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Heart failure is an illness that requires life-long treatment and often affects everyday aspects of a person’s life. Self-care is a significant part of the treatment. Good self-care resources make it possible for people with heart failure to make the lifestyle changes they often need to maintain or improve their level of health. Self-care means having knowledge of and being able to recognize the symptoms and signs of deterioration that can occur with heart failure, so that the person can take appropriate measures – and it also means knowing when it is time to seek professional help. The significance of self-care for heart failure has increased and will increase even more in the future, when monitoring one’s condition will be left more and more to the people themselves and those who take care of them. The object of the study was to learn what self-care measures people with heart failure say they apply in everyday life. The quantitative method of a questionnaire study (The European Heart Failure Self-Care Behaviour Scale) was used. Of the 94 people registered at a heart failure unit who were asked to complete the questionnaire, 58 of them consented. The results showed that more than 95% of the people with heart failure applied the recommended self-care measure of taking the medicines prescribed by their doctor. Many also applied the self-care measures of taking a rest during the day (83%) and taking it easy when they felt out of breath (78%). On the other hand, the self-care measures of daily weight control were applied only by 41%, daily exercise by only 48% and salt and fluid restrictions by only 59%. The self-care measures of contacting a doctor/nurse when noticing problems or symptoms of deterioration were applied by only 36% of those who felt out of breath and by only 43% of those who felt increased fatigue. The conclusion is that there is a need to improve the knowledge about and confidence in self-care treatment for people with heart failure. One way of achieving this is to show that people with heart failure check for symptoms and apply measures in their homes as part of the treatment and that this leads to an increased quality of life.

Heart failure is a common and serious chronic condition, which can be as ‘malignant’ as most forms of cancer (Stewart, MacIntyre, Hole, Capewell, & McMurray, 2001). Recent estimates are that around 40,000 men and 45,000 women are living with heart failure in Scotland (Stewart, MacIntyre, Capewell, & McMurray, 2003). Heart failure is significantly influenced by socioeconomic factors, with people on lower incomes being more likely to develop, and die faster from, heart failure (McAlister et al, 2004). There is a growing body of research on the experience of living with heart failure, however, none provides serious consideration of the role of socioeconomic factors in impacting the experience of heart failure, and some qualitative research may actually obscure such factors. There were two main aims in this thesis. One was to explore how qualitative research methods can better consider the relationship between experience and broader context, such as the influence of socio-economic factors on health. The other aim was to examine the experiences of people as they live with and die from heart failure in ways that situate their accounts in the broader context of their lives. An initial research study, on which I was the main researcher, focused on the experiences of 30 people living with advanced heart failure. These people, their carers and key health professionals were interviewed, where possible, three times over a six months period. This thesis re-examines that study, focusing on 20 of those participants, for which a total of 122 interviews were conducted. I used a dialogical approach to see whether the socioeconomic context of heart failure for these respondents, could be captured through exploring experiences, performance, relationships, discourses and institutional practices, the social processes that mediate the relationship between socioeconomic disadvantage and chronic diseases were explored. This offers important learning in relation to the experience of living with heart failure, along with the experience of providing care. The findings highlight the need to broaden our view of chronic illness beyond biomedical approaches, and grow our methodological approaches along with that, in order to develop knowledge and practice that has relevance for people who live with and die from heart failure.

Le remodelage ventriculaire gauche (RVG) est un processus complexe qui intervient après un infarctus du myocarde chez 30% des patients en dépit des meilleurs traitements connus actuellement. Le but de mon travail de thèse consistait à identifier les déterminants moléculaires du RVG dans le but de mieux en comprendre les mécanismes physiopathologiques. Pour cela, nous avons étudié les modifications post-traductionnelles des protéines contractiles du VG et en particulier, la phosphorylation et la O-N-acétylglucosaminylation (O-GlcNAc). Nous nous sommes ensuite particulièrement intéressés à la troponine T (TnT) pour laquelle nous avons ainsi pu mettre en évidence une diminution de la phosphorylation au niveau de la sérine 208 au niveau du VG et du plasma chez le rat, suggérant que cela pourrait être un marqueur du RVG post-infarctus. Pour cette étude, nous avons travaillé en collaboration avec l’unité INSERM U644 de Rouen sur un modèle expérimental d’insuffisance cardiaque. L’infarctus du myocarde est induit chez le rat par ligature de la branche descendante de l’artère coronaire gauche, les rats témoins subissant l’intervention mais sans ligature. Dans un premier temps, nous avons réalisé une étude globale du phosphoprotéome du VG en phase tardive du RVG (2 mois post-ligature). Pour cela, les protéines extraites du VG ont été séparées par électrophorèse bidimensionnelle puis colorées au Pro-Q®Diamond (spécifique des protéines phosphorylées) puis au Sypro®Ruby (spécifique des protéines totales). Par analyse bioinformatique, nous avons mis en évidences 69 spots polypeptidiques présentant des modulations de phosphorylation. Nous avons donc analysé ces spots par spectrométrie de masse et avons identifié 30 protéines correspondant à 53 spots polypeptidiques présentant des modulations de phosphorylation. Parmi ces protéines, nous avons choisi de nous concentrer et d’étudier 6 protéines contractiles : la TnT, l’alpha-tropomyosine 1 (α-Tm 1), la desmine, l’αB-crystalline et les chaînes légères de myosine 1 et 2 (MLC). Pour chacune de ces protéines, nous avons identifié le type d’acide aminé responsable de la phosphorylation et quantifié les modulations de phosphorylation dans le VG des rats insuffisants cardiaques (IC). De manière intéressante, nous avons observé que le VG des animaux IC présentait une diminution significative de la phosphorylation sur les résidus sérine pour l’α-Tm 1, la TnT et la MLC-2 et sur les résidus de tyrosine pour l’αB-crystalline ainsi qu’une augmentation significative de la phosphorylation sur les résidus tyrosine pour la MLC-1 et sur les résidus de sérines pour la desmine, confirmant ainsi les résultats obtenus en électrophorèse bidimensionnelle. Afin de compléter l’analyse des modifications post-traductionnelles, nous avons étudié les modifications de O-GlcNAc pour chacune de ces protéines. Nous avons ainsi observé une diminution significative de la O-GlcNAcylation de l’α-Tm 1, de la desmine et l’αB crystalline ainsi qu’une augmentation de la O-GlcNAcylation de la MLC-3 et de la TnT. Par ailleurs, nous avons pu corréler ces modulations de phosphorylation et de O-GlcNAcylation avec des modulations de l’activité des enzymes impliquées dans ces modulations. En effet, par analyse bioinformatique de la séquence de la TnT et par recherche bibliographique nous avons mis en évidence que la protéine kinase C et la protéine phosphatase 2A pourrait être impliquées dans ces modulations de phosphorylation. Nous avons alors mis en évidence une diminution de l’activité de la protéine kinase C epsilon dans le VG des rats IC mais sans variation de l’activité de la protéine phosphatase 2A. Par ailleurs, nous avons mis en évidence une augmentation de l’activité de la O-GlcNAc transférase et une diminution de l’activité de la O-GlcNAcase dans le VG des rats IC. [...] / Despite significant improvements in management of myocardial infarction (MI), left ventricular remodelling (LVR) remains a major complication and a strong predictor of both heart failure (HF) and death after MI. Although several variables, such as MI size, have been identified as risk factors, LVR remains difficult to predict in clinical practice. Better prediction could allow an individualized approach with more intense therapy and follow-up for such high-risk patients. The aim of my work is to identify molecular determinants of LVR to have a better understanding of physiopathological mechanisms of LVR. For that purpose, we studied post-translational modifications of contractile proteins in particular, phosphorylation and O-N-acetylglucosaminylation (O-GlcNAc). Then, we studied particularly troponin T (TnT) for which we could highlight a decrease of phosphorylation of serine 208 in LV and plasma of MI-rats. These results suggest that the level of circulating phosphorylated troponin T could be new biomarker of LVR and may help to predict the development of heart failure after MI. For this study, we worked in collaboration with INSERM unit U644 at Rouen using an experimental model of HF. MI was induced in rat by left coronary ligation and, the control rats undergoing the surgery without ligation. Initially, we performed differential phosphoproteomic study of LV in the late phase of the LVR (2 months post-MI). For this purpose, LV proteins were extracted and separated by two-dimensional electrophoresis. Gels were first stained by Pro-Q®Diamond (specific of phosphorylated proteins) and then by Sypro®Ruby (specific of total proteins). By bioinformatic analysis, we showed that 69 polypeptidic spots were modulated for their phosphorylation levels. We analyzed these spots by mass spectrometry and identified 30 proteins corresponding to 53 spots with modulationof phosphorylation. Among these proteins, we have chosen to study 6 contractile proteins: TnT, alpha-tropomyosin 1 (Tm-α1), desmin, αB-crystallin and myosin light chains 1 and 2 (MLC). For each described proteins, we have validated the modulation of phosphorylation and determined the aminoacid involved in the phosphorylation modulation using immunoprecipitation techniques with specific antibodies against the proteins and phospho-Tyrosine, -Threonine and –Serine antibodies confirming the screening performed by 2D-electrophoresis for the detection of phosphoproteins. We observed a significant decrease of phosphorylation on serine for Tm-α1, TnT and MLC-2 and on tyrosine residues for αB-crystallin as well as a significant increase in phosphorylation on tyrosine for MLC-1 and on serine residues for desmin, thus confirming the results obtained in two-dimensional electrophoresis. In order to complete analysis of the post-translational modifications, we studied the modifications of O-GlcNAc for each one of these proteins. We thus observed a significant decrease in O-GlcNAcylation of Tm-α1, αB-crystallin and desmin as well as an increase in O-GlcNAcylation of the MLC-3 and TnT. In addition, we have correlated these modulations of phosphorylation and O-GlcNAcylation levels with modulations of the activity of enzymes implied in these modulations. Indeed, by bioinformatic analysis of the TnT sequence and literature review, we highlighted that the protein kinase C and the protein phosphatase 2A could be implied in these modulations. We observed a decrease of protein kinase C epsilon isoform expression in the LV of MI- rats without modulation of protein phosphatase 2A activity. In addition, we showed an increase in the activity of O-GlcNAc transferase and a decreaseof O-GlcNAcase activity in LV of MI rats. [...]

Heart failure (HF) is a complex, debilitating disease that affects approximately 6.5 million Americans (Ades et al., 2013). HF is a large reason for hospital readmissions, and subsequently, a major contributor to rising health care costs. Unfortunately, there is no cure for HF, but various interventions such as cardiac rehabilitation (CR) have been employed to help patients manage the symptoms. However, the lack of patients ever being referred to cardiac rehabilitation is disturbing. Healthcare providers play an essential role in providing education about heart failure and CR, and thus should be knowledgeable about these principles themselves. Therefore, the aim of this project is to evaluate data from a survey sent to nurse practitioners (NPs) regarding whether HF patients are being referred to CR appropriately, and if barriers are limiting use of CR programs. This was a descriptive, nonexperimental study with a survey design seeking to understand if NP providers are following evidence-based guidelines when treating HF patients and if providers consider CR programs to be an appropriate treatment tool. A survey questionnaire was distributed to NPs who are members of Coalition of Arizona Nurses in Advanced Practice (CAZNAP). Data from 27 surveys were used for analysis. Results showed that nurse practitioner respondents felt they had a good understanding of heart failure education and diagnosis. A majority also considered CR to be a useful tool for HF patients, and all agreed that health care providers affect CR enrollment and participation rates. A mere nine respondents (33%) reported being introduced to the outcomes and benefits of CR in their graduate education. Findings also confirmed previous work suggesting that providers are not adequately referring HF patients to CR, as 33% of NPs reported they have never referred a patient to CR. With respect to these findings, it is important to identify methods to assist providers with proper education about CR and its referral methods. As supported by the literature review, improved referral rates to CR can lead to better management and health outcomes for HF patients. Therefore, further research is needed to identify interventions that promote increased CR referral rates.

A Research report submitted to the Faculty of Health Sciences, Department of Internal Medicine, University of the Witwatersrand, Johannesburg, in partial fulfillment of the requirements for the Degree of Master of Medicine in the Division of Cardiology. 2017 / INTRODUCTION The field of medicine has been challenged by the dual epidemic of heart failure and renal insufficiency. There is an increasing need to identify these patients at an early stage so as to delay progression to renal damage. Furthermore there is a lack of local data assessing the relationship between heart failure and renal dysfunction. AIMS • To identify the prevalence of renal dysfunction in patients attending the heart failure clinic at Charlotte Maxeke Johannesburg Academic hospital (Cardiorenal syndrome Type II) • To evaluate the relationship between severity of heart failure and severity of renal dysfunction • To compare heart failure with reduced ejection fraction (HFREF) variables between patients with and without renal dysfunction. METHODOLOGY This study is a single center retrospective study of patients attending Charlotte Maxeke Johannesburg Academic Hospital Heart Failure Clinic. Heart failure patients included in this study were those with an ejection fraction < 50% as this is an accepted definition for HFREF. Patients with HFREF were analyzed specifically for the following; presence of renal dysfunction, Ejection Fraction (EF), Systolic Blood Pressure (SBP), Diastolic Blood Pressure (DBP), Haemoglobin (HB), New York Heart Association (NYHA) functional class, furosemide dose , six minute walk test (6MWT) and Minnesota Living with Heart Failure Questionnaire (MLFQ) score . Presence of renal dysfunction was identified based on the glomerular filtration rate (eGFR) value of less than 60ml/min/1.73m2 as this is the threshold eGFR below which complications of renal impairment appear. The eGFR was calculated using the Modification of Diet in Renal Disease (MDRD) abbreviated formula: (186.3 X serum creatinine) -1.154 x (age) -0.203 x (0.742 if female) x (1.212 if African) The control group consisted of patients attending the clinic who did not have renal dysfunction. RESULTS A total 242 files were reviewed. Forty-two files were excluded from the study due to lack of adequate study data recorded in the file. Data was collected and entered into a database, which was analyzed using the Statistics/Data Analysis Program (STATA) Version 10.0. The mean age of the study group was 53.3 years (SD± 15.05) with the youngest subject being 21 years old and the oldest subject aged 85 years. The mean SBP was 119mmHg and the mean DBP was 75mmHg. The mean eGFR was 72.01 ml/min/1.73m2. The overall prevalence of low eGFR (<60ml/min/1.73m2) in the sample population was 34.5 %. The prevalence in female and male patients with a low eGFR was 35% and 33.6% respectively. Analysis of MLFQ, 6MWT, DBP and age yielded a positive correlation with eGFR, which was statically significant (p<0.05). An insignificant correlation was obtained comparing eGFR with SBP (p=0.07), EF (p=0.69) and HB (p=0.79). The Analysis of Variance Test (ANOVA), showed a significant correlation between eGFR values across the different NYHA functional classes (p 0.012). Thus it was found that the higher the NYHA class (clinically worse) was associated with worse renal function. The mean eGFR for NYHA I was 77.05 ml/min/1.73m2, for NYHA II was 70.61 ml/min/1.73m2, for NYHA III was 64.13 ml/min/1.73m2 and NYHA IV was 50.02 ml/min/1.73m2. DISCUSSION The overall prevalence of low eGFR (<60ml/min/1.73m2) in this study was 34.5%, a finding consistent with international trials. The majority of patients in this study were in NYHA functional class I or II, thereby highlighting the fact that renal dysfunction is common in heart failure patients and starts early. Statistically significant values were also obtained between eGFR and 6MWT, MLFQ, furosemide dose, age and DBP. The patients with higher 6MWT have better effort tolerance, thereby classifying their heart failure as milder. This in effect confirms that higher eGFR patients have higher effort tolerance. Higher MLFQ scores and higher furosemide doses are inversely correlated to eGFR. The more subjective symptoms you have, and the higher doses of furosemide you need, is a reflection of the severity of the heart failure. With regards to age, there is a normal physiological decline in eGFR with increasing age. In this study a statistically significant negative correlation between eGFR and NYHA was found. Thus a higher NYHA class is associated with worse renal function. This suggests that the clinically more advanced the patient, the poorer the renal function. Also, the prevalence of low eGFR (<60ml/min/1.73m2) within each NYHA class, as expected, increased with increasing NYHA class. It was 27% for NYHA I, 38% for NYHA II, 40% for III, while class IV had 80% of low eGFR prevalence CONCLUSION The findings of this study confirm that the cardio-renal syndrome is common in a local cohort of heart failure patients. The study also suggests that renal dysfunction starts in the early stages of heart failure (NYHA I/II) and becomes more prevalent in patients with more advanced stages of heart failure. These findings highlight the need to treat heart failure patients early after presentation and more appropriately if we are to decrease complications such as renal dysfunction, thereby improving morbidity and mortality. / MT2018

A dissertation submitted to the Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, in fulfillment of the requirements for the degree of Master of Science in Medicine Johannesburg, 2005 / ABSTRACT INTRODUCTION The risk of cardiovascular disease in patients with end stage renal disease (ESRD) is far greater than in the general population. Amongst patients with ESRD, the prevalence of coronary artery disease (CAD) and congestive heart failure is approximately 40% compared with 5-12% in the general population. The excess risk is caused by multiple traditional and non-traditional risk factors for ischaemic heart disease present in these patients. There is little information on CAD and its risk factors in black haemodialysis patients as most of these studies were carried out in the white population. This study is therefore aimed at determining the risk factors for atherosclerosis in Black and non-black (White and Indian) South African patients on haemodialysis. METHODS Fifty-eight black patients and twenty-six non-black patients on haemodialysis were recruited. Sixty-three age and sex matched controls (staff, students and kidney donors) were also recruited. Fasting venous blood samples were drawn for measurement of Creactive protein, homocysteine, Lp (a), serum lipids and adiponectin. Carotid intima-media thickness and plaque occurrence was measured by B-mode ultrasonography. Echocardiography was used to determine LVH. vi RESULTS Haemodialysis (HD) patients had significantly lower total cholesterol, LDL cholesterol and triglycerides compared with controls (p<0.001; p= 0.042). Hs-CRP, adiponectin and homocysteine levels were significantly higher in patients compared with controls (p< 0.001). The prevalence of plaques was significantly higher among HD patients (32%) compared with controls (7%) X2 = 60.72 p< 0.001. LVMI was significantly higher among HD patients (194.25± 7.69gm/m2) compared with controls (93.21 ± 3.27 gm/m2) p < 0.001. No significant difference between patients (Black or Asian/White) and controls with respect to CIMT was found. CVD risk factors in black haemodialysis patients and black controls showed a similar pattern to the whole study population combined. Risk factors associated with CIMT on regression analysis were total cholesterol, LDL-cholesterol, age, Hs-CRP, family history of CKD. Risk factors associated with plaque occurrence on logistic regression analysis were age, systolic blood pressure, male gender, smoking, calcium phosphate product and serum phosphate. CONCLUSION HD patients have a high prevalence of traditional and non-traditional risk factors for atherosclerosis and this is independent of race. Traditional risk factors like lipids were much lower in ESRD patients. HD patients showed a high prevalence of atherosclerosis as measured by increased carotid intima-media thickness and plaque occurrence in carotid arteries. Hs-CRP correlated significantly with a surrogate marker of atherosclerosis (CIMT).

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