Medicine (St Vincent's) - Theses
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ItemAdvanced characterisation of pulmonary hypertension: Assessment of right ventricular diastolic function and pulmonary artery wave reflection( 2016)Pulmonary hypertension is the net haemodynamic consequence of a wide variety of underlying pathologies. As disease progresses, right ventricular systolic dysfunction may develop. However, by the time this occurs, prognosis is poor. Like the situation in the left ventricle, chronically increased right ventricular afterload first leads to right ventricular hypertrophy and hypothetically, diastolic dysfunction. Although there is some evidence from animal models for this, human data is limited. Theoretically, the identification of right ventricular diastolic dysfunction may assist in the earlier diagnosis of pulmonary hypertension. This thesis provides evidence that right ventricular diastolic dysfunction does exist in the setting of pulmonary hypertension, that it occurs earlier than systolic dysfunction, and that it can be identified by invasive pressure measurement in the right ventricular cavity. Although echocardiography provides a useful way to assess left ventricular diastolic function, data presented here will show that currently available echocardiographic measurement of right ventricular diastolic function may not be sensitive enough to detect abnormal function. The secondary hypothesis tested is that a pressure/time analysis of pulmonary wave reflection can provide additional information in the assessment of patients with pulmonary hypertension. Data suggests that a metric of wave reflection, the pulmonary augmentation index, is closely associated with standard measures of right ventricular afterload, and therefore may not add value. However, the time to wave reflection is related to the site of obstruction in the pulmonary circulation and could theoretically assist in identifying disease aetiology.
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ItemAetiology of structural and functional remodelling of the right ventricle in endurance athletes( 2010)Endurance exercise training results in changes in cardiac structure and function which have been more thoroughly characterised for the left ventricle (LV) than for the right ventricle (RV). Recent evidence suggests that intense prolonged exercise may result in myocardial dysfunction which predominantly affects the RV, and that chronic RV remodelling may represent a substrate for ventricular arrhythmias in athletes. The reasons underlying the predilection towards RV dysfunction with intense prolonged exercise and the variation between individuals in its occurrence are not known, but may include haemodynamic, neurohormonal and genetic factors. This work seeks to describe the acute and chronic effects of strenuous exercise on the RV. Changes in RV function are described relative to LV function in both endurance athletes and non-athletes. Whereas most previous investigations of cardiac function in athletes have been performed at rest, a key element of this thesis is the exploration of changes in haemodynamics and myocardial function during exercise. To enable thorough assessment of RV function, established and novel echocardiographic measures are validated against cardiac magnetic resonance imaging values. A comprehensive description of resting cardiac morphology is used to demonstrate that, relative to non-athletes, cardiac remodelling is greater in endurance athletes and that the remodelling is greater for the RV than the LV. As a potential explanation for this ventricular asymmetry, systolic wall stress was quantified during acute exercise and determined to increase to a greater extent in the RV than the LV. As a potential modulator of the load on the RV during exercise, exercise-induced pulmonary vascular changes are described by studying the pulmonary transit of agitated contrast (PTAC). Relationships between the extent of PTAC and both RV afterload and structure were identified and measures which may predict favourable RV afterload are proposed. The effect of intense prolonged exercise of differing durations was assessed and it was determined that myocardial dysfunction of the RV, but not the LV, is common and increases with exercise duration. Parameters determined during acute exercise testing were not predictive of RV dysfunction following intense prolonged exercise. In subsequent chapters, potential neurohormonal, inflammatory and genetic explanations for acute and chronic RV dysfunction in endurance athletes are explored, but do not appear to account for RV abnormalities in athletes. This thesis serves to expand the current understanding of RV function in athletes by demonstrating that RV remodelling is profound and is influenced by the differential acute haemodynamic influences of exercise on the right ventricle. RV function should be considered in future studies in which the clinical consequences of athletic cardiac remodelling are assessed.