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Thesis (M.S.)--University of Akron, Dept. of Chemical and Biomedical Engineering, 2009. / "May, 2009." Title from electronic thesis title page (viewed 8/2/2009) Advisor, Bruce C. Taylor; Committee members, Daniel B. Sheffer, Dale H. Mugler; Department Chair, Daniel B. Sheffer; Dean of the College, George K. Haritos; Dean of the Graduate School, George R. Newkome. Includes bibliographical references.

Heart failure has a significant impact on mortality and morbidity. Dilated cardiomyopathy (DCM) is the third most common cause of heart failure and the most common reason for heart transplantation. Familial DCM is known to be caused by mutations in the LMNA gene encoding lamins A and C. New methods to enhance cardiac contractility would be beneficial in the treatment or prevention of heart failure. The focus of this thesis was to evaluate the mechanisms of altered contractility in two mouse models: the LMNA knockout model (homozygous, Lmna-/-; heterozygous, Lmna+/-) generated by targeted deletion of the lmna gene, and the model of enhanced contractility due to cardiac alpha1A-adrenergic receptor (???1A-AR) overexpression (A1A1). Previous studies have found altered nuclear-desmin connections in lamin A/C deficient mice. It was proposed that these alterations result in ???defective force transmission???, which leads to DCM. Studies in this thesis have supported this hypothesis. Studies of isolated single cardiomyocytes from mice aged 4-6 weeks demonstrated abnormal cell morphology and contractile dysfunction in Lmna-/- cardiomyocytes, while Lmna+/- cells showed no overt phenotype. Excitation-contraction coupling experiments and forcecalcium studies in skinned fibers excluded altered calcium kinetics as a primary cause of DCM in this model, but there was evidence of reduced sarcomere numbers and reduced sarcomere lengths as a contributor to reduce force generation in Lmna-/- and Lmna+/- mice. Previous in vivo studies showed that A1A1 mice had enhanced contractility with the absence of hypertrophy. Studies on isolated single cardiomyocytes from A1A1 mice aged 8-12 weeks showed reduced contractility in the absence of ???1A-AR stimulation, but an exaggerated response to ???1A-AR stimulation. In contrast isolated isovolumic Langendorff perfused A1A1 hearts without ???1A-AR stimulation replicated the enhanced contractility observed in vivo. These studies are consistent with down-regulation of contractility due to the hyperactivity of the overexpressed ???1A-AR in vivo, which only becomes evident in isolated cells without ???1A-AR stimulation due to the loss of functional receptor numbers during isolation. Sufficient spontaneously active ???1A-ARs are preserved in the isolated Langendorff heart preparation to ensure maximum contractility driven by increase calcium release.

Heart failure has a significant impact on mortality and morbidity. Dilated cardiomyopathy (DCM) is the third most common cause of heart failure and the most common reason for heart transplantation. Familial DCM is known to be caused by mutations in the LMNA gene encoding lamins A and C. New methods to enhance cardiac contractility would be beneficial in the treatment or prevention of heart failure. The focus of this thesis was to evaluate the mechanisms of altered contractility in two mouse models: the LMNA knockout model (homozygous, Lmna-/-; heterozygous, Lmna+/-) generated by targeted deletion of the lmna gene, and the model of enhanced contractility due to cardiac alpha1A-adrenergic receptor (???1A-AR) overexpression (A1A1). Previous studies have found altered nuclear-desmin connections in lamin A/C deficient mice. It was proposed that these alterations result in ???defective force transmission???, which leads to DCM. Studies in this thesis have supported this hypothesis. Studies of isolated single cardiomyocytes from mice aged 4-6 weeks demonstrated abnormal cell morphology and contractile dysfunction in Lmna-/- cardiomyocytes, while Lmna+/- cells showed no overt phenotype. Excitation-contraction coupling experiments and forcecalcium studies in skinned fibers excluded altered calcium kinetics as a primary cause of DCM in this model, but there was evidence of reduced sarcomere numbers and reduced sarcomere lengths as a contributor to reduce force generation in Lmna-/- and Lmna+/- mice. Previous in vivo studies showed that A1A1 mice had enhanced contractility with the absence of hypertrophy. Studies on isolated single cardiomyocytes from A1A1 mice aged 8-12 weeks showed reduced contractility in the absence of ???1A-AR stimulation, but an exaggerated response to ???1A-AR stimulation. In contrast isolated isovolumic Langendorff perfused A1A1 hearts without ???1A-AR stimulation replicated the enhanced contractility observed in vivo. These studies are consistent with down-regulation of contractility due to the hyperactivity of the overexpressed ???1A-AR in vivo, which only becomes evident in isolated cells without ???1A-AR stimulation due to the loss of functional receptor numbers during isolation. Sufficient spontaneously active ???1A-ARs are preserved in the isolated Langendorff heart preparation to ensure maximum contractility driven by increase calcium release.

Functional garments for physiological sensing purposes have been utilized in several disciplinesi.e. sports, firefighting, military and medical. In most of the cases textile electrodes (Textrodes)embedded in the garment are employed to monitor vital signs and other physiologicalmeasurements. Electrical Bioimpedance (EBI) is a non-invasive and effective technology that canbe used for detection and supervision of different health conditions. In some specific applicationssuch as body composition assessment EBIS has shown encouraging results proving good degreeof effectiveness and reliability. In a similar way Impedance Cardiography (ICG) is anothermodality of EBI primarily concerned with the determination of Stroke Volume SV, indices ofcontractility, and other aspects of hemodynamics.EBI technology in the previously mentioned modalities can benefit from a integration with agarment; however, a successful implementation of EBI technology depends on the goodperformance of textile electrodes. The main weakness of Textrodes is a deficient skin-electrodeinterface which produces a high degree of sensitivity to signal disturbances. This sensitivity canbe reduced with a suitable selection of the electrode material and an intelligent and ergonomicgarment design that ensures an effective skin-electrode contact area.This research work studies the performance of textile electrodes and garments for EBIspectroscopy for Total Body Assessment and Transthoracic Electrical Bioimpedance (TEB) forcardio monitoring. Their performance is analyzed based on impedance spectra, estimation ofparameters, influence of electrode polarization impedance Zep and quality of the signals using asreference Ag/AgCl electrodes. The study includes the analysis of some characteristics of thetextile electrodes such as conductive material, skin-electrode contact area size and fabricconstruction.The results obtained in this research work present evidence that textile garments with a dry skinelectrodeinterface like the ones used in research produce reliable EBI measurements in bothmodalities: BIS for Total Body Assessment and TEB for Impedance Cardiography. Textiletechnology, if successfully integrated, may enable the utilization of EBI in both modalities andconsequently implementing wearable applications for home and personal health monitoring. / <p>QC 20121213</p>

Exaggerated cardiovascular reactivity (CVR) to stress has been implicated in the increased risk for cardiovascular disease (CVD) in individuals with posttraumatic stress disorder (PTSD), yet mixed results have been reported. The CVR research may have been confounded by underrepresentation of women, few studies using sophisticated cardiovascular measurement, and a lack of analyses of PTSD symptom clusters. The purpose of the present study was to examine if young civilian women (M ± SD = 29.89±7.33) with PTSD (n=17) demonstrate greater CVR than women with depression (n=12) or no mental illness controls (n=18), and to explore the relationships between CVR and PTSD symptom clusters. Participants were 56% Caucasian, 21% African American, 19% Hispanic, and 4% other. Systolic and diastolic blood pressure (SBP and DBP), heart rate (HR), and impedance cardiography derived cardiac output (CO) and total peripheral resistance (TPR) were utilized to examine CVR during speech preparation/delivery and math tasks. Between-group effects were observed during speech preparation - specifically, lower DBP reactivity for the PTSD group compared to the depression group (p < .05). Between-group effects were also evident during speech delivery, with a trend toward lower DBP reactivity for the PTSD group than the depression group (p <.08), higher CO reactivity for the PTSD group than controls (p <.01), and lower TPR reactivity for the PTSD group than the depression (p <.01) and control groups (p <.01). PTSD severity scores for DSM-IV-TR and DSM-5 were used as independent predictors of CVR in multiple regressions variables. The DSM-IV analysis did not provide significant associations. The DSM-5 yielded significant associations of avoidance and arousal clusters with SBP reactivity during math, a significant association avoidance with DBP reactivity during math, and significant associations of avoidance and arousal with HR reactivity during math. Further exploration of PTSD symptom clusters may provide a clearer picture of the relationship between PTSD/CVR. Higher reactivity and lower reactivity may both be associated with risk for CVD, albeit through separate mechanisms.

Thesis (Ph. D.)--University of Washington, 1999. / Vita. Includes bibliographical references (leaves 109-117).

Impedance cardiography is an important tool in determining a person's hemodynamic properties. The makers obtained through thoracic impedance have been shown to be of great importance when monitoring critical care patients. Technological developments have made this process noninvasive and ambulatory, opening up new possibilities for potential use. A study was conducted by remotely monitoring healthy subjects (n=5), who performed an 8-minute mild-to-moderate aerobic exercise protocol, followed up by a four minute cognitive stress test. Testing was conducted onsite at Kennedy Space Center in association with the National Aeronautics and Space Administration using the MW1000A (MindWare Technologies LTD, Gahanna, OH) ambulatory impedance cardiography monitoring (ICG) device. The current study was conducted in order to establish the test-retest reliability of the ICG during aerobic exercise and cognitive stress across a 2 week period. For the purpose of this study Heart Rate (HR), Left Ventricular Ejection Time (LVET) Stroke Volume (SV), Cardiac Output (CO), and Pre-Ejection Period (PEP) were acquired and analyzed during three phases. The phases were, walking on a level treadmill, walking at incline, and an at rest mental arithmetic stress test. Testing has shown that the MW1000A device can provide accurate ambulatory impedance cardiography monitoring with no significant difference between testing intervals. The simple application of electrodes makes this device easy to use and requires little training. Its non-invasive properties render employing ICG both a simple and effective means of determining the hemodynamic properties of a subject.

Obstructive Sleep Apnea Hypopnea Syndrome (OSAHS) is a breathing disorder characterized by recurrent episodes of upper airway collapse during sleep. Measuring cardiac function in OSAHS patients may provide information to help delineate not only chronic effects of autonomic imbalance and ventricular loading in the diseases state, but also possible beneficial effects of clinical treatments. Objectives (Study 1): The aim of this study was to determine the reproducibility of select cardiac variables when monitoring a simulated sleep apnea event using a new improved bioimpedance cardiography system. Methods: Fifteen apparently healthy males were tested on three different days in a protocol requiring their performance of two 15 sec and two 30 sec forced and sustained inspiratory efforts against a closed epiglottis (Müeller Maneuver-MM). Results: Changes in cardiac output (CO), heart rate (HR), stroke volume (SV), myocardial contractility index (MCI) and systemic vascular resistance (SVR) were similar during 15 sec and 30 sec MM in all three days. During 30 sec MM, these changes in cardiac function were pronounced in comparison to the minimal variations observed for the 15 sec MM challenge test. Objectives (Study 2): The aim of this study was to characterize the cardiac responses to negative intrathoracic pressure in OSAHS patients with and without hypertension versus healthy subjects. Methods: Two groups of 10 OSAHS patients, one without HTN and one with HTN were compared with a control group. Each subject underwent two 30 sec (MM) as previously described. Results: During MM, there were similar changes in SV, HR and SVR in all three groups. CO was lower during MM in controls compared to OSAHS groups, whereas MCI decreased during MM in both controls and OSAHS+HTN groups (-7.5% and -1.7%, respectively) compared with an increase in OSAHS group (11.8%). During a Post-MM, both OSAHS groups showed return of cardiac responses toward their pre-MM baseline within 30 sec. Conclusions: The new bioimpedance cardiograph evaluated in this study was found to be reliable for measuring acute changes in cardiac responses to this breathing challenge test. OSAHS may cause acute changes in selected cardiac parameters during and immediately after a breathing challenge test. / Ph. D.

Made available in DSpace on 2015-07-22T20:50:42Z (GMT). No. of bitstreams: 0 Previous issue date: 2009-11-25. Added 1 bitstream(s) on 2015-08-11T03:25:54Z : No. of bitstreams: 1 Publico-11760a.pdf: 1069601 bytes, checksum: 88c7a2d10e394e1888e3b93a69070de4 (MD5). Added 1 bitstream(s) on 2015-08-11T03:25:54Z : No. of bitstreams: 2 Publico-11760a.pdf: 1069601 bytes, checksum: 88c7a2d10e394e1888e3b93a69070de4 (MD5) Publico-11760b.pdf: 1959621 bytes, checksum: 2665d88fb8fec237d73fdc84aa78a26a (MD5) / Introdução: A insuficiência cardíaca congestiva (ICC) descompensada pode ser definida como a evidência de sinais e sintomas de insuficiência cardíaca (IC) ao repouso e representa estado de ativação neuro-hormonal intensa, secundária ao déficit de perfusão renal. Regurgitações valvares funcional mitral e tricúspide são causas reversíveis de diminuição de fluxo sanguíneo sistêmico eficaz. O impacto de tais regurgitações sobre o débito cardíaco, sobre o conteúdo de fluido torácico, sobre as dimensões de câmaras cardíacas e sobre a função do aparato valvular pode ser monitorado de forma não-invasiva, antes e após a otimização do tratamento clínico. Objetivo: Avaliar o papel das regurgitações valvares funcional mitral e tricúspide como causas reversíveis de redução do débito cardíaco em ICC descompensada, e que acompanham a disfunção ventricular sistólica em miocardiopatias isquêmica e não-isquêmica. Métodos: catorze pacientes do sexo masculino (66 ± 8 anos de idade), fração de ejeção (24 ± 5%) secundária às miocardiopatias isquêmica (71%) e não-isquêmica (29%), apresentaram ICC descompensada com evidência clínica de regurgitações valvares mitral e tricúspide, foram avaliados por Bioimpedância cardíaca e ecocardiografia antes e uma semana após otimização de tratamento clínico. Resultados: o tratamento farmacológico de ICC descompensada foi acompanhado de redução de peso corpóreo de 82,9 a 76 kg (P<0,01), elevação no índice cardíaco (de 2,1 para 2,6 L/min/m2; P<0,01), redução na pressão sistólica da artéria pulmonar (de 58 para 35 mm Hg; P<0,001), conteúdo de fluido torácico (de 39 para 32 kOhm; P<0,001) e resistência vascular sistêmica (de 1633 para 1209 dinas/seg/cm5; P<0.001). A melhora dessas regurgitações incluiu redução nas dimensões das câmaras atriais esquerda e direita (de 27 para 24 cm2 e de 26 para 23 cm2, respectivamente; (P<0,001), diminuição das regurgitações mitral e tricúspide detectadas pelo Doppler colorido (P < 0,01), do volume regurgitante mitral (de 105 para 65 ml; P<0,001), e do tamanho efetivo do orifício regurgitante mitral (de 0,8 para 0,6 cm2; P<0,01). Conclusões: Na ICC descompensada, as regurgitações funcionais mitral e tricúspide contribuem para redução do débito cardíaco, aumento do conteúdo fluido torácico e da resistência vascular sistêmica, simultaneamente ao aumento de câmaras atriais e do orifício valvar, os quais podem ser melhorados com tratamento clínico. A bioimpedância cardíaca e a ecocardiografia fornecem avaliação seriada não-invasiva de parâmetros hemodinâmicos e função valvar nestes pacientes. / Objective: We hypothesized that functional mitral and tricuspid valvular incompetence (MR and TR, respectively) are reversible causes of reduced cardiac output in decompensated heart failure (DF) that accompanies systolic dysfunction in ischemic or nonischemic cardiomyopathy. Background: DF, defined as signs and symptoms of heart failure at rest, is rooted in a salt-avid state transduced by neurohormonal activation secondary to impaired renal perfusion. Functional MR and TR are reversible causes of reduced systemic blood flow. Their impact on cardiac output, thoracic fluid content, cardiac chamber dimensions, and valvular apparatus function can be monitored noninvasively, before and after optimized medical management. Methods: Fourteen male subjects (66 ± 8 years old) with reduced ejection fraction (24 ± 5%) secondary to ischemic (71%) or nonischemic (29%) cardiomyopathy, who developed DF with clinical evidence of mitral (MR) and tricuspid (TR) valvular incompetence, were each assessed by bioimpedance and echocardiography before and 1 week after optimized medical management restored compensated failure. Results: Pharmacologic elimination of DF was accompanied by a reduction in body weight (p<0.01). Hemodynamic improvements included a rise in cardiac index (2.1 to 2.6 L/min/m2; p<0.01) and a reduction in predicted pulmonary artery systolic pressure (58 to 35 mm Hg; p<0.001), thoracic fluid content (39 to 32 kOhm; p<0.001), and systemic vascular resistance (1633 to 1209 dynes/sec/cm5; p<0.001). Improvements in functional MR and TR included reductions in left and right atrial areas (27 to 24 cm and 26 to 23 cm2, respectively; p<0.001), color-flow grading of MR and TR severity (p<0.01), mitral regurgitant volume (105 to 65 mL; p<0.001), and effective MR orifice size (0.8 to 0.6 cm2; p<0.01). Conclusions: In DF, functional MR and TR contribute to reduced cardiac output, increased thoracic fluid content, and systemic vascular resistance, together with enlarged atria and valvular orifice size, which can be improved by medical management. Bioimpedance and echocardiography provide for serial noninvasive assessments of hemodynamic status and valvular function in such cases. / TEDE / BV UNIFESP: Teses e dissertações