Dissertations / Theses on the topic 'Saphenous Vein Graft Disease'
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1
Li, Jun. "Pre-existing intimal hyperplasia and overexpression of TGF-ß1 in saphenous vein grafts before myocardial revascularization in humans: implications for aortocoronary saphenous vein graft disease." Ulm : Univ. Ulm , Med. Fak, 2001. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-8610.
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Ohnaka, Motoaki. "Effect of microRNA-145 to prevent vein graft disease in rabbits by regulation of smooth muscle cell phenotype." Kyoto University, 2014. http://hdl.handle.net/2433/192144.
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The final publication is available at http://dx.doi.org/10.1016/j.jtcvs.2013.11.054. Motoaki Ohnaka, Akira Marui, Kenichi Yamahara, Kenji Minakata, Kazuhiro Yamazaki, Motoyuki Kumagai, Hidetoshi Masumoto, Shiro Tanaka, Tadashi Ikeda, Ryuzo Sakata, Effect of microRNA-145 to prevent vein graft disease in rabbits by regulation of smooth muscle cell phenotype, The Journal of Thoracic and Cardiovascular Surgery, Volume 148, Issue 2, August 2014, Pages 676-682.e2, ISSN 0022-5223.Kyoto University (京都大学)
0048
新制・課程博士
博士(医学)
甲第18544号
医博第3937号
新制||医||1006(附属図書館)
31444
京都大学大学院医学研究科医学専攻
(主査)教授 木村 剛, 教授 野田 亮, 教授 瀬原 淳子
学位規則第4条第1項該当
3
PRANDI, FRANCESCA. "Identification of early pathophysiological events underlying venous coronary bypass stenosis by a mechano-biology approach." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2014. http://hdl.handle.net/10281/50493.
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Saphenous vein graft disease represents an unresolved problem in coronary artery bypass grafting. After surgery, progressive modification in the vein wall occurs, leading to occlusion of the graft lumen. This process, called intima hyperplasia, involves the participation of vein-resident cells as well as the recruitment of vein-extrinsic cells. Arterial wall strain has recently emerged as one of the factor that can contribute to the pathogenesis of the vein graft disease. Therefore, in collaboration with Department of Bioengineering, Politecnico di Milano we developed a culture system for the ex vivo pressure stimulation of vein segments. This new ex vivo vein culture system is able to reproduce the wall strain typical of the arterial circulation. The ex vivo vein culture system (ECVS) adopted in this project has been validated and proved as a valuable, reliable, easy handling and versatile tool for studying arterial pressure events triggered in VGD.
The biological data achieved confirm an important contribution of the arterial-like wall strain in SV structural and biochemical changes, activation of vessel resident cells and in the expression of molecular signals involved in the pathogenesis of IH.
Using this system, we found that either venous- or arterial-specific pressure regimens induced vein pro-pathologic commitment involving upregulation of Matrix Metallo-Proteases 2/9, and induction of microRNAs-21/146a/221. By contrast, arterial-like pressure caused a significant morphological rearrangement of the vein, a suppression of Tissue Inhibitor of Metallo Protease-1, an enhanced expression of TGF-β1 and BMP-2 mRNAs and, finally, the upregulation of microRNAs-138/200b/200c. In coronary-pressure stimulated vessels, the density of the adventitial vasa vasorum was significantly increased. This was accompanied by an increased presence of cells co-expressing NG2, CD44 and SM22α markers in the adventitia, identifying them as multipotent mesenchymal cells/smooth muscle cells progenitors with a pericyte origin. An increase in Histone H3 Lysine 4 methylation and histone H4 Lysines 9/16 acetylation levels was finally found in adventitial cells and vasa vasorum. The present findings suggest a mechanistic role of the arterial-like pulsatile pressure in reinforcement of SV-resident cells pro-pathologic commitment in vein bypass failure, by activation of mechanical-dependent transcriptional circuitries and of pericyte-derived cells located in the vessel adventitia.
The ultimate goal of this project is to find a treatment that can prevent, avoid or reduce the incidence of the vein graft disease in patients subjected to bypass surgery with saphenous vein. This treatment could include one or more targets identified in this work focusing on the early stage of the pathological adaptation of the SV to the new hemodynamic environment.
4
Cornelissen, Jacqueline. "Saphenous vein bypass graft occlusion : signalling pathways and apoptosis." Thesis, University of the West of England, Bristol, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.431153.
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Crook, Martin. "Mechanisms of monocyte adhesion to human saphenous vein." Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324233.
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WADA, KENTARO, TOMOYUKI NODA, KENICHI HATTORI, HIDEKI MAKI, AKIRA KITO, and HIROFUMI OYAMA. "AIR VENT OF VEIN GRAFT IN EXTRACRANIAL-INTRACRANIAL BYPASS SURGERY." Nagoya University School of Medicine, 2012. http://hdl.handle.net/2237/16744.
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Gopakumar, Bhaskaran Nair. "Molecular strategies to inhibit vein graft disease." Thesis, University of Leeds, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.426787.
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Dreifaldt, Mats. "Conduits in coronary artery bypass grafting surgery : Saphenous vein, radial and internal thoracic arteries." Doctoral thesis, Örebro universitet, Institutionen för hälsovetenskap och medicin, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-33265.
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A novel technique for saphenous vein (SV) graft harvesting, the No-touch technique (NT), has been developed at the Dept. of Cardiovascular surgery, Örebro University hospital. With NT the SV is harvested with a pedicle of surrounding tissue. This avoids graft spasm and eliminates the need for distension. The surrounding tissue acts as a structural support and is a rich source of vaso-dilating agents. A randomized controlled trial (RCT) has shown a significantly higher patency rate for NT SV grafts compared to SV grafts harvested with conventional technique (CT). This thesis evaluates some of the properties of the surrounding tissue and compares patency rates between NT SV and radial artery (RA) grafts and patency rates for internal thoracic artery (ITA) grafts harvested with and without surrounding tissue. Paper I investigated vasa vasorum (VV) in SV grafts and showed that the NT preserves an intact VV whereas CT does not. This could be one of the mechanisms underlying the improved patency for NT SV grafts. Paper II evaluated VV and associated nitric oxide (NO) in SV and arterial grafts. SV grafts showed a higher number and larger VV, which correlated with NO production, compared to arterial grafts. NT SV grafts showed higher activity for e-NOS compared to CT SV grafts. Paper III is a RCT comparing patency rates between NT SV and RA grafts, three years after surgery, showing a significantly higher patency rate for NT SV grafts. Paper IV is a RCT comparing patency rates for ITA graft harvested with and without surrounding tissue and did not show any difference between graft preparations. In conclusion, the NT for SV graft harvesting preserves an intact vasa vasorum and associated NO production. NT SV grafts show a higher patency rate than RA grafts. Harvesting of ITA with or without surrounding tissue does not affect patency rate.
9
Paul, Timir, Samit Bhatheja, Hemang Panchal, Shimin Zheng, Subhash Banerjee, Sunil V. Raso, Luis Guzman, et al. "Outcomes of Saphenous Vein Graft Intervention With and Without Embolic Protection Device: A Comprehensive Review and Meta-Analysis." Digital Commons @ East Tennessee State University, 2017. https://dc.etsu.edu/etsu-works/2771.
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Background: Current guidelines give a class I recommendation to use of embolic protection devices (EPD) for saphenous vein graft (SVG) intervention; however, studies have shown conflicting results. The objective of this meta-analysis is to compare all-cause mortality, major adverse cardiovascular events, myocardial infarction (MI), or target vessel revascularization in SVG intervention with and without EPD.
Methods and Results: Literature was searched through October 2016. Eight studies (n=52 893) comparing SVG intervention performed with EPD (n=11 506) and without EPD (n=41 387) were included. There was no significant difference in all-cause mortality (odds ratio [OR], 0.79; confidence interval [CI], 0.55–1.12; P=0.19), major adverse cardiovascular events (OR, 0.73, CI, 0.51–1.05; P=0.09), target vessel revascularization (OR, 1.0; CI, 0.95–1.05; P=0.94), periprocedural MI (OR, 1.12; CI, 0.65–1.90, P=0.69), and late MI (OR, 0.80; CI, 0.52–1.23; P=0.30) between the 2 groups. Sensitivity analysis excluding CathPCI Registry study showed no difference in periprocedural MI, late MI, and target vessel revascularization; however, it favored EPD use in all-cause mortality and major adverse cardiovascular events. Further sensitivity analysis including only observational studies revealed no difference in all-cause mortality, major adverse cardiovascular events, target vessel revascularization, and late MI. Additional analysis after excluding CathPCI Registry study revealed no difference in outcomes.
Conclusions: This study including 52 893 patients suggests no apparent benefit in routine use of EPD during SVG intervention in the contemporary real-world practice. Further randomized clinical trials are needed in current era to evaluate long-term outcomes in routine use of EPD, and meanwhile, current guideline recommendations on EPD use should be revisited.
10
Kauhanen, Petteri. "Vascular regulation of hemostasis and fibrinolysis : with special focus on vein graft disease." Helsinki : University of Helsinki, 2001. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/kauhanen/.
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Rautio, T. (Tero). "Primary saphenous vein insufficiency:prospective studies on diagnostic duplex ultrasonography and treatment with endovenous radiofrequency-resistive heating." Doctoral thesis, University of Oulu, 2002. http://urn.fi/urn:isbn:9514267230.
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Abstract
The purpose of the present research was (I-II) to evaluate the effects of
clinical, hand-held Doppler (HHD) and duplex ultrasonographic examinations on the
planning of operative procedure for primary varicose veins, (III) to assess the
feasibility, safety and efficacy of endovenous saphenous vein obliteration with
radiofrequency-resistive heating and (IV) to compare endovenous saphenous vein
obliteration with conventional stripping operation in terms of short-term
recovery and costs.
Sixty-two legs (in 49 consecutive patients) and 142 legs (in 111
consecutive patients) with primary uncomplicated varicose veins were examined
clinically and with HHD and duplex ultrasonography for planning the subsequent
treatment. At the saphenous-femoral junction (SFJ) and at the saphenous-popliteal
junction (SPJ), sensitivity was 56-64% and 23%, specificity 93-97% and 96%,
positive predictive value 97-98% and 43% and negative predictive value 44-45% and
91%, respectively. In 9% of the cases, the treatment plan was modified on the
basis of the duplex ultrasound findings. The present study showed that, in
primary uncomplicated varicose veins, the accuracy of HHD is
unsatisfactory.
Thirty legs of 27 patients with varicose veins were treated using an
endovenous catheter (Closure® System, VNUS Medical Technologies, Inc.,
Sunnyvale,
CA), which was inserted under ultrasound guidance via a percutaneous puncture or
a skin incision. The persistence of vein occlusion and complications potentially
attributable to the endovenous treatment were assessed at 1-week, 6-week,
3-month, 6-month and 1-year follow-up visits. By the time of the last follow-up
visit, occlusion of the treated segment of the LSV had been achieved in 22
(73.3%) legs. Persisting patency or recanalization of LSV was detected in 8 legs
(26.7%). Postoperative complications included saphenous nerve paresthesia in 3
legs (10%) and thermal skin injury in one limb (3.3%).
Twenty-eight selected patients admitted for operative treatment of varicose
veins in the tributaries of the primary long saphenous were randomly assigned to
endovenous obliteration (n = 15) or stripping operation (n = 13). The patients
were followed up for 7-8 weeks postoperatively and examined by duplex
ultrasonography. The comparison of costs included both direct medical costs and
costs due to lost of productivity. All operations were successful, and the
complication rates were similar in the two groups. The sick leaves were
significantly shorter in the endovenous obliteration group [6.5 (SD 3.3) vs. 15.6
(SD 6.0), 95 % CI 5.4 to 12.9, p < 0.001, t-test]. When
the
value of the lost working days was included, the endovenous obliteration was
societally cost-saving.
12
GAROFFOLO, GLORIA. "Cell- and Tissue-based mechanosensation in programming and progression of coronary vein graft disease." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2021. http://hdl.handle.net/10281/304792.
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Nonostante generalmente si preferisca utilizzare i condotti arteriosi, la grande vena safena (SV) rimane indispensabile per il bypass aortocoronarico, specialmente nella malattia coronarica multi-vasale. È stato scoperto che il rimodellamento precoce causato da alterazioni meccaniche a carico della parete del vaso gioca un ruolo chiave nella malattia da trapianto di vena safena. Il meccanismo rimane, tuttavia, sconosciuto. Lo scopo di questo lavoro è quello di dimostrare l'esistenza di un effetto meccanico nel fallimento dell'innesto venoso, dovuto ai cambiamenti nelle condizioni emodinamiche che si verificano a seguito del trapianto in posizione coronarica. I segmenti di vena safena di pazienti sottoposti a bypass coronarico sono stati stimolati all’interno di un bioreattore in grado di mimare le condizioni emodinamiche venose o coronariche. Cellule muscolari lisce e cellule progenitrici avventiziali derivate dalla vena safena umana sono state stimolate meccanicamente in vitro utilizzando lo strumento Flexcell. La differenziazione pro-patologica delle cellule residenti nella vena, derivante dall'esposizione al flusso coronarico, è causata da un fenomeno meccano-percettivo. In particolare, le cellule avventiziali vengono attivate a seguito del rilascio di Trombospondina-1 da parte delle cellule muscolari lisce nelle vene esposte al flusso coronarico, suggerendo così una connessione tra lo stress meccanico sperimentato dalla parete vascolare e il rimodellamento del bypass. Inoltre, un'analisi dell'arricchimento genico dei trascritti differenzialmente modulati dallo stress meccanico, ha rivelato il coinvolgimento di un circuito trascrizionale meccano-sensitivo (HIPPO/YAP/TEAD pathway) nelle cellule stimolate meccanicamente. Questi risultati suggeriscono l'esistenza di un effetto "meccano-paracrino" dovuto al stress di parete negli innesti di vena safena. Sia il reclutamento delle cellule progenitrici avventiziali, sia il loro differenziamento verso il fenotipo fibrotico, sono eventi potenzialmente coinvolti nell’insorgenza della malattia da trapianto di vena safena.Despite the preferred application of arterial conduits, the greater saphenous vein (SV) remains indispensable for coronary artery bypass grafting (CABG), especially in multi-vessel coronary artery disease. Early remodeling induced by altered wall mechanics has been recognized to play a key role in SV graft disease. The mechanism remains, however, unknown. The aim of this work was to unveil the existence of a mechanical effect in SV graft failure, due to changes in the hemodynamic conditions occurring in SV grafts after transplantation into coronary position. SV segments from patients receiving coronary artery bypass grafts were stimulated in a coronary ‘pulse-duplicator’ bioreactor with either CABG or venous hemodynamic conditions. Human saphenous vein derived-smooth muscle cells (SMCs) and adventitial progenitors (SVPs) were mechanically stretched in vitro using Flexcell Tension System. The pro-pathological differentiation of resident cells in the vein, resulting from exposure to coronary flow, derives from a mechano-perception phenomenon. In particular, adventitial cells are activated by the release of Thrombospondin-1 by stretched smooth muscle cells in the veins exposed to coronary flow, thus suggesting a connection between the mechanical stress experienced by the vascular wall and the remodeling of the bypass. In addition, a gene enrichment analysis of transcripts up/downmodulated by mechanical stress revealed the involvement of a mechanosensing transcriptional circuitry (HIPPO/YAP/TEAD pathway) in cells stimulated with the cyclic strain. These findings suggest the existence of a ‘mechano-paracrine’ effect due to CABG-specific wall strain in SV grafts. This process has consequences for recruitment of adventitial progenitor cells, and a fibrotic-like process possibly involved in pathologic programming of SV graft failure.
13
Nishio, Hiroomi. "MicroRNA-145-loaded poly(lactic-co-glycolic acid) nanoparticles attenuate venous intimal hyperplasia in a rabbit model." Kyoto University, 2019. http://hdl.handle.net/2433/242371.
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PARMA, LAURA. "INTRAPLAQUE ANGIOGENESIS AND THERAPEUTIC TARGETING OF ANGIOGENESIS." Doctoral thesis, Università degli Studi di Milano, 2020. http://hdl.handle.net/2434/777113.
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In this thesis we have investigated different approaches to block intraplaque angiogenesis in atherosclerosis. Intraplaque angiogenesis is a physiological response to the increased oxygen demand in the plaque but also has adverse effects by facilitating intraplaque hemorrhage and influx of inflammatory mediators, resulting in plaque instability and consequent rupture. To study this phenomenon we used in vitro assays as well as the accelerated atherosclerosis vein graft model in ApoE3*Leiden mice, a unique model in which the formed plaque shows characteristics that highly resemble human atherosclerotic lesions, including intraplaque angiogenesis and hemorrhage and a high inflammatory cell content. We focused on different approaches to restore plaque stability via improving intraplaque oxygen levels as well as via blocking different growth factors signaling. Moreover we studied the effects of our treatments on the interaction between angiogenesis and inflammation both in vitro and in vivo.
15
Swenne, Christine Leo. "Wound Infection Following Coronary Artery Bypass Graft Surgery : Risk Factors and the Experiences of Patients." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7168.
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Campos, Luciene Cristina Gastalho. "Identificação e caracterização de proteínas modificadas em enxertos de veias safenas humanas arterializadas no modelo ex vivo." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-16122008-174047/.
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A revascularização cardíaca utilizando a ponte de safena é um procedimento bastante utilizado para restabelecer o fluxo coronariano. Apesar do sucesso deste procedimento, a patência deste enxerto pode chegar a menos de 50% em 10 anos. Atribui-se parte deste insucesso a variações no processo adaptativo à nova condição hemodinâmica, onde o shear stress e o estiramento aumentados podem estar interferindo na função endotelial e vascular. Este processo envolve a participação de diversas proteínas e o estudo de como elas participam conjuntamente é uma importante abordagem para entender as alterações fisiológicas e patológicas que ocorrem no enxerto vascular. Neste trabalho, tecnologias proteômicas, gel 2-D e ICAT, foram utilizadas para identificar as proteínas que são modificadas nas fases precoces da arterialização do enxerto venoso. Foi utilizado um sistema ex vivo de perfusão controlada, desenvolvido em nosso laboratório, onde a veia safena humana foi cultivada tanto em regime hemodinâmico venoso (5 mL/min) e arterial (50 mL/min, 80 mmHg) por 24 horas. Dentre as proteínas identificadas, a maioria apresenta funções estruturais como, por exemplo, -actina de músculo liso, CRP1, colágeno VI, tropomiosina, miosina, desmina e vimentina. Para avaliação funcional foram selecionadas a -SMA e a CRP. A -SMA mostrou-se diminuída nas fases mais precoces da arterialização venosa, com quase desaparecimento após 3 dias da cirurgia, seguido de um aumento nos períodos subseqüentes. A CRP3 mostrou-se com expressão predominantemente arterial tanto em amostra humana como de rato. A arterialização de segmentos venosos induziu a expressão da CRP3, sendo dependente do aumento do estiramento (stretch) nas células musculares lisas e não do aumento do shear stress na superfície endotelial. Coletivamente, neste trabalho caracterizamos duas proteínas que foram modificadas durante o processo de arterialização e/ou adaptação da veia à condição hemodinâmica arterial. As proteínas identificadas contribuirão para o melhor entendimento do processo de arterialização venosa e poderão ser testadas como novos alvos terapêuticos para melhorar a patência destes enxertosCoronary artery bypass surgery by saphenous vein graft is still widely used to revascularization of ischemic heart. Despite the success of this procedure, about 50% occlude after 5-10 years. The vein graft is subjected to increased tensile stress and the adaptive vein response to the arterial hemodynamic condition may predispose to bypass occlusion. Several proteins are modulated during arterialization, the understanding of the molecular changes of this process may be useful to new therapeutics approaches development attempting to increase vein graft patency. In this work, proteomics plataform, gel 2-D and ICAT, were used to identify the proteins that are modified in the early stages of vein graft rterialization. Human saphenous vein were cultured in an ex vivo flow through system in both venous (5 ml / min) and arterial (50 ml / min, 80 mm Hg) hemodymanic conditions for 24 hours. The identified proteins were related to cell structural function, such as -SMA, CRP1, collagen VI, tropomyosin, myosin, desmin and vimentin. To functional characterization, -SMA and CRP were selected. In rat vein arterialization model, - SMA showed to be decreased during the early stages of arterialization and almost disappeared after 3 days of surgery. Later on, -SMA-positive cells increase reaching similar expression levels of normal jugular vein. The expressiom of CRP3 showed to be predominantly to arterial beds both in human and rat. When vein segment were submitted to arterial hemodynamic condition, it was observed a significant induction of CRP3 expression. Interestingly, the increase of CRP3 is dependent of stretch stimulus in smooth muscle cells while shear stress did not modify its expression in endothelial cells. Collectively, we successfully identified proteins differentially expressed during the vein arterialization by using proteomic technique. -SMA and CRP3 were modified in vein segments exposed to arterial hemodynamic condition and efficiently discriminate smooth muscle cell phenotype. The identified proteins will contribute to the better understanding of the venous arterialization process and may be tested as new therapeutic targets for improving the patency these grafts
17
Roberts, A. C., J. Gohil, L. Hudson, K. Connolly, P. Warburton, R. Suman, P. O'Toole, et al. "Aberrant Phenotype in Human Endothelial Cells of Diabetic Origin: Implications for Saphenous Vein Graft Failure?" 2015. http://hdl.handle.net/10454/10083.
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yesType 2 diabetes (T2DM) confers increased risk of endothelial dysfunction, coronary heart disease, and vulnerability to vein graft failure after bypass grafting, despite glycaemic control. This study explored the concept that endothelial cells (EC) cultured from T2DM and nondiabetic (ND) patients are phenotypically and functionally distinct. Cultured human saphenous vein- (SV-) EC were compared between T2DM and ND patients in parallel. Proliferation, migration, and in vitro angiogenesis assays were performed; western blotting was used to quantify phosphorylation of Akt, ERK, and eNOS. The ability of diabetic stimuli (hyperglycaemia, TNF-α, and palmitate) to modulate angiogenic potential of ND-EC was also explored. T2DM-EC displayed reduced migration (~30%) and angiogenesis (~40%) compared with ND-EC and a modest, nonsignificant trend to reduced proliferation. Significant inhibition of Akt and eNOS, but not ERK phosphorylation, was observed in T2DM cells. Hyperglycaemia did not modify ND-EC function, but TNF-α and palmitate significantly reduced angiogenic capacity (by 27% and 43%, resp.), effects mimicked by Akt inhibition. Aberrancies of EC function may help to explain the increased risk of SV graft failure in T2DM patients. This study highlights the importance of other potentially contributing factors in addition to hyperglycaemia that may inflict injury and long-term dysfunction to the homeostatic capacity of the endothelium.
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Li, Jun [Verfasser]. "Pre-existing intimal hyperplasia and overexpression of TGF-β1 [TGF-beta-1] in saphenous vein grafts before myocardial revascularization in humans : implications for aortocoronary saphenous vein graft disease / presented by Jun Li." 2001. http://d-nb.info/1001068564/34.
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"Novel vascular markers and therapeutic strategies for the prevention of vein graft failure in a pig model of carotid artery-saphenous vein interposition grafting." 2009. http://library.cuhk.edu.hk/record=b5894197.
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Kang, Ning.Thesis (M.Phil.)--Chinese University of Hong Kong, 2009.
Includes bibliographical references.
Abstract also in Chinese.
Abstracts --- p.i
Abbreviations --- p.v
List of Figures and Tables --- p.vii
Contents --- p.viii
Chapter Chapter 1: --- Introduction --- p.1
Chapter 1. --- Saphenous vein graft patency after coronary artery bypass grafting --- p.1
Chapter 2. --- Mechanism of vein graft failure and therapeutic strategies --- p.8
Chapter 2.1 --- Mechanism --- p.15
Chapter 2.2 --- Therapeutic strategies --- p.18
Chapter 3. --- Summary --- p.22
Chapter 4. --- References --- p.23
Chapter Chapter 2: --- Animal model and laboratory investigations --- p.34
Chapter 1. --- Surgical procedure --- p.35
Chapter 2. --- Postoperative management --- p.37
Chapter 3. --- Adenoviral-mediated gene transfer ex vivo for gene therapy study --- p.38
Chapter 4. --- Laboratory investigations --- p.39
Chapter 5. --- Statistical analysis --- p.40
Chapter 6. --- Summary --- p.41
Chapter 7. --- References --- p.41
Chapter Chapter 3: --- "Impact of osteopontin expression in vein grafts on VSMC migration, proliferation, and neointimal formation" --- p.42
Chapter 1. --- Introduction --- p.42
Chapter 2. --- Methods and materials --- p.43
Chapter 3. --- Results --- p.43
Chapter 4. --- Discussion --- p.49
Chapter 5. --- Summary --- p.52
Chapter 6. --- References --- p.53
Chapter Chapter 4: --- Potential Role of gene therapy in prevention of vein graft failure --- p.56
Chapter 1. --- Vectors --- p.56
Chapter 2. --- "Reporter gene, timing and titer" --- p.57
Chapter 3. --- Candidate genes --- p.58
Chapter 4. --- Summary --- p.64
Chapter 5. --- References --- p.66
Chapter Chapter 5: --- Conclusions --- p.70
Acknowledgements --- p.72
20
Jackson, C. D., K. Barnes, Shervanthi Homer-Vanniasinkam, and A. J. Turner. "Expression and localization of human endothelin-converting enzyme-1 isoforms in symptomatic atherosclerotic disease and saphenous vein." 2006. http://hdl.handle.net/10454/3922.
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NoEndothelln-converting enzyme (ECE-1) is a critical enzyme in the production of the potent vasoconstrictor peptide endothelin (ET-1). It has previously been shown that the levels of both ET-1 and ECE-1 are raised in atherosclerosis, but the possible relevance of the isoforms of ECE-1 in these changes has not yet been investigated. The aim of this study was to examine the expression of the ECE-1a and ECE-1c isoforms in human atherosclerotic pathologies. Immunohistochemical analysis was carried out on sections from atherosclerotic and non-atherosclerotic vascular tissue using a combination of ECE-1 isoform-specific antibodies, anti-¿-actin antibodies to identify smooth muscle cells (SMC) and anti-CD68 antibodies to identify macrophages. ECE-1 isoform expression was also examined in cultured SMC and in macrophages isolated from human blood. Results indicated differences in isoform expression in atherosclerotic lesions, with distinct patterns of staining for ECE-1 a and ECE-1 c. ECE-1 c immunoreactivity was seen in macrophages, and also correlated with actin staining. ECE-1a was also localized to macrophages and SMC. Results of this study suggest that these local changes influence the expression patterns of the ECE-1 isoforms within individual cell types. Correlation of these isoform expression patterns with the stage of atherosclerosis could provide novel indicators of disease progression.
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Δαμέλου, Αναστασία. "Η εκτίμηση με οπτική συνεκτική τομογραφία των ένοχων βλαβών μοσχευμάτων ασθενών με οξύ στεφανιαίο σύνδρομο και προηγηθείσα αορτοστεφανιαία παράκαμψη." Thesis, 2013. http://hdl.handle.net/10889/6231.
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Στο συγκεκριμένο ερευνητικό πρωτόκολλο μελετήθηκαν οι πιθανές ένοχες βλάβες σε φλεβικά μοσχεύματα ασθενών με οξέα στεφανιαία σύνδρομα με τη μέθοδο της Οπτικής Συνεκτικής Τομογραφίας (OCT).
• Οι αθηροσκληρωτικές βλάβες των φλεβικών μοσχευμάτων έχουν μελετηθεί in vivo με τη μέθοδο της αγγειοσκόπησης και της ενδαγγειακής υπερηχογραφίας (IVUS). Απεναντίας, η απεικόνιση των μοσχευμάτων με τη μέθοδο της OCT, η οποία χαρακτηρίζεται από σημαντικά μεγαλύτερη διακριτική ικανότητα σε σχέση με το IVUS και βελτιωμένη διεισδυτική ικανότητα συγκρινόμενη με την αγγειοσκόπηση, δεν έχει μελετηθεί συστηματικά.
• Μέθοδος: Η απεικόνιση των ένοχων βλαβών των μοσχευμάτων πραγματοποιήθηκε, κατόπιν αγγειογραφίας τους, με τη μέθοδο χωρίς απόφραξη της OCT σε ασθενείς με ασταθή στηθάγχη (UA), έμφραγμα μυοκαρδίου με ανάσπαση του διαστήματος ST (STEMI) και έμφραγμα μυοκαρδίου χωρίς ανάσπαση του διαστήματος ST (non-STEMI). Ο ινώδης ιστός, ο λιπώδης ιστός, οι εναποθέσεις ασβεστίου, ο θρόμβος και η ρήξη της πλάκας ορίστηκαν σύμφωνα με τα κριτήρια απεικόνισης στοιχείων για την OCT, όπως περιγράφηκαν και στο γενικό μέρος.
• Αποτελέσματα: Απεικονίστηκαν 28 φλεβικά μοσχεύματα (μέσης ηλικίας 14.6 ετών) σε 26 ασθενείς. Οι βλάβες χαρακτηρίστηκαν ως σύμπλοκες αγγειογραφικά σε ποσοστό 96.4%, ενώ εμφάνιζαν εξέλκωση σε ποσοστό 32.1% και θρόμβο σε ποσοστό 21.4%. Η OCT αποκάλυψε ινολιπώδη σύσταση σε όλες τις βλάβες, εναπόθεση ασβεστίου στο 32.1% των βλαβών, ρήξη πλάκας σε ποσοστό 60.7% και παρουσία θρόμβου σε ποσοστό 46.4%. Η παρουσία του θρόμβου ήταν προοδευτικά συχνότερη ανάμεσα στις ομάδες ανάλογα με το κλινικό τους σύνδρομο (UA έως STEMI, p=0.003, UA έναντι εμφράγματος μυοκαρδίου, p=0.006). Η λεπτή ινώδης κάψα καταγράφηκε οριακά συχνότερα στους ασθενείς με οξύ έμφραγμα μυοκαρδίου (UA έναντι εμφράγματος μυοκαρδίου, p=0.06, STEMI 100% έναντι non-STEMI 53.3% έναντι UA 20%, p=0.03). Βλάβες με στοιχεία ευθρυπτότητας, όπως απεικονίζονταν στην OCT παρουσιάζονταν σε ποσοστό 67.9%, χωρίς όμως συσχέτιση με την κλινική εικόνα.
• Συμπέρασμα: Οι ένοχες βλάβες φλεβικών μοσχευμάτων μεγάλης ηλικίας ασθενών με οξέα στεφανιαία σύνδρομα, όπως αυτές απεικονίζονται στην OCT, εμφανίζουν ινολιπώδη σύσταση, σχετικά λεπτή ινώδη κάψα, ρήξη πλάκας και θρόμβο που συσχετίζονται με το κλινικό φάσμα των οξέων στεφανιαίων συνδρόμων. Αυτά οδηγούν στο συμπέρασμα ότι οι ίδιοι μηχανισμοί αθηροσκλήρωσης που οδηγούν στην εμφάνιση οξέων στεφανιαίων συνδρόμων στα γηγενή στεφανιαία αγγεία, είναι πιθανόν να ενέχονται και στην πρόκληση οξέων στεφανιαίων συνδρόμων λόγω αποτυχίας των φλεβικών μοσχευμάτων.This study sought to assess, with optical coherence tomography (OCT), presumably culprit atherosclerotic lesions of saphenous vein grafts (SVGs) in patients with acute coronary syndromes (ACS). Background: Atherosclerotic lesions of SVGs have been studied in vivo with angioscopy and intravascular ultrasound. However, imaging with OCT, which has a higher resolution than intravascular ultrasound and better penetration than angioscopy, has not been conducted systematically. Methods Using a nonocclusive OCT technique, we performed angiography and OCT of culprit SVG lesions in patients with unstable angina (UA), ST-segment elevation myocardial infarction (STEMI), and non-STEMI. Fibrous and fatty tissue, calcification, thrombus, and plaque rupture were defined according to OCT objective criteria. Results: Twenty-eight SVGs (average age 14.6 years) in 26 patients were imaged. Lesions on angiography were complex (96.4%), with ulceration in 32.1% and thrombus in 21.4%. OCT disclosed a fibrofatty composition in all lesions, calcification in 32.1%, plaque rupture in 60.7%, and thrombus in 46.4%. Thrombus was progressively more frequent across groups (UA to STEMI, p=0.003; UA vs. myocardial infarction, p=0.006). A thin fibrous cap was marginally more frequent in myocardial infarction patients (UA vs. myocardial infarction, p=0.06; STEMI 100% vs. non-STEMI 53.3% vs. UA 20%, p=0.03). OCT features of friability were present in 67.9% of SVGs not correlating with clinical presentation. Conclusions: OCT of culprit lesions of old SVGs in patients with ACS demonstrates fibrofatty composition, relatively thin fibrous cap, plaque rupture, and thrombus, which correlate with the clinical spectrum of ACS. This suggests that similar mechanisms with native vessels’ atherosclerosis may be involved in SVG-related ACS.