Treatments aimed at modifying cardiac substrate utilisation are designed to improve metabolic efficiency. In the fasting state, the heart mainly relies on fatty acid oxidation for its energy production. The heart can adapt to metabolise glucose, lactate and amino acids depending on the predominate milieu and demands placed upon it. A shift from fatty acid oxidation to carbohydrate oxidation leads to a lower oxygen consumption per unit of adenosine triphosphate produced. It is this concept of improving cardiac efficiency by a reduction in oxygen demand that underpins the use of metabolic manipulating agents as a therapeutic strategy in heart failure. Cardiac energy starvation is increasingly recognised as playing a central role in the pathophysiology of heart failure. Alterations in substrate utilisation thus underlie the hope that metabolic manipulating agents will be of benefit in heart failure of both ischaemic and non-ischaemic origin. This metabolic shift is achieved by promoting glucose utilisation and reducing the utilisation of fatty acids. This leads to a greater production of adenosine triphosphate per unit of oxygen consumed. With an ongoing demand for treatment options in ischaemic heart disease and the growing burden of chronic heart failure, new treatment modalities beyond contemporary therapy warrant consideration. This thesis aims to investigate the short term effects of metabolic manipulation on changes in cardiac energetic status, cardiac function, efficiency and substrate utilisation.

No description available.

Thiamin is a required coenzyme in the production of energy to fuel myocardial contraction. Therefore, thiamin deficiency (TD) may contribute to myocardial weakness by limiting the available energy for myocyte contraction. Previous studies report a wide range for the prevalence of TD in patients with heart failure (HF) (3% to 91%). These trials are limited by their small sample size, indirect measurement of thiamin status, exclusion criteria, and their focus on hospitalized patients. Therefore, this study determined the prevalence of TD in a large (n=100) group of ambulatory patients with HF, using high performance liquid chromotography. The prevalence of TD ([thiamin pyrophosphate (TPP)] ≤ 180 nM/l erythrocytes) was found to be 7%. TD was not related to furosemide use, dietary thiamin intake, severity of the HF, or age. More investigation into the factors that may influence development of TD in ambulatory patients with HF is warranted.

Thiamin is a required coenzyme in energy producing reactions that subsequently fuel myocardial contraction. Therefore, thiamin deficiency (TD) might contribute to the reduction in myocardial function observed in patients with heart failure (HF) by limiting the available energy and subsequently aggravating cardiac performance. While the prevalence of TD as well as the impact of supplementation has been examined in patients with HF, none of these studies to date has examined the impact of TD on clinical outcomes. Therefore, this study investigated the associations between erythrocyte [TPP] levels and outcomes in ambulatory patients with HF. Time-to-event probabilities were found to be not significant for acute decompensated heart failure, mortality, all-cause hospitalizations, arrhythmias, myocardial infarctions and other adverse events. Further investigations into the longer term impact of TD on outcomes and the effects of thiamin supplementation as an adjunct therapy in delaying the disease progression are needed.

Thiamin is a required coenzyme in the production of energy to fuel myocardial contraction. Therefore, thiamin deficiency (TD) may contribute to myocardial weakness by limiting the available energy for myocyte contraction. Previous studies report a wide range for the prevalence of TD in patients with heart failure (HF) (3% to 91%). These trials are limited by their small sample size, indirect measurement of thiamin status, exclusion criteria, and their focus on hospitalized patients. Therefore, this study determined the prevalence of TD in a large (n=100) group of ambulatory patients with HF, using high performance liquid chromotography. The prevalence of TD ([thiamin pyrophosphate (TPP)] ≤ 180 nM/l erythrocytes) was found to be 7%. TD was not related to furosemide use, dietary thiamin intake, severity of the HF, or age. More investigation into the factors that may influence development of TD in ambulatory patients with HF is warranted.

Thiamin is a required coenzyme in energy producing reactions that subsequently fuel myocardial contraction. Therefore, thiamin deficiency (TD) might contribute to the reduction in myocardial function observed in patients with heart failure (HF) by limiting the available energy and subsequently aggravating cardiac performance. While the prevalence of TD as well as the impact of supplementation has been examined in patients with HF, none of these studies to date has examined the impact of TD on clinical outcomes. Therefore, this study investigated the associations between erythrocyte [TPP] levels and outcomes in ambulatory patients with HF. Time-to-event probabilities were found to be not significant for acute decompensated heart failure, mortality, all-cause hospitalizations, arrhythmias, myocardial infarctions and other adverse events. Further investigations into the longer term impact of TD on outcomes and the effects of thiamin supplementation as an adjunct therapy in delaying the disease progression are needed.

Diss. (sammanfattning) Uppsala : Uppsala universitet, 2005. / Härtill 4 uppsatser.

Thesis (MHSc--Health Science) -- Auckland University of Technology, 2004. / Some appendices not included in e-thesis. Also held in print (166 leaves, 30 cm.) in Akoranga Theses Collection. (T 362.19612900993 HOR)

Thesis (Ph. D.)--Case Western Reserve University, 2008. / Frances Payne Bolton [School of Nursing]. Includes bibliographical references.

Thesis (Ph. D.)--West Virginia University, 2009. / Title from document title page. Document formatted into pages; contains ix, 146 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 139-146).