Background Myocardial Infarction (MI) is one of the major diseases which cause death in the world nowadays. In Hong Kong, 27.7 persons per 100,000 population died from AMI during the years 2007 to 2009. The rate for recurrent MI is also very high and the mortality rate is even higher for recurrent MI cases than first MI attack. Meanwhile, modern lifestyles and convenience brought about by advancements in technology have led to unhealthy lifestyles which is a risk factor for recurrent MI. Prevention of recurrent MI has become highly important and a worldwide public health issue. Patient education is the process by which health professionals provide information to patients or the public aiming to enhance their awareness and, therefore, alter their unhealthy behavior in order to improve their health status. Even nowadays, patient education is a common approach to disease prevention and health promotion in developed countries. Currently, many developed countries use patient education for disease prevention and health promotion. Many studies have investigated the effect of patient education on recurrent MI prevention resulting from proper behavioral change, and some decreases have resulted in recurrent MI after giving patient education. However, there is a gap in the current literature regarding the specialized meta-analysis in the evaluation of effectiveness of patient education conducted within three months or earlier. In other words, the efficiency of patient education to prevent recurrent MI has seldom been assessed. Although there have been a few systemic reviews about patient education in the past, the focus of these studies was not on recurrent MI, but obesity and diabetes. In addition, they discuss the issues in a qualitative manner, and omit calculations of the relative risk or summarized odds ratio. Therefore, this meta-analysis aims to generate statistics on the evaluation of the positive impact resulting from early patient education on recurrent MI prevention. Aim The current study aimed to assess the effect of early post-MI education in preventing the recurrence of myocardial infarction. Objective The current systematic review aimed to evaluate the relation between the occurrence of recurrent MI, which is evidenced by hospitalization, in addition to consultation with medical professionals, and the provision of early patient education. Method Studies were identified through searching e-databases including MEDLINE (Ovid), PUBMED, Cochrane library and EMBASE. Two reviewers searched the databases independently. Keywords included “recurrent heart attack”, “recurrent myocardial infarction”, “post MI education”, “prevention of myocardial infarction”, “cardiac rehabilitation on MI” when searching the databases. Only studies fulfilling the inclusion criteria were chosen in this meta-analysis. Randomized control trials were selected and included in meta-analysis after the screening and filtering process. Other study methods such as case control study and cohort study were not included in this meta-analysis. All studies selection included in this meta-analysis had to follow strictly the PRISMA 2009 guideline. Quality assessments were also performed by using CONSORT 2010 checklists. Results Eight randomized controlled trials were selected for this meta-analysis. The meta-analysis evaluated the effect of receiving early patient education on prevention of future recurrence of MI by comparing with control subjects. Patients who received early patient education showed a reduction of risk of recurrent myocardial infarction by 3% to 100%; the summarized relative risk of the interventional group was 0.80compared with the control group. This means there resulted a 20% reduction in recurrent MI. Conclusion Early patient education was shown to have a positive effect on the prevention of recurrent MI in this meta-analysis. Compared with the usual care in today’s hospital and medical system, we should provide more early patient education to patients with myocardial infarction for recurrent MI prevention. In light of this meta-analysis, I recommend the government to invest more funds and manpower in patient education at both hospital and clinical levels. / published_or_final_version / Public Health / Master / Master of Public Health

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.