Academic literature on the topic 'Scar remodeling'
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Journal articles on the topic "Scar remodeling"
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Costa, Andréa Monte Alto, Simone Peyrol, Luís Cristóvão Pôrto, Jean-Pierre Comparin, Jean-Louis Foyatier, and Alexis Desmoulière. "Mechanical Forces Induce Scar Remodeling." American Journal of Pathology 155, no. 5 (1999): 1671–79. http://dx.doi.org/10.1016/s0002-9440(10)65482-x.
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Ludwig, Irene H., and Alan Y. Chow. "Scar remodeling after strabismus surgery." Journal of American Association for Pediatric Ophthalmology and Strabismus 4, no. 6 (2000): 326–33. http://dx.doi.org/10.1067/mpa.2000.107899.
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Singh, Yashbir, Deepa Shakyawar, and Weichih Hu. "Non-ischemic endocardial scar geometric remodeling toward topological machine learning." Proceedings of the Institution of Mechanical Engineers, Part H: Journal of Engineering in Medicine 234, no. 9 (2020): 1029–35. http://dx.doi.org/10.1177/0954411920937221.
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Scar tissues have been important factors in determining the progression of myocardial diseases and the development of adverse cardiac failure outcomes. Accurate segmentation of the scar tissues can be helpful to the clinicians for risk prediction and better evaluation of cardiovascular diseases. Our goal is to apply topology data analysis toward machine learning algorithms to confirm the geometry of scar tissue, in addition to gaining better visualization and quantification of the scar tissue present. We have introduced architecture for integrating geometry in the form of topology toward machine learning. Morphological image processing was carried out to define the regions of the endocardial wall. We implemented convolutional neural networks on delayed enhancement cardiac computed tomography images for the recognition of scar tissue. Segmented two-dimensional images were stacked up to build the geometry of the scar area for visualization purposes. Mathematical calculations were executed for the validation of the scar tissue in addition to performing morphological image processing and marking the scar tissue present on the endocardial wall of the left ventricular. We applied convolutional neural network over convolution and pooling the layers with small sizes; we achieved 89.23% accuracy, 91.11% sensitivity, and 87.75% specificity, and found the dissimilarity distance between the normal endocardial tissue distances to be 9.37. This new concept in this study contributes toward a better understanding of scar structure and transmural variation of the endocardial wall of the left ventricular.
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Tepper, Ronnie, Yoram Beyth, Zvi Klein, and Rami Aviram. "Postmyomectomy sonographic imaging: uterus remodeling and scar repair." Archives of Gynecology and Obstetrics 280, no. 3 (2009): 509–11. http://dx.doi.org/10.1007/s00404-009-0967-6.
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Lee, Sang-jun, Dong-Hye Suh, Ji Min Lee, Kye-Yong Song, and Hwa Jung Ryu. "Dermal Remodeling of Burn Scar by Fractional CO2 Laser." Aesthetic Plastic Surgery 40, no. 5 (2016): 761–68. http://dx.doi.org/10.1007/s00266-016-0686-x.
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Duerr, Georg D., Naziha Elhafi, Toktam Bostani, et al. "Comparison of Myocardial Remodeling between Cryoinfarction and Reperfused Infarction in Mice." Journal of Biomedicine and Biotechnology 2011 (2011): 1–10. http://dx.doi.org/10.1155/2011/961298.
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Myocardial infarction is associated with inflammatory reaction leading to tissue remodeling. We compared tissue remodeling between cryoinfarction (cMI) and reperfused myocardial infarction (MI) in order to better understand the local environment where we apply cell therapies. Models of closed-chest one-hour ischemia/reperfusion MI and cMI were used in C57/Bl6-mice. The reperfused MI showed rapid development of granulation tissue and compacted scar formation after 7 days. In contrast, cMI hearts showed persistent cardiomyocyte debris and cellular infiltration after 7 days and partially compacted scar formation accompanied by persistent macrophages and myofibroblasts after 14 days. The mRNA of proinflammatory mediators was transiently induced in MI and persistently upregulated in cMI. Tenascin C and osteopontin-1 showed delayed induction in cMI. In conclusion, the cryoinfarction was associated with prolonged inflammation and active myocardial remodeling when compared to the reperfused MI. These substantial differences in remodeling may influence cellular engraftment and should be considered in cell therapy studies.
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Holmes, J. W., H. Yamashita, L. K. Waldman, and J. W. Covell. "Scar remodeling and transmural deformation after infarction in the pig." Circulation 90, no. 1 (1994): 411–20. http://dx.doi.org/10.1161/01.cir.90.1.411.
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Astakhova, M. I., E. S. Golovneva, L. V. Astakhova, I. A. Astakhov, and E. N. Ignatieva. "REGULATION OF MICROCIRCULATION DURING REMODELING OF SKIN SCAR UNDER INFLUENCE OF LASER." Medical academic journal 19, no. 1S (2019): 144–45. http://dx.doi.org/10.17816/maj191s1144-145.
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An experimental study was fulfilled on 15 laboratory mail rats. After normotrophic skin scar modeling, the scar tissue was once exposed to high-intensive red, near or far infrared laser in comparable modes. Microcirculation parameters were assessed with laser Doppler flowmetry. It was found that the nature of microcirculation response to high-intensive laser irradiation substantially depended on the laser wavelength and its penetrating depth. Laser resurfacing of the skin scar with CO2 laser in early period led to blood stasis in the vessels and decrease in the vascular wall tone against the background of sympathetic influence increase. The red and near-infrared lasers caused the increased arterial blood inflow and venular outflow, with local regulation by myogenic tone prevailing.
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Sun, Daniel, and Tatjana C. Jakobs. "Structural Remodeling of Astrocytes in the Injured CNS." Neuroscientist 18, no. 6 (2011): 567–88. http://dx.doi.org/10.1177/1073858411423441.
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Astrocytes respond to all forms of CNS insult and disease by becoming reactive, a nonspecific but highly characteristic response that involves various morphological and molecular changes. Probably the most recognized aspect of reactive astrocytes is the formation of a glial scar that impedes axon regeneration. Although the reactive phenotype was first suggested more than 100 years ago based on morphological changes, the remodeling process is not well understood. We know little about the actual structure of a reactive astrocyte, how an astrocyte remodels during the progression of an insult, and how populations of these cells reorganize to form the glial scar. New methods of labeling astrocytes, along with transgenic mice, allow the complete morphology of reactive astrocytes to be visualized. Recent studies show that reactivity can induce a remarkable change in the shape of a single astrocyte, that not all astrocytes react in the same way, and that there is plasticity in the reactive response.
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Snider, J. Caleb, Lance A. Riley, Noah T. Mallory, et al. "Targeting 5-HT 2B Receptor Signaling Prevents Border Zone Expansion and Improves Microstructural Remodeling After Myocardial Infarction." Circulation 143, no. 13 (2021): 1317–30. http://dx.doi.org/10.1161/circulationaha.120.051517.
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Background: Myocardial infarction (MI) induces an intense injury response that ultimately generates a collagen-dominated scar. Although required to prevent ventricular rupture, the fibrotic process is often sustained in a manner detrimental to optimal recovery. Cardiac myofibroblasts are the cells tasked with depositing and remodeling collagen and are a prime target to limit the fibrotic process after MI. Serotonin 2B receptor (5-HT 2B ) signaling has been shown to be harmful in a variety of cardiopulmonary pathologies and could play an important role in mediating scar formation after MI. Methods: We used 2 pharmacological antagonists to explore the effect of 5-HT 2B inhibition on outcomes after MI and characterized the histological and microstructural changes involved in tissue remodeling. Inducible 5-HT 2B ablation driven by Tcf21 MCM and Postn MCM was used to evaluate resident cardiac fibroblast- and myofibroblast-specific contributions of 5-HT 2B , respectively. RNA sequencing was used to motivate subsequent in vitro analyses to explore cardiac fibroblast phenotype. Results: 5-HT 2B antagonism preserved cardiac structure and function by facilitating a less fibrotic scar, indicated by decreased scar thickness and decreased border zone area. 5-HT 2B antagonism resulted in collagen fiber redistribution to thinner collagen fibers that were more anisotropic, enhancing left ventricular contractility, whereas fibrotic tissue stiffness was decreased, limiting the hypertrophic response of uninjured cardiomyocytes. Using a tamoxifen-inducible Cre, we ablated 5-HT 2B from Tcf21 -lineage resident cardiac fibroblasts and saw similar improvements to the pharmacological approach. Tamoxifen-inducible Cre-mediated ablation of 5-HT 2B after onset of injury in Postn -lineage myofibroblasts also improved cardiac outcomes. RNA sequencing and subsequent in vitro analyses corroborate a decrease in fibroblast proliferation, migration, and remodeling capabilities through alterations in Dnajb4 expression and Src phosphorylation. Conclusions: Together, our findings illustrate that 5-HT 2B expression in either cardiac fibroblasts or activated myofibroblasts directly contributes to excessive scar formation, resulting in adverse remodeling and impaired cardiac function after MI.
Dissertations / Theses on the topic "Scar remodeling"
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Nelson, Charles A. L. "Relationship between the transmural distribution of myocardial scar and ventricular function /." [St. Lucia, Qld.], 2004. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe18564.pdf.
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Qurashi, Abrar Ahmad. "Neuronal remodeling in Drosophila melanogaster with WAVE/SCAR complex and its implication in cognitive functions." Université Louis Pasteur (Strasbourg) (1971-2008), 2006. http://www.theses.fr/2006STR13112.
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La morphogenèse neurale et la plasticité neuronale dépendent du remodelage du cytosquelette d’actine et sont induits en réponse à des signaux extra cellulaires qui sont interprétés par la famille des petites Rho GTPases. Pendant ma thèse, j’ai cherché à comprendre comment les voies de signalisations en aval des protéines Rac, petites Rho GTPases, sont utilisés pour réguler la morphogenèse neurale et la plasticité structurelle. Récemment, le complexe WAVE/SCAR, un ensemble de cinq protéines conservées durant l’évolution [WAVE (SCAR), PIR121 (Sra-1 or CYFIP), Hem-2 (NAP1 or Kette),Abi et HSPC300] a été identifié comme le lien essentiel entre Rac1 et Arp2/3 (un complexe moléculaire induisant la polymérisation d’actine). Les premières études suggéraient que Rac1 agissait en dissociant le complexe WAVE/SCAR conduisant à la libération et à l’activation de la protéine WAVE (SCAR). Des études ultérieures proposent un autre mode d’action et suggèrent que le complexe WAVE/SCAR ne se dissocie pas mais qu’à la place il est nécessaire dans son ensemble pour localiser et activer la protéine WAVE (SCAR). Au cours de ma thèse, j’ai utilisé la drosophile comme modèle pour étudier la fonction et le mode d’action du complexe WAVE/SCAR au cours de différents processus du développement neuronal comme la navigation axonale et le développement synaptique. J’ai plus particulièrement isolé des mutants du gène HSPC300 et caractérisé génétiquement et moléculairement cette protéine. Ensuite, j’ai étudié le rôle des autres membres du complexe WAVE/SCAR, ce qui m’a permis de proposer un modèle expliquant comment les divers signaux reçus par les différents membres du complexe sont interprétés. Pendant ma thèse, j’ai démontré que WAVE (SCAR), Kette et HSPC300 forment aussi un complexe chez la drosophile. J’ai observé que toutes ces protéines sont très fortement exprimées dans le système nerveux et tout particulièrement dans les neurones du système nerveux central et les neurones moteurs. De manière intéressante, j’ai observé que muter n’importe quel membre du complexe conduit toujours à des défauts similaires non seulement au niveau du guidage et de la croissance axonale mais aussi au niveau de la morphologie des jonctions neuromusculaires. Nous avons ensuite recherché les raisons de cette similarité phénotypique. Par des expériences de génétique et de biochimie, nous avons démontré que la perte d’un des composants du complexe conduit à l’instabilité des autres composants ce qui fournit une base physique à la similarité des phénotypes observés avec les différentes mutations individuelles. De manière intéressante, les mutations individuelles des composants du complexe n’affectent pas seulement la stabilité des autres membres mais aussi les voies de signalisations en aval. Par exemple, muter n’importe quel membre du complexe WAVE/SCAR a un effet sur la signalisation de CYFIP vers une autre protéine FMRP (Fragile X Mental Retardation Protein : une proteine impliquée dans la mémoire et l’apprentissage chez les humains). De la même manière, la signalisation SCAR-Arp2/3 est affectée par toutes les différentes mutation individuelles. Nous avons aussi étudié la fonction de ce complexe dans le développement de l’oeil de drosophile et montré qu’il contrôle notamment la morphologie et l’intégrité des différents types cellulaires, photorécepteurs (neurones) y inclus. En conclusion, j’ai démontré que le complexe WAVE/SCAR se trouve au centre (physiquement et fonctionnellement) de nombreuses voix de signalisations impliquées et dans le développement de nombreux types cellulaires. Ainsi mon travail s’inscrit dans la lignée des études qui supportent que la régulation de différents évènements morphogénétiques passent par un même noyau de signalisation. Enfin, ma thèse suggère que les autre petites Rho GTPases Rac2 et Mtl sont elles aussi impliqués dans plasticité et la croissance synaptiqueNeuronal morphogenesis and plasticity during development as well as in cognitive functions rely on actin cytoskeleton remodeling in response to extra-cellular signals that are interpreted by Rho family of small GTPases. The key subject of my thesis is to understand how signaling pathways downstream of Rac proteins, members of the Rho GTPase family, are utilized to orchestrate distinct aspects of neuronal morphogenesis and structural plasticity. WAVE/SCAR complex, an evolutionarily-conserved assembly of five proteins: WAVE (SCAR), PIR121 (CYFIP), Hem-2 (Kette), Abi and HSPC300 has emerged as a critical link between Rac1 and Arp2/3, molecular complex triggering actin nucleation. During my thesis I have used Drosophila melanogaster as a model system to understand the physiological significance of WAVE/SCAR complex. We have elucidated its role in neuronal actin remodeling underlying axon as well synapse development. Specifically, I have isolated mutations in the HSPC300 gene, and present its detailed characterization both at genetic and biochemical level. My thesis work provides evidence that in Drosophila melanogater SCAR, CYFIP, Kette and HSPC300 associate together to form a complex. All these proteins are highly expressed in the embryonic nervous system and show strong accumulation in central and motor neurons. Interestingly, in many processes examined, there are striking similarities between the phenotypes resulting from the mutations in any member of the complex, for example defects in axon path-finding, axon growth and Neuromuscular Junction (NMJ) morphology, thus demonstrating their pivotal roles for precise neuronal development. By biochemical and genetic experiments, we demonstrated that loss of any of the complex components leads to instability in other components. Therefore, the results provide an unequivocal reason for the common pathological condition noticed in single mutation of the WAVE/SCAR complex. Interestingly, mutation in individual components of the complex not only affects the stability of other complex components but also affects the multiple downstream pathways associated with them. For example, mutation in any component of the complex has an impact on CYFIP signaling to the Fragile X Mental Retardation Protein (FMRP) implicated in learning and memory in humans. Thus, our results identify the Drosophila WAVE/SCAR complex as a multifunctional unit orchestrating different pathways and aspects of neuronal connectivity and support an emerging theme: different aspects of xv morphogenesis may involve the regulation of common core signaling pathways. Additionally, my thesis also demonstrates the interaction of all three Racs (Rac1, Rac2 and Mtl) with CYFIP and suggests their requirement during NMJ growth and plasticity
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Aubin, Marie-Claude. "Étude de la fonction vasculaire et du remodelage cardiaque avant l’établissement de l’obésité et de la dyslipidémie chez les rats femelles Sprague-Dawley recevant une diète riche en gras." Thèse, 2009. http://hdl.handle.net/1866/3569.
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Des lacunes existent au niveau des connaissances concernant les modifications cardiovasculaires manifestées avant l’établissement d’obésité et en absence d’hyperlipidémie. Dans cette optique, la présente étude a testé l'hypothèse générale qui stipule que l’administration d’une diète riche en gras pour une période de 8 semaines chez les rats femelles influence négativement la fonction et le remodelage cardiaque, avant le développement de l’obésité et en absence d’hyperlipidémie et d’hyperglycémie. Afin de répondre à cette problématique, des rats femelles Sprague-Dawley ont été assignés à une diète standard (SD; 12,5% lipides, kcal) ou riche en gras (HF; 42% lipides, kcal) pour une période de 8 semaines. Cette durée était insuffisante pour induire le développement d’une dyslipidémie ou une augmentation significative de la masse corporelle chez les animaux HF(329±14g) comparativement aux rates SD (300±10g). Toutefois, une hypertension artérielle s’est développée chez les rates HF (130±4 vs 108±6 mmHg, p<0,05), accompagnée d’une altération des relaxations aortiques dépendantes de l’endothélium (relaxation maximale : 22±5% versus 53±8%, pour les animaux HF et SD respectivement, p<0,05). L’administration orale chronique de l’antioxydant resvératrol (RES; 20 mg·kg-1·jr-1) a prévenu le développement de ces altérations pathologiques, attestant d’une implication du stress oxydant. Au niveau cardiaque, le RES n’a toutefois pas inhibé le développement de fibrose périvasculaire secondaire à l’administration de la diète riche en gras.
Suite à une insulte d’ischémie-reperfusion, la taille (SD : 0,29±0,09 versus HF : 0,32±0,13 cm), l’épaisseur (SD : 0,05±0,02 versus HF : 0,06±0,01 cm) et le contenu en
collagène α1 type 1 (SD : 0,21±0,04 versus HF : 0,20±0,04 unités arbitraires/mm2) de la
cicatrice du coeur infarci des rats HF étaient comparables au coeur infarci des rats SD. Malgré ces similitudes, le taux de décès était significativement (p<0,05) plus élevé chez les rats HF (56%) comparativement aux rats SD (5%). L’approche par électrophysiologie a démontré que l’administration de la diète riche en gras était associée à une augmentation (p<0,05) du nombre d’extrasystoles ventriculaires induites. Cette élévation de l’incidence était associé à une hyperinnervation sympathique fonctionnelle, tel que démontré par une
élévation (p<0,05) de la densité des fibres neurofilament-M (HF : 2830±250 versus SD :
2020±260 μm2/mm2) et de la protéine de l’hydroxylase de la tyrosine. La fonctionnalité des jonctions intercellulaires était également atteinte, caractérisée par une latéralisation et
internalisation de connexine 43 ainsi qu’une diminution de l’expression de connexine 40 au niveau des disques intercalaires. Ainsi, avant l’établissement de l’obésité et d’une dyslipidémie, les rats femelles modestement hypertendus présentent un phénotype arythmogénique cardiaque en partie dû à une hyperinnervation sympathique et une expression altérée concomitante de la
distribution et de l’expression des jonctions intercellulaires. L’absence de symptômes cliniques d’obésité dans la présente étude ne fournit aucun indice au clinicien quant à la susceptibilité accrue aux arythmies ventriculaires. Ainsi, en présence d’une hypertension artérielle modérée chez un patient non-obèse, une mesure de l’activité sympathique par la quantification des niveaux circulants de catécholamines pourrait être bénéfique afin de détecter les patients à risque de mort subite.Knowledge is insufficient regarding cardiovascular modifications occurring prior to the development of overt obesity and dyslipidemia. In this regard, the present project aimed at testing the hypothesis stipulating that the administration of a high fat diet for an 8-week period in female rats can adversely influence cardiac function and remodeling prior to the development of overt obesity, and in the absence of hyperlipidemia and hyperglycaemia. To directly examine these issues, normal female Sprague-Dawley rats were fed a standard (SD; 12.5% lipid, kcal) or a high-fat diet (HF; 42% lipids, kcal) for 8 weeks. This regimen was insufficient to induce a significant gain in body mass in HF rats (329±14g) as compared to SD rats (300±10g), or any variation in the lipid profile. By contrast, systemic arterial hypertension developed in high fat fed rats (130±4mmHg versus SD, 108±6mmHg, p<0.05), additionally to a significant decrease in acetylcholine-mediated maximal relaxation of isolated aortic rings (HF, 22±5%) compared to rats fed a standard diet (53±8%, p<0.05). Chronic oral administration of the antioxidant resveratrol (RES; 20 mg·kg-1·d-1) prevented the development of both pathological alterations, attesting to the implication of oxidative stress. However, it failed to attenuate the perivascular fibrosis that developed following the administration of the high-fat diet. Following ischemia/reperfusion injury, scar length (SD, 0.29±0.09 versus HF, 0.32±0.13 cm), thickness (SD, 0.05±0.02 versus HF, 0.06±0.01 cm) and collagen α1 type 1 content (SD, 0.21±0.04 versus HF, 0.20±0.04 arbitrary units/mm2) in the infarcted heart of rats fed a high fat diet were similar to infarcted normal rats. Despite these findings, the rate of death was significantly increased (p<0.05) in female rats fed a high fat diet (56%) compared to rats fed a standard diet (5%). An electrophysiology approach revealed that normal female rats fed a high fat diet had an increased incidence (p<0.05) of induced ventricular extrasystoles. In addition, these hearts presented a functional sympathetic hyperinnervation, as reflected by the increased density of neurofilament-M immunoreactive fibres (SD, 2020±260 versus HF, 2830±250 μm2/mm2; p<0.05) and increased protein expression of tyrosine hydroxylase. The gap junction function was also impaired, characterized by lateralization and internalization of connexine 43, and a decreased expression of connexine 40 in intercalated discs of rats fed a high fat diet. Thus, prior to the development of overt obesity and dyslipidemia, female rats with modest hypertension exhibit an arrhythmogenic cardiac phenotype due in part to sympathetic hyperinnervation and a concomitant aberrant pattern of gap junctional protein expression and distribution. The lack of significant clinical manifestations of obesity in the present study does not enable clinicians to suspect the increased susceptibility to ventricular arrhythmias. Hence, in presence of modest hypertension in a non-obese patient, evaluation of the sympathetic activity by the assessment of circulating catecholamine could be helpful in detecting patients at high risk for sudden death.
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Proulx, Cindy. "L’implication du Stromal Cell-derived Factor-1 alpha dans le remodelage cardiaque une semaine après un infarctus du myocarde." Thèse, 2008. http://hdl.handle.net/1866/2707.
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L’injection de cellules souches provenant de la moelle osseuse est reconnue pour améliorer la fonction ventriculaire ainsi que le remodelage cicatriciel après un infarctus du myocarde (IM). Le Stromal Cell-derived factor-1 alpha (SDF-1 alpha), une chimiokine induite par l’ischémie cardiaque, représente une grande importance en raison de son rôle dans le recrutement de cellules inflammatoires et de cellules souches de la moelle osseuse vers les sites endommagés. Quoique les recherches sur le rôle de la chimiokine SDF-1 alpha dans le remodelage ventriculaire se multiplient, son implication dans la phase aiguë du remodelage reste inexplorée. Le but de la présente étude est de déterminer l’effet du SDF-1 alpha sur la taille de la cicatrice, l’hypertrophie cardiaque ainsi que la fonction ventriculaire chez des rats et des souris une semaine après un IM. La stratégie utilisée implique l’administration de l’AMD3100 (1 mg/kg, 24 heures après l’IM, pendant 6 jours), l’antagoniste sélectif du récepteur du SDF-1 alpha, le CXCR4. Ce récepteur est couplé à une protéine G alpha i et induit la migration et la prolifération cellulaire. Chez les rats du groupe IM, l’expression de la chimiokine a été détectée surtout dans les cellules musculaires lisses et les cellules endothéliales des vaisseaux cicatriciels. Le profil d’expression de la chimiokine dans le cœur infarci indique un gradient de concentration vers la cicatrice. Une semaine après l’IM, le traitement avec l’AMD3100 a diminué la taille de la cicatrice, résultant en une amélioration de la fonction ventriculaire et une diminution de l’élévation de l’expression de l’ARNm de l’ANP dans le ventricule gauche non infarci (VGNI). Chez les souris, le traitement avec l’AMD3100 a engendré les mêmes effets, soit une diminution de la taille de la cicatrice ainsi qu’une amélioration de la fonction ventriculaire. La réduction de la taille de la région infarcie chez les souris traitées avec l’AMD3100 est associée avec une atténuation de l’infiltration des neutrophiles dans la région ischémique. Ces résultats suggèrent que le blocage pharmacologique de l’axe SDF-1 alpha/CXCR4 lors de la phase aiguë du remodelage ventriculaire après un IM diminue la taille de la cicatrice et améliore la fonction ventriculaire, en partie, par la diminution de la réaction inflammatoire.The injection of bone marrow stem cells in the infarcted heart was shown to improve ventricular function and scar remodelling. The chemokine Stromal Cell-derived factor-1 alpha (SDF-1 alpha) is implicated in the migration of inflammatory and bone marrow derived stem cells to damaged region. Despite a local increase of SDF-1 alpha expression in the damaged myocardium, the biological impact of the chemokine during the acute phase of remodelling in the ischemic heart remains undefined. Therefore, the present study examined the role of SDF-1 alpha on scar expansion, cardiac hypertrophy and ventricular function in rats following myocardial infarction (MI) via administration of AMD3100 (1 mg/kg, 24 hours post-MI and continued for 6 days) a selective antagonist of the SDF-1 alpha receptor, CXCR4. This receptor is coupled to a G alpha i protein and induced migration and proliferation of cells. In 1-week post-MI rats, chemokine expression was detected in smooth muscle and endothelial cells of blood vessels residing in the infarcted region. An SDF-1 alpha gradient towards the infarcted region was detected in the post-MI rat heart. In 1-week post-MI rats, AMD3100 therapy reduced scar size, concomitantly improved left ventricular function and partially supressed the elevated expression of ANP mRNA in the non-infarcted left ventricule. Preliminary studies on mice showed that the reduced infarct size in AMD3100-treated post-MI mice was associated with an attenuation of neutrophil infiltration in the ischemic region. These data highlight the novel observation that pharmacological antagonism of the SDF-1 alpha/CXCR4 axis during the acute phase of repartive fibrosis post-MI attenuated scar expansion and improved ventricular function in part via attenuation of the inflammatory response.
Books on the topic "Scar remodeling"
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Dilsizian, Vasken, Ines Valenta, and Thomas H. Schindler. Myocardial Viability Assessment. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199392094.003.0021.
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Heart failure may be a consequence of ischemic or non-ischemic cardiomyopathy. Etiologies for LV systolic dysfunction in ischemic cardiomyopathy include; 1) transmural scar, 2) nontransmural scar, 3) repetitive myocardial stunning, 4) hibernating myocardium, and 5) remodeled myocardium. The LV remodeling process, which is activated by the renin-angiotensin system (RAS), stimulates toxic catecholamine actions and matrix metalloproteinases, resulting in maladaptive cellular and molecular alterations5, with a final pathway to interstitial fibrosis. These responses to LV dysfunction and interstitial fibrosis lead to progressive worsening of LV function. Established treatment options for ischemic cardiomyopathy include medical therapy, revascularization, and cardiac transplantation. While there has been continuous progress in the medical treatment of heart failure with beta-blockers, angiotensin-converting enzyme (ACE) inhibition, angiotensin II type 1 receptor (AT1R) blockers, and aldosterone to beneficially influence morbidity and mortality, the 5-years mortality rate for heart failure patients remains as high as 50%. Revascularization procedures include percutaneous transluminal coronary artery interventions (PCI) including angioplasty and endovascular stent placement and coronary artery bypass grafting (CABG). Whereas patents with heart failure due to non-coronary etiologies may best benefit from medical therapy or heart transplantation, coronary revascularization has the potential to improve ventricular function, symptoms, and long term survival, in patients with heart failure symptoms due to CAD and ischemic cardiomyopathy.
Book chapters on the topic "Scar remodeling"
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Weber, Karl T. "Infarct Scar. Living Tissue." In Cardiac Remodeling and Failure. Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9262-8_23.
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Ogawa, Rei. "Mechanobiology of Cutaneous Scarring." In Textbook on Scar Management. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44766-3_2.
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AbstractThe last phase of cutaneous wound healing produces the scar. Under normal circumstances, the immature scar then undergoes the scar maturation process over several months. This process involves tissue remodeling, which associates with a natural decrease in the inflammation and the numbers of blood vessels, collagen fibers, and fibroblasts. However, sometimes the scar maturation process is not properly engaged because inflammation continues in the scar. Consequently, the immature scar stage is prolonged. This results in the pathological scars called hypertrophic scars and keloids. Many factors that prolong the inflammatory stage have been identified. However, multiple lines of evidence acquired in recent years suggest that mechanical force can be an important cause of pathological scar development.
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Liu, Wei. "Emerging Technologies in Scar Management: Remodeling of Post-surgical Linear Scar Using Microplasma Radiofrequency." In Textbook on Scar Management. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44766-3_53.
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AbstractLinear scar is a common problem in all fields of surgery as it leads to unpleasant appearance that is not socially acceptable. In particular, linear scars in the exposed areas such as face, neck, and upper extremities cause significant psychological disturbance to patients who need proper medical assistance to release their suffering. The author proposed tissue remodeling strategy on an existed linear scar using FMRT (fractional microplasma radiofrequency technology) to render gross view of a linear scar less visible or non-visible by changing the scar tissue architecture. Similar concept is also applied to the intervention of an early-stage wound to significantly alter the natural process of wound healing via FMRT-mediated change of the histological architecture of a wound, and thus to prevent the formation of a grossly visible linear scar. This chapter introduces the general background information, FMRT concept, and its application on linear scar treatment and prevention with the presentation of several typical cases.
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Ogawa, Rei. "Ideal Wound Closure Methods for Minimizing Scarring After Surgery." In Textbook on Scar Management. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44766-3_21.
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AbstractWound-healing phenomena are the result of a cascade of complex biochemical events that can be categorized into four general overlapping phases: coagulation, inflammation, proliferation, and remodeling. Significantly, all four phases of wound healing are influenced by both intrinsic and extrinsic mechanical forces. These mechanical forces provoke chronic inflammation of the dermis, namely, the unceasing influx and activation of inflammatory cells, the persistent generation of blood vessels and nerve fibers, and the constant production of collagen by the activated fibroblasts. This chronic inflammation blocks the conversion of the granulation tissue into dermis-like tissue by the remodeling process and results in an immature hypertrophic scar that is red, elevated, hard, and painful. These observations suggest that, to prevent pathological scarring after surgery, it is necessary to ensure that the sutures cause the wound edges to adhere to each other without any tension, even when strong extrinsic forces are placed on the wound. This will allow the granulation tissue to convert smoothly into dermis-like tissue, thereby yielding minimal scarring. Another way to prevent pathological scar formation in high-tension areas is to use zigzag suturing techniques such as the Z-plasty.
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Moortgat, Peter, Mieke Anthonissen, Ulrike Van Daele, Jill Meirte, Tine Vanhullebusch, and Koen Maertens. "Shock Wave Therapy for Wound Healing and Scar Treatment." In Textbook on Scar Management. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44766-3_55.
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AbstractShock Wave Therapy (SWT) meets all the requirements for the ideal non-invasive scar treatment. It is safe, well tolerated by patients, cost-effective, easy to apply, has low complication rates, and can be used in an outpatient setting. The overall effect of SWT is an improvement of tissue homeostasis, accompanied by an improvement of the tissue self-healing abilities, and it seems to focus on inducing tissue regeneration and matrix remodeling in vivo by means of mechanotransduction.SWT has a beneficial effect on wound healing and is characterized by an upregulation of the angio-active factors as nitric oxide (NO) and vascular endothelial growth factor (VEGF) leading to induced angiogenesis. A downregulation of alpha-SMA expression, myofibroblast phenotype, TGF-β1 expression, fibronectin, and collagen type I are measured after SWT on scars, leading to improvement of several relevant scar parameters like height, pliability, vascularity, and pigmentation, and thus ameliorating function.For a full treatment outline, the energy flux density (EFD), the number of pulses, the pulse frequency, and the number and interval of treatments are the most relevant parameters. The EFD for soft tissue indications is typically in the range of 0.08–0.25 mJ/mm2, while scars and fibrosis are treated with an EFD ranging between 0.15 and 0.33 mJ/mm2. These settings seem to be ideal to induce the optimal cell responses for each indication.All the presented findings are fundamental knowledge for further investigation of SWT to reduce the fibrous component in regenerating and remodeling tissues. However, the full potential of SWT in wound healing and scar treatment needs further unraveling.
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Darby, Ian A., and Alexis Desmoulière. "Scar Formation: Cellular Mechanisms." In Textbook on Scar Management. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44766-3_3.
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AbstractFibroblasts are key players in the maintenance of skin homeostasis and in orchestrating physiological tissue repair. Fibroblasts secrete and are embedded in a sophisticated extracellular matrix, and a complex and interactive dialogue exists between fibroblasts and their microenvironment. In addition to the secretion of the extracellular matrix, fibroblasts and myofibroblasts secrete extracellular matrix remodeling enzymes, matrix metalloproteinases and their inhibitors, and tissue inhibitors of metalloproteinases and are thus able to remodel the extracellular matrix. Myofibroblasts and their microenvironment form a network that evolves during tissue repair. This network has reciprocal actions affecting cell differentiation, cell proliferation, cell quiescence, or apoptosis and has actions on growth factor bioavailability by binding, sequestration, and activation. Mechanical forces also play a role in regulating the myofibroblast phenotype as cells are subjected to mechanical stress and mechanical signaling is activated. Innervation is also involved in both skin repair processes and differentiation of myofibroblasts. In pathological situations, for example, in excessive scarring, the dialogue between myofibroblasts and their microenvironment can be altered or disrupted, leading to defects in tissue repair or to pathological scarring, such as that seen in hypertrophic scars. Better understanding of the intimate dialogue between myofibroblasts and their local microenvironment is needed and will be important in aiding the identification of new therapeutic targets and discovery of new drugs to treat or prevent aberrant tissue repair and scarring.
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"Chapter 18 SCAR REMODELING WITH FAT GRAFTING AFTER BURN INJURY." In Fat Injection, edited by Sydney R. Coleman, Riccardo F. Mazzola, and Lee L. Q. Pu. Georg Thieme Verlag, 2018. http://dx.doi.org/10.1055/b-0038-149554.
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Abboud, Nicolas, and Marwan Abboud. "Power-Assisted Liposuction Mammaplasty (PALM): A Short Scar Mammaplasty in Gigantomastia." In Enhanced Liposuction - New Perspectives and Techniques [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.98816.
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Breast reduction has been widely studied throughout the years, with different types of resection and breast reshaping techniques being described based on one or two pedicles. This chapter introduces the combination of parenchymal resection and liposuction to treat Gigantomastia, leaving a short scar. Liposuction improves breast remodeling, whereas breast glandular resection and repositioning enhances the upper pole fullness. The Power-Assisted Liposuction Mammaplasty (P.A.L.M.) technique is a safe and reliable procedure, insuring an optimal vascularization to the breast through the preservation of the central, superior and lateral pedicle, thus reducing the complication rate. In this chapiter we emphasize the importance of the preoperative markings, considered as essential for optimal results.
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Mankiewicz, Kimberly A., and Leonard K. Seibold. "Wound Healing In Glaucoma." In Complications of Glaucoma Surgery. Oxford University Press, 2013. http://dx.doi.org/10.1093/oso/9780195382365.003.0013.
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The goal of wound healing in most surgeries is to bring the injured tissue back to its original state to prevent the wound from reopening. However, in glaucoma surgery, the goal is to have incomplete wound healing. Scar formation prevents the filtering mechanism and bleb from functioning properly, leading to poor pressure control and failure of the surgery. However, if there is too little wound healing, surgical failure may be marked by overfiltration and hypotony. Several modulators are currently used in conjunction with glaucoma surgery, and new targets are under investigation to improve our ability to control the healing process. Normal wound healing occurs in 3 phases: the inflammatory phase, the proliferative/repair phase, and the remodeling phase. In the inflammatory phase, blood cells and plasma proteins are released around the wound site. These proteins attract other wound healing factors, such as cytokines and growth factors. White blood cells are also recruited to the site, clearing out undesired cellular debris through phagocytosis. Additionally, platelet aggregation and fibrin clot formation occur. In the proliferative/repair phase, fibroblasts, crucial cells for tissue repair and scarring, begin reforming the extracellular matrix (ECM) and other components of connective tissue. Angiogenesis also occurs, and the wound begins to close. In the final phase, blood vessels are resorbed and fibroblasts disperse. Fibroblasts produce matrix metalloproteinases that, along with collagen and elastin, allowing for wound remodeling and scar formation. The modulators used in glaucoma surgery, as well as new agents in development, disrupt various aspects of this cycle. Use of topical corticosteroids in conjunction with filtering surgery is a routine part of postoperative management and has been for many decades. Corticosteroids blunt the wound healing response by altering the inflammatory phase through reducing the amount of inflammatory cells and cytokines that migrate to the wound site. Corticosteroids also prevent the complexing and conversion of inflammatory mediators, as well as reduce vascular permeability to limit mobility of wound healing factors to the wound site.
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Castelvecchio, Serenella, Raffaella Molfetta, Andrea Garatti, and Lorenzo Menicanti. "Coronary artery bypass grafting with surgical ventricular reconstruction." In State of the Art Surgical Coronary Revascularization, edited by Naresh Trehan and Yasir Abu-Omar. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198758785.003.0074.
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The increase in left ventricular volume after a myocardial infarction is a component of the remodelling process leading to heart failure and it is associated with poor clinical outcomes. Hence, the current management strategy for ischaemic left ventricular dysfunction has been aimed to reverse the remodelling process by medical therapy, devices and/or surgical strategies. Surgical ventricular reconstruction, usually combined with myocardial revascularization, has been introduced as an optional therapeutic strategy aimed to reduce the left ventricle through the exclusion of the scar tissue. Surgical ventricular reconstruction is recommended in selected heart failure patients, especially if a postoperative left ventricular end-systolic volume index less than 70 mL/m2 can be predictably achieved, because a smaller residual volume is associated with improved survival. This chapter briefly discusses the rationale to surgically reverse left ventricular remodelling, the technique, and the indications to the best of the authors’ knowledge, coming from one of the centres with the most experience in SVR worldwide.
Conference papers on the topic "Scar remodeling"
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Nagel, Thomas, and Daniel J. Kelly. "Compaction and Anisotropy Induced by Remodeling of the Collagen Network’s State of Tension-Compression Transition." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53399.
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Extracellular matrix remodeling is ubiquitous in connective, musculoskeletal and cardiovascular tissues. The collagen network can thereby not only remodel its orientation [1] but also its stress-free configuration. This stress-free configuration can be described by the so-called transition stretch — the stretch above which a fiber begins to bear load. Remodeling of collagen crimp has been shown to be involved in long bone growth [2], contracture, scar pathologies, collagen gel compaction and can be cell mediated or occur via cell-independent mechanisms [3, 4, 5].
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Richardson, William J., and Jeffrey W. Holmes. "Do Infarcts Really Expand or Compact? Relationship Between Changing Material Properties and Apparent Infarct Remodeling." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14411.
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Myocardial infarction (MI) is a leading cause of mortality and morbidity with over 600,000 new Americans suffering an MI each year [1]. Following infarction, damaged muscle is gradually replaced by collagenous scar tissue, while undamaged (remote) myocytes remodel due to altered load. Remodeling of both the infarcted and remote myocardium are important determinants of cardiac function and the risk of progression to heart failure.
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Shehata, Monda L., Jan Skrok, Dirk Lossnitzer, et al. "Myocardial Scar In Pulmonary Hypertension: Relationship To Pulmonary Hemodynamics, Right Ventricular Function And Remodeling." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5536.
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Fomovsky, Gregory M., and Jeffrey W. Holmes. "Evolution of Scar Mechanical Properties During Myocardial Infarct Healing in Rat." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176422.
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The mechanics of healing myocardial infarcts are an important determinant of post-infarction left ventricular (LV) function and remodeling. Large animal infarct models are well studied; healing infarct scars have been shown to be mechanically and structurally anisotropic [1], and this anisotropy may help preserve LV function during some stages of healing [2]. At the same time, it has been suggested that the rat model of myocardial infarction is more similar to humans in the range of infarct sizes and observed LV dysfunction [3]. However, in the rat model, infarct mechanics and their effect on the overall LV function have not been described so far.
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Trubelja, Alen, John W. MacArthur, Joseph J. Sarver, et al. "Bioengineered SDF-1a Analogue Delivered as an Angiogenic Therapy Significantly Normalizes Elastic and Viscoelastic Material Properties of Infarcted Cardiac Muscle." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14602.
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Heart disease is a leading cause of death worldwide, and coronary heart disease causes 1 of every 6 deaths in the United States [1]. Following a myocardial infarction, scar tissue gradually replaces myocardium that is lost through a process of collagen deposition and an increase in tensile strength of the tissue [2]. This leads to infarct expansion, adverse ventricular remodeling and dysfunction, and ultimately heart failure. Dilation of the left ventricle (LV) leads to increased LV wall stress and is ultimately responsible for adverse ventricular remodeling. LV dilation causes stretching and thereby increased wall stress, prohibiting cardiomyocytes from effectively contracting, which leads to further dilation, and ultimately a decrease in cardiac pump efficiency [3]. Previously, it has been shown that using a tissue filler to modify the material properties of an infarct limits the process of ventricular remodeling [4]. Angiogenesis is another mechanism by which adverse ventricular remodeling can be limited. Previously, our group developed engineered stromal cell-derived factor-1α (ESA), a computationally designed analog of an established endothelial progenitor cell chemokine, SDF-1α, and demonstrated that ESA injection enhances LV function by promoting angiogenesis and retains the native properties of the extracellular matrix (ECM) [5] [6]. In this study, we propose that injection of ESA to infarcted cardiac muscle improves the tensile strength and viscoelastic properties of ventricular muscle.
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Discher, Dennis, and Adam Engler. "Mesenchymal Stem Cell Injection After Myocardial Infarction Improves Myocardial Compliance." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176754.
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Cellular therapy for myocardial injury has improved ventricular function in both animal and clinical studies, though the mechanism of benefit is unclear. This study was undertaken to examine the effects of cellular injection after infarction on myocardial elasticity. Coronary artery ligation of Lewis rats was followed by direct injection of human mesenchymal stem cells (MSC) into the acutely ischemic myocardium. Two weeks post-infarct, myocardial elasticity was mapped by atomic force microscopy. MSC-injected hearts near the infarct region were two-fold stiffer than myocardium from non-infarcted animals but softer than myocardium from vehicle-treated infarcted animals. After eight weeks, the following variables were evaluated: MSC engraftment and left ventricular geometry by histologic methods; cardiac function with a pressure-volume conductance catheter; myocardial fibrosis by Masson trichrome staining; vascularity by immunohistochemistry; and apoptosis by TUNEL assay. The human cells engrafted and expressed a cardiomyocyte protein but stopped short of full differentiation and did not stimulate significant angiogenesis. MSC-injected hearts showed significantly less fibrosis than controls, as well as less left ventricular dilation, reduced apoptosis, increased myocardial thickness, and preservation of systolic and diastolic cardiac function. In summary, MSC injection after myocardial infarction did not regenerate contracting cardiomyocytes but reduced the stiffness of the subsequent scar and attenuated post-infarction remodeling, preserving some cardiac function. Improving scarred heart muscle compliance could be a functional benefit of cellular cardiomyoplasty.
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Tang, Dalin, Chun Yang, Tal Geva, Glenn Gaudette, and Pedro J. del Nido. "Regenerated Contracting Myocardium May Improve Post-Surgery Right Ventricle Function: Patch Comparison Using MRI-Based Two-Layer Anisotropic Models of Human Right and Left Ventricles." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19067.
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Patients with repaired Tetralogy of Fallot (ToF), a congenital heart defect which includes a ventricular septal defect and severe right ventricular outflow obstruction, account for the majority of cases with late onset RV failure. The current surgical approach, which includes pulmonary valve replacement/insertion (PVR), has yielded mixed results. One reason for the unpredictable results is that the PVR surgery only addresses pulmonary regurgitation. New surgical options including scar tissue reduction and RV remodeling have been proposed in order to improve RV function recovery [1]. Various RV reconstruction techniques are being investigated, including patch design (materials, sizes, and shapes) and myocardium regeneration techniques which have the potential that viable myocardium may be regenerated or placed in the patch area [2,4]. Wald and Geva et al. investigated effects of regional dysfunction on global RV function in patients with repaired ToF and reported that localized dysfunction in the region of the RV outflow tract patch adversely affects global RV function and regional measures, and may have important implications for patient management [5]. Recent advances in computational modeling have made it possible for computer-simulated procedures (virtual surgery) to be used in clinical decision-making process to replace empirical and often risky clinical experimentation to examine the efficiency and suitability of various reconstructive procedures and patch design in diseased hearts [4]. In this paper, cardiac magnetic resonance imaging (CMR)-based two-layer active anisotropic models of human right and left ventricles (RV/LV) were constructed to compare three different patch materials and investigate the potential improvement of regenerated contracting myocardium on RV function after PVR surgery: Patch 1 – Dacron scaffold; Patch 2 – pericardium treated with gluteraldehyde; Patch 3 – viable contracting myocardium (not currently available but represents future direction). The 3D CMR-based RV/LV/Patch combination models were solved to obtain 3D ventricular deformation and stress/strain distributions for accurate assessment of RV mechanical conditions and function. The computational models were validated by CMR data and then used to assess the effect of patch material properties with the ultimate goal of improving recovery of RV function after surgery.
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Rajabi-Jaghargh, Ehsan, Mahesh K. Krishnamoorthy, and Rupak K. Banerjee. "Longitudinal Effect of Pressure Drop on the Intima-Media Thickening of the Venous Segment of the Arteriovenous Fistula." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14478.
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Venous stenosis is one of the primary causes of the arteriovenous fistula (AVF) maturation-failure and is characterized by vasoconstriction and significant intima-media thickening (IMT). Although the hemodynamic endpoints are believed to play a crucial role in the pathogenesis of venous stenosis, the exact mechanism behind this is unclear. Our hypothesis is that the changes in the pressure drop over time (Δp′) can influence the remodeling factors in AVFs: changes in luminal diameter (ΔDh) and IMT. Curved (C-AVF; n = 3) and straight (S-AVF; n = 3) AVFs were created between the femoral arteries and veins of 3 pigs. CT-scan and ultrasound were utilized to numerically evaluate the flow field, and thus pressure drop in AVFs at 2D (D: days), 7D, and 28D post-surgery. For each AVF, IMT was also measured at 4 histological blocks along the vein. For the C-AVF, the pressure drop consistently decreased over time (from 18.32 mmHg at 2D to 4.58 mmHg at 28D), while opposite trend was found for the S-AVF (from 12.91 mmHg at 2D to 24.49 mmHg at 28D). The Δp′ was negative at all the histology blocks for C-AVF which showed the reduction in the resistance over time due to dilation (positive ΔDh) and outward hypertrophy of the venous segment (positive ΔDh/IMT). In contrast, Δp′ was mostly positive for the S-AVF which showed the increase in the resistance due to vasoconstriction (negative ΔDh) and inward hypertrophy (negative ΔDh/IMT). Thus, measuring Δp′ at the successive post-surgery time points can provide important information on the remodeling behavior of AVFs. Also, creating AVFs in a surgical configuration that can result in negative Δp′ and thus favorable remodeling could influence the life expectancy of the dialysis patients.
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Scotti, Christine M., Ender A. Finol, Siddharth Viswanathan, et al. "Computational Fluid Dynamics and Solid Mechanics Analyses of a Patient-Specific AAA Pre- and Post-EVAR." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-62352.
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The establishment of a new pathway for blood flow immediately following endovascular aneurysm repair (EVAR) results in morphological changes and remodeling of the aneurismal sac. While EVAR is a minimally invasive surgical intervention, failure of the endovascular graft (EVG) may occur in which there is downstream migration and endoleak formation, creating a repressurization of the aneurismal sac and an increased risk of rupture. While the mechanism of aneurysm rupture and EVG failure is fundamental in nature, the factors that most significantly contribute to the end result are not yet fully understood. Mechanically, both are the consequence of an exerted force or disturbance exceeding the strength of a given material, whether it is the aneurismal arterial wall or the interaction that exists between the graft and wall. Embedded within this causal relationship are the contributions of arterial wall remodeling, intraluminal thrombus formation, and the dynamics that exists within the lumen. Several studies have been performed to examine these factors individually as they affect shear stress, the development of vortices, and the mechanical stress experienced along the arterial wall. However, a complete investigation is needed to study an anatomically realistic geometry operating under physiological conditions. The computational analyses conducted in this investigation address the confluence of these factors as they are modeled within an accurate patient-specific abdominal aortic aneurysm (AAA) reconstructed from CT scan data prior to and after EVAR. Our results verify the pressure-dominated characteristic of the flow and the negligible contribution of the dynamic and frictional force components; both are in good agreement with previously published results for analytical estimation of flow-induced forces in EVGs. [1]
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Fan, Rong, Michael S. Sacks, Ahmed Bayoumi, John E. Mayer, Christopher M. Hobson, and William R. Wagner. "Optimization of Engineered Ovine Pulmonary Heart Valve Leaflet Tissue Shape for Single Leaflet Replacement." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80824.
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Pulmonary valve (PV) replacement surgery is a treatment option for patients with a congenitally defective pulmonary outflow track. While a tissue engineered approach offers many potential advantages, develop of such a valve involves a complex process of optimization. As an intermediate step, we have used a single leaflet replacement surgical model to further our understanding of the in-vivo remodeling process. A critical step is to determine the deformed shape of the replacement PV leaflet under transvalvular pressure. Key factors in this process are: the scaffold anisotropic mechanical properties, optimal thickness, and the exact initial leaflet shape. We have used electrospun poly (ester urethane) ureas (ES-PEUU) scaffolds since they exhibit mechanical properties very similar to the native PV. In this work we present a design framework of the optimal leaflet shape determination utilizing a single sheet of ES-PEUU for single leaflet replacement surgery via finite element (FE) simulation. The mechanical properties of ES-PEUU scaffold for leaflet replacement were obtained from biaxial in-plane tension experiments. Generalized Fung-type hyperelastic constitutive model [1] was implemented into a commercial FE software package to simulate the deformation of ES-PEUU scaffolds under pressure. By perturbing the initial shape of leaflet and simulating its quasi-static deformation under PV diastolic loading, the optimal shape of unloaded leaflet was determined by comparing the deformed shape of leaflet obtained from FE simulation of TEPV with the one from microCT scan of a native ovine PV. In-vitro test of PV after single leaflet replacement was also conducted to validate the developed method.