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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.

Technological advances for treatment of congenital heart disease (CHD) have led to decreases in mortality over the past thirty years. Persistent morbidity into adolescence and adulthood necessitates regular medical follow-up and the influence of ongoing physical health issues on the teens emotional health merits clinician and researcher attention. Employing interpretive description research methodology, 22 interviews with teens aged 13-17 years were analyzed to understand how adolescents with CHD describe everyday life and relate to questions about quality of life (QOL). Although the majority of these teens viewed themselves as normal, CHD was a part of their everyday life that they situated into the foreground or background of their lives, as it suited their needs. These teens spoke of QOL issues in a concrete manner focusing on physical activity limitations and their need to fit in. Further discussion of these issues must be undertaken as adolescents with CHD transition to adulthood.

The traditional PI3K pathway relies on agonist mediated stimulation of PI3Kα through RTKs and PI3Kγ through GPCRs, which stimulate downstream enzymes such as Akt. This pathway has been found to be important in cardiomyocytes and cardiofibroblasts for regulating cardiac morphology and function. However, evidence has suggested that this traditional pathway does not fully represent the PI3K signaling cascade. We demonstrated that PI3Kγ regulates calcium through kinase independent interactions. PI3KγKO hearts rapidly develop systolic dysfunction and dilated cardiomyopathy in response to pressure overload due to excess matrix metalloproteinase mediated degradation of N-cadherin adhesion complexes. We also show a connection between the PI3K/PTEN and Casein Kinase 2, an enzyme that deactivates PTEN. Finally, our results demonstrate crosstalk between GPCRs and PI3Kα via transactivation of growth factor receptors. Our results provide insight into the regulation and the complexity of the PI3K/PTEN pathway. / Experimental Medicine

Thesis (M.S.)--University of Hawaii at Manoa, 2006. / Includes bibliographical references (leaves 95-98). / 105 leaves, bound ill. 29 cm

Left ventricular hypertrophy (LVH) in response to pressure overload is associated with increased cardiovascular morbidity and mortality, making its prevention an important therapeutic goal. The role of a calcineurin-dependent molecular pathway in the induction of pressure-overload LVH is controversial. The present study tested the hypothesis that, in the setting of LV pressure overload, activation of the systemic renin-angiotensin system was necessary for activation of this calcineurin pathway. Mild LV pressure overload was induced in male Wistar rats by abdominal aortic constriction (AAC) or transverse aortic arch constriction (TAC), producing well-matched pressure gradients of 37 ?? 8 and 35 ?? 15 mmHg, respectively. Tight transverse aortic arch constriction (TTAC) in additional animals produced a pressure gradient of 75 ?? 15 mmHg. Only AAC increased plasma renin concentration and activated the calcineurin pathway, indicated by increased nuclear NFAT3 content. Plasma renin concentration and nuclear NFAT3 content were unchanged in TAC and TTAC animals. AAC animals developed more LVH 21 days post-banding than TAC and TTAC animals: the slope of the relationship between LV/body weight ratio and systolic blood pressure was much steeper in AAC animals than the combined TAC and TTAC animals (20x10-6 versus 5x10-6, p<0.001). Treatment with the calcineurin inhibitor FK506 did not significantly alter the slope of this relationship in the combined TAC and TTAC animals (8x10-6), but FK506 abolished this relationship in AAC animals (-5x10-6, R =0.0003). These data indicate that activation of the calcineurin pathway occurs only in high-renin hypertension, providing an additional stimulus to LVH induction. Calcineurin plays no role in the induction of LVH in low-renin hypertension, which is much more common clinically.