at highest risk to undergo restenosis. Lesions that are long, very severely stenosed, incompletely dilated or in small coronary arteries are also at high-risk for restenosis. Overall, about one-third of all patients who have a successful PTCA will have restenosis. At least one-third of these will have no symptoms that are interpreted as ischemia. Therefore, the definition of restenosis has to be by angiography. There is no other way to make a definition at present. There are no medical treatments that are proven to prevent restenosis. Currently the only acceptable treatment is a repeat dilation or another interventional procedure.
Coronary arteries
Lumen (anatomy)
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Lumen (anatomy)
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The success of PTCA is limited by late restenosis, which occurs in 30-50% of all cases, chiefly within the first six months after the intervention. Restenosis is due to the proliferation of smooth muscle cells and especially to overproduction of extracellular matrix in the arterial wall. The coronary intervention is followed by a not fully defined constrictive process of wound healing, so-called remodeling. Various alternative intervention techniques were investigated but did not show any clear advantage concerning restenosis compared to PTCA. Although the rate of restenosis is reduced by stent implantation, which hinders remodeling, the remaining intimal hyperplasia often leads to restenosis. In spite of promising results in animal models, to date no effective human pharmacological therapy has been found to prevent restenosis. To determine whether antioxidants, endovascular radiation or gene therapy show any benefit will require further, larger trials.
Intimal hyperplasia
Coronary restenosis
Neointimal hyperplasia
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Coronary angiography is the necessary investigation in the diagnostic complex of patients with ischemic heart disease (IHD). The use of trans-radial access makes it possible to do the angiography without hospitalization. The algorithm of coronary angiography in day-time clinic was proposed. Non-hospital angiography in 15 patients was successful. It is the first time this method has been used in this country.
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In-stent restenosis after interventional treatment remains an unsolved and important clinical problem. The proliferation and migration of arterial smooth muscle cells are key events frequently followed by vascular restenosis after angioplasty and continuous inflammation may also be the other important factor for the restenosis after stenting. Study of the pathogenesis of restenosis may find some potentially novel therapeutic pathways for attenuating in-stent restenosis.
Pathogenesis
Coronary restenosis
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Restenosis after percutaneous transluminal coronary angioplasty is a critical factor limiting the usefulness of this procedure. It has been reported to occur in 25% to 50% of patients averaging 33%. In the majority of patients it appears within 6 months after procedure. Some clinical, angiographic and procedural factors can predict higher incidence of restenosis--they are discussed in the article. Main mechanisms which result in restenosis are intimal hyperplasia and smooth muscle cellular proliferation. Exercise thallium-201 scintigraphy and coronary angiography are the best methods in diagnosis of restenosis. The prevention and the therapy of restenosis appear as a difficult problems. Successful pharmacological approach doesn't exist until now. In about 50% of patients with restenosis coronary angioplasty is repeated with the same success and restenosis rate as in the first angioplasty.
Intimal hyperplasia
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In-stent restenosis represents the major limitation for stenting procedures. In-stent restenosis is the renarrowing o f the artery lumen within a stent predominantly due to excessive growth of neointimal hyperplasia. Clinical studies have found that stent design is a key determinant in the propensity o f stents to cause restenosis, indicating a vital link between the biomechanics o f stents and the development of the disease. The ISAR-STEREO Trial specifically assessed the effect o f strut thickness on restenosis outcome and found that for the same stent design, a thinner strut stent was associated with a significant reduction o f angiographic and clinical restenosis compared to the same stent with a thicker strut. The main objective o f this study is to use the finite element method to simulate these stenting procedures, and to examine the stresses induced within the stented arterial vessel walls by the stents, thus enabling the mechanical stimuli for in-stent restenosis to be identified.
Finite element models o f thin and thick strut stents were developed and the stents were deployed in various stenosed vessel geometries such that the stresses induced within the stented vessels by the two stents could be compared. The stresses were examined at the end o f stent deployment, to determine the mechanical stimuli for acute damage, and again at stent unloading, to determine the long term stimuli for in-stent restenosis. The stress analyses were used to determine the level of vascular injury caused to the artery by different strut thickness stents.
The finite element studies successfully identified differences between the mechanical loading of the arterial tissue in the vessels stented with the two different stents. The higher restenosis rate of the thicker strut stent, reported in the ISAR-STEREO clinical study, was found to be the result of the higher luminal gain achieved by the thicker strut stent, due to the lower recoil of the stent structure when both stents were expanded to the same initial lumen diameter. Further stenting analyses, however, found that the thicker strut stent resulted in a lower percentage of volume stressed at high levels compared with the thinner strut stent when it was expanded to the same final lumen diameter. This suggests that a thicker strut stent may in fact have the potential to be expanded to an optimal diameter whereby the in-stent restenosis is minimised. Therefore, it is proposed that the use of preclinical testing tools, such as finite element modelling, could be used to predetermine the deployment protocol and optimum luminal gain of a particular stent design in order to minimise the mechanical stimuli for in-stent restenosis.
Lumen (anatomy)
Intimal hyperplasia
Neointimal hyperplasia
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Lipoprotein (a) [Lp(a)] is an independent genetically determined marker of coronary artery disease. It is present in the atheromatous plaque with a molecular structure similar to that of plasminogen. Its role in postangioplasty restenosis is a possibility but is controversial. A population of 103 coronary patients underwent angioplasty with control coronary angiography before the 6th month; there were 53 good results and 50 cases of restenosis. The Lp(a) was measured by immunonephelemetry (threshold value of 250 mg/l). A subgroup with Lp(a) concentrations > 250 mg/l was identified. The average concentrations of Lp(a) in the two groups without restenosis (368 +/- 350 mg/l) and with restenosis (418 +/- 434 mg/l) were not statisticaly different (p = 0.2). When cases with Lp(a) > 250 mg/l were considered alone, the tendency to higher average concentrations of Lp(a) in the group with restenosis (777 +/- 424 mg/l) compared with the group without restenosis (656 +/- 340 mg/l) was more clear-cut but did not achieve statistical significance (p = 0.08). The individual scatter of Lp(a) being very wide (83 to 1,450 mg/l in the group without restenosis and 90 to 1,740 mg/l in the group with restenosis), it is impossible to predict restenosis from this parameter in a given individual. No correlations were observed between the different lipid fractions and restenosis. The extension of the lesions and the angioplasty site did not correlate with restenosis in this study. The authors conclude: 1) that the Lp(a) concentration has no individual predictive value for restenosis; 2) individuals with Lp(a) concentrations > 250 mg/l have an increased risk of restenosis (NS); 3) these results confirm other recent publications; and 4) further research into the isoforms of Lp(a) in each group could provide interesting data.
Lipoprotein(a)
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