Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.659029
Title: Pathophysiological mechanisms of hypertensive left ventricular hypertrophy : optimising regression
Author: Burns, Joanna
Awarding Body: University of Leeds
Current Institution: University of Leeds
Date of Award: 2013
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Abstract:
The central theme throughout this work is the relationship between neuroendocrine factors, including the sympathetic nervous system (SNS), and the renin-angiotensin-aldosterone system (RAAS) and left ventricular mass (LVM) in essential hypertension (EBT). Chapter 1 begins by defining EBT, outlining its prevalence and complications, including left ventricular hypertrophy (L VB), and summarises possible aetiological mechanisms felt to be important in its development. Methods currently available to assess hypertensive LVB and sympathetic drive are outlined, followed by a review of factors known to influence LVM, with particular emphasis given to human trials linking L VM with neuroendocrine pathways. Chapter 2 outlines the two core methodological techniques common to both major studies of this thesis- namely, microneurography to quantify sympathetic drive and cardiac magnetic resonance imaging (Cardiac MRI) to quantify LVM. Chapter 3 describes a prospective study planned to determine whether or not the magnitude of sympathetic nerve hyperactivity was related to LVM in subjects who had a broad range of both arterial blood pressures and L VM. This study showed for the first time in patients with EHT that L VM is significantly related to central sympathetic nerve hyperactivity regardless of whether associated clinical L VB exists. These findings are consistent with the theory that sympathetic activation in hypertension is a significant mechanism leading to increased LVM. Chapter 4 supports this hypothesis fmiher, by describing a prospectively randomised trial designed to investigate whether L VH regression would be greater using a therapeutic strategy specifically designed to reduce neuroendocrine activity compared to one that did not. This study showed that the magnitude of L VB regression achieved by inhibiting neuroendocrine pathways was greater than that produced by comparable blood pressure (BP) reduction alone. Chapter 5 critically appraises the key findings of this thesis in the context of current work. Future planned directions for work in this field are also briefly discussed.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.659029  DOI: Not available
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