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Release of Cardiac Biomarkers and Inflammatory Response during Cardiopulmonary Bypass: Comparison of Different Biocompatible Materials Used in Cardiopulmonary BypassSohn, Namseok 26 August 2008 (has links)
Coronary Artery Bypass Grafting (CABG) is an effective and invasive cardiac surgery to salvage blocked coronary artery. Cardiopulmonary bypass (CPB) is usually applied to support circulation during temporary cardiac arrest. Studies have demonstrated that cardiac injury, inflammation, and oxidative stress could be induced during CABG with CPB. We conducted two studies to investigate the release of cardiac biochemical markers and inflammatory response as well as to compare the effect of different coating biomaterial of CPB on the induction of inflammation and oxidative stress during CPB. We investigated the release patterns and the serum levels of cardiac markers as well as inflammatory markers in patients undergoing elective CABG at different time points after initiation of CPB. In this study, we demonstrated that cardiac markers such as creatine kinase isoenzyme MB (CK-MB), and cardiac troponin I (cTnI) and inflammatory markers such as tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and high sensitivity C-reactive protein (hsCRP) were highly elevated after CPB. Moreover, we confirmed that cTnI is still a better biochemical marker for cardiac injury than others following CABG with CPB. Other nonspecific but highly sensitive markers such as lactate dehydrogenase (LDH), lactate, TNF-alpha, IL-6, and hsCRP could be potential surrogate markers for evaluation of cardiac injury following CPB. Based on these findings, we conducted a further investigation to demonstrate our hypothesis that different biocompatible materials used in CPB may affect the inflammation and oxidative stress differently. Biocompatible materials are thinly coated on CPB tubes to provide similar environment like endothelial cells during cardiac surgery. There are several biocompatible materials available in the market. Each of them has unique characteristics. Inflammatory response is one of the bodys fundamental defense mechanisms against foreign invaders. However, inappropriate or excessive response can lead to harmful, potentially life-threatening consequences due to severe inflammatory tissue destruction. CPB-induced inflammatory response can be one of the factors, which can affect surgical outcomes. Depending on the presence of different biocompatible materials in CPB circuits, the degree of immunoreactions can be varied. In this study, we analyzed hsCRP, an acute phase protein, and tau protein, a marker of neurocognitive deficiency. Furthermore we analyzed inflammatory cytokines including TNF-alpha, IL-6, IL-10, and interferon-gamma (IFN-gamma) to evaluate the levels of inflammation. Serum levels of oxidized nitric oxide as a marker of oxidative stress were also assessed. We demonstrated that different biocompatible material has different impacts on inflammation and oxidative stress. In the aspect of anti-inflammation, heparin-coated biocompatible material is better than others whereas surface-modifying additives biocompatible material is worse than others. Overall, different coating biomaterial of CPB results in various inflammatory response. In terms of oxidative stress, we did not observe significant difference between different biomaterial-coated CPB. Read more
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A Spectral Deferred Correction Method for Solving Cardiac ModelsBowen, Matthew M. January 2011 (has links)
<p>Many numerical approaches exist to solving models of electrical activity in the heart. These models consist of a system of stiff nonlinear ordinary differential equations for the voltage and other variables governing channels, with the voltage coupled to a diffusion term. In this work, we propose a new algorithm that uses two common discretization methods, operator splitting and finite elements. Additionally, we incorporate a temporal integration process known as spectral deferred correction. Using these approaches,</p><p>we construct a numerical method that can achieve arbitrarily high order in both space and time in order to resolve important features of the models, while gaining accuracy and efficiency over lower order schemes.</p><p>Our algorithm employs an operator splitting technique, dividing the reaction-diffusion systems from the models into their constituent parts. </p><p>We integrate both the reaction and diffusion pieces via an implicit Euler method. We reduce the temporal and splitting errors by using a spectral deferred correction method, raising the temporal order and accuracy of the scheme with each correction iteration.</p><p> </p><p>Our algorithm also uses continuous piecewise polynomials of high order on rectangular elements as our finite element approximation. This approximation improves the spatial discretization error over the piecewise linear polynomials typically used, especially when the spatial mesh is refined. </p><p>As part of these thesis work, we also present numerical simulations using our algorithm of one of the cardiac models mentioned, the Two-Current Model. We demonstrate the efficiency, accuracy and convergence rates of our numerical scheme by using mesh refinement studies and comparison of accuracy versus computational time. We conclude with a discussion of how our algorithm can be applied to more realistic models of cardiac electrical activity.</p> / Dissertation Read more
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Magnetic Resonance Phase Velocity Mapping of Cardiac DyssynchronyDelfino, Jana G. 24 May 2007 (has links)
Cardiac resynchronization therapy (CRT) has recently emerged as an effective treatment option for heart failure patients with dyssynchrony. Patients have traditionally been chosen for CRT based on a prolonged QRS interval. However, this selection method is far from ideal, as approximately 30% of those receiving CRT do not show any clinical improvement.
Tissue Doppler imaging (TDI) suggests that one of the best predictors of response to CRT is the underlying level of mechanical dyssynchrony in the myocardial wall prior to CRT. As a result, there has been growing interest in direct imaging of the myocardial wall. Because myocardial contraction is a complex, three-dimensional movement, providing an accurate picture of myocardial wall motion can be challenging. Echocardiography initially emerged as the modality of choice, but the long list of limitations (limited echocardiographic windows, one direction of motion, poor reproducibility) has fostered interest in exploring the use of MR for myocardial wall imaging. Although MR presents some unique drawbacks (expensive equipment, longer imaging times), it is able to overcome many of the limitations of TDI. In particular, Phase Velocity Mapping (MR PVM) can provide a complete, three-directional description of motion throughout the entire myocardial wall at high spatial and temporal resolution.
The overall goal of this project was to develop a patient-selection method for CRT based on myocardial wall velocities acquired with MR PVM. First the image acquisition and post-processing protocols for MR PVM imaging of myocardial tissue were developed. A myocardial motion phantom was used to verify the accuracy of, and optimize the acquisition parameters for, the developed MR PVM sequence. Excellent correlation was demonstrated between longitudinal myocardial velocity curves acquired with the optimized MR PVM sequence and Tissue Doppler velocities. A database describing the normal myocardial contraction pattern was constructed. A small group of dyssynchrony patients was compared to the normal database, and several areas of delayed contraction were identified in the patients. Furthermore, significantly higher levels of dyssynchrony were detected in the patients than the normal volunteers. Finally, a method for computing transmural, endocardial, and epicardial, radial strains and strain rates from MR PVM velocity data was developed Read more
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Genetic analysis of dilated cardiomyopathy in the great daneHerbst, Stephanie Michelle 15 May 2009 (has links)
The domestic dog, Canis familiaris, with over 450 naturally-occurring hereditary
diseases, serves as a valuable model organism for study of the genetics underlying many
human hereditary diseases. Approximately half of the diseases that afflict the dog are
clinically very similar to various human hereditary diseases. Several cardiac diseases are
in this category. Our laboratory is interested in cardiac diseases because they are
common causes of death in the human and are also a widespread problem in many
breeds of dog. The specific focus of my work is on understanding the genetics of dilated
cardiomyopathy (DCM).
DCM is a disease characterized by enlargement of the left ventricle leading to an
inability of the heart to pump sufficient blood to the body. It is one of the most common
cardiac diseases in the dog and has a high mortality. The Great Dane is the second most
commonly affected breed. It is seen in many families of Great Danes, and this suggests
that DCM has a genetic component. The mode of inheritance of DCM in the Great Dane
is currently unknown, although studies have reported both autosomal recessive and
autosomal dominant transmission. Many different genes cause DCM, indicating the complexity of the disease.
These typically produce proteins that are involved in the sarcomere or cytoskeletal
components, leading to problems with contraction or cardiac cell integrity.
In order to identify causative or susceptibility genes for DCM in the Great Dane,
a whole-genome linkage screen was conducted in a family of Great Danes. One
candidate gene, gamma-sarcoglycan (SGCG), was identified through linkage and
sequenced in affected and unaffected dogs. Sequencing data revealed no mutations in the
coding regions of SGCG, most likely excluding it as a candidate gene for DCM.
Continued evaluation of this gene and others, both in sequence content and additional
properties such as epigenetic effects, protein structure, and interaction with other genes
will increase understanding of DCM in both the dog and the human. Read more
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A CLINICO-NEUROPATHOLOGICAL STUDY ON BRAIN DEATHTAKAHASHI, AKIRA, HASHIZUME, YOSHIO, UJIHIRA, NOBUKO 25 November 1993 (has links)
名古屋大学博士学位論文 学位の種類 : 博士(医学)(論文) 学位授与年月日:平成5年4月6日 氏平伸子氏の博士論文として提出された
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Design of mold to yield elastomeric membrane whose shape and size, when inflated, is similar to the shape of the human heartLagu, Amit Vinayak 15 November 2004 (has links)
Nearly five million Americans are living with heart failure and 550,000 new cases are diagnosed each year in the US. Amongst the new approaches to develop a better solution for Congestive Heart Failure, Ventricular Recovery (VR) holds the most promise. A team, under the guidance of Dr. Criscione in the Cardiac Mechanics Lab at Texas A&M University, is currently developing an investigative device which aims to assist in VR by restoration of physiological strain patterns in the myocardial cells. The contribution of this thesis has been towards the development of a molding apparatus that yields a polymeric membrane whose shape, when inflated, is similar to the shape of the human heart. This membrane would surround the epicardial surface of the heart, when used for the device being discussed and in particular for the prototypes being developed. Contribution also includes a testing apparatus that measures the inflation of a membrane and simulation to predict the behavior of isotropic ellipsoids upon inflation.
After unsuccessful implementations of two processing techniques, the successful design, fabrication implementation and attachment method meets the design criteria and is based on a thermoforming technique. Inflation profiles for membranes developed using this technique were studied at different pressures, with the axis length as variable. At 1kpa, which is the normal coronary arterial pressure, the membrane with an axis length of 140mm was found to show a shape which is similar to the shape of the human heart. In order to better understand and predict the shape an isotropic ellipsoidal membrane would take upon inflation without experimentation, simulations were carried out. Successful conversion of ellipsoidal geometry, with a few degrees of freedom as parameters, aided in simulation. Read more
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The clinical reasoning of expert acute care registered nurses in pre-cardiopulmonary arrest events /Ashcraft, Alyce Louise Smithson. January 2001 (has links)
Thesis (Ph. D.)--University of Texas at Austin, 2001. / Vita. Includes bibliographical references (leaves 405-423). Available also in a digital version from Dissertation Abstracts.
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High performance wireless bio-impedance measurement systemLe, Kelvin 03 February 2015 (has links)
Electrical and Computer Engineering / A high performance, wireless bio-impedance measurement system has been designed for the purpose of monitoring essential electrical properties of the heart during cardiac ablation. The system is broken into three parts: a spring-loaded device to house a tetrapolar surface probe and sensors, a wireless bio-impedance measurement system, and a desktop base station for graphical data display and acquisition. The system is specifically designed for a tetrapolar-electrode configuration where the two outer electrodes served as a current source operating at 20 kHz with an amplitude of 100 µArms and the two inner electrodes served as voltage sensing electrodes. In addition, the system also has a dedicated channel for current sense. The system is designed to be modular and reconfigurable for different measurement needs. Epochs of both discrete voltage and current samples generated by the voltage-controlled current source are processed using a digital signal processing algorithms to generate admittance measurements. In addition to the admittance’s magnitude and phase, pressure, electrocardiogram (EKG), and temperature (two channels) data are also acquired. The measurements are then wirelessly transmitted from the bio-impedance measurement system to a base station where data are processed and viewed graphically. The final system updates the admittance, pressure, EKG, and two temperature channels at 320 Hz, consumes less than 3 W, and has percent of measurement errors of 7 % and 2 % for capacitive and resistive measurements in the range of 100 pF to 10000 pF and 300 Ω to 1600 Ω, respectively. Instrument design, calibration, verification, and modeling are at the heart of this thesis. In the future, the instrument will be deployed for various bio-impedance measurements that require a high degree of linearity, precision, and a wide input range. / text Read more
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The clinical reasoning of expert acute care registered nurses in pre-cardiopulmonary arrest eventsAshcraft, Alyce Louise Smithson 28 August 2008 (has links)
Not available / text
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Mechanisms of ski-induced apoptosis in cardiac fibroblasts and myofibroblastsDavies, Jared 01 September 2015 (has links)
One of the hallmarks of chronic cardiac disease is the excessive formation of fibrous extracellular matrix. This inappropriate remodeling is mediated in large part by cardiac fibroblasts and phenoconverted myofibroblasts. The protooncoprotein Ski has previously been described as possessing anti-fibrotic properties within the myocardium, in addition to triggering apoptosis when overexpressed. In the current study, we found that overexpression of Ski results in a set of distinct morphological and biochemical changes within primary cardiac myofibroblasts that is indicative of apoptosis. Its upregulation is associated with the expression of pro-apoptotic factors such as Bax and Bak, as well as caspase-9 and -7. In all, our results indicate that Ski triggers a pro-death mechanism in primary rat cardiac myofibroblasts that is mediated through the intrinsic apoptotic pathway. The survival of these cells appears to be prolonged by a pro-survival autophagic response as apoptosis is hastened when autophagy is inhibited. The observed cell death response is likely working in parallel with the previously observed anti-fibrotic properties of Ski within this cell type. As myofibroblast cells are the engines of matrix expansion in heart failure, we suggest that using Ski or a projected Ski-mimetic to induce graded apoptosis in myofibroblasts within the failing heart may be a novel therapeutic mechanism of controlling cardiac fibrosis. / October 2015 Read more
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