Heart disease including ischemic heart disease is the highest contributor to death and morbidity in the western world. The studies presented were conducted to determine possible pathways of protection of the heart against ischemia/reperfusion. We employed adenovirus mediated over-expression of Methionine sulfoxide reductase A (MsrA) in primary neonatal rat cardiac myocytes to determine the effect of this enzyme in protecting against hypoxia/reoxygenation. Cells transfected with MsrA encoding adenovirus and subjected to hypoxia/reoxygenation exhibited a 45% decrease in apoptosis as compared to controls. Likewise total cell death as determined by levels of Lactate Dehydrogenase (LDH) release was dramatically decreased by MsrA overexpression. The initial hypothesis that led to our testing sulindac was based on the fact that the S epimer of sulindac was a substrate for MsrA and that this compound might function as a catalytic anti-oxidant based on a reaction cycle that involved reductio n to sulindac sulfide followed by oxidation back to sulindac. To test this we examined the protective effect of sulindac in hypoxia re-oxygenation in both cardiac myocytes in culture and using a Langendorff model of myocardial ischemia. Using this model of myocardial ischemia we showed that pre-incubation of hearts with sulindac, or the S and R epimers of sulindac resulted in protection against cell death. We present several lines of evidence that the protective effect of sulindac is not dependent on the Msr enzyme system nor does it involve the well established role of sulindac as a Cyclooxygenase (COX) inhibitor. Numerous signaling pathways have been implicated in myocardial protective mechanisms, many of which require fluctuations in ROS levels as initiators or mediators. / Sulindac shows very good potential as a preconditioning agent that could induce tissue protection against oxidative damage.Blocking of preconditioning pathways by administration of the PKC blocker chelerythine abrogated the ischemic protection afforded by sulindac. Secondly, an end-effector of preconditioning, inducible nitric oxide synthase (iNOS),was found to be induced by greater than 5 fold after 48 h prior feeding sulindac. / by Ian Moench. / Thesis (Ph.D.)--Florida Atlantic University, 2008. / Includes bibliography. / Electronic reproduction. Boca Raton, Fla., 2008. Mode of access: World Wide Web.

Tam Wing Yin. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2004. / Includes bibliographical references (leaves 82-100). / Abstracts in English and Chinese. / English abstrac --- p.I / 中文摘要 --- p.VI / Glossary --- p.X / Chapter Chapter 1. --- Background: / Chapter 1.1. --- Coronary heart disease in Hong Kong --- p.1 / Chapter 1.2. --- Coronary heart disease and atherosclerosis --- p.2 / Chapter 1.3. --- Pathogenesis of atherosclerosis --- p.2 / Chapter 1.4. --- Risk factors for atherosclerosis --- p.5 / Chapter 1.5. --- Homocysteine --- p.6 / Chapter 1.6. --- Folate --- p.10 / Chapter 1.7. --- Vitamin B12 --- p.13 / Chapter 1.8. --- Adhesion Molecules --- p.14 / Chapter 1.9. --- Phytoestrogen --- p.17 / Chapter 1.10. --- Secondary prevention of coronary artery disease --- p.20 / Chapter Chapter 2. --- "Heart disease, Danshen and Gegen in Chinese medicine" / Chapter 2.1. --- The record of Cardiac symptoms in Chinese Medicine --- p.24 / Chapter 2.2. --- Danshen (Salvia Miltriorrhiza) --- p.25 / Chapter 2.3. --- Gegen (Radix Pueraria) --- p.28 / Chapter Chapter 3. --- Surrogate atherosclerotic markers / Chapter 3.1. --- Flow-mediated dilatation of brachial artery (FMD) --- p.31 / Chapter 3.2. --- Carotid intima media thickness (IMT) --- p.32 / Chapter Chapter 4. --- Method / Chapter 4.1. --- Rational of the study --- p.33 / Chapter 4.2. --- Clinical protocol --- p.35 / Chapter 4.3. --- Measurement of plasma homocysteine --- p.38 / Chapter 4.4. --- Measurement of folate and vitamin B12 --- p.40 / Chapter 4.5. --- Measurement of soluble cellular adhesion molecules (CAMs) --- p.41 / Chapter 4.6. --- Measurement of plasma enterolactone --- p.43 / Chapter 4.7. --- Measurement of plasma hs-C-reactive protein --- p.44 / Chapter 4.8. --- Other laboratory tests --- p.45 / Chapter 4.9. --- High resolution ultrasound imaging --- p.46 / Chapter 4.10. --- Statistical analysis --- p.49 / Chapter 4.11. --- My contribution to this joint project --- p.49 / Chapter Chapter 5. --- Results / Chapter 5.1. --- Recruitment and outcomes of subjects --- p.51 / Chapter 5.2. --- Baseline characteristics --- p.53 / Chapter 5.3. --- Medical history and treatment received in the study subjects --- p.54 / Chapter 5.4. --- Safety profiles --- p.55 / Chapter 5.5. --- Severe adverse events --- p.56 / Chapter 5.6. --- Lipid profiles --- p.57 / Chapter 5.7. --- Secondary endpoints --- p.58 / Chapter 5.8. --- Primary endopoints --- p.59 / Chapter 5.9. --- The effect of statin usage on the primary endpoints / Chapter 5.10. --- The major determinant of the change in FMD by multivariate logistic regression / Chapter 5.11. --- Progress of lipid profiles and primary endpoints in the open label phase / Chapter Chapter 6. --- Discussion / Chapter 6.1. --- Brachial FMD --- p.66 / Chapter 6.2. --- Carotid IMT --- p.69 / Chapter 6.3. --- Brachial GTN --- p.70 / Chapter 6.4. --- Lipid-lowering effect --- p.72 / Chapter 6.5. --- Phytoestrogen --- p.72 / Chapter 6.6. --- Folate --- p.73 / Chapter 6.7. --- Vitamin B12 and glucose --- p.76 / Chapter 6.8. --- Summary of possible anti-atherogenic mechanism of D&G --- p.76 / Chapter 6.9. --- Placebo effect --- p.77 / Chapter 6.10. --- Safety profile --- p.77 / Chapter 6.11. --- Limitation of the study and suggestion of solution --- p.77 / Chapter 6.12. --- Suggestions and ummary of the future work --- p.79 / Chapter Chapter 7. --- Conclusions --- p.81 / References --- p.82

Chung, Jennifer Siu Toye. / "June 2008." / Thesis (M.Phil.)--Chinese University of Hong Kong, 2008. / Includes bibliographical references (leaves 145-157). / Abstracts in English and Chinese, some text in appendix also in Chinese. / Abstract of Thesis in English --- p.i / Abstract of Thesis in Chinese --- p.iii / Acknowledgments --- p.v / List of Tables --- p.xi / List of Figures --- p.xiii / List of Abbreviations --- p.xiv / List of Publications and Presentations related to Thesis --- p.xvi / Contributions related to Thesis --- p.xvii / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Introduction of the Thesis --- p.1 / Chapter 1.2 --- Review on Coronary Heart Disease --- p.3 / Chapter 1.2.1 --- Definition of Coronary Heart Disease --- p.3 / Chapter 1.2.2 --- Risk factors for the development of Coronary Heart Disease --- p.3 / Chapter 1.2.3 --- Worldwide Figures for Coronary Heart Disease --- p.9 / Chapter 1.2.4 --- Coronary Heart Disease in Asia Pacific --- p.10 / Chapter 1.2.5 --- Coronary Heart Disease in Hong Kong --- p.11 / Chapter 1.3 --- Dyslipidaemia --- p.14 / Chapter 1.3.1 --- Lipid Transport and Lipoprotein Metabolism --- p.14 / Chapter 1.3.2 --- Definition and Classification of Dyslipidaemia --- p.16 / Chapter 1.3.3 --- Coronary Heart Disease and Dyslipidaemia --- p.17 / Chapter 1.3.4 --- Lifestyle Modifications for the Management of Dyslipidaemia --- p.19 / Chapter 1.3.4.1 --- Dietary Measures --- p.20 / Chapter 1.3.4.2 --- Cigarette Smoking --- p.23 / Chapter 1.3.4.3 --- Physical Activity --- p.24 / Chapter 1.3.4.4 --- Weight Control --- p.25 / Chapter 1.3.5 --- Lipid-lowering Drug Therapy for Dyslipidaemia --- p.29 / Chapter 1.3.5.1 --- Statins --- p.31 / Chapter 1.3.5.2 --- Bile Acid Sequestrants --- p.35 / Chapter 1.3.5.3 --- Fibrates --- p.36 / Chapter 1.3.5.4 --- Ezetimibe --- p.37 / Chapter 1.3.5.5 --- Nicotinic Acid Group --- p.38 / Chapter 1.4 --- International Guidelines for Dyslipidaemic Management --- p.39 / Chapter 1.4.1 --- National Service Framework for Coronary Heart Disease (UK) --- p.39 / Chapter 1.4.1.1 --- National Service Framework Lipid-lowering Goals --- p.40 / Chapter 1.4.1.2 --- The Joint British Societies' Guidelines --- p.41 / Chapter 1.4.1.3 --- Achievement of the NSF Lipid Profile Targets --- p.42 / Chapter 1.4.2 --- National Cholesterol Education Program (United States) --- p.43 / Chapter 1.4.2.1 --- The Third Report of the National Cholesterol Education Program --- p.43 / Chapter 1.4.2.2 --- Review of Clinical Trials --- p.43 / Chapter 1.4.2.3 --- Low-Density Lipoprotein Cholesterol Goal Targets --- p.46 / Chapter 1.4.2.4 --- Compliance with the NCEP ATP III Guidelines --- p.48 / Chapter 1.4.3 --- Dyslipidaemic Guidelines for Study --- p.51 / Chapter 1.5 --- Clinical Pharmacy Services --- p.52 / Chapter 1.5.1 --- The Healthcare System in Hong Kong --- p.52 / Chapter 1.5.2 --- Clinical Pharmacy Services in Hong Kong --- p.54 / Chapter 1.5.3 --- Examples of successful Clinical Pharmacy Services --- p.55 / Chapter 1.5.3.1 --- Hypertension Clinic --- p.55 / Chapter 1.5.3.2 --- Diabetes Mellitus Clinic --- p.56 / Chapter 1.5.3.3 --- Smoking Cessation Clinic --- p.57 / Chapter 1.5.3.4 --- Anticoagulation Clinic --- p.57 / Chapter 1.5.3.5 --- Haematology-oncology Clinic --- p.57 / Chapter 1.5.4 --- Pharmacist-managed Lipid Clinics --- p.58 / Chapter 1.6 --- Objective & General Aims of the Study --- p.60 / Chapter 1.6.1 --- Objectives --- p.60 / Chapter 1.6.2 --- Study Hypothesis --- p.60 / Chapter 1.6.3 --- General Aims of the Study --- p.60 / Chapter Chapter 2 --- Methodology of Study --- p.62 / Chapter 2.1 --- Background Setting --- p.62 / Chapter 2.2 --- Subject Selection and Recruitment --- p.62 / Chapter 2.3 --- Intervention and Control Groups --- p.63 / Chapter 2.4 --- Validation of Survey --- p.67 / Chapter 2.5 --- Data Collection --- p.67 / Chapter 2.6 --- Outcome Measures --- p.68 / Chapter 2.6.1 --- Lipid value changes --- p.68 / Chapter 2.6.2 --- Compliance rate with medications --- p.68 / Chapter 2.6.3 --- Patient satisfaction survey assessment --- p.69 / Chapter 2.6.4 --- Time spent and Cost of clinical pharmacist --- p.69 / Chapter 2.7 --- Statistical Analysis --- p.70 / Chapter 2.7.1 --- Sample Size Calculation --- p.70 / Chapter 2.7.2 --- Methods of Statistical Analysis --- p.71 / Chapter Chapter 3 --- Results of Study --- p.72 / Chapter 3.1 --- Recruitment Details --- p.72 / Chapter 3.2 --- Demographic Characteristics of Patients --- p.73 / Chapter 3.3 --- Drug Therapy of Patients during Study Period --- p.75 / Chapter 3.4 --- LDL-C Lowering Potency of Statin Doses Prescribed --- p.80 / Chapter 3.5 --- Coronary Heart Disease Risk Category of Patients --- p.84 / Chapter 3.6 --- Lipid Profile Changes --- p.85 / Chapter 3.7 --- NCEP ATP III LDL-C Goal Attainment --- p.87 / Chapter 3.8 --- Relationship between Patient Characteristics and LDL-C Goal Attainment --- p.91 / Chapter 3.9 --- Compliance with Medications --- p.94 / Chapter 3.10 --- Pharmacist Intervention --- p.98 / Chapter 3.10.1 --- Range of Pharmacist Intervention --- p.98 / Chapter 3.10.2 --- Time spent by Pharmacist --- p.100 / Chapter 3.10.2.1 --- Time spent on Documentation --- p.100 / Chapter 3.10.2.2 --- Time spent on Direct Communication with Patients --- p.101 / Chapter 3.10.3 --- Cost of Clinical Pharmacy Service at the Lipid Clinic --- p.102 / Chapter 3.10.3.1 --- Cost of Pharmacist Involvement --- p.102 / Chapter 3.10.3.2 --- Potential Healthcare Cost Saving --- p.103 / Chapter 3.11 --- Clinical Pharmacy Service Satisfaction Survey --- p.105 / Chapter 3.11.1 --- Validation of Survey --- p.105 / Chapter 3.11.2 --- Questionnaire Survey for Intervention and Control Groups --- p.107 / Chapter 3.11.3 --- Physician Questionnaire Survey on Clinical Pharmacy Service --- p.110 / Chapter Chapter 4 --- Discussion --- p.111 / Chapter 4.1 --- Clinical Outcomes of Study --- p.111 / Chapter 4.1.1 --- Changes in Lipid Parameters --- p.111 / Chapter 4.1.2 --- Reduction in CHD risk --- p.113 / Chapter 4.1.3 --- Attainment in NCEP ATP III LDL-C goals --- p.114 / Chapter 4.1.4 --- Predictors for LDL-C Goal Attainment --- p.117 / Chapter 4.2 --- Drug-related Problems --- p.119 / Chapter 4.2.1 --- Statin Dosing and LDL-C Lowering Potency --- p.119 / Chapter 4.2.2 --- Adherence to Drug Therapy --- p.121 / Chapter 4.2.3 --- Polypharmacy --- p.126 / Chapter 4.2.4 --- Adverse Drug Events and Drug Interactions --- p.129 / Chapter 4.2.5 --- Patient Busy Lifestyle --- p.131 / Chapter 4.3 --- Role of Clinical Pharmacist --- p.133 / Chapter 4.3.1 --- Role of Pharmacist --- p.133 / Chapter 4.3.2 --- Multidisciplinary Team --- p.135 / Chapter 4.3.3 --- Healthcare Cost Saving --- p.137 / Chapter 4.4 --- Limitations of Study --- p.139 / Chapter 4.5 --- Further Study --- p.142 / Chapter Chapter 5 --- Conclusion --- p.144 / Chapter 5.1 --- Conclusion of Study --- p.144 / Bibliography --- p.145 / Appendices --- p.158 / Appendix I Data collection form --- p.158 / Appendix II Information sheet on study protocol to patient --- p.160 / Appendix III Patient consent form for study --- p.164 / Appendix IV Framingham risk scoring system for male --- p.165 / Appendix V Framingham risk scoring system for female --- p.166 / Appendix VI Patient educational leaflet --- p.167 / Appendix VII Physician-pharmacist communication sheet --- p.169 / Appendix VIII Telephone checklist --- p.170 / Appendix IX Questionnaire survey provided to Intervention Group --- p.172 / Appendix X Questionnaire survey provided to Control Group --- p.174 / Appendix XI Questionnaire survey provided to Physicians --- p.176

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.