Relevant bibliographies by topics / Coronary vasculature

Academic literature on the topic 'Coronary vasculature'

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Published: 4 June 2021
Last updated: 25 May 2024

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Journal articles on the topic "Coronary vasculature"

1

TAYLOR, R. "Smoking and the coronary vasculature." Journal of Molecular and Cellular Cardiology 18 (1986): 23. http://dx.doi.org/10.1016/s0022-2828(86)80553-3.

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2

Kapuria, Subir, Tyler Yoshida, and Ching-Ling Lien. "Coronary Vasculature in Cardiac Development and Regeneration." Journal of Cardiovascular Development and Disease 5, no. 4 (December 17, 2018): 59. http://dx.doi.org/10.3390/jcdd5040059.

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Functional coronary circulation is essential for a healthy heart in warm-blooded vertebrates, and coronary diseases can have a fatal consequence. Despite the growing interest, the knowledge about the coronary vessel development and the roles of new coronary vessel formation during heart regeneration is still limited. It is demonstrated that early revascularization is required for efficient heart regeneration. In this comprehensive review, we first describe the coronary vessel formation from an evolutionary perspective. We further discuss the cell origins of coronary endothelial cells and perivascular cells and summarize the critical signaling pathways regulating coronary vessel development. Lastly, we focus on the current knowledge about the molecular mechanisms regulating heart regeneration in zebrafish, a genetically tractable vertebrate model with a regenerative adult heart and well-developed coronary system.
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Kassab, Ghassan S. "The Coronary Vasculature and its Reconstruction." Annals of Biomedical Engineering 28, no. 8 (August 2000): 903–15. http://dx.doi.org/10.1114/1.1308494.

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4

Lin, Kai, and James C. Carr. "MR Imaging of the Coronary Vasculature." Radiologic Clinics of North America 53, no. 2 (March 2015): 345–53. http://dx.doi.org/10.1016/j.rcl.2014.11.003.

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Roux, Sebastien, Jean-Paul Clozel, Walter Fischli, and Herbert Kuhn. "Isoproterenol Impairs the Rat Coronary Vasculature." Journal of Cardiovascular Pharmacology 19, no. 4 (April 1992): 525–31. http://dx.doi.org/10.1097/00005344-199204000-00008.

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Fushimi, Etsuko, Takashi Saito, Yasutsugu Kudo, Tohru Abe, Yutaka Kimura, Kazuhito Takahashi, and Mamoru Miura. "Endothelial injury in reperfused coronary vasculature." Journal of Molecular and Cellular Cardiology 24 (May 1992): 163. http://dx.doi.org/10.1016/0022-2828(92)90514-z.

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de Beer, Vincent J., Shawn B. Bender, Yannick J. Taverne, Fen Gao, Dirk J. Duncker, M. Harold Laughlin, and Daphne Merkus. "Exercise limits the production of endothelin in the coronary vasculature." American Journal of Physiology-Heart and Circulatory Physiology 300, no. 5 (May 2011): H1950—H1959. http://dx.doi.org/10.1152/ajpheart.00954.2010.

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We previously demonstrated that endothelin (ET)-mediated coronary vasoconstriction wanes with increasing exercise intensity via a nitric oxide- and prostacyclin-dependent mechanism (Ref. 23). Therefore, we hypothesized that the waning of ET coronary vasoconstriction during exercise is the result of decreased production of ET and/or decreased ET receptor sensitivity. We investigated coronary ET receptor sensitivity using intravenous infusion of ET and coronary ET production using intravenous infusion of the ET precursor Big ET, at rest and during continuous treadmill exercise at 3 km/h in 16 chronically instrumented swine. In the systemic vasculature, Big ET and ET induced similar changes in hemodynamic parameters at rest and during continuous exercise at 3 km/h, indicating that exercise does not alter ET production or receptor sensitivity in the systemic vasculature. In the coronary vasculature, infusion of ET resulted in similar dose-dependent decreases in coronary blood flow and coronary venous oxygen tension and saturation at rest and during exercise. In contrast, administration of Big ET resulted in dose-dependent decreases in coronary blood flow, as well as coronary venous oxygen tension and saturation at rest. These effects of Big ET were significantly reduced during exercise. Altogether, our data indicate that continuous exercise at 3 km/h attenuates ET-mediated coronary vasoconstriction through reduced production of ET from Big ET rather than through reduced ET sensitivity of the coronary vasculature. The decreased ET production during exercise likely contributes to metabolic coronary vasodilation.
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Xiao, Ruoxiu, Jian Yang, Mahima Goyal, Yue Liu, and Yongtian Wang. "Automatic Vasculature Identification in Coronary Angiograms by Adaptive Geometrical Tracking." Computational and Mathematical Methods in Medicine 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/796342.

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As the uneven distribution of contrast agents and the perspective projection principle of X-ray, the vasculatures in angiographic image are with low contrast and are generally superposed with other organic tissues; therefore, it is very difficult to identify the vasculature and quantitatively estimate the blood flow directly from angiographic images. In this paper, we propose a fully automatic algorithm named adaptive geometrical vessel tracking (AGVT) for coronary artery identification in X-ray angiograms. Initially, the ridge enhancement (RE) image is obtained utilizing multiscale Hessian information. Then, automatic initialization procedures including seed points detection, and initial directions determination are performed on the RE image. The extracted ridge points can be adjusted to the geometrical centerline points adaptively through diameter estimation. Bifurcations are identified by discriminating connecting relationship of the tracked ridge points. Finally, all the tracked centerlines are merged and smoothed by classifying the connecting components on the vascular structures. Synthetic angiographic images and clinical angiograms are used to evaluate the performance of the proposed algorithm. The proposed algorithm is compared with other two vascular tracking techniques in terms of the efficiency and accuracy, which demonstrate successful applications of the proposed segmentation and extraction scheme in vasculature identification.
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Westerhof, Nico, Christa Boer, Regis R. Lamberts, and Pieter Sipkema. "Cross-Talk Between Cardiac Muscle and Coronary Vasculature." Physiological Reviews 86, no. 4 (October 2006): 1263–308. http://dx.doi.org/10.1152/physrev.00029.2005.

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The cardiac muscle and the coronary vasculature are in close proximity to each other, and a two-way interaction, called cross-talk, exists. Here we focus on the mechanical aspects of cross-talk including the role of the extracellular matrix. Cardiac muscle affects the coronary vasculature. In diastole, the effect of the cardiac muscle on the coronary vasculature depends on the (changes in) muscle length but appears to be small. In systole, coronary artery inflow is impeded, or even reversed, and venous outflow is augmented. These systolic effects are explained by two mechanisms. The waterfall model and the intramyocardial pump model are based on an intramyocardial pressure, assumed to be proportional to ventricular pressure. They explain the global effects of contraction on coronary flow and the effects of contraction in the layers of the heart wall. The varying elastance model, the muscle shortening and thickening model, and the vascular deformation model are based on direct contact between muscles and vessels. They predict global effects as well as differences on flow in layers and flow heterogeneity due to contraction. The relative contributions of these two mechanisms depend on the wall layer (epi- or endocardial) and type of contraction (isovolumic or shortening). Intramyocardial pressure results from (local) muscle contraction and to what extent the interstitial cavity contracts isovolumically. This explains why small arterioles and venules do not collapse in systole. Coronary vasculature affects the cardiac muscle. In diastole, at physiological ventricular volumes, an increase in coronary perfusion pressure increases ventricular stiffness, but the effect is small. In systole, there are two mechanisms by which coronary perfusion affects cardiac contractility. Increased perfusion pressure increases microvascular volume, thereby opening stretch-activated ion channels, resulting in an increased intracellular Ca2+transient, which is followed by an increase in Ca2+sensitivity and higher muscle contractility (Gregg effect). Thickening of the shortening cardiac muscle takes place at the expense of the vascular volume, which causes build-up of intracellular pressure. The intracellular pressure counteracts the tension generated by the contractile apparatus, leading to lower net force. Therefore, cardiac muscle contraction is augmented when vascular emptying is facilitated. During autoregulation, the microvasculature is protected against volume changes, and the Gregg effect is negligible. However, the effect is present in the right ventricle, as well as in pathological conditions with ineffective autoregulation. The beneficial effect of vascular emptying may be reduced in the presence of a stenosis. Thus cardiac contraction affects vascular diameters thereby reducing coronary inflow and enhancing venous outflow. Emptying of the vasculature, however, enhances muscle contraction. The extracellular matrix exerts its effect mainly on cardiac properties rather than on the cross-talk between cardiac muscle and coronary circulation.
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Taylor, Adam Michael, Joe McAleer, and Quenton Wessels. "Novel bilateral bifurcation of the coronary vasculature." Anatomy & Cell Biology 54, no. 1 (March 31, 2021): 132–35. http://dx.doi.org/10.5115/acb.20.241.

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Dissertations / Theses on the topic "Coronary vasculature"

1

Wade, Steven. "The effects of perhexiline on the rat coronary vasculature /." Title page, and summary only, 1996. http://web4.library.adelaide.edu.au/theses/09SB/09sbw121.pdf.

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Thesis (B. Sc.(Hons.))--University of Adelaide, Dept. of Physiology, 1997?
"Running title: Perhexiline: effects on vasculature, contractility and the role of endothelium." Includes bibliographical references.
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2

Reeves, Katherine Ann. "The cardiovascular actions of the isopropyl ester and other synthetic derivatives of palmitoyl carnitine." Thesis, University of Bath, 1995. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260252.

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3

Zatta, Amanda J., and n/a. "Adenosine and the Coronary Vasculature in Normoxic and Post-Ischaemic Hearts." Griffith University. School of Health Science, 2004. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20051130.124230.

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While previous research into the pathogenesis of ischaemic and reperfusion injuries has focussed on the cardiac myocyte, there is increasing evidence for a crucial role for coronary vascular injury in the genesis of the post-ischaemic phenotype [1-3]. Post-ischaemic vascular injury may be manifest as a transient or sustained loss of competent vessels, impairment of vascular regulatory mechanisms, and ultimately as the 'no-reflow' phenomenon (inability to sufficiently reperfuse previously ischaemic tissue despite the removal of the initial obstruction or occlusion). It is now appreciated that the earliest distinguishing feature of various forms of vascular injury (including atherosclerosis and infarction) is 'endothelial dysfunction', which is the marked reduction in endothelial-dependent relaxation due to reduced release or action of endothelial nitric oxide (NO). Importantly, vascular injury may worsen myocardial damage in vivo [4,5], significantly limiting tissue salvage and recovery. The pathogenesis of post-ischaemic vascular injury and endothelial dysfunction is incompletely understood, but has generally been considered to reflect a cardiovascular inflammatory response, neutrophils playing a key role. However, while blood-borne cells and inflammatory elements are undoubtedly involved in the 'progression' of vascular injury [6,7], accumulating evidence indicates that they are not the primary 'instigators' [8]. It should be noted that a wealth of controversial findings exists in the vascular injury literature and mechanisms involved remain unclear. Indeed, multiple mechanisms are likely to contribute to post-ischaemic vascular injury. Adenosine receptors are unique in playing a role in physical regulation of coronary function, and also in attenuating injury during and following ischaemia. While the adenosine receptor system has been extensively investigated in terms of effects on myocardial injury [9,10], little is known regarding potential effects of this receptor system on post-ischaemic coronary vascular injury. This thesis initially attempts to further our understanding of the role of adenosine in normal coronary vascular function, subsequent chapters assess the effect of ischaemia-reperfusion on vascular function, and adenosine receptor modification of vascular dysfunction in the isolated asanguinous mouse heart. Specifically, in Chapter 3 the receptor subtype and mechanisms involved in adenosine-receptor mediated coronary vasodilation were assessed in Langendorff perfused mouse and rat hearts. The study revealed that A2A adenosine receptors (A2AARs) mediate coronary dilation in the mouse vs. A2B adenosine receptors (A2BARs) in rat. Furthermore, responses in mouse involve a sensitive endothelial-dependent (NO-dependent) response and NO-independent (KATP-mediated) dilation. Interestingly, the ATP-sensitive potassium channel component predominates over NO-dependent dilation at moderate to high agonist levels. However, the high-sensitivity NO-dependent response may play an important role under physiological conditions when adenosine concentrations and the level of A2AAR activation are low. In Chapter 4 the mechanisms regulating coronary tone under basal conditions and during reactive hyperaemic responses were assessed in Langendorff perfused mouse hearts. The data support a primary role for KATP channels and NO in mediating sustained elevations in flow, irrespective of occlusion duration (5-40 s). However, KATP channels are of primary importance in mediating initial flow adjustments after brief (5-10 s) occlusions, while KATP (and NO) independent processes are increasingly important with longer (20-40 s) occlusion. Evidence is also presented for compensatory changes in KATP and/or NO mediated dilation when one pathway is blocked, and for a modest role for A2AARs in reactive hyperaemia. In Chapter 5 the impact of ischaemia-reperfusion on coronary function was examined, and the role of A1 adenosine receptor (A1AR) activation by endogenous adenosine in modifying post-ischaemic vascular function was assessed in isolated buffer perfused mouse hearts. The results demonstrate that ischaemia does modify vascular control and signficantly impairs coronary endothelial dilation in a model devoid of blood cells. Additionally, the data indicate that post-ischaemic reflow is significantly determined by A2AAR activation by endogenous adenosine, and that A1AR activation by endogenous adenosine protects against this model of vascular injury. Following from Chapter 5, the potential of A1, A2A and A3AR activation by exogenous and endogenous agonists to modulate post-ischaemic vascular dysfunction was examined in Chapter 6. Furthermore, potential mechanisms involved injury and protection were assessed by comparing effects of adenosine receptors to other 'vasoprotective' interventions, including anti-oxidant treatment, Na+/H+ exchange (NHE) inhibition, endothelin (ET) antagonism, and 2,3-butanedione monoxime (BDM). The data acquired confirm that post-ischaemic endothelial dysfunction is reduced by intrinsic A1AR activation, and also that exogenous A3AR activation potently reduces vascular injury. Protection appears unrelated to inhibition of ET or oxidant stress. However, preliminary data suggest A3AR vasoprotection may share signalling with NHE inhibition. Finally, the data reveal that coronary reflow in isolated buffer perfused hearts is not a critical determinant of cardiac injury, suggesting independent injury processes in post-ischaemic myocardium vs. vasculature. Collectively, these studies show that adenosine has a significant role in regulating coronary vascular tone and reactive hyperaemic responses via NO and KATP dependent mechanisms. Ischaemia-reperfusion modifies vascular control and induces significant endothelial dysfunction in the absence of blood, implicating neutrophil independent injury processes. Endogenous adenosine affords intrinsic vasoprotection via A1AR activation, while adenosinergic therapy via exogenous A3AR activation represents a new strategy for directly protecting against post-ischaemic vascular injury.
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Page, Henry Askew. "An investigation into the role of TMEM16A in the coronary vasculature." Thesis, St George's, University of London, 2017. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.754073.

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Introduction: Failure of coronary blood vessels to adequately supply cardiac myocytes with oxygen underlies ischaemic heart disease and ultimately myocardial infarction. Therefore, it is important to determine the factors that regulate coronary blood flow. Activation of Ca2+-activated chloride channels depolarises vascular smooth muscle cells sufficiently to cause Ca2+ influx through voltage-dependent channels and contraction of the cell. TMEM16A is the main molecular candidate for these channels. Hypothesis: TMEM16A is expressed in rat coronary arteries where it regulates vascular smooth muscle contraction. In coronary arteries from hypertensive rats the level of expression, and function of TMEM16A is altered. Methods: Quantitative polymerase chain reaction and immunodetection techniques assessed TMEM16A expression. Whole-cell patch clamp techniques were used to measure currents from freshly isolated rat coronary artery vascular smooth muscle cells (VSMCs). Wire myography and Langendorff perfused heart setup assessed coronary artery contractility and coronary blood flow respectively. Microelectrode impalement of rat coronary artery segments were combined with wire myography for membrane potential measurements. Results: TMEM16A was identified at mRNA and protein levels in rat coronary artery smooth muscle and TMEM16A-specific blockers attenuated the vasoconstricting effects of U46619 and 5-HT. These pharmacological agents also reduced the membrane depolarising effects of U46619 in sharp microelectrode studies and enhanced coronary flow in Langendorff set-ups. TMEM16A transcript was increased in coronary arteries from spontaneously hypertensive rats while the sensitivity to U46619 and 5HT was also increased in these vessels. This increased sensitivity was diminished in the presence of a novel TMEM16A inhibitor. Conclusion: TMEM16A is expressed in rat coronary arteries, where chloride is essential for optimal contraction and novel inhibitors of TMEM16A drastically effect vascular function. The expression of TMEM16A, contractility, and sensitivity to novel inhibitors of TMEM16A are all altered in coronary arteries from hypertensive rats.
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5

Zatta, Amanda J. "Adenosine and the Coronary Vasculature in Normoxic and Post-Ischaemic Hearts." Thesis, Griffith University, 2004. http://hdl.handle.net/10072/367305.

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While previous research into the pathogenesis of ischaemic and reperfusion injuries has focussed on the cardiac myocyte, there is increasing evidence for a crucial role for coronary vascular injury in the genesis of the post-ischaemic phenotype [1-3]. Post-ischaemic vascular injury may be manifest as a transient or sustained loss of competent vessels, impairment of vascular regulatory mechanisms, and ultimately as the 'no-reflow' phenomenon (inability to sufficiently reperfuse previously ischaemic tissue despite the removal of the initial obstruction or occlusion). It is now appreciated that the earliest distinguishing feature of various forms of vascular injury (including atherosclerosis and infarction) is 'endothelial dysfunction', which is the marked reduction in endothelial-dependent relaxation due to reduced release or action of endothelial nitric oxide (NO). Importantly, vascular injury may worsen myocardial damage in vivo [4,5], significantly limiting tissue salvage and recovery. The pathogenesis of post-ischaemic vascular injury and endothelial dysfunction is incompletely understood, but has generally been considered to reflect a cardiovascular inflammatory response, neutrophils playing a key role. However, while blood-borne cells and inflammatory elements are undoubtedly involved in the 'progression' of vascular injury [6,7], accumulating evidence indicates that they are not the primary 'instigators' [8]. It should be noted that a wealth of controversial findings exists in the vascular injury literature and mechanisms involved remain unclear. Indeed, multiple mechanisms are likely to contribute to post-ischaemic vascular injury. Adenosine receptors are unique in playing a role in physical regulation of coronary function, and also in attenuating injury during and following ischaemia. While the adenosine receptor system has been extensively investigated in terms of effects on myocardial injury [9,10], little is known regarding potential effects of this receptor system on post-ischaemic coronary vascular injury. This thesis initially attempts to further our understanding of the role of adenosine in normal coronary vascular function, subsequent chapters assess the effect of ischaemia-reperfusion on vascular function, and adenosine receptor modification of vascular dysfunction in the isolated asanguinous mouse heart. Specifically, in Chapter 3 the receptor subtype and mechanisms involved in adenosine-receptor mediated coronary vasodilation were assessed in Langendorff perfused mouse and rat hearts. The study revealed that A2A adenosine receptors (A2AARs) mediate coronary dilation in the mouse vs. A2B adenosine receptors (A2BARs) in rat. Furthermore, responses in mouse involve a sensitive endothelial-dependent (NO-dependent) response and NO-independent (KATP-mediated) dilation. Interestingly, the ATP-sensitive potassium channel component predominates over NO-dependent dilation at moderate to high agonist levels. However, the high-sensitivity NO-dependent response may play an important role under physiological conditions when adenosine concentrations and the level of A2AAR activation are low. In Chapter 4 the mechanisms regulating coronary tone under basal conditions and during reactive hyperaemic responses were assessed in Langendorff perfused mouse hearts. The data support a primary role for KATP channels and NO in mediating sustained elevations in flow, irrespective of occlusion duration (5-40 s). However, KATP channels are of primary importance in mediating initial flow adjustments after brief (5-10 s) occlusions, while KATP (and NO) independent processes are increasingly important with longer (20-40 s) occlusion. Evidence is also presented for compensatory changes in KATP and/or NO mediated dilation when one pathway is blocked, and for a modest role for A2AARs in reactive hyperaemia. In Chapter 5 the impact of ischaemia-reperfusion on coronary function was examined, and the role of A1 adenosine receptor (A1AR) activation by endogenous adenosine in modifying post-ischaemic vascular function was assessed in isolated buffer perfused mouse hearts. The results demonstrate that ischaemia does modify vascular control and signficantly impairs coronary endothelial dilation in a model devoid of blood cells. Additionally, the data indicate that post-ischaemic reflow is significantly determined by A2AAR activation by endogenous adenosine, and that A1AR activation by endogenous adenosine protects against this model of vascular injury. Following from Chapter 5, the potential of A1, A2A and A3AR activation by exogenous and endogenous agonists to modulate post-ischaemic vascular dysfunction was examined in Chapter 6. Furthermore, potential mechanisms involved injury and protection were assessed by comparing effects of adenosine receptors to other 'vasoprotective' interventions, including anti-oxidant treatment, Na+/H+ exchange (NHE) inhibition, endothelin (ET) antagonism, and 2,3-butanedione monoxime (BDM). The data acquired confirm that post-ischaemic endothelial dysfunction is reduced by intrinsic A1AR activation, and also that exogenous A3AR activation potently reduces vascular injury. Protection appears unrelated to inhibition of ET or oxidant stress. However, preliminary data suggest A3AR vasoprotection may share signalling with NHE inhibition. Finally, the data reveal that coronary reflow in isolated buffer perfused hearts is not a critical determinant of cardiac injury, suggesting independent injury processes in post-ischaemic myocardium vs. vasculature. Collectively, these studies show that adenosine has a significant role in regulating coronary vascular tone and reactive hyperaemic responses via NO and KATP dependent mechanisms. Ischaemia-reperfusion modifies vascular control and induces significant endothelial dysfunction in the absence of blood, implicating neutrophil independent injury processes. Endogenous adenosine affords intrinsic vasoprotection via A1AR activation, while adenosinergic therapy via exogenous A3AR activation represents a new strategy for directly protecting against post-ischaemic vascular injury.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Health Sciences
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6

Kneale, Barry J. "The influence of gender on forearm resistance vessel function." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312451.

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Kmetz, John George II. "Differential Regulation of TRPV1 Channels in the Murine Coronary Vasculature by H2O2." Kent State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=kent1398336723.

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8

Ellwood, Amanda Jane. "5-hydroxytryptamine receptor agonism and antagonism in guinea-pig and rabbit coronary vasculature." Thesis, King's College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.264337.

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Goyal, Ayush. "Vasculature reconstruction from 3D cryomicrotome images." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:aa9e500b-a0a4-48f3-8cb8-e75bbcc775e9.

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Background: Research in heart disease can be aided by modelling myocardial hemodynamics with knowledge of coronary pressure and vascular resistance measured from the geometry and morphometry of coronary vasculature. This study presents methods to automatically reconstruct accurate detailed coronary vascular anatomical models from high-resolution three-dimensional optical fluorescence cryomicrotomography image volumes for simulating blood flow in coronary arterial trees. Methods: Images of fluorescent cast and bead particles perfused into the same heart comprise the vasculature and microsphere datasets, employed in a novel combined approach to measure vasculature and simulate a flow model on the extracted coronary vascular tree for estimating regional myocardial perfusion. The microspheres are used in two capacities - as fiducial biomarker point sources for measuring the image formation in order to accurately measure the vasculature dataset and as flowing particles for measuring regional myocardial perfusion through the reconstructed vasculature. A new model-based template-matching method of vascular radius estimation is proposed that incorporates a model of the optical fluorescent image formation measured from the microspheres and a template of the vessels’ tubular geometry. Results: The new method reduced the error in vessel radius estimation from 42.9% to 0.6% in a 170 micrometer vessel as compared to the Full-Width Half Maximum method. Whole-organ porcine coronary vascular trees, automatically reconstructed with the proposed method, contained on the order of 92,000+ vessel segments in the range 0.03 – 1.9 mm radius. Discrepancy between the microsphere perfusion measurements and regional flow estimated with a 1-D steady state linear static blood flow simulation on the reconstructed vasculature was modelled with daughter-to-parent area ratio and branching angle as the parameters. Correcting the flow simulation by incorporating this model of disproportionate distribution of microspheres reduced the error from 24% to 7.4% in the estimation of fractional microsphere distribution in oblique branches with angles of 100°-120°.
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Davis, Griffith M. "Exposure to Nanomaterials Results in Alterations of Inflammatory and Atherosclerotic Signaling Pathways in the Coronary Vasculature of Wildtype Rodents." Thesis, University of North Texas, 2018. https://digital.library.unt.edu/ark:/67531/metadc1248468/.

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Cardiovascular disease (CVD) is the leading cause of death for people of most ethnicities on a global scale, and countless research efforts on the pathology of CVD has been well-characterized over the years. However, advancement in modern technologies, such as nanotechnology, has generated environmental and occupational health concerns within the scientific community. Current investigation of nanotoxicity calls into question the negative effects nanomaterials may invoke from their environmental, commercial, and therapeutic usage. As a result, further research is needed to investigate and characterize the toxicological implications associated with nanomaterial-exposure and CVD. We investigated the toxicity of multi-walled carbon nanotubes (MWCNT) and titanium dioxide (TiO2), which are two prominently used nanomaterials that have been previously linked to upregulation of inflammatory and atherogenic factors. However, the mechanistic pathways involved in these nanomaterials mediating detrimental effects on the heart and/or coronary vasculature have not yet been fully determined. Thus, we utilized two different routes of exposure in rodent models to assess alterations in proinflammatory and proatherogenic signaling pathways, which are represented in contrast throughout the dissertation. In our MWCNT study, we used C57Bl/6 mice exposed to MWCNTs (1 mg/m3) or filtered air (FA-Controls), via inhalation, for 6 hr/d for 14d. Conversely, intravenous TiO2 was administered to F344 male fisher rats, following 24h and 28d post-exposure to a single injection of TiO2-NPs (1 mg/kg), compared to control animals. MWCNT-exposed endpoints investigated the alterations in cholesterol transport, such as lectin-like oxidized low-density lipoprotein receptor (LOX)-1 and ATP-binding cassette transporter (ABCA)-1, inflammatory markers [tumor necrosis factor (TNF)-α], interleukin (IL)-1β/IL-6, nuclear-factor kappa-light-chain-enhancer of activated B cells (NF-κB) and signaling factors involved in activation of the pathway, as well as intracellular/vascular adhesion molecule(s) (VCAM-1, ICAM-1), and miRNAs (miR-221/-21/-1), associated with CVD, were analyzed in cardiac tissue and coronary vasculature. Cardiac fibrotic deposition, matrix-metalloproteinases (MMP)-2/9, and reactive oxygen species (ROS) were also assessed. TiO2-exposure endpoints also involved alterations on cholesterol transport proteins via LOX-1 and ABCA-1, factors of inflammation, namely intracellular macrophages and interleukin (IL)-1β, MMP-2/9 activity and protein expression, fibrotic deposition, and ROS generation were analyzed via quantitative detection or histologically in both cardiac tissue and coronary vasculature. Results from both studies found alterations in fibrotic deposition, upregulation in LOX-1 expression and MMP-2/9 activity, and ROS generation; with a concurrent decrease in ABCA-1 expression in cardiac tissue and coronary vasculature. Individually, MWCNT-exposed endpoints had shown induction of cardiac TNF-α, MMP-9, IκB Kinase (IKK)-α/β, and miR-221 mRNAs; as well as increased coronary expression of TNF-α and VCAM-1. TiO2 studies found increases in IL-1β and MMP-9 protein expression, as well as intracellular macrophage induction. Both studies also found, through pre-treatment of NADPH oxidase inhibitor, apocynin, resulted in attenuation of nanomaterial-exposure mediated ROS production; with nitric oxide synthase inhibitor, L-NNA, also showing attenuation, but only in our MWCNT-exposed inhalation study. The results from both studies have demonstrated, through different routes of administration, exposures, and rodent models; that exposure to nanomaterials can mediate signaling pathways involved in initiation and/or progression of CVD.
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Books on the topic "Coronary vasculature"

1

Tomanek, Robert J. Coronary Vasculature. Boston, MA: Springer US, 2013. http://dx.doi.org/10.1007/978-1-4614-4887-7.

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Tomanek, Robert J. J. Coronary Vasculature: Development, Structure-Function, and Adaptations. Springer, 2014.

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Coronary Vasculature: Development, Structure-Function, and Adaptations. Springer, 2012.

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Tomanek, Robert J. Coronary Vasculature: Development, Structure-Function, and Adaptations. Springer, 2012.

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Tomanek, Robert J. Coronary Vasculature: Development, Structure-Function, and Adaptations. Springer, 2012.

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Cahill, Thomas J., and Paul R. Riley. Epicardial and coronary vascular development. Edited by Miguel Torres. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0009.

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The coronary circulation is essential for human life. In embryonic development, abnormal formation of the coronary vasculature can cause death in utero or after birth. In adulthood, atherosclerosis of the coronary arteries is the commonest cause of death worldwide. The last decade has witnessed significant strides forward in our understanding of coronary development. Multiple sources of coronary endothelial cells have been identified using genetic tools for fate mapping. The epicardium, the outermost layer of the developing heart, has emerged as both a source of cell progenitors and key signalling mediators. Knowledge of the specific genes underlying formation, function, and heterogeneity of the epicardium is expanding. Significant challenges remain, however, in understanding the spatiotemporal signalling patterns required for organized migration, differentiation, and patterning of the vasculature. In addition, dissecting how coronary development is perturbed in patients with congenital coronary anomalies is a major ongoing focus of research.
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O'Gorman, Daniel Joseph. Abnormalities of the coronary vasculature in the hypertrophied guinea pig heart. 1994.

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Kahn, S. Lowell. Balloon Anchor Techniques for Sheath, Guide Catheter, and Stent Advancement and to Facilitate Chronic Total Occlusion Traversal. Edited by S. Lowell Kahn, Bulent Arslan, and Abdulrahman Masrani. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199986071.003.0061.

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Advancement of a sheath or guide catheter into a small, diseased or angled branch vessel such as the superior mesenteric artery or renal artery can be difficult. Similarly, there are times when placement of a sheath up and over a sharply angulated aortic bifurcation can present a challenge. Obtaining a sheath position at or beyond a stenotic or occlusive lesion may be critical for delivering a stent, particularly with the inherent risk of dislodgment associated with balloon-expandable stents. The use of balloons as anchors has been described most commonly in the coronary vasculature, but it can have an important role in peripheral and visceral applications. This chapter discusses the utility of balloons as an anchor to advance a sheath or stent to a target location.
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Banerjee, Amitava, and Kaleab Asrress. Screening for cardiovascular disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0351.

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Screening involves testing asymptomatic individuals who have risk factors, or individuals who are in the early stages of a disease, in order to decide whether further investigation, clinical intervention, or treatment is warranted. Therefore, screening is classically a primary prevention strategy which aims to capture disease early in its course, but it can also involve secondary prevention in individuals with established disease. In the words of Geoffrey Rose, screening is a ‘population’ strategy. Examples of screening programmes are blood pressure monitoring in primary care to screen for hypertension, and ultrasound examination to screen for abdominal aortic aneurysm. The effectiveness and feasibility of screening are influenced by several factors. First, the diagnostic accuracy of the screening test in question is crucial. For example, exercise ECG testing, although widely used, is not recommended in investigation of chest pain in current National Institute for Health and Care Excellence guidelines, due to its low sensitivity and specificity in the detection of coronary artery disease. Moreover, exercise ECG testing has even lower diagnostic accuracy in asymptomatic patients with coronary artery disease. Second, physical and financial resources influence the decision to screen. For example, the cost and the effectiveness of CT coronary angiography and other new imaging modalities to assess coronary vasculature must be weighed against the cost of existing investigations (e.g. coronary angiography) and the need for new equipment and staff training and recruitment. Finally, the safety of the investigation is an important factor, and patient preferences and physician preferences should be taken into consideration. However, while non-invasive screening examinations are preferable from the point of view of patients and clinicians, sometimes invasive screening tests may be required at a later stage in order to give a definitive diagnosis (e.g. pressure wire studies to measure fractional flow reserve in a coronary artery). The WHO’s principles of screening, first formulated in 1968, are still very relevant today. Decision analysis has led to ‘pathways’ which guide investigation and treatment within screening programmes. There is increasing recognition that there are shared risk factors and shared preventive and treatment strategies for vascular disease, regardless of arterial territory. The concept of ‘vascular medicine’ has gained credence, leading to opportunistic screening in other vascular territories if an individual presents with disease in one territory. For example, post-myocardial infarction patients have higher incidence of cerebrovascular and peripheral arterial disease, so carotid duplex scanning and measurement of the ankle–brachial pressure index may be valid screening approaches for arterial disease in other territories.
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Covic, Adrian, Mugurel Apetrii, Luminita Voroneanu, and David J. Goldsmith. Vascular calcification. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0120_update_001.

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Vascular calcification (VC) is a common feature of patients with advanced CKD and it could be, at least in part, the cause of increased cardiovascular mortality in these patients. From a morphologic point of view, there are at least two types of pathologic calcium phosphate deposition in the arterial wall—namely, intima calcification (mostly associated with atherosclerotic plaques) and media calcification (associated with stiffening of the vasculature, resulting in significantly adverse cardiovascular outcomes). Although VC was viewed initially as a passive phenomenon, it appears to be a cell-mediated, dynamic, and actively regulated process that closely resembles the formation of normal bone tissue, as discovered recently. VC seems to be the result of the dysregulation of the equilibrium between promoters and inhibitors. The determinants are mostly represented by altered calcium and phosphorus metabolism, secondary hyperparathyroidism, vitamin D excess, high fibroblast growth factor 23, and high levels of indoxyl sulphate or leptin; meanwhile, the inhibitors are vitamin K, fetuin A, matrix G1a protein, osteoprotegerin, and pyrophosphate. A number of non-invasive imaging techniques are available to investigate cardiac and vascular calcification: plain X-rays, to identify macroscopic calcifications of the aorta and peripheral arteries; two-dimensional ultrasound for investigating the calcification of carotid arteries, femoral arteries, and aorta; echocardiography, for assessment of valvular calcification; and, of course, computed tomography technologies, which constitute the gold standard for quantification of coronary artery and aorta calcification. All these methods have a series of advantages and limitations. The treatment/ prevention of VC is currently mostly around calcium-mineral bone disease interventions, and unproven. There are interesting hypotheses around vitamin K, Magnesium, sodium thiosulphate and other potential agents.
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Book chapters on the topic "Coronary vasculature"

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Tomanek, Robert J. "Coronary Anomalies." In Coronary Vasculature, 101–21. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4887-7_6.

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Tomanek, Robert J. "General Concepts of Blood Vessel Formation and Remodeling." In Coronary Vasculature, 1–23. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4887-7_1.

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Tomanek, Robert J. "Myocardial Ischemia and Infarction." In Coronary Vasculature, 189–220. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4887-7_10.

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Tomanek, Robert J. "Cardiac Hypertrophy." In Coronary Vasculature, 221–46. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4887-7_11.

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Tomanek, Robert J. "Therapy for the Coronary Circulation." In Coronary Vasculature, 247–66. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4887-7_12.

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Tomanek, Robert J. "Prenatal Coronary Morphogenesis." In Coronary Vasculature, 25–46. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4887-7_2.

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Tomanek, Robert J. "Postnatal Coronary Morphogenesis and Growth." In Coronary Vasculature, 47–57. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4887-7_3.

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Tomanek, Robert J. "Structure–Function of the Coronary Hierarchy." In Coronary Vasculature, 59–81. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4887-7_4.

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Tomanek, Robert J. "Historical Perspectives." In Coronary Vasculature, 83–100. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4887-7_5.

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Tomanek, Robert J. "Aging." In Coronary Vasculature, 123–41. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4887-7_7.

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Conference papers on the topic "Coronary vasculature"

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Soroushmehr, S. M. R., A. Bafna, S. Sinha, B. Nallamothu, K. Ward, and K. Najarian. "Quantitative measurement of vasculature in coronary angiogram videos." In 2016 IEEE-EMBS International Conference on Biomedical and Health Informatics (BHI). IEEE, 2016. http://dx.doi.org/10.1109/bhi.2016.7455863.

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Chen, Jenny, Jessica S. Coogan, Hyun Jin Kim, and Charles A. Taylor. "Pressure and Flow Characterization for Different Idealized Models of Stenotic Coronary Arteries." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19329.

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Coronary artery disease is one of the leading causes of death worldwide. This year, an estimated 785,000 Americans will have a new coronary attack [1]. Treatment of coronary artery disease varies from medication alone to cardiovascular surgery. Treatment regimens depend on the number and hemodynamic significance of stenoses present. In this study, we created idealized models of stenotic coronary arteries with varying geometric properties and simulated flow and pressure in coronary stenoses using a novel computational method including a three-dimensional model of an idealized coronary artery coupled to a lumped parameter model of the heart at the inlet and a lumped parameter model of the distal coronary vasculature at the outlet.
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Banerjee, Rupak K., Lloyd H. Back, Martin R. Back, and Young I. Cho. "Linking Measurements of Coronary Flow Reserve in Patients During Angioplasty Procedures to Myocardial Perfusion Using Computational Hemodynamics." In ASME 2000 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/imece2000-2613.

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Abstract Computational hemodynamics was used to determine the connection between measurements of coronary flow reserve (CFR) and myocardial perfusion in patients with obstructive disease during angioplasty. The 32 patient group (Wilson et al. 1988) had single-vessel, single-lesions with either unstable angina pectoris or stable angina, but no known abnormalities that might affect the vasodilator capacity of the arteriolar vasculature. The patients’ maximal vasodilation-distal perfusion pressure curve (CFR- P ˜ r h ) was uniquely determined by the intersections of measured values of CFR and computed values of P ˜ r h for the native and residual lesions after percutaneous transluminal coronary balloon angioplasty (PTCA) supplying blood to the same vasculature. Extrapolation of this nearly linear curve to its origin gave a zero-flow mean pressure P ˜ r o of about 20 mm Hg, close to a value of 18 mm Hg known to be associated with ischemia in the subendocardium of dog hearts (Bache and Schwartz, 1982). The corresponding value of P ˜ r h of about 55 mm Hg in the native lesions coincided with the level proposed by Brown et al. 1984 to cause ischemia in the subendocardium of human hearts.
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Wang, Roy, Rudolph L. Gleason, and Luke Brewster. "Diameter Constriction Reduces Intramural Circumferential Stress Gradient in the Vein Under Arterial Pressures." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80797.

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Coronary and peripheral artery diseases are a leading cause of morbidity and mortality in developed countries. For severe cases, surgical intervention to bypass the disease using autologous vessels continues to be the preferred choice of treatment. These bypass vessels are typically obtained from the venous vasculature. Despite the superior long-term patency of veins over synthetic grafts, one-year failure rates approach 30–40% in both the coronary and peripheral systems [1–2]. Still, bypass surgery remains the recommended therapy for most persons with severe arterial blockages [3]. As the number of bypass procedures increase and patients receiving bypasses live longer, improving the lifetime of bypass grafts is increasingly important.
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Boutsianis, Evangelos, Thomas Frauenfelder, Hitendu Dave, Jurg Grunenfelder, Simon Wildermuth, Gregor Zund, Marko Turina, Dimos Poulikakos, and Yiannis Ventikos. "Cardiovascular Haemodynamic Simulations of Anatomically Accurate Coronaries." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-42728.

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The present study is devoted to the investigation of the pulsatile blood flow within the first few vessels of the Left Coronary Artery (LCA) vasculature of an anatomically accurate porcine coronary tree. Transient computational fluid dynamics simulations were performed under realistic pulsatile volume inflow boundary conditions. The numerical results have provided a comprehensive collection of information regarding the haemodynamics within the LCA and its major branches, namely the Left Anterior Descending (LAD) and the Left Circumflex (LCX) arteries. The underlying principle of developing computational techniques, which would eventually allow for the realistic simulation of the vascular haemodynamics of patients, lies on the capacity of such tools for predictive diagnostics and non-invasive, hence simulation-based, surgical planning.
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Meglan, Dwight A., Bryan P. Bergeron, Ryan S. Bardsley, John M. Galeotti, and Cameron N. Riviere. "Techniques for Avoidance of Coronary Vasculature during Epicardial Needle Insertions with a Miniature Robotic Walker." In the 3rd International Conference. New York, New York, USA: ACM Press, 2017. http://dx.doi.org/10.1145/3068796.3068799.

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Sherknies, Denis, Jean Meunier, and Jean-Claude Tardif. "3D heart motion from single-plane angiography of the coronary vasculature: a model-based approach." In Medical Imaging 2004, edited by J. Michael Fitzpatrick and Milan Sonka. SPIE, 2004. http://dx.doi.org/10.1117/12.534629.

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Wahle, Andreas, Steven C. Mitchell, Mark E. Olszewski, Ryan M. Long, and Milan Sonka. "Accurate visualization and quantification of coronary vasculature by 3D/4D fusion from biplane angiography and intravascular ultrasound." In EOS/SPIE European Biomedical Optics Week, edited by Israel Gannot, Yuri V. Gulyaev, Theodore G. Papazoglou, and Christiaan F. P. van Swol. SPIE, 2001. http://dx.doi.org/10.1117/12.413790.

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Bonert, Michael, Jerry G. Myers, Stephen E. Fremes, and C. Ross Ethier. "Influence of Graft/Host Diameter Ratio on the Hemodynamics in Sequential ITA Anastomoses." In ASME 2000 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/imece2000-2612.

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Abstract Multivessel grafting with internal thoracic artery (ITA) conduits may improve the long-term results of coronary surgery for patients with multivessel coronary disease. Sequential ITA grafting has been increasingly used as a means of allowing a single ITA to revascularize a greater amount of the myocardium (Izzat et al, 1994). In this procedure, the graft first supplies blood to a coronary artery via a side-to-side anastomoses and then delivers blood to a second site in the coronary vasculature through an end-to-side anastomosis. However, it is unclear if the complex geometry and hemodynamic patterns in the side-to-side anastomosis contribute to the development of intimal hyperplasia, as reported for end-to-side anastomoses (Bassiouny et al. 1992). In a previous study we studied the hemodynamics of side-to-side anastomosis when graft and host diameters are equal (Bonert et al., 1999). In this study, we examined the wall shear stress (WSS) characteristics in idealized models of a “parallel” and a “diamond” side-to-side anastomoses for the case in which the graft diameter is substantially larger than the host diameter (Lei et al., 1996). Regions of specific interest were those exhibiting low WSS and rapidly changing WSS (high spatial WSS gradient) both of which have been suggested to promote intimal hyperplasia.
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de Tullio, Marco D., Roberto Verzicco, Luciano Afferrante, and Giuseppe Pascazio. "Fluid Mechanics of Deformable Aortic Prostheses." In ASME 2010 3rd Joint US-European Fluids Engineering Summer Meeting collocated with 8th International Conference on Nanochannels, Microchannels, and Minichannels. ASMEDC, 2010. http://dx.doi.org/10.1115/fedsm-icnmm2010-31148.

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The simultaneous replacement of a diseased aortic valve, aortic root and ascending aorta with a composite graft equipped with a prosthetic valve is a nowadays standard surgical approach in which the Valsalva sinuses of the aortic root are sacrificed and the coronary arteries are reconnected directly to the graft (Bentall procedure). In practice, two different polyethylene terephthalate (Dacron) prostheses are largely used by surgeons: a standard straight graft and a graft with a bulged portion that better reproduces the aortic root anatomy (Valsalva graft). The aim of the present investigation is to study the effect of the graft geometry, with its pseudo-sinuses, on the the flowfield, with particular attention to the coronary entry-flow, and on the stress concentration at the level of coronary-root anastomoses during the cardiac cycle. A bi-leaflet mechanical valve with curved leaflets is considered, attached to the two different prostheses. Two cylindrical channels, reproducing the very early coronary vasculature are connected to the grafts. An accurate three-dimensional numerical method, based on the immersed boundary technique, is proposed to study the flow inside deformable geometries. Direct numerical simulations of the flow inside the prostheses under physiological pulsatile inflow conditions are presented. The dynamics of the leaflets (considered rigid) is obtained by a fully-coupled fluid-structure-interaction approach, while a weak-coupled approach is employed for the deforming roots, in order to reduce the computational cost, using optimized solvers for both the fluid and structural problems. The Dacron material is modeled as orthotropic, with an inversion of the material properties in longitudinal and circumferential direction for the skirt region of the Valsalva prosthesis. Coronary perfusion is reproduced modulating in time the porosity, and thus the resistance, of the coronary channels. The results indicate that while the pseudo-sinuses do not significantly influence the coronary entry-flow, their presence allows for smaller levels of stresses at the level of coronary-root anastomoses, potentially reducing post-operative complications.
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