Dissertations / Theses on the topic 'Cardiovascular system Diseases Australia Prevention'

[Truncated abstract] Indigenous Australians suffer cardiovascular disease (CVD) at a rate six times greater than the general population in Australia and while the incidence of CVD has been reduced dramatically amongst the majority of non-indigenous Australians and amongst Indigenous populations in other countries in the last 30 years, there has been little change in the figures for Aboriginal Australians, showing that heart health campaigns have little impact, for this group of people. Aims : The principal aims of this study were firstly, to determine and record the barriers to the development and delivery of CVD prevention programs amongst Indigenous Australians and secondly, to develop an alternative, effective and culturally sensitive method of delivering heart health messages. Methods and results : The study was qualitative research undertaken in three South-West towns of Western Australia where the incidence of CVD was high amongst the Aboriginal community members. The use of semi-formal interviews, informal individual consultation, observation, and focus groups were methods implemented to obtain information. The first phase of the research was to identify the barriers which affected the Aboriginal Health Workers’ ability to deliver specialist educational programs. Questionnaires and interviews with the Aboriginal Health Workers and other health professionals in the towns, and community focus groups were undertaken in this phase of the study. The second phase of the research was aimed at developing an alternative strategy for delivering heart health messages. The focus changed to adopt more traditional ways of passing on information in Indigenous communities. The idea of small gatherings of friends or family with a trusted community member presenting the health message was developed. The third phase of the research was to implement this new approach. Lay educators who had been identified within focus groups and by Aboriginal Health Workers were trained in each of the towns and a protocol involving discussions of health issues, viewing a video on CVD, produced by the National Heart Foundation, sharing in a ‘heart healthy’ lunch and partaking in a ‘heart health’ knowledge game which was developed specifically for the gatherings. Several of these gatherings were held in each of the towns and they became known as ‘HeartAware parties’.

Polyphenols are naturally-occurring phytochemicals, which form an integral part of the human diet. Results from epidemiological studies have associated polyphenol intake with reduced risk of cardiovascular diseases. Previous human intervention studies suggested that dietary polyphenols exert their cardioprotective effects through their antioxidant and anti-inflammatory effects. While most in vitro experiments have not accounted for the bioavailability and metabolism of these polyphenols, our work has provided direct evidence, using quercetin, that metabolic transformation, together with bioavailability, exert profound effects on bioactivity. We examined the effect of quercetin and its major metabolites on the production of pro-inflammatory eicosanoids by human leukocytes. Studies comparing free radical scavenging, antioxidant activity and eicosanoid production demonstrate that there are different structural requirements for antioxidant and anti-inflammatory activity. We also investigated the effect of metabolic transformation on flavonoid bioactivity by comparing the activity of quercetin and its major metabolites to inhibit inflammatory eicosanoid production from human leukocytes. Quercetin was a potent inhibitor of leukotriene B4 formation in leukocytes (IC50 ~ 2µM), and its activity was dependent on specific structural features, particularly the 2,3 double bond of the C ring. Functionalisation of the 3'-OH group with either methyl or sulfate reduced inhibitory activity up to 50% while a glucuronide substituent at the 3-OH effectively removed the leukotriene B4 inhibitory activity. The major quercetin metabolite quercetin-3'-O-sulfate retained considerable lipoxygenase inhibitory activity (IC50 ~ 7 µM) while quercetin-3-O-glucuronide maintained antioxidant activity but had no lipoxygenase inhibitory activity at physiologically relevant concentrations. We conclude that structural modification of quercetin due to metabolic transformation had a profound effect on bioactivity, and that the structural features required for antioxidant activity of 8 quercetin and related flavonoids were unrelated to those required for inhibition of inflammatory eicosanoids.

Background: Cardiovascular disease is the leading cause of mortality and morbidity in the world and has something to do with daily diet. The polyphenol is the most abundant compound in daily diet, including grape. The red wine was rich in polyphenol because of composing much grape. Early study has already confirmed the “French Paradox” in cardiovascular protection power, which shed light on the dietary modulation on disease. Objective: The main objective of the study was to evaluate the effect of products containing polyphenol such as red wine extract, grape juice and grape extract tablets or powder on cardiovascular disease risk factors. It mainly examined relationship between polyphenol and serum lipid in addition to blood pressure. Methods: Studies working on effects of grape extract products on cardiovascular disease were searched from electronic resources MEDLINE and EMBASE. Nine clinical controlled trials were identified through PubMed and Ovid. CONSORT guideline and Jadad Score were used to appraise the quality of trials. Weighing two assessment guidelines, a total of three studies were in good quality, one was in bad quality while the rest four were fair to middle. Results: The changes before and after intervention on serum lipid and blood pressure were contradictory. Some studies found polyphenol was statistically significant protective factors, while some did not find it siginificant but still showed a protective effect. One study found polyohenol had no effect on cardiovascular disease risk factors. Conclusion: The prevention of polyphenol was not consistent in nine trials and there is no sufficient and strong evidence supporting its cardiovascular protection effect given that the study design of each trial differed. It was not recommeded to use grape polyphenol as cardiovascular protect products. There were limitations and weakness of current study on the association of polyphenol and cardiovascular disease. Further research on this topic is required, both in vivo and in vitro.
published_or_final_version
Public Health
Master
Master of Public Health

Background Cardiovascular disease (CVD) is the worldwide leading cause of death among non-communicable diseases and results in a huge burden of mortality and morbidity. China, a rapidly growing East Asian country, has the world largest population and is facing an increasing burden. Incidence of CVD is lower in China than in Western countries. There are more strokes, especially hemorrhagic strokes, but less coronary heart disease (CHD) in China than in Western countries. Statin, a first-choice drug for lowering low-density lipoprotein cholesterol (LDL-C), has been shown to be effective in preventing CVD and is widely used in Western countries. However, it is not known whether the same can be applied to Asian countries, where the incidence of CVD is lower and ischemic events are rarer. The aim of this systematic review is to evaluate the effectiveness of statin for prevention of CVD in East Asian populations. Methods A systematic review was conducted by searching for randomized controlled trials from 3 databases (PubMed, MEDLINE and Cochrane Trial) for prevention of CVD comparing statin with usual care or placebo in East Asian population. Data on CVD events (deaths, CHD and cerebrovascular events, rehospitalization and revascularization) and serum lipid levels (total cholesterol (TC), LDL-C, high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG)) were extracted. Risk ratios of CVD events and change in serum lipid level were tabulated. The relationship between change in serum lipid level and mortality and incidence of CVD events were also explored. Results Fourteen studies were included, with most of them (9 studies) done in Japan. Overall, statins did not significantly reduce risk of mortality, CHD events, cerebrovascular events, revascularization and rehospitalization due to CHD. However, statins consistently lowered the risk of angina-related rehospitalization by 53% (95% confidence interval (CI) 23% to 71%) and 64% (95% CI 11% to 86%) respectively in 2 studies. There was a consistent reduced risk of composite CVD events by 34% (95% CI 5% to 55%) to 54% (95% CI 6% to 41%) in 4 studies for secondary prevention. In terms of change in lipid levels, TC and LDL-C were significantly reduced by 8% to 31% and 14% to 41% respectively with statin treatment. Change in HDL-C and TG were not consistent across studies. Lowering of TC and LDL-C level was correlated with the reduction in composite CVD and CHD events. Conclusion The use of statins in East Asian populations to prevent CVD may not be as effective as in Western countries, because of the lower baseline risk and different patterns of CVD. As the prevalence of CVD risk factors increases, the incidence of CVD will increase and the pattern of CVD may change, so careful monitoring is needed. More importantly, most of the studies included had small sample sizes, short follow-up periods and/or low methodological quality, which might contribute to the inconsistent findings. A further large-scale randomized controlled trial should be done to confirm the benefits of statins among Chinese.
published_or_final_version
Public Health
Master
Master of Public Health

Background: Research studies in recent years suggested possible role of dark chocolate in preventing cardiovascular diseases due to its high flavonal and procyanidins contents. Whether there is clear clinical benefit and the mechanisms mediating such benefits is controversial. Objective: This systematic review aims to comprehensively examine the current clinical evidence regarding effectiveness and the possible mechanisms of chocolate in reducing the risk and / or surrogate markers of cardiovascular diseases. Methods: Comprehensive electronic literature search was performed using Ovid, Medline and Cochrane database. Only English language literatures published during year 1950 - 2010 were reviewed. All intervention studies and observational studies of adult human subjects taking white or dark chocolate in relation to outcomes of cardiovascular risk were included. All review articles and meta-analysis were also included. Clinical diagnosis of cardiovascular disease and surrogate markers including blood pressure, vascular endothelial function as measured by flowed mediated vasodilation, and blood biomarkers such as lipid profile were studied as outcome variables. Results: The review outlines recent observational and interventional studies and meta-analysis to give an overview of the topic. For observational studies, a cohort studies and two case control studies were found. The observational studies showed that dark chocolate consumption was inversely associated with blood pressure, cardiovascular mortality and C-reactive protein. All interventional studies searched showed that dark chocolate increased FMD and improved platelet function. However, the effects of cocoa on intermediate outcomes such as blood pressure, antioxidant capacity and inflammatory marker changes were inconsistent among interventional studies. Three interventional studies indicated that there was a dose-dependent improvement in immediate outcome variables after 1 month or even 2 hours acute consumption of dark chocolate with procyanidins or cocoa drink with flavonol. However, publication bias and potential conflict of interests may be a potentially important factor in interpreting study results in the current literature. Conclusions: There are some clinical and scientific evidences that consumption of dark chocolate produces positive cardiovascular benefits. A small amount of dark chocolate may be good for the heart. However, gaps in our knowledge such as a lack of long-term RCT in clinical outcomes must be filled in before recommending habitual dark chocolate consumption for reduction of cardiovascular risk.
published_or_final_version
Community Medicine
Master
Master of Public Health

The disparity in life expectancy between Indigenous and non-Indigenous populations, including within high-income countries, is driven by a heightened risk of cardio-metabolic diseases. The current study recruited independent panels of experts in Indigenous cardio-metabolic health from Australia, New Zealand and the United States, in order to establish local consensus opinion and initiate dialogue on appropriate prevention strategies. Therefore, a three-round Delphi process was used to consolidate and compare the opinions of 60 experts, 20 from each country. Round one, the experts were asked twelve open-ended questions across six domains: (i) prevention; (ii) consultation; (iii) educational resources; (iv) societal issues; (v) workforce issues; (vi) culture and family. Round two, the experts completed a structured questionnaire based on results from the first round, in which they ranked items according to their importance. Final round, the experts were asked to re-rank the same items after receiving summary feedback about the rank ordering from the previous round. Several themes emerged common to all three countries: (i) socio-economic and education inequalities should be addressed; (ii) educational, behaviour change and prevention strategies should address physical environmental determinants and be responsive to the local context, including being culturally appropriate; and (iii) cultural appropriateness can be achieved through consultation with Indigenous communities, cultural competency training, use of Indigenous health workers, and use of appropriate role models. These findings highlight several key priorities that can be used to initiate dialogue on appropriate prevention strategies. Such strategies should be contextualized to the local Indigenous populations.

Thesis (MSc (Biomedical Technology))--Cape Peninsula University of Technology, 2016.
Cardiovascular diseases (CVD) are the leading cause of global mortality, of which over 75% occurred in low- and middle-income countries such as South Africa. The lipid profile, specifically decreased levels of high density lipoprotein cholesterol (HDL-C), elevated triglyceride levels and the presence of small-dense low density lipoprotein (sdLDL) has been reported associated with CVD. An increased number of sdLDL is also common in metabolic syndrome (MetS), visceral obesity and diabetes mellitus, the last a known risk factor for CVD. The modification of low density lipoprotein (LDL) size, or number of sdLDL particles, has been reported to significantly reduce CVD risk, but not conclusively so and needs further investigation. In this regard, sdLDL particles are seldom estimated routinely for clinical use because of financial and other limitations. Currently, an alternative approach for estimating sdLDL is to use equations derived from routine lipid measures, as has been proposed by several groups. However, there is a need for extensive evaluation of this equation across different ethnic and disease groups, especially since reports showed an inadequate performance of the equation in a Korean population. The aim of this study was to assess the performance of a recently proposed equation for the estimation of sdLDL in healthy and diabetic mixed ancestry South Africans. Furthermore, we also investigated the role of sdLDL as a cardiometabolic risk factor, as measured against known risk factors such as the glycemic and lipid profiles.

Thesis (MScMedSc)--Stellenbosch University, 2015.
ENGLISH ABSTRACT: It is well-established that transient activation of the β-adrenergic signalling pathway with ligands such as isoproterenol, formoterol and dobutamine, elicits cardioprotection against subsequent long periods of ischaemia. Initially the focus was on the β1- and β2-adrenergic receptors (β1-AR, β2-AR), but recently the β3-AR also emerged as a potential target in the treatment of heart disease. In heart failure, β1- and β2-AR are typically known to be down-regulated while β3-ARs, on the other hand, are up-regulated (Moniotte et al., 2001). Thus, it has become important to examine the significance of the β3-AR and its downstream signalling under similar states of stress. It has been shown that β3-AR stimulation is resistant to short term agonist-promoted desensitization in vitro and in vivo (Liggett et al., 1993) and after being activated, this receptor is able to convey continual intracellular signals (Lafontan et al., 1994). Thus, it could be an ideal target for therapeutic intervention, also in ischaemic heart disease. We hypothesized that selective β3-AR stimulation during ischaemia / reperfusion may be cardioprotective, whereas selective inhibition of this receptor may prove useful in the end stages of sustained ischaemia and early reperfusion. Methods: The isolated working rat heart, subjected to 35 min of regional ischaemia (RI) and 60 min reperfusion was used as model. The β3-AR agonist (BRL37344) (1 μM) or antagonist (SR59230A) (0.1 μM) were applied as follows: (i) before 35 min RI (PT), (ii) during the last 10 min of RI (PerT) and /or (iii) at the onset of reperfusion (PostT) and (iv) administration of BRL37344 during the last 10 min of RI BRL37344 (PerT) was followed by SR59230A during first 10 min of reperfusion SR59230A (Post). The contribution of nitric oxide synthase (NOS) in β3-AR was assessed, using the non-specific NOS inhibitor, L-NAME (50 μM). Endpoints were functional recovery and infarct size. In another set of experiments BRL37344 and SR59230A were applied according to the same protocols, but the left ventricle was dissected from the heart and freeze clamped at 10 min reperfusion for Western blot analysis of extracellular signal-regulated kinase (ERK p44/p42), protein kinase B (PKB/Akt), glycogen synthase kinase-3β (GSK-3β), and endothelial nitric oxide synthase (eNOS). Data were analyzed with one or two-way analysis of variance (ANOVA). Results: Administration of the selective β3-AR agonist (BRL37344) (1μM) before 35 min RI (BRL37344 (PT), significantly reduced infarct size when compared to the non-pretreatment group (NPT) (21.43±2.52 vs 43.17±1.20, p < 0.001). BRL37344 had similar effects on infarct size when applied during the last 10 min of regional ischaemia BRL37344 (PerT) (14.94±2.34, vs NPT, p < 0.001) or at the onset of reperfusion BRL37344 (PostT) (19.06±1.81, vs NPT, p < 0.001). When BRL37344 was applied as a (PerT+PostT) strategy, infarct size was once again significantly reduced (20.55±2.01 vs 43.17±1.20, p <0.001). In contrast, administration of the β3-antagonist SR59230A according to the same protocol did not reduce infarct size and values similar to those of untreated hearts (NPT) were obtained. Surprisingly, when BRL37344 was applied during the last 10 min of regional ischaemia followed by the administration of the β3-AR antagonist (SR59230A) at the onset of reperfusion, [BRL37344 (PerT) & SR59230A (PostT)], infarct size was significantly reduced to 20.78±3.02 (p <0.001 vs NPT and SR59230A (PerT + PostT). Involvement of nitric oxide (NO) was shown since the reduction in infarct size elicited by BRL37344 was totally abolished by, L-NAME, when administered in combination with BRL37344 for 10 minutes prior to RI or at the onset of reperfusion for 10 minutes (% infarct size: 41.48±3.18 and 35.75±3.54, p <0.001 vs BRL37344 (PT) and BRL37344 (PostT), respectively. Western blot results show that PKB/Akt is activated by BRL37344 regardless of the time of administration. The intervention BRL37344 (PerT+PostT), exhibited the most significant phosphorylation of PKB/Akt (fold increase: 14.2±3.71, p<0.01 vs NPT and p<0.05 vs BRL37344 (PostT). In addition, BRL37344 (PT), (PerT), (PostT) and [BRL37344 (PerT) +SR59230A (PostT)] showed significant activation of this kinase (2.92±0.22, 5.54±0.43, 4.73±0.47, and 6.60±0.78, respectively). ERKp44/p42 however, was not significantly activated by any of the treatments. Phosphorylation of eNOS and GSK-3β was significant only in the BRL37344 (PerT+PostT) and [BRL37344 (PerT) + SR59230A (PostT)] groups. The activation of eNOS-S-1177 in the BRL37344 (PerT+PostT) group was (2.82±0.46, p<0.01 and 0.05 vs NPT and BRL37344 (PostT), respectively) and in the [BRL37344 (PerT) + SR59230A (PostT)] group was (2.26±0.48, p<0.05 vs NPT). A very significant increased phosphorylation of GSK-3β was seen in the same two groups (68.8±7.73, p<0.001 vs NPT and 25.5±5.42 vs NPT, p<0.05, respectively). Conclusion: β3-AR has potent cardioprotective effects when administered either before, during and after ischaemia during early reperfusion as indicated by the reduction in infarct size as well as activation of PKB, GSK-3β and eNOS. These beneficial effects can be linked to NO production through activation of eNOS.
AFRIKAANSE OPSOMMING: Dit is bekend dat verbygaande aktivering van die β-adrenerge seinpad, met ligande soos isoproterenol, formoterol en dobutamien, die hart teen daaropvolgende lang periodes van iskemie beskerm. Aanvanklik was die fokus op die β1- en β2-adrenerge reseptore (β1-AR, β2-AR); maar onlangs is ook die β3-AR as 'n potensiële teiken in die behandeling van hartsiektes ge-eien. In hartversaking, is dit bekend dat β1- en β2-AR afreguleer word, terwyl β3-ARs, aan die ander kant, opreguleer word (Moniotte et al., 2001). Dit het dus belangrik geword om die belang van die β3-AR en sy stroomaf seinpad onder soortgelyke strestoestande te ondersoek. Dit is bewys dat β3-AR stimulasie teen korttermyn agonis geïnduseerde desensitisering in vitro en in vivo bestand is (Liggett et al., 1993) en wanneer geaktiveer, is hierdie reseptor in staat om intrasellulêre seine voortdurend oor te dra (Granneman, 1995). Dit kan dus ‘n ideale teiken vir terapeutiese intervensie wees, ook in iskemiese hartsiekte. Ons hipotetiseer dat selektiewe β3-AR stimulasie tydens iskemie / reperfusie kardiobeskermende mag wees, terwyl selektiewe inhibisie van hierdie reseptor effektief kan wees in die eindstadia van volgehoue iskemie en vroeë herperfusie. Metodes: Die geïsoleerde werkende rothart, onderwerp aan 35 min van streeksiskemie (SI) en 60 min herperfusie, is as model gebruik. Die β3-AR agonis (BRL37344) (1μM) of antagonis (SR59230A) (0.1 μM), is as volg toegedien: (i) voor 35 min SI (PT), (ii) gedurende die laaste 10 min van SI (PerT) en / of (iii) tydens die aanvang van herperfusie (PostT) en (iv) gedurende die laaste 10 min van SI is BRL toediening BRL37344 (PerT) gevolg deur SR59230A tydens die eerste 10 min van herperfusie SR59230A (Post). Die rol van stikstofoksiedsintase (NOS) in β3-AR is met behulp van die nie-spesifieke NOS inhibitor, L-NAME (50 μM) ondersoek. Eindpunte was funksionele herstel tydens herperfusie en infarktgrootte. In 'n ander reeks eksperimente is BRL37344 en SR59230A volgens dieselfde protokolle toegedien, maar die linker ventrikel is uit die hart gedissekteer na 10 min herperfusie en gevriesklamp vir Western klad analise van ekstrasellulêre-sein gereguleerde kinase (ERK p44/p42), proteïen kinase B (PKB/Akt), glikogeen sintase kinase-3β (GSK-3β), en endoteel stikstofoksied- sintase (eNOS). Data is met een of twee-rigting variansie analise (ANOVA) ontleed. Resultate: Administrasie van die selektiewe β3-AR agonis (BRL37344) (1μM) voor 35 min SI BRL37344 (PT), het die infarktgrootte beduidend verminder vergeleke met die nie-behandelde groep (NPT) (21.43±2.52 vs 43.17±1.20, p<0.001). BRL37344 het ‘n soortgelyke effek op infarktgrootte wanneer dit gedurende die laaste 10 min van streeksiskemie BRL37344 (PerT) (14.94±2.34, vs NPT, p<0.001) of by die aanvang van herperfusie (BRL37344 (PostT) (19.06±1.81, vs NPT, p<0.001) toegedien word. Wanneer BRL37344 as 'n (PerT+PostT) strategie toegedien is, was infarktgrootte weereens beduidend verlaag (20.55±2.01 vs 43.17±1.20, p<0.001). In teenstelling hiermee, het administrasie van die β3-antagonis SR59230A volgens dieselfde protokol, nie infarktgrootte verminder nie en waardes soortgelyk aan dié van onbehandelde harte (NPT) is verkry. Interessant, wanneer BRL37344 gedurende die laaste 10 min van streeksiskemie toegedien is, gevolg deur die administrasie van die β3-AR antagonis (SR59230A) by die aanvang van herperfusie, [BRL37344(PerT) & SR59230A(PostT)], was infarktgrootte aansienlik verminder tot 20.78±3.02 (p<0.001 vs NPT en SR59230A (PerT+PostT). Die betrokkenheid van stikstofoksied (NO) is waargeneem deurdat die vermindering in infarktgrootte ontlok deur BRL37344, heeltemal deur L-NAME opgehef is, wanneer dit in kombinasie met BRL37344 vir 10 minute voor SI of by die aanvang van herperfusie vir 10 minute toegedien is (% infarktgrootte: 41.48±3.18 en 35.75±3.54, p<0.001 vs BRL37344 (PT) en BRL37344 (PostT) onderskeidelik). Western kladresultate toon dat PKB/Akt deur BRL37344 geaktiveer word ongeag die tyd van die administrasie. Die intervensie BRL37344 (PerT+PostT), toon die mees beduidende fosforilering van PKB/Akt (voudige toename: 14.2±3.71, p<0.01 vs NPT en p<0.05 vs BRL37344 (PostT). Daarbenewens het BRL37344 (PT), (PerT), (PostT) en [BRL37344 (PerT) + SR59230A (PostT)] ook beduidende aktivering van hierdie kinase tot gevolg gehad (2.92±0.22, 5.54±0.43, 4.73±0.47 en 6.60±0.78, onderskeidelik). ERKp44/p42 is egter nie deur enige van die behandelings geaktiveer nie. Fosforilering van eNOS en GSK-3β was net beduidend in die BRL37344 (PerT+PostT) en [BRL37344 (PerT) + SR59230A (PostT)] groepe. Die aktivering van eNOS-S-1177 was beduidend in die BRL37344 (PerT+PostT) en [BRL37344 (PerT) + SR59230A (PostT)] groepe. 'n Baie beduidende toename in fosforilering van GSK-3β is in dieselfde twee groepe (68.8±7.73, p<0.001 en 25.5±5.42, p<0.05 vs NPT onderskeidelik) waargeneem. Gevolgtrekking: β3-AR het kragtige kardiobeskermende effekte wanneer dit, hetsy voor, tydens en na iskemie gedurende vroeë herperfusie toegedien word, soos deur die vermindering in infarktgrootte sowel as die aktivering van PKB, GSK-3β en eNOS aangedui is. Hierdie voordelige effekte kan aan NO produksie deur aktivering van eNOS gekoppel word.

Orientador: Otávio Rizzi Coelho
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: Hipertensão arterial sistêmica (HAS) é uma importante causa evitável de morbidade e mortalidade cardiovascular. Vários estudos apontam para o aumento de sua prevalência no mundo e baixo controle pressórico, mas existem poucos dados referentes as comunidades ribeirinhas. Esta pesquisa compara a prevalência, consciência, tratamento e controle de HAS entre população urbana e ribeirinha em Porto Velho, região Amazônica, assim como avalia outros fatores de risco cardiovascular. Foi conduzido um estudo transversal, fundamentado em inquérito domiciliar em indivíduos de 35 a 80 anos, recrutados entre julho e dezembro de 2013. Realizado entrevista com questionário padronizado, medidas de pressão arterial (PA), peso, altura e circunferência abdominal (CA). HAS foi definido através de indivíduos que relataram ter a doença, ou prescritos para uso de medicações anti-hipertensivas ou aqueles que tinham PA sistólica ? 140 mmHg ou PA diastólica ? 90 mmHg, na média de duas medidas usando dispositivo digital automático. Consciência foi baseada em autorrelatos, tratamento no uso de medicamento anti-hipertensivo, e controle foi definido quando indivíduos apresentavam PA menor do que 140/90 mmHg. Foi calculado índice de massa corpórea (IMC) e CA para avaliação de obesidade e obesidade abdominal. Também foi avaliado, através de autorrelatos, a taxa de diabetes, dislipidemia, tabagismo. Entre 1410 participantes, 750 (53,19%) tinham HAS e 473 (63,06%) eram cientes do diagnóstico. Daqueles que tinham consciência do diagnóstico, a maioria 404 (85.41%) recebia tratamento farmacológico, mas a taxa de controle foi baixa. As percentagens de prevalência e tratamento foram maiores na área urbana, respectivamente, (55,48% vs. 48,87%)(p=0,02) e (61,25% vs. 52,30%)(p<0,01). A consciência de HAS foi maior na área ribeirinha (61,05% vs. - 67,36%)(p<0,01), mas as taxas de controle, tanto entre todos os hipertensos quanto naqueles que faziam tratamento farmacológico, foram similares, respectivamente, (22,11% vs. 23,43%)(p=0,69) e (33,88% vs. 34,32%) (p=0,77). Não houve diferença significativa no sobrepeso (40,93% vs. 40,28%)(p=0,73); obesidade (19,10% vs 19,63%)(p=0,68) e tabagismo (18,56% vs. 16,76%)(p=0,09). Cerca de metade dos participantes apresentavam HAS. A prevalência foi mais alta nos urbanos, mas a diferença para os ribeirinhos foi pequena. Dos indivíduos hipertensos, tanto na área urbana quanto ribeirinha, menos de um quarto tinham HAS controlada
Abstract: High blood pressure (hypertension) is a major preventable cause of cardiovascular morbidity and mortality. Several studies indicate to the increase its prevalence in the world and low control rate, but there are few data on the riverside communities. This research compares the prevalence, awareness, treatment and control of hypertension between urban and riverside population in Porto Velho, the Amazon region, as well as evaluating other cardiovascular risk factors. A cross-sectional study was conducted, based on a household survey in individuals 35-80 years recruited between July and December 2013. Directed interview with standardized questionnaire, blood pressure measurements (PA), weight, height and waist circumference (WC). Hypertension was defined by individuals who reported having the disease, or prescribed for use of antihypertensive medications or those who had systolic blood pressure ? 140 mmHg or diastolic BP ? 90 mmHg, the mean of two measurements using automatic digital device. Awareness was based on self-reports, treatment in the use of antihypertensive medication, and control was defined as a BP ? 140/90 mm Hg. We calculated body mass index (BMI) and WC for assessing obesity and abdominal obesity. We also assessed through self-report, the rate of diabetes, dyslipidemia, smoking. Among 1410 participants, 750 (53.19%) had hypertension and 473 (63.06%) were aware of their diagnosis. Of those who were aware of the diagnosis, 404 (85.41%) received pharmacological treatment, but the control rate was low. The percentages of prevalence and treatment were higher in urban areas, respectively (55.48% vs. 48.87%) (p = 0:02) and (61.25% vs. 52.30%) (p <0.01). Awareness was higher in the riverside area (61.05% vs. 67.36%) (p <0.01), but control rates, both among all hypertensive patients and in those who were pharmacological treatment were similar, respectively, (22.11% vs . 23.43%) (p = 0.69) and (33.88% vs. 34.32%) (p = 0.77). - There was no significant difference in the overweight (40.93% vs. 40.28%) (p = 0.73); obesity (19.10% vs. 19.63%) (p = 0.68) and smoking (18.56% vs. 16.76%) (p = 0.09). Hypertension prevalence was higher in the urban population than in the riverside population. Of the hypertensive individuals in both areas, < 25% had controlled blood pressure
Doutorado
Clinica Medica
Doutor em Clínica Médica

[Truncated abstract] Vitamin E is comprised of a family of tocopherols (TOH) and tocotrienols. The most studied of these is [alpha]-tocopherol ([alpha]-TOH), as this form is retained within the body and any deficiency of vitamin E is corrected with this supplement. [alpha]-TOH is a lipid-soluble antioxidant required for the preservation of cell membranes and potentially acts as a defense against oxidative stress. Individuals who have a primary vitamin E deficiency such as low birth weight infants, secondary vitamin E deficiency due to fat malabsorption such as in abetalipoproteinaemia, or a genetic defect in TOH transport require supplementation. There is debate as to whether vitamin E supplementation in other patient groups is required. Vitamin E supplementation has been recommended for persons with FHBL, a rare disorder of lipoprotein metabolism that leads to low serum [alpha]-TOH and decreased LDL cholesterol and apolipoprotein B concentrations. We examined the effect of truncated apoB variants on vitamin E metabolism and oxidative stress in persons with heterozygous FHBL. We used HPLC with electrochemical detection to measure [alpha]- and [gamma]-TOH in serum, erythrocytes, and platelets, and GC-MS to measure urinary F2-isoprostanes and TOH metabolites as markers of oxidative stress and TOH intake, respectively. Erythrocyte [alpha]-TOH was decreased, but we observed no differences in lipid-adjusted serum TOHs, erythrocyte [gamma]-TOH, platelet [alpha]- or [gamma]-TOH, urinary F2-isoprostanes, or TOH metabolites. Taken together, our findings do not support the recommendation that persons with heterozygous FHBL should receive vitamin E supplementation. ... Sesame lignans are natural components of sesame seed oil and there is evidence that these lignans can inhibit CYP450 enzymes, in particular, those responsible for vitamin E metabolism. We hypothesised that sesame seed ingestion would increase serum [gamma]-TOH, lower plasma lipids and inhibit platelet function in human subjects with at least one cardiovascular risk factor. We used HPLC with electrochemical detection to measure [alpha]- and -TOH in serum and GC-MS to measure F2-isoprostanes and TOH metabolites as markers of oxidative stress and TOH intake, respectively. We used high-sensitive C-reactive protein as a measure of systemic inflammation. Platelet function was assessed using the PFA-100 platelet aggregation assay. Although serum [gamma]-TOH increased by 17%, we observed no effect on lipid metabolism, markers of inflammation, oxidative stress or platelet function following treatment with ~25 g/day sesame seeds for five weeks. Our findings challenge the hypothesis that sesame seed ingestion provides beneficial cardiovascular effects. In summary, we have studied the metabolism and transport of both [alpha]- and [gamma]-TOH in humans to evaluate the requirements for supplementation and the effects of vitamin E on platelet function and CYP3A4 activity. Specialised techniques using HPLC were developed to measure serum and cellular TOH concentrations both in supplemented and un-supplemented individuals. We also used GCMS to provide a sensitive, accurate assessment of TOH metabolites and midazolam pharmacokinetics in humans after vitamin E supplementation. We have examined the role vitamin E has on important biochemical endpoints, with emphasis on the implications for TOH supplementation in subjects at risk of CVD.

Dissertation (PhD)--University of Stellenbosch, 2005.
ENGLISH ABSTRACT: Activation of the NO-cGMP pathway is associated with myocardial protection against ischaemia/reperfusion injury. However, high-cholesterol diets alter function of this pathway and these alterations have been implicated in both ischaemic/reperfusion injury and the development of ischaemic heart disease. Little is known about the effects of supplements such as Red Palm Oil (RPO) on the myocardial NO-cGMP-signalling pathway. RPO consists of saturated, mono-unsaturated and poly-unsaturated fatty acids and is rich in antioxidants such as β-carotene and Vitamin E (tocopherols and tocotrienols). The aims of this study were: 1) to determine whether dietary RPO-supplemention protects against ischaemia/reperfusion injury in rats fed a standard rat chow (control) and cholesterol-enriched diets and 2) if so, to investigate possible mechanisms for this protection. Male Long-Evans rats were fed a standard rat chow or a standard rat chow plus cholesterol and/or RPO-supplementation for 6 weeks. Myocardial functional recovery was measured and hearts were freeze-clamped for determination of myocardial phospholipid, cAMP/cGMP concentrations, total myocardial nitric oxide concentrations, lipid hydroperoxide production and superoxide dismutase- and nitric oxide synthase activity in isolated rat hearts subjected to 25 minutes of normothermic total global ischaemia. In addition, the degree of phosphorylation of extracellular signal-regulated kinase (ERK), p38, c-Jun N-terminal protein kinase (JNK) and protein kinase B (PKB/Akt) was investigated. Furthermore, the effect of RPO-supplementation on caspase-3 activation and poly (ADP-ribose) polymerase (PARP)-cleavage in hearts subjected to ischaemia and reperfusion was also investigated. Our data show that dietary RPO-supplementation protects the hearts of rats on a standard rat chow (control) and hypercholesterolaemic diet against ischaemia/reperfusion injury as reflected by improved aortic output recovery. Increased intracellular cardiomyocyte NO concentrations as observed in control hearts supplemented with RPO after 120 minutes hypoxia may contribute to the elevated cGMP concentration and may confer some of the cardioprotection to the ischaemic/reperfused heart. Although improved functional recovery with RPO-supplementation of a high-cholesterol diet was also associated with an increase in intracellular cardiomyocyte NO production after hypoxia compared to the non-hypoxic conditions, it could not be linked to increased NO-cGMP signalling. These data are in agreement with other studies, which showed that high-cholesterol diet impairs NO-cGMP signalling and confirms our hypothesis that elevated cGMP concentrations may not be the only mechanism of protection. We have also shown that RPOsupplementation caused increased phosphorylation of p38 and PKB, reduced phosphorylation of JNK and attenuation of PARP cleavage, which may contribute to the protection of the cell against apoptosis. Based on our results we propose that the myocardial protection offered by RPO-supplementation of rats on a normal and hypercholesterolaemic diet may be associated with either its antioxidant characteristics and/or changes in the fatty acid composition of the myocardium during ischaemia/reperfusion. Furthermore, we demonstrated for the first time that RPO-supplementation protects the isolated perfused working rat heart during reperfusion from ischaemia/reperfusion-induced injury through a MAPK-dependent pathway.
AFRIKAANSE OPSOMMING: Aktivering van die NO-cGMP sein transduksie pad word geassosieer met miokardiale beskerming teen isgemie/herperfusie skade. Hoë cholesterol diëte verander egter die funksie van die pad en hierdie veranderings speel ‘n rol in beide isgemie/herperfusie besering en die ontwikkeling van isgemiese hartsiekte. Daar is egter min inligting beskikbaar oor die uitwerking van aanvullings soos rooi palm olie (RPO) op die miokardiale NO-cGMP sein transduksie pad. RPO bevat versadigde, mono-onversadigde en poli-onversadigde vetsure en is ryk aan anti-oksidante nl. β-karotene en vitamien E (tokoferole en tokotriënole). Die doelwitte van hierdie studie was: 1) om vas te stel of ‘n RPO-aanvulling beskerming bied teen isgemie/herperfusie besering in rotte wat gevoed is met ‘n standaard rotmengsel (kontrole) en cholesterol-verrykte dieet en 2) indien wel, om moontlike meganismes van beskerming te ondersoek. Long-Evans manlike rotte is vir 6 weke gevoer met ‘n standaard rotmengsel of ‘n standaard rotmengsel plus cholesterol en/of RPO-aanvulling. Miokardiale funksionele herstel is gemeet en harte is gevriesklamp vir die bepaling van miokardiale fosfolipied, cAMP/cGMP, totale stikstofoksied, lipied hidroperoksied, superoksied dismutase en stikstofoksied sintase in geïsoleerde rotharte wat vir 25 minute onderwerp was aan normotermiese totale globale isgemie. Hiermee saam is die graad van fosforilering van ekstrasellulêre sein gereguleerde kinase (ERK), p38 mitogeen-geaktiveerde proteïen kinase (p38 MAPK), c-Jun-N-terminale proteïenkinase (JNK) en proteïen kinase B (PKB/Akt) ondersoek, asook kaspase-3 aktivering en poli (ADP-ribose) polimerase (PARP) kliewing in harte blootgestel aan isgemie en herperfusie. Ons resultate toon dat RPO-aanvulling van rotte op ‘n normale en hipercholesterolemiese dieet die hart beskerm soos getoon deur verbeterde herstel van aortiese uitset. Verhoogde intrasellulêre miokardiale NO vlakke in kontrole harte met ‘n RPO-aanvulling wat blootgestel was aan 120 minute hipoksie, mag bygedra het tot die verhoogde cGMP vlakke en beskerming van die hart tydens isgemie en herperfusie. Alhoewel verbeterde funksionele herstel met RPO-aanvulling van ‘n hoë cholesterol dieet ook geassosieer is met ‘n toename in intrasellulêre miokardiale NO produksie ná hipoksiese toestande, kon dit nie verbind word met verhoogde aktivering van die NOcGMP sein transduksie pad nie. Hierdie resultate stem ooreen met ander studies wat aangetoon het dat hoë-cholesterol diëte die NO-cGMP seinpad onderdruk. Hierdie bevinding bevestig ons hipotese dat verhoogde cGMP vlakke moontlik nie die enigste beskermingsmeganisme is nie. Ons resultate het ook gewys dat RPO-aanvulling fosforilering van p38 en PKB/Akt verhoog, fosforilering van JNK verminder en PARP kliewing onderdruk. Dit dui op beskerming van die sel teen apoptose. Ons resultate dui aan dat die miokardiale beskerming wat RPO-dieet aanvulling bied moontlik geassosieer kan word met sy anti-oksidant eienskap en/of veranderinge in die vetsuur samestelling van die miokardium tydens isgemie/herperfusie. Ons het ook vir die eerste keer bewys dat RPO-aanvulling die geïsoleerde geperfuseerde werkende rothart gedurende herperfusie beskerm teen isgemie/herperfusie besering deur die aktivering en/of deaktivering van die MAPK afhanklike pad.

Gao, Ni.
Thesis (M.Phil.)--Chinese University of Hong Kong, 2009.
Includes bibliographical references (leaves 133-153).
Abstracts also in Chinese.
ACKNOWLEDGEMENTS
TABLE OF CONTENT --- p.1
LIST OF FIGURES AND TABLES --- p.4
List of Figures --- p.4
List of Tables --- p.5
ABSTRACT --- p.6
中文摘要 --- p.9
ABBREVIATIONS --- p.11
Chapter CHAPTER 1 - --- BACKGROUND REVIEW AND HYPOTHESIS --- p.13
Chapter 1.1 --- Overview of Peritoneal dialysis --- p.13
Chapter 1.2 --- Peritoneal dialysis in Hong Kong --- p.16
Chapter 1.3 --- Cardiovasular Disease in PD patients --- p.18
Chapter 1.3.1 --- Arterial disease --- p.21
Chapter 1.3.2 --- Left ventricular hypertrophy --- p.23
Chapter 1.4 --- Malnutrition in PD patients --- p.26
Chapter 1.5 --- Fluid overload in PD patients: a cause and a result of CVD --- p.28
Chapter 1.5.1 --- Overview --- p.28
Chapter 1.5.2 --- Fluid overload and residual renal function --- p.29
Chapter 1.5.3 --- Fluid overload and hypertension --- p.30
Chapter 1.5.4 --- Fluid overload and malnutrition --- p.32
Chapter 1.5.5 --- Assessment of fluid status in PD patient --- p.33
Chapter 1.6 --- Peritoneal transport as the cause of fluid overload --- p.36
Chapter 1.6.1 --- Structure of peritoneum --- p.36
Chapter 1.6.2 --- Structural alteration of peritoneal membrane in PD --- p.37
Chapter 1.6.3 --- Ultrafiltration dysfunction --- p.38
Chapter 1.6.4 --- Peritoneal transport and outcome of PD patients --- p.40
Chapter 1.6.5 --- Fluid overload and peritoneal transport --- p.41
Chapter 1.6.6 --- Peritoneal transport and malnutrition --- p.42
Chapter 1.6.7 --- Assessment of peritoneal transport --- p.44
Chapter 1.7 --- Closing the circle: Arterial stiffness as a cause of high peritoneal transport? --- p.47
Chapter 1.7.1 --- Vascular function and anatomy --- p.47
Chapter 1.7.2 --- Atherosclerosis --- p.49
Chapter 1.7.3 --- Atherosclerosis and Endothelial Dysfunction --- p.50
Chapter 1.7.4 --- Atherosclerosis and Extracellular Matrix --- p.53
Chapter 1.7.5 --- Arterial stiffness and renal function --- p.54
Chapter 1.7.6 --- Arterial stiffness in PD --- p.55
Chapter 1.7.7 --- Arterial stiffness and clinical outcome --- p.55
Chapter 1.7.8 --- Assessment of arterial stiffness --- p.57
Chapter 1.8 --- An overall construct --- p.61
Chapter 1.9 --- Hypothesis --- p.63
Chapter CHAPTER 2 - --- GENERAL METHODOLOGY --- p.65
Chapter 2.1 --- Radiographic Parameters of Intravascular Volume Status --- p.65
Chapter 2.2 --- Pulse Wave Velocity Study --- p.69
Chapter 2.3 --- Dialysis adequacy study --- p.72
Chapter 2.4 --- Peritoneal equilibration test (PET) --- p.73
Chapter 2.5 --- Assessment of nutritional status --- p.75
Chapter CHAPTER 3 - --- Radiographic Parameters of Intravascular Volume Status as a Prognostic Marker in Chinese Peritoneal Dialysis Patients --- p.77
Chapter 3.1 --- Introduction --- p.77
Chapter 3.2 --- Patients and Methods --- p.78
Chapter 3.3 --- Results --- p.81
Chapter 3.4 --- Conclusion --- p.90
Chapter CHAPTER 4 - --- Longitudinal Changes of Radiographic Parameters as the Prognostic Marker of Chinese Peritoneal Dialysis Patients --- p.91
Chapter 4.1 --- Introduction --- p.91
Chapter 4.3 --- Results --- p.95
Chapter 4.4 --- Conclusions --- p.104
Chapter CHAPTER 5 - --- "The Relation between Arterial Pulse Wave Velocity, Peritoneal Transport Characteristics, and Radiological Parameters of Intravascular Volume Status in Chinese peritoneal dialysis patients" --- p.105
Chapter 5.1 --- Introduction --- p.105
Chapter 5.2 --- Patients and Methods --- p.106
Chapter 5.3 --- Results --- p.110
Chapter 5.4 --- Conclusions --- p.119
Chapter CHAPTER 6 - --- DISCUSSION --- p.120
Chapter 6.1 --- Methodology --- p.120
Chapter 6.2 --- Results --- p.123
Chapter 6.3 --- Further Directions of Research --- p.131
Chapter 6.4 --- Conclusions --- p.132
REFERENCE --- p.133
PUBLICATIONS RELATED TO THIS WORK --- p.154
Index Publication --- p.154
Abstract --- p.154

Conclusions: In the same number of people treated, the number of CVD events avoided for the overall risk approach is always larger than that of the blood pressure approach. The additional benefits of overall risk approach compared with the blood pressure approach decreases as the percentage of people from the total population is increased. If the current practice and hypertension guidelines in China are shifted to the overall risk approach, many more CVD events could be avoided with the same resources used.
Methods: The sample used in the analyses includes a subsample of 38,673 persons from the 2002 China National Nutrition and Health Survey, who were 30-74 years old, without previous CVD, and had data on all major CVD risk factors. CVD risks of the patients selected by each approach are predicted using suitable risk prediction equation. The RRR of anti-hypertensive drug treatment derived from meta-analyses of RCTs. The difference in the absolute effectiveness between the two approaches is used to quantify how many more CVD events can be prevented in 1000 people treated by the ORA as compared to the BPA.
Objective: To estimate and compare the number of major cardiovascular events that could be avoided by shifting the blood pressure approach to the overall risk approach if the same percentage of people in a large, representative Chinese population is treated with anti-hypertensive drugs.
Results: When 2.5%, 5.5%, 10.1%, 15.5%, 20.7%, 25.7% or 33.0% of the 38,673 subjects were treated by anti-hypertensive drugs by using the two approaches respectively, 22 (95%CI: 17∼28), 13 (11∼16), 9 (8∼10), 7 (6∼8), 6 (5∼7), 5 (4∼6), or 4 (3∼4) more CVD events could be avoided in every 1000 people treated if the blood pressure approach is shifted to the overall risk approach, which is in general a 15% to 25% increase in CVD events prevented.
Qin, Ying.
Adviser: Jin Ling Tang.
Source: Dissertation Abstracts International, Volume: 73-02, Section: B, page: .
Thesis (Ph.D.)--Chinese University of Hong Kong, 2010.
Includes bibliographical references (leaves 116-121).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [201-] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstract also in Chinese.

To Man Yin.
Thesis (M.Phil.)--Chinese University of Hong Kong, 2006.
Includes bibliographical references (leaves 85-105).
Abstracts in English and Chinese.
Abstract (in English) --- p.i
(in Chinese) --- p.iv
Acknowledgements --- p.vi
Publications --- p.viii
Table of Contents --- p.ix
List of Tables --- p.xii
List of Figures --- p.xiii
List of Abbreviations --- p.xiv
Chapter CHAPTER 1: --- General Introduction --- p.1
Chapter Section 1.1 --- Background and Clinical Application of Anthracylines --- p.1
Chapter Section 1.2 --- DOX-induced Cardiotoxicity --- p.3
Chapter 1.2.1 --- Types of Cardiotoxicity --- p.4
Chapter 1.2.1.1 --- Acute Cardiotoxicity --- p.4
Chapter 1.2.1.2 --- Chronic Cardiotoxicity --- p.5
Chapter 1.2.2 --- Subcellular Effects of DOX --- p.6
Chapter 1.2.2.1 --- Ultrastructural Lesions --- p.6
Chapter 1.2.2.2 --- Effects on Mitochondrial Functions --- p.7
Chapter 1.2.2.3 --- Effects on Sarcoplasmic reticulum (SR) Functions --- p.8
Chapter Section 1.3 --- Mechanisms of DOX-induced Cardiotoxicity --- p.8
Chapter 1.3.1 --- Formation of Free Radicals --- p.9
Chapter 1.3.1.1 --- Generation of Free Radicals by DOX --- p.10
Chapter 1.3.1.2 --- Cardiac damage by Free radicals --- p.12
Chapter 1.3.2 --- Induction of Apoptosis --- p.14
Chapter 1.3.2.1 --- Characteristics and Pathway of Apoptosis --- p.14
Chapter 1.3.2.2 --- Mitochondria and Apoptosis --- p.15
Chapter 1.3.2.3 --- Caspases and Apoptosis --- p.17
Chapter 1.3.2.4 --- Apoptosis and DOX-induced Cardiotoxicity --- p.18
Chapter Section 1.4 --- Strategies to Reduce DOX-induced Cardiotoxicity --- p.19
Chapter 1.4.1 --- Dosage optimization and Schedule modification --- p.19
Chapter 1.4.2 --- Anthracycline Analogues --- p.21
Chapter 1.4.3 --- Cardioprotective Agents --- p.21
Chapter Section 1.5 --- Thrombopoietin --- p.23
Chapter CHAPTER 2: --- Hypotheses and Objectives --- p.30
Chapter CHAPTER 3: --- Methodology --- p.33
Chapter Section 3.1 --- Methods --- p.33
Chapter 3.1.1 --- Culture of Rat H9C2 Myoblast Cell Line and Primary Neonatal Rat Cardiomyocytes --- p.33
Chapter 3.1.1.1 --- Maintenance of Cell Line --- p.33
Chapter 3.1.1.2 --- Culture of Primary Neonatal Rat Cardiomyocytes --- p.34
Chapter 3.1.2 --- Effects of Thrombopoietin on Cell Viability of Rat H9C2 Myoblast Cell Line and Beating Rates of Primary Rat Cardiomyocytes --- p.35
Chapter 3.1.2.1 --- Cell Viability assay --- p.35
Chapter 3.1.2.2 --- Beating Rate of Primary Beating Cardiomyocytes --- p.36
Chapter 3.1.3 --- Effects of Thrombopoietin on the Protection against DOX-induced Heart Injury In Vivo --- p.36
Chapter 3.1.3.1 --- Animals --- p.36
Chapter 3.1.3.2 --- Experimental Protocol --- p.37
Chapter 3.1.3.3 --- Echocardiography --- p.38
Chapter 3.1.3.4 --- Blood Cell Counts --- p.39
Chapter 3.1.3.5 --- Histopathology --- p.39
Chapter 3.1.4 --- Effects of Thrombopoietin on Apoptosis and Mitochondrial Integrity of Rat H9C2 Myoblast Cell Line and Apoptosis In Vivo --- p.40
Chapter 3.1.4.1 --- Determination of Externalized Phosphatidylserine --- p.40
Chapter 3.1.4.2 --- Determination of Active Caspase-3 Expression --- p.41
Chapter 3.1.4.3 --- Assessment of Mitochondrial Integrity --- p.42
Chapter 3.1.4.4 --- TUNEL assay --- p.43
Chapter 3.1.5 --- Statistical Analysis --- p.44
Chapter CHAPTER 4: --- Effects of Thrombopoietin on Cell Viability of Rat H9C2 Myoblast Cell Line and Beating Rates of Primary Neonatal Rat Cardiomyocytes --- p.46
Chapter Section 4.1 --- Results --- p.46
Chapter 4.1.1 --- Effects of TPO on DOX-induced Cell Death --- p.46
Chapter 4.1.2 --- Effects of TPO on the Beating Rates of Primary Cardiomyocytes --- p.47
Chapter Section 4.2 --- Discussion --- p.47
Chapter CHAPTER 5： --- Effects of Thrombopoietin on the Protection Against DOX-induced Heart Injury In Vivo --- p.54
Chapter Section 5.1 --- Results --- p.54
Chapter 5.1.1 --- General Observations and Survival --- p.54
Chapter 5.1.2 --- Blood Cell Counts --- p.55
Chapter 5.1.3 --- Cardiac Functions by Echocardiography --- p.56
Chapter 5.1.4 --- Gross Anatomic Changes and Pathology of the Myocardium --- p.57
Chapter Section 5.2 --- Discussion --- p.58
Chapter CHAPTER 6: --- Effects of Thrombopoietin on Apoptosis and Mitochondrial Integrity of H9C2 Cell Line and Apoptosis In Vico --- p.69
Chapter Section 6.1 --- Results --- p.69
Chapter 6.1.1 --- Determination of Externalized Phosphatidylserine --- p.69
Chapter 6.1.2 --- Determination of Active Caspase-3 Activity --- p.70
Chapter 6.1.3 --- Assessment of Mitochondrial Membrane Potential --- p.70
Chapter 6.1.4 --- Determination of Apoptosis by TUNEL assay --- p.72
Chapter Section 6.2 --- Discussion --- p.72
Chapter CHAPTER 7： --- General Discussion and Conclusion --- p.83
References --- p.85

Bibliography: leaves 192-212.
xv, 212 leaves ; 30 cm.
The present study investigates the relationships between fetal growth, as manifest in size and shape at birth, and later blood pressure and blood lipids, in an Australian cohort. Data on these outcomes for cohort members at age 8 years are available from a previous study. Birth details (body weight, placental weight, head circumference, chest circumference and length) are abstracted from hospital records. In addition, a follow up of cohort members is undertaken to collect new data pertaining to the two cardiovascular risk factors at 20 years of age. Socio-economic circumstances are characterised at birth, age 8 and age 20.
Thesis (Ph.D.)--University of Adelaide, Dept. of Public Health, 1997?

After adjusted for the effect of baseline MCE risk and reduction in SBP, the multivariate meta-regression showed baseline SBP was not significantly related to the RD for all the relevant outcomes examined (p>0.22) except MCE (p=0.0226). However, the baseline MCE risk remained significantly related to the RD for all the outcomes (p<0.01) except CHD (p=0.1011). The reduction in SBP remained significantly related to the RD for deaths due to CVD, MCE, CHF and stroke (p<0.01) but not to the RD for all-cause death (p=0.3788) and CHD (p=0.8755).
Conclusions. This study showed that baseline CVD risk and reduction in blood pressure were strongly and consistently related to the absolute effect of treatment and surprisingly the baseline blood pressure was not. The findings lend direct support to the overall risk approach to primary prevention and suggest that contrary to conventional wisdom and current practice, the overall CVD risk rather than blood pressure alone should be used to identify and treat people to prevent major CVD events through anti-hypertensive drugs. These findings suggest that anti-hypertensive drugs should be given to those who have a high future CVD risk rather than high blood pressure alone so as to achieve better cost-effectiveness of anti-hypertensive drugs for primary prevention.
Data extraction and analyses: Two reviewers independently abstracted data on baseline variables, variables that determine methodological quality, and outcomes. The following main outcomes were assessed: all-cause deaths, deaths due to cardiovascular disease, death due to causes other than CVD, major cardiovascular events (MCE), congestive heart failure (CHF), stroke, and coronary heart disease (CHD).
Key words. hypertension, antihypertensive drugs, cardiovascular disease, meta-analysis, systematic review, randomized controlled trial, primary prevention, baseline risk, evidence based medicine
Meta-analysis was used to obtain the overall odds ratio (OR) and risk difference (RD). Forest plots, bubble plots and funnel plots were used to show the results visually or to check biases. Meta-regression was used to identify factors that may independently determine the effect of antihypertensive drugs. The control CVD risk, initial mean blood pressure and reduction in blood pressure were examined.
Method. Identification of studies: The databases searched included ACP Journal Club, Cochrane Database of Systematic Reviews, Database of Abstracts of Reviews of Effects, Cochrane Central Register of Controlled Trials, MEDLINE, EMBASE, Cumulative Index to Nursing & Allied Health Literature, Chinese Medical Current Contents to identify relevant studies between 1966 and 2005. We also examined references from relevant trials, reviews and meta-analyses. For trials to be included in this review, they have to have the following characteristics: (1) essential hypertension in patients of any age, sex and race; (2) treatment intervention is antihypertensive drugs; (3) control intervention is a placebo or no treatment; (4) endpoint outcomes are all-cause death and major cardiovascular events; and (5) randomized controlled trials.
Objective. Although the overall risk approach to cardiovascular disease (CVD) primary prevention has been widely adopted, direct evidence that supports this policy is however weak and in some aspects lacking. Importantly, there is no direct evidence to show, between blood pressure and CVD risk, which is a better predictor of the absolute benefit from anti-hypertensive drugs. The evidence that the absolute benefit increases as the future CVD risk increases does not necessarily mean that treating high risk people will be more cost-effective than treating hypertensive people as blood pressure may also be positively related to treatment benefit. The high risk approach would be preferable only when we can show with strong evidence that blood pressure is not related to the absolute benefit of treatment or the CVD risk is much more strongly related to the benefit than blood pressure. We thus conducted this systematic review to examine the evidence from randomized controlled trials to directly show how blood pressure and CVD risk are related to the absolute benefit from anti-hypertensive drugs and compare the capability of the two factors in predicting the benefit. The stronger predictor should be a better indicator for identifying those who should be treated with anti-hypertensive drugs.
Results. Twenty-two eligible randomized controlled trials with a total of 55,448 participants were identified from 1967 to 2004. The average follow-up was 45.6 months ranging from 13 to 84 months. The combined RD and OR for all-cause deaths, deaths due to CVD, MCE, CHF, Stroke and CHD were all statistically significant, showing a consistent and considerable reduction in the risk of these outcomes due to the treatment of anti-hypertensive drugs (p<0.01).
Jiang, Yu.
"September 2007."
Adviser: Jin Ling Tang.
Source: Dissertation Abstracts International, Volume: 69-08, Section: B, page: 4657.
Thesis (Ph.D.)--Chinese University of Hong Kong, 2007.
Includes bibliographical references (p. 107-115).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstract in English and Chinese.
School code: 1307.

目的：針對心血管初級預防，世界各國均推薦某一年齡段人群全部測量膽固醇以估算心血管病發病風險。此舉耗費高且非必須，本研究旨在建立並驗證一個新型的选择性膽固醇篩查模型，用以篩查需藥物治療之高危人群，并在成本效益方面與其它篩查模型相比較。
方法：本模型具體采用兩步法：首先利用一個足夠高的假設膽固醇值代入心血管病風險預測方程，用以系統性的高估絶大多數人的心血管病風險；其次只有假設心血管病風險高於推薦治療閾值時，該個體才需要測量膽固醇，並進行實際心血管病風險分析。
英国健康调查和中国营养与健康调查是本次研究的合适数据。我們首先探索最優的假設膽固醇值，尋找到最後膽固醇值之後，我們將繼續測試我們的新型膽固醇篩查模型，在不同的治療閾值下，表現是否穩定。我們以靈敏度，特異度和徐篩查人群為指標，比較我們模型與全民篩查模型和英國NICE 選擇篩查模型相比較。之後我們估算在中英人群中應用該篩查模型，所需耗費的成本和可預防心血管事件數。
结果：與全名篩查模型相比，我們的模型靈敏度相若但可以節省80%左右的篩查費用。模型的靈敏度主要取決於所採用的假設膽固醇值，與所用風險預測方程，治療閾值和人群心血管風險分佈無關。當以均數加2 倍標準差作為假設膽固醇值時，靈敏度可達到97.5%左右，特異度可以達到90%左右，符合預期。模型應用於中國人群得到的結果類似。值得註意的是，在中國人群中，即使不測量膽固醇，模型靈敏度亦接近95%。此外，將膽固醇篩查項目限制于男性50-84歲，女性60-84 歲年齡段可以進一步減少篩檢費用。在人群影響方面，我們模型可預防心血管事件數比全名篩查模型略少，但成本大大降低。英國NICE 模型適用於某些特定情況，但並非全部。
結論：我們的新型篩查模型靈敏度與全民篩查模型相若，但可以節省大量篩查費用。在资源匮乏地区，可考虑在某一特定年龄段运用我们的模型已达到进一步减少费用的效果。如果本研究结果得到进一步数据证实，對於中國人群而言，膽固醇測量可能並非心血管風險評估所必須。
Objectives
Since the mid 1990s, most guidelines on primary prevention of cardiovascular disease (CVD) have recommended regular cholesterol measurement for all adults or those above a certain age (which is known as mass screening). Cholesterol measurement comprises a large cost of CVD prevention and is not necessarily required in those who do not need drug intervention. In order to reduce this cost, we have developed a new selective cholesterol screening model in order to determine whose cholesterol should be measured for drug prevention. The model was evaluated and compared with other widely adopted models in basic model performance as well as cost effectiveness.
Methods
The new model has two steps. In the first step, we purposely over-estimated the majority of respondents’ CVD risk by substituting a sufficiently high hypothetical cholesterol value in the risk estimation. We then recommend cholesterol measurement only to those with the estimated CVD risk above a predetermined risk threshold for drug treatment. In the second step, the CVD risk is re-estimated based on the individual’s real cholesterol consentration. Those with a risk above the treatment threshold are recommended for drug treatment.
We evaluated the performance of our two-step model with data from the Health Survey for England and re-evaluated it with data from the China Nutrition and Health Survey 2002. By varying the hypothetical cholesterol values and treatment thresholds in CVD risk, we assessed the sensitivity, specificity and proportion of the population who need to measure cholesterol and compared it with the US mass screening model and the UK NICE selective screening model. We further compared the costs and CVD events avoided in the compared screening programmes. We also examined how the age restriction should be set in cholesterol screening programmes.
Results
As compared to mass screening, our new model can achieve a high sensitivity and save some 80% the cost of cholesterol measurements. The sensitivity depends mainly on the hypothetical cholesterol level used and seems independent of population’s CVD risk, treatment cut-off values and risk prediction model. The model performed well in almost all the conditions tested. When the hypothetical cholesterol was set at MEAN+2SD, the resulting sensitivity of our selective screening model was almost always above 95% and close to the expected 97.5%. The sensitivity was only compromised slightly if cholesterol is not measured at all for the Chinese population. Furthermore, in order to save more costs, cholesterol measurement could be better restricted to men aged 50-84 and women 60-84 years regardless of the screening model used. In CVD events prevented, mass screening is always the best but our model can prevent almost as many. In costs, mass screening is always the most expensive but our model can save all or most of the cost. The NICE selective model can perform as well as our model only when it is used in an appropriate manner and in certain circumstances.
Conclusion
Our new cholesterol screening model has a high sensitivity which is comparable to that of universal screening programs but can save most of the cost on cholesterol measurements. In where resources are particular sparse, our model can also perform well by applying it only to certain age groups, which will further save cholesterol measurement costs. Cholesterol measurement could even be completely avoided for the Chinese population if our findings can be re-confirmed correct with more updated data.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Hu, Xuefeng.
Thesis (Ph.D.)--Chinese University of Hong Kong, 2012.
Includes bibliographical references (leaves 114-121).
Abstract also in Chinese.
Abstract (in English) --- p.i
Abstract (in Chinese) --- p.iv
Acknowledgements --- p.vi
Abbreviations used in the thesis --- p.viii
List of Tables --- p.xvi
List of Figures --- p.xviii
List of Boxes --- p.xix
Chapter 1. --- Introduction --- p.1
Chapter 1.1 --- The burden of cardiovascular disease --- p.1
Chapter 1.2 --- Primary prevention of CVD --- p.2
Chapter 1.3 --- The high-risk individual strategy for CVD primary prevention --- p.3
Chapter 1.3.1 --- The high risk individual strategy is effective --- p.4
Chapter 1.3.2 --- The high risk individual strategy is cost-effective --- p.4
Chapter 1.4 --- Who should be treated with drugs? --- p.5
Chapter 1.4.1 --- The single risk factor strategy --- p.5
Chapter 1.4.2 --- The overall CVD risk strategy --- p.7
Chapter 1.4.3 --- Scope of CVD primary prevention --- p.8
Chapter 1.5 --- Methods for assessing the CVD risk --- p.9
Chapter 1.6 --- Current strategies for cholesterol measurements --- p.10
Chapter 1.6.1 --- United States National Cholesterol Education Program --- p.13
Chapter 1.6.2 --- American Heart Association CVD and Stroke prevention guideline --- p.14
Chapter 1.6.3 --- The U.S. Preventive Services Task Force guideline --- p.15
Chapter 1.6.4 --- New Zealand guideline 2003 --- p.16
Chapter 1.6.5 --- Australian guideline 2009 --- p.17
Chapter 1.6.6 --- The Joint British Society guideline-2 --- p.17
Chapter 1.6.7 --- UK Department of Health guideline on vascular check --- p.18
Chapter 1.6.8 --- China Blood Lipid Modification Guideline 2007 --- p.18
Chapter 1.6.9 --- Summary of the reviewed guidelines --- p.19
Chapter 1.7 --- Rationale for a selective screening model --- p.20
Chapter 1.8 --- The UK NICE model --- p.22
Chapter 1.9 --- Objectives of this study --- p.24
Chapter 2 --- Methods --- p.25
Chapter 2.1 --- The new cholesterol screening model --- p.25
Chapter 2.2 --- Framework for evaluating the new screening model --- p.27
Chapter 2.3 --- Indexes for evaluating the basic performance of screening models --- p.28
Chapter 2.3.1 --- Sensitivity, specificity and % need cholesterol measurement --- p.28
Chapter 2.3.2 --- Sensitivity analysis for model performance --- p.29
Chapter 2.3.2.1 --- Using different hypothetical cholesterol values --- p.29
Chapter 2.3.2.2 --- Using different treatment cut-off thresholds --- p.30
Chapter 2.3.2.3 --- Using different populations --- p.30
Chapter 2.3.2.4 --- Using different risk equations --- p.31
Chapter 2.4 --- Data --- p.31
Chapter 2.4.1 --- The Health Survey for England --- p.31
Chapter 2.4.1.1 --- Background and aim of the survey --- p.31
Chapter 2.4.1.2 --- Survey design --- p.32
Chapter 2.4.1.2.1 --- Sampling Frame --- p.32
Chapter 2.4.1.2.2 --- Weighting variables --- p.33
Chapter 2.4.1.3 --- Data collection --- p.33
Chapter 2.4.1.3.1 --- Blood cholesterol --- p.34
Chapter 2.4.1.3.2 --- Blood pressure --- p.34
Chapter 2.4.1.3.3 --- Smoking --- p.34
Chapter 2.4.1.3.4 --- History of CVD and diabetes --- p.34
Chapter 2.4.1.3.5 --- Treatment history --- p.35
Chapter 2.4.2 --- The 2002 China National Nutrition and Health Survey --- p.35
Chapter 2.4.2.1 --- Survey design --- p.36
Chapter 2.4.2.2 --- Data collection --- p.36
Chapter 2.4.2.2.1 --- Blood pressure --- p.36
Chapter 2.4.2.2.2 --- Blood cholesterol --- p.38
Chapter 2.4.2.2.3 --- Smoking --- p.38
Chapter 2.4.2.2.4 --- History of CVD, diabetes and drug treatment --- p.38
Chapter 2.4.3 --- Subjects eligible for analysis in this study --- p.38
Chapter 2.5 --- CVD risk prediction --- p.43
Chapter 2.5.1 --- The Framingham risk equation for the UK population --- p.43
Chapter 2.5.2 --- The Asian equation for the Chinese population --- p.44
Chapter 2.5.3 --- Adjusting for cholesterol and blood pressure --- p.45
Chapter 2.5.4 --- Deriving the hypothetical cholesterol --- p.46
Chapter 2.6 --- Identifying the appropriate age ranges for cholesterol measurement --- p.47
Chapter 2.7 --- Comparing various screening models and options --- p.47
Chapter 2.7.1 --- Compared screening models and options --- p.47
Chapter 2.7.1 --- Indices for the performance of the screening options --- p.49
Chapter 2.7.2 --- Costs of different screening options --- p.50
Chapter 2.7.2.1 --- Components of screening cost from societal perspective --- p.50
Chapter 2.7.2.1.1 --- Cost for inviting people for data collection --- p.50
Chapter 2.7.2.1.2 --- Cost for the full risk assessment --- p.51
Chapter 2.7.2.1.3 --- Treatment cost --- p.51
Chapter 2.7.2.1.4 --- Cost saved for avoided CVD events --- p.52
Chapter 2.7.2.2 --- Components of screening cost from health system’s perspective --- p.52
Chapter 2.7.3 --- Number of CVD events avoidable --- p.53
Chapter 2.8 --- Statistical analysis --- p.54
Chapter 2.8.1 --- Descriptive analysis --- p.54
Chapter 2.8.2 --- Cross-tabulation analysis --- p.54
Chapter 2.8.3 --- Survey data analysis --- p.54
Chapter 3 --- Results --- p.57
Chapter 3.1 --- Description of data --- p.57
Chapter 3.1.1 --- The UK population --- p.57
Chapter 3.1.1.1 --- Sumamry of CVD risk and risk factors --- p.57
Chapter 3.1.1.2 --- Distribution of age --- p.57
Chapter 3.1.1.3 --- Distribution of blood pressure and blood cholesterol --- p.58
Chapter 3.1.1.4 --- Distribution of the predicted 10-year CVD risk --- p.62
Chapter 3.1.1.5 --- Relation between the risk threshold and age --- p.63
Chapter 3.1.2 --- The Chinese population --- p.65
Chapter 3.1.2.1 --- Summary of CVD risk and risk factors --- p.65
Chapter 3.1.2.2 --- Distribution of age --- p.65
Chapter 3.1.2.3 --- Distribution of blood pressure and blood cholesterol --- p.66
Chapter 3.1.2.4 --- Distribution of the predicted 10-year CVD risk --- p.69
Chapter 3.1.2.5 --- Relation between the risk threshold and age --- p.70
Chapter 3.2 --- Performance of our new screening model --- p.72
Chapter 3.2.1 --- Performance according to cholesterol values in the UK population --- p.72
Chapter 3.2.2 --- Performance according to treatment cut-offs in the UK population --- p.73
Chapter 3.2.3 --- Performance according to cholesterol values in the Chinese population --- p.73
Chapter 3.2.4 --- Performance according to the risk cut-offs in the Chinese population --- p.74
Chapter 3.2.4 --- Performance using different risk equations --- p.76
Chapter 3.3 --- Comparison with other existing screening models --- p.77
Chapter 3.3.1 --- Performance of the 3 models within an age-restricted UK population --- p.79
Chapter 3.3.2 --- Performance of the 3 models within an age-restricted Chinese population --- p.81
Chapter 3.3.3 --- Performance of the 3 models in the entire UK population --- p.83
Chapter 3.3.4 --- Performance of the 3 models in the entire Chinese population --- p.84
Chapter 3.3.5 --- Costs of various screening options --- p.87
Chapter 3.3.6 --- Number of CVD events avoidable of the screening programmes --- p.92
Chapter 4 --- Discussion --- p.96
Chapter 4.1.1 --- Performance at different hypothetical cholesterol values --- p.96
Chapter 4.1.2 --- Performance at various treatment cut-off thresholds --- p.97
Chapter 4.1.3 --- Performance with different risk equations --- p.98
Chapter 4.1.4 --- Performance in different populations --- p.99
Chapter 4.1.5 --- Performance with different survival functions --- p.99
Chapter 4.2 --- Further modifications of the model --- p.100
Chapter 4.2.1 --- A model without any cholesterol measurement --- p.100
Chapter 4.2.2 --- Age restriction for selective models --- p.102
Chapter 4.2.3 --- Our model with potential personalized treatment cut-off --- p.103
Chapter 4.2.4 --- Three key things to ensure model performance in other population --- p.104
Chapter 4.3 --- CVD events preventable --- p.105
Chapter 4.3.1 --- Importance of age restriction --- p.105
Chapter 4.3.2 --- Limitations of the NICE model --- p.106
Chapter 4.4 --- Costs of different screening models --- p.107
Chapter 4.4.1 --- Cost from different perspectives --- p.107
Chapter 4.4.2 --- Cholesterol measurement cost and routine data collection --- p.108
Chapter 4.4.3 --- Cost components --- p.109
Chapter 4.4.4 --- Ways to reduce cholesterol measurement costs --- p.109
Chapter 4.4.5 --- Costs and gain of the missing 2.5% high risk individuals --- p.109
Chapter 4.5 --- Strengths and limitations of this study --- p.110
Chapter 4.6 --- Recommendations --- p.113
References --- p.114

D.Litt. et Phil.
This research investigated the effectiveness of the treatment programme used by the South African Recurrent Coronary Prevention Project (SARCPP) in reducing the risk of not only recurrent heart disease, but also of original occurrence of heart disease. Heart disease can often be attributed to lifestyle factors such as obesity, high fat content diets and smoking (Friedman & Ulmer, 1995 and Richards & Baker, 1988). Another lifestyle risk factor of heart disease is Type A behaviour, as first discovered by Rosenman and Friedman (1959). Type A behaviour is made up of various components, such as hostility, time urgency and insecurity. The SARCPP has effectively reduced Type A behaviour in past studies (Venter, 1993; Viljoen, 1993; MacLennan, 1994 and Webster, 1994) and it has been found that reducing Type A behaviour through this programme increases high density lipoproteins and decreases total triglycerides, thus decreasing physiological risk factors of heart disease (Wolff, Thoresen, Viljoen, & Venter, 1994). The SARCPP thus far had only been used with Type A persons who had already suffered a form of heart disease, such as myocardial infarction and angina pectoris (here called "unhealthy" Type As). Other interventions have been used to decrease Type A behaviour in subjects who had not yet suffered heart disease (or "healthy" Type As). A leading researcher in this field is Ethel Roskies (1979-1990). Due to ineffective measurement and ineffective treatment programmes, her attempts were not successful, though. This research study applied the treatment used in the SARCPP to both "healthy" and "unhealthy" Type As and it was found that it was as successful in reducing Type A behaviour in both the "healthy" subjects as in the "unhealthy" subjects. Not only was global Type A behaviour as measured by the Videotaped Structured Interview decreased in the treatment groups, but so were the components of Hostility, Time Urgency and Insecurity (although Insecurity was not decreased in the "unhealthy" subjects). The tendency by the subjects to repress angry feelings was reduced in both "unhealthy" and "healthy" subjects, as was cynical hostility in the "healthy" subjects. It was found that the "unhealthy" subjects had significantly more State and Trait anxiety before the treatment took place than the "healthy" subjects and that the treatment reduced that anxiety in the "unhealthy" subjects significantly. Depression was decreased in both "healthy" and "unhealthy" subjects. Thus, the treatment programme of the SARCPP was effective in reducing coronary-prone behavioural factors and can be used as both prevention in recurrence and prevention in original occurrence of heart disease.

Dissertation
The aim of this study was to determine the knowledge of persons with hypertension in a selected geographical area regarding cardiovascular risk factors in order to make recommendations for patient education. A quantitative, non-experimental, descriptive study was done in the form of a survey using a questionnaire as measuring instrument. The population was hypertensive patients from selected private medical practices in the western part of KwaZulu-Natal and the bordering eastern part of the Free State. Convenience sampling was used and 46 respondents participated in the study. Only 16 (35%) of the respondents achieved a percentage on or above the competency indicator of 50%. Respondents performed worst in questions where definitions, for example hypertension, were assessed. Recommendations for a patient education document, nursing practice and further research were made.
Health Studies
M.A. (Health Studies)

Chan, Po Tai.
Thesis (Ph.D.)--Chinese University of Hong Kong, 2011.
Includes bibliographical references (leaves 128-150).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstract also in Chinese; some appendixes in Chinese.