Cardiovascular disease is the number one reason for emergency room visits in the United States. Understanding the different pathologies of the cardiovascular system is crucial when trying to prescribe proper treatment or intervention. In order best understand these issues proper computer simulations would be necessary. Due to the fact that every patient is different. Being able to analysis and properly simulate each patients data individually to better understanding their specific case is necessary for patient specific interventions. In order to achieve such requirement we propose a new method of mesh generation to better map patient specific geometries. This new framework takes a set of points in a 3D space and generates a 2D NURBS mesh. Insuring a smooth and accurate representation of the patient specific geometry will allow for more specific incite to possible medical issues that may arise. This NURBS based mesh can be then used to run either finite element analysis, computational fluid dynamics, or even fluid solid interactions. Running these patient-specific valve simulations using isogementric modeling is what will allow us to have patient specific treatments and intervention.

The projects of this thesis examine the complex interaction between isotonic exercise, functional capacity, exercise-induced myocardial ischaemia, severity of regurgitation and left ventricular function in patients with significant chronic mitral regurgitation. The concept of left ventricular contractile reserve, i.e. the ability of the left ventricle to increase its contractility and decrease its end systolic volume with isotonic exercise, is explored. In patients with chronic isolated mitral regurgitation without coronary disease, isotonic exercise was associated with a slight decrease in left ventricular end diastolic volume but a marked decrease in end systolic volume, resulting in a significant increase in the stroke volume and ejection fraction. Early after uncomplicated mitral valve repair surgery, there was a significant decrease in the left ventricular ejection fraction with a proportion of the patients developing left ventricular dysfunction despite a normal pre-operative ejection fraction. When different pre-operative echocardiographic indices of left ventricular function were evaluated for their ability to predict left ventricular function after mitral valve repair, the exercise indices were found to be superior to resting indices. Left ventricular end systolic volume immediately after exercise was found to be the best predictor. The optimal cut-off was at 25 ml/m2, which had a sensitivity and specificity of 83% in predicting early post-operative left ventricular dysfunction. Exercise indices appeared to be superior to resting indices in identifying patients with persistent left ventricular dysfunction &lt1 year after mitral valve repair. The concept of contractile reserve was further examined by estimating the left ventricular stroke work from simplified pressure-volume loops, which were constructed from non-invasively obtained parameters with geometric assumptions. Left ventricular stroke work immediately after exercise, but not at rest, was found to be significantly lower in patients with latent left ventricular dysfunction. Patients without latent ventricular dysfunction had similar increases in stroke work with exercise compared with healthy normal subjects. The ability of the left ventricle to increase its stroke work with exercise, a measure of the contractile reserve, was correlated with the left ventricular ejection fraction after mitral valve repair. A numerical model was constructed using the clinical data as input parameters. The results from the numerical model were similar to that obtained from the clinical study, testifying that the observation made in the clinical study was valid and independent of the geometric assumptions made in constructing the simplified pressure-volume loops. Left ventricular pressure-volume loops under different loading conditions were plotted from simultaneously measured left ventricular pressure and volume to measure the left ventricular end systolic elastance (Ees) and preload recruitable stroke work relationship (MSW). Despite normal or near normal haemodynamics at rest, a significant proportion of the study patients were found to have impaired left ventricular contractility, as measured by Ees, consistent with a state of latent left ventricular dysfunction. Exercise indices of left ventricular function were better correlated with Ees and MSW than resting indices. There were highly significant inverse relationships between end systolic volume index immediately after exercise and Ees and MSW. Moreover, there was a significant powered relationship between MSW and exercise left ventricular ejection fraction. There was no such relationship between Ees or MSW and any of the resting echocardiographic indices of left ventricular function. Furthermore, the optimal diagnostic cut-off level of end systolic volume index after exercise at 25 ml/m2 accurately identified those with impaired left ventricular contractility as defined by an Ees of &gt 2 mmHg/ml. In patients with chronic organic mitral regurgitation with ejection fraction of &lt 50%, objectively measured functional capacity, VO2max, was correlated with exercise cardiac output, patient age and gender but not to the severity of the mitral regurgitation or the resting left ventricular function. The VO2max of these patients were significantly lower than that of age and gender-matched healthy controls despite these patients' relative lack of subjective symptoms. There were significant individual variations in the response of the severity of the mitral regurgitation to isotonic exercise. Patients whose regurgitant stroke volume increased had a lower exercise cardiac output than those whose regurgitant stroke volume decreased. Such variability was also seen with the response of the left ventricular function to exercise. Patients whose left ventricular end systolic volume increased with exercise, i.e. patients with a limited contractile reserve, had a lower exercise cardiac output and lower VO2max than those whose end systolic volume decreased with exercise. The determinants of exercise capacity were then examined in patients with functional mitral regurgitation and left ventricular dysfunction. VO2max of these patients was correlated with exercise cardiac output and exercise left ventricular ejection fraction, a situation similar to that seen in patients with organic mitral regurgitation and normal left ventricular function. Furthermore, indices of left ventricular systolic function at rest and pulsed wave Doppler indices of diastolic function showed no significant correlations with VO2max. The determinants of VO2max remained unchanged in these patients after four weeks of supervised exercise training. The four weeks of exercise training resulted in a significant decrease in left ventricular end systolic volume, a trend towards an increase in left ventricular ejection fraction and some restoration of the contractile reserve. The total exercise time almost doubled. However, this dramatic improvement in total exercise time was accompanied only by non-significant increases in VO2max and left ventricular ejection fraction. Therefore, the benefits of exercise training in these patients may involve more than just central mechanisms. Exercise induced myocardial ischaemia may also contribute to a limited left ventricular contractile reserve in patients with mitral regurgitation. Electrocardiographic changes at rest are commonly seen in patients with mitral regurgitation due to mitral valve prolapse. These resting electrocardiographic changes make exercise electrocardiography uninterpretable for exercise-induced ischaemia. Exercise electrocardiographic changes are also commonly encountered in these patients despite the absence of coronary artery disease and a normal resting electrocardiogram, making exercise electrocardiography unreliable as a non-invasive screening test for coronary artery disease. In these patients, exercise echocardiography was slightly more sensitive but significantly more specific in diagnosing significant coronary artery disease. The overall accuracy and the positive predictive value were significantly higher for exercise echocardiography than for exercise electrocardiography. The &quotcost-effectiveness&quot of different diagnostic strategies for coronary artery disease in patients with mitral valve prolapse was examined based on the results of the clinical study. Strategies involving exercise electrocardiography as part of the screening test were costly and were associated with a high false negative rate. Strategies involving exercise echocardiography were more accurate and less costly but the initial costs of exercise echocardiography for all patients meant that the overall costs were still considerable. Assessing the pre-test probability of coronary artery disease in these patients and using exercise echocardiography as the initial test for patients with at least a moderate pre-test probability of coronary artery disease seemed to result in the best compromise between cost and effectiveness. The studies of this thesis have shown that a limited cardiac contractile reserve is a sign of latent ventricular dysfunction in patients with chronic mitral regurgitation. The presence of a limited contractile reserve can be used to predict left ventricular dysfunction after mitral valve repair. The concept of a limited contractile reserve is further supported by the finding of a limited increase in left ventricular stroke work with exercise from a theoretical as well as a numerical model of left ventricular pressure-volume loops. Exercise echocardiographic indices show better correlations to invasively measured Ees and MSW than resting indices. VO2max in these patients is determined more by their ability to increase their forward cardiac output with exercise and not by the regurgitant volumes. Exercise training in patients with left ventricular dysfunction and functional mitral regurgitation results in some restoration of contractile reserve. Exercise echocardiography is also a reliable and cost-effective test in the non-invasive screening for coronary artery disease in these patients. Based on the results of the studies in the thesis, one can incorporate exercise echocardiography as one of the important assessment tools in the management of patients with significant mitral regurgitation as it allows measurement of left ventricular volumes and assessment of contractile reserve. Further studies are needed to examine whether a policy of monitoring of contractile reserve in these patients to guide therapy and surgical referral will result in a better preservation of long term left ventricular function, an improvement in functional capacity and patient outcome.

<p>During a cardiac cycle the cardiac walls change between contracted and relaxed and the valves open and close in response to pressure changes. This master thesis is a study of the changes in heart movement pattern caused by intravenous injections of Ca2+ or Nitroprusside. At Stanford University radiopaque markers have been surgically implanted in the walls and in the mitral valve of ovine hearts and 3D coordinates for each marker have been constantly measured during the cardiac cycle. By using MatLab, the volume and pressure of the left ventricle and several parameters related to the opening kinematics of the mitral valve have been analyzed. The results show, among others, that both Ca2+ and Nitroprusside reduce the volume and pressure of the left ventricle and that both substances decrease the size of the mitral annular ring. It was also shown that Ca2+ delays the opening of the mitral valve.</p>

During a cardiac cycle the cardiac walls change between contracted and relaxed and the valves open and close in response to pressure changes. This master thesis is a study of the changes in heart movement pattern caused by intravenous injections of Ca2+ or Nitroprusside. At Stanford University radiopaque markers have been surgically implanted in the walls and in the mitral valve of ovine hearts and 3D coordinates for each marker have been constantly measured during the cardiac cycle. By using MatLab, the volume and pressure of the left ventricle and several parameters related to the opening kinematics of the mitral valve have been analyzed. The results show, among others, that both Ca2+ and Nitroprusside reduce the volume and pressure of the left ventricle and that both substances decrease the size of the mitral annular ring. It was also shown that Ca2+ delays the opening of the mitral valve.

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Mitral valve prolapse is the most commonly occurring cardiac condition. It is a benign condition which affects as many as 10% of the population. Some patients have symptomatic mitral valve prolapse. This condition is referred to as mitral valve prolapse syndrome. Symptoms include: chest pain, tachycardia, palpitations, fatigue, dizziness, shortness of breath, headaches, low exercise tolerance, feelings of anxiety, panic attacks, and mood swings. These symptoms adversely effect the patient's quality of life.The purpose of this study was to investigate the response of patients with mitral valve prolapse syndrome to treatment that includes the accepted treatment for panic disorder, and to determine the roles of self-efficacy and of level of spousal support in enhancing the ability of identified patients to cope with mitral valve prolapse syndrome.Thirty-one subjects initially agreed to participate in this study. Of these subjects, fifteen left the study. The leading causes of dropout were lack of spousal support and multiple role stress. The remaining sixteen subjects completed the study. Subjects were randomly divided into three treatment conditions, individual multimodal therapy, couples multimodal therapy, and a waiting list/control group. Treatment consisted of attending a five session psychoeducational program and completing prescribed exercises at home between sessions. The first two sessions examined self-care lifestyle changes that patients could make to alleviate symptoms. The remaining three sessions focused on the over reactiveness of the autonomic nervous system for these patients and the efficacy of learned relaxation procedures. Dependent measures included a Symptom Checklist, Anxiety Sensitivity, Strength and Magnitude of Self-Efficacy and Strength and Magnitude of Interactive Efficacy.Data was analyzed in a two-step process. First, it was analyzed using a multiple single case design format. This was followed by a quantitative analysis of grouped data. In general, the multiple single case design complemented the quantitative analysis. Individual findings in the multiple single case design indicated issues for future research.Participation in treatment was found to aid in decreasing global physical symptoms, decreasing anxiety sensitivity symptoms, and increasing the subject's confidence in her ability to manage her symptoms. The increased level of self-confidence was related significantly to decreasing global physical symptoms. There was a weak, non-statistically significant correlation between increased confidence of self-efficacy and decreased anxiety sensitivity symptoms. Participation in couples multimodal treatment or any treatment was not significantly linked to increased interactive efficacy. Increased interactive efficacy was correlated with increased self-efficacy and decreased global physical symptoms. / Department of Counseling Psychology and Guidance Services

Atrial fibrillation is the most common sustained arrhythmia; however, its mechanism is not well understood. Several conditions such as valvular disease, heart failure, and hypertension predispose to atrial fibrillation. Identifying the electrophysiological substrate in these clinical conditions would yield insight into the mechanism of atrial fibrillation and aid in developing strategies to prevent or cure it. Rheumatic mitral stenosis is associated with high prevalence of atrial fibrillation. While atrial stretch itself may be adequate to explain the occurrence of atrial fibrillation in this population, it is not known if the disease process would remodel the atria so as to increase its propensity. Chapters 2 and 3 present the results of the studies evaluating the substrate for atrial fibrillation in both the left and right atria in rheumatic mitral stenosis. These studies have demonstrated extensive conduction abnormalities both regional and site specific associated with low voltage area and scar. Despite the prolonged atrial refractoriness, the propensity for atrial fibrillation was increased; lending support to the theory that structural remodelling associated with conduction abnormalities plays a greater role in the substrate predisposing to atrial fibrillation. Chapters 4 and 5 present the results of the studies evaluating the immediate effects of chronic atrial stretch reversal on the atrial electrical remodelling. These studies demonstrated that immediately after percutaneous mitral commissurotomy there was decrease in P wave duration, improvement in site specific conduction delay and conduction velocity associated with increase in the voltage. However, there was no change in atrial refractoriness. Chapter 6 studies the substrate long-term after reduction of stretch. There was further increase in conduction velocity and voltage associated with decrease in atrial refractoriness and conduction delay across the crista terminalis. These observations suggest that strategies aimed at reducing atrial stretch in different disease conditions would potentially decrease the burden or prevent atrial fibrillation. There is mounting evidence of the effect of stretch on the atria; however, the effect of stretch on the triggers of atrial fibrillation has not been evaluated before. Chapter 7 and 8 present the results of the study examining the effect of acute and chronic stretch on human pulmonary veins. Simultaneous pacing of the right ventricle and pulmonary vein induced acute stretch. The effect of chronic stretch was evaluated in patients with mitral stenosis. The atrial refractoriness was abbreviated in acute stretch while it was prolonged in the chronic form. Nevertheless, both resulted in marked pulmonary vein conduction abnormalities that were pronounced with chronic stretch and extra-stimuli. Additionally, structural remodelling was seen with chronic stretch. These abnormalities implicate stretch in the milieu for re-entry and pulmonary vein arrhythmogenesis in conditions predisposed to atrial fibrillation. In summary, this thesis has evaluated the effects of stretch on the substrate and triggers of atrial fibrillation. It provides evidence for the importance of structural changes and the associated abnormalities in conduction in predisposing to atrial fibrillation. These observations may be important in the development of tools to treat, cure and prevent atrial fibrillation. / Thesis (Ph.D.) -- University of Adelaide, School of Medicine, 2008