Mindin (Spondin 2) is a highly conserved extracellular matrix protein of the Mindin-F-spondin family and a regulator of host innate immunity. Despite its expression in the heart, its role in cardiac stress response is unknown. The objective of this study was to determine the role of mindin following myocardial infarction (MI). C57/BL6 wild-type (mindin+/+) or mindin knockout (mindin-/-) mice were randomized to permanent left anterior descending (LAD) coronary artery ligation or sham operation. Mindin expression level increased maximally on day 7 post MI, but returned to baseline by day 28. Mindin-/- mice showed reduced mortality, rupture rate, cardiac MMP-9/-2 activities, NF-kB activation, cytokines and macrophage recruitment. We concluded that mindin is a significant contributor to mortality and acute adverse remodeling post MI, partly through its unique attributes of innate immune regulator and inhibitor of angiogenesis. Mindin may function as a potential biomarker or therapeutic target post MI.

Mindin (Spondin 2) is a highly conserved extracellular matrix protein of the Mindin-F-spondin family and a regulator of host innate immunity. Despite its expression in the heart, its role in cardiac stress response is unknown. The objective of this study was to determine the role of mindin following myocardial infarction (MI). C57/BL6 wild-type (mindin+/+) or mindin knockout (mindin-/-) mice were randomized to permanent left anterior descending (LAD) coronary artery ligation or sham operation. Mindin expression level increased maximally on day 7 post MI, but returned to baseline by day 28. Mindin-/- mice showed reduced mortality, rupture rate, cardiac MMP-9/-2 activities, NF-kB activation, cytokines and macrophage recruitment. We concluded that mindin is a significant contributor to mortality and acute adverse remodeling post MI, partly through its unique attributes of innate immune regulator and inhibitor of angiogenesis. Mindin may function as a potential biomarker or therapeutic target post MI.

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

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Zusammenfassung der Arbeit Dissertation zur Erlangung des akademischen Grades Dr. med. Zusammenhang zwischen dem sozioökonomischem Status und der Entwicklung akuter ST – Strecken – Elevations – Myokardinfarkte eingereicht von Susanne Seide, geb. Gärtner, 02.12.1979 in München angefertigt am Institut für Herz- und Kreislaufforschung des Klinikum Links der Weser Bremen Klinik für Kardiologie und Angiologie Senator Wessling Strasse 1 28277 Bremen Betreuer: Prof. Dr. med. Rainer Hambrecht eingereicht im Februar 2015 An der Entwicklung der koronaren Herzkrankheit und dem damit verbundenen Auftreten akuter ST – Strecken – Elevations – Myokardinfarkte sind neben klassischen Risikofaktoren wie Bluthochdruck, Rauchen, Diabetes mellitus, Übergewicht und Fettstoffwechselstörungen andere Faktoren, wie Alter, Geschlecht, Bewegungsmangel und der psychosoziale Status beteiligt. Frühere Untersuchungen haben darüber hinaus gezeigt, dass die Entwicklung kardiovaskulärer Erkrankungen in einem Zusammenhang mit dem sozioökonomischen Hintergrundes steht. Inwieweit die Zugehörigkeit zu einer bestimmten sozialen Schicht Einfluss auf die Infarktrate der Bremer Bevölkerung hat, und ob es Unterschiede im Risikoprofil, in der Behandlung und Prognose von Patienten aus unterschiedlichen sozialen Milieus gibt, sollte mit dieser Arbeit untersucht werden. Hierzu wurden Daten von 2062 Patienten aus dem STEMI Register des Herzzentrums Bremen ausgewertet. Die Patienten aus dem Stadtgebiet Bremen wurden anhand der Postleitzahl ihrer Heimatadresse einer von vier Gruppen zugeordnet. Hiernach wurde für sie ein hoher sozioökonomischer Status (G1), ein intermediär hoher sozioökonomischer Status (G2), ein intermediär niedrig sozioökonomischer Status (G3) oder ein niedriger sozioökonomischer Status (G4) ermittelt. Der sozioökonomische Status der jeweiligen Gruppe wurde mit Hilfe des so genannten „Bremer Benachteiligungsindexes“, einem Maß für die soziale Stellung eines Stadtteiles, und anhand von Einkommensstatistiken der Bremer Stadtteile bestimmt. Die vier Gruppen wurden hinsichtlich ihrer Infarktinzidenzen verglichen. Innerhalb der Patientengruppen wurden Baselinecharakteristika (Alter zum Infarktzeitpunkt, Geschlecht, Vorerkrankungen, kardiovaskuläre Risikofaktoren), Surrogat – Parameter der Krankheitsausprägung (Mehrgefäßerkrankung, hämodynamische Stabilität, linksventrikuläre Ejektionsfraktion nach Myokardinfarkt), und der Therapie (PTCA, ACVB – Operation, Door – to – balloon Zeiten und Medikamentengabe) sowie Prognosedaten (30 Tage – Mortalität, 5 Jahres – Überleben) erhoben und die Gruppen anhand dieser Ergebnisse miteinander verglichen. Die wesentlichen Ergebnisse lassen sich wie folgt zusammenfassen: ➢ Die alters- und geschlechtsadjustierte Inzidenz akuter transmuraler Myokardinfarkte war in den sozial benachteiligten Bremer Stadtteilen signifikant höher als in Stadtbezirken mit geringerer Benachteiligung (G1: 47 ± 5 STEMIs pro 100.000 Einwohner pro Jahr versus G4: 66 ± 5 STEMIs pro 100.000 Einwohner pro Jahr; p < 0,01). ➢ Insbesondere junge Menschen waren von diesem sozialen Abwärtsgradienten betroffen (18 – 49 Jahre RR G4 2,01 versus 65 – 79 Jahre RR G4: 1,39). ➢ Herzinfarktpatienten aus sozial benachteiligten Stadtteilen waren zum Infarktzeitpunkt signifikant jünger (G1: 67±13 Jahre versus G4: 63±13 Jahre; p = 0,026), häufiger Raucher (G1: 35,9% versus G4: 51,2%; p < 0,01) und übergewichtig (G1:.15,3% BMI > 30 kg/qm versus G4: 26,1% BMI > 30 kg/qm; p < 0,01). ➢ Bezüglich der Infarktschwere und der Therapie zeigten sich keine wesentlichen Unterschiede zwischen den Gruppen (Mehrgefäßerkrankung G1: 62,4% versus G4: 57,0%; p = 0,27; Killip – Stadium III/IV G1: 12,5% versus G4: 13,0%; p = 0,84; LVEF nach Myokardinfarkt < 30% G1: 6,0% versus G4: 7,6%; p = 0,4; primäre PTCA G1: 89,8% versus G4: 89,8%; p = 0,92; ACVB - Operation G1: 11,6% versus G4: 12,6%; p = 0,13; Door – to – balloon Zeit G1: 54±38 min. versus G4 52±41 min.; p = 0,74; ASS G1: 94,4% versus G4: 94,7%; p = 0,64; ADP – Antagonist G1: 90,0% versus G4: 93,8%;p = 0,23; Betablocker G1 82,8% versus G4 83,9%; p = 0,25; Statin G1: 85,8% versus G4: 86,4%; p = 0,97; ACE – Hemmer oder AT1 – Rezeptorantagonisten G1: 77,4% versus G4: 79,3%; p = 0,90). ➢ Die alters– und geschlechtsadjustierte inhospitale Mortalität war in allen Gruppen vergleichbar hoch (G1: 4,8% versus G4: 3,9%; p = 0,3), für Patienten aus den sozioökonomisch am stärksten benachteiligten Stadtgebieten zeigte sich aber ein starker Trend hin zu einem geringeren 5 Jahres – Überleben (G4 versus G1: HR 1,55, 95% KI 0,98-2,5, p = 0,067). Die Ergebnisse dieser Studie demonstrieren, dass das relative Risiko für einen ST – Strecken – Elevations – Myokardinfarkt mit abnehmendem sozioökonomischem Status der Bevölkerung steigt, und dass das kardiovaskuläre Risikoprofil von Patienten aus sozioökonomisch benachteiligten Stadtteilen ausgeprägter ist. Trotz gleicher Initialtherapie aller STEMI Patienten, unabhängig von der sozialen Herkunft, haben diejenigen aus sozioökonomisch benachteiligten Wohnbezirken eine deutlich schlechtere Prognose. Daher besteht unseres Erachtens vor allem in den sozioökonomisch benachteiligten Stadtteilen nicht nur in Bremen ein erhöhter Handlungsbedarf hinsichtlich konsequenter primär– und sekundärpräventiver Maßnahmen.

Background:  Peri-operative myocardial infarction (PMI) may be under- and/or mis-diagnosed because WHO criteria are often not met and creatinine kinase (CK/CK-MB) ratios can be difficult to interpret.  Cardiac troponin (cTn) I is the most sensitive and specific marker of myocardial cell necrosis but is not yet widely available. Aims: 1.  To examine the use of pre-operative risk indices, including ASA score, POSSUM score and Goldman’s cardiac risk index and compare these with peri-operative cTnI rise. 2.  To compare cTnI levels with CK/CK-MB levels peri-operatively in the diagnosis of MI. 3.  To explore the role of the fibrinolytic system in patients undergoing emergency surgery for ruptured aneurysm and relate this to cTnI levels. 4.  To examine the use of the polymerase chain reaction (PCR) in the identification of bacteraemia and to relate this to systemic endotoxin levels and septic episodes. Methods:  Prospective observational study of 67 patients undergoing aortic surgery (29 elective AAA, 31 emergency AAA, 7 aorto-occlusive).  cTnI and endotoxin were measured pre-operatively and at 6, 24, 48, 72 and 96 hours post­operatively.  Blood for PCR was also collected at these time points.  CK and CK-­MB were measured where cTnI was detectable.  Fibrinolytic markers were measured up to 24 hours post operatively.  Clinical, septic, ECG and cardiac events were prospectively documented. Results:  ASA score was correlated with perioperative cTnI rise.  Over 50%<i> </i>of patients undergoing emergency, and more than a quarter undergoing elective, aortic surgery will suffer myocardial injury as determined by cTnI rise.  This is accompanied by CK/ CK-MB ratio in less than a fifth of cases.  eTnI rise is associated with inhibition of fibrinolysis with emergency AAA repair.  No relationships were observed with the presence of bacterial DNA, endotoxin response and sepsis.

Myocardial infarction is the most common cause of heart failure and remains one of the leading causes of morbidity and mortality in humans. Stem cells are important in the maintenance and repair of adult tissues. Hoechst effluxing cells, termed side population cells are a rare subset of cells found in adult tissues that are highly enriched for stem and progenitor cell activity. Recent studies have suggested that Sca-1+/CD31- cardiac side population cells are capable of differentiation into cardiomyocytes in vitro. However, the response of cardiac side population cells to myocardial injury remains unknown in vivo. In this study, we directly transplanted Sca-1+/CD31- cardiac side population cells into an acutely infarcted mouse heart. After two weeks, the transplanted cells were found to express cardiomyocyte or endothelial cell markers. Importantly, when these cells were transplanted into a remote nonischemic part of the heart after MI, they were able to migrate to the damaged myocardium. Consistent with these cells homing property, we found that SDF-1α, a chemotactic chemokine and its receptor, CXCR4 were up-regulated in the damaged myocardium and on Sca-1+/CD31- cardiac SP cells respectively following an acute myocardial infarction. We further showed that SDF-1α was able to induce migration of Sca-1+/CD31- cardiac side population cells in vitro. Our results have therefore suggested that Sca-1+/CD31- cardiac side population cells are able to migrate to damaged myocardium from non-ischemic myocardium and differentiate into cardiomyocytes as well as endothelial cells in the acutely infarcted mouse heart. We postulate that the SDF-1α/CXCR4 interaction may play an important role in the migration of these cells. Understanding and enhancing these processes may hold enormous potential possibilities for therapeutic myocardial regeneration for the treatment of cardiovascular disease.

Diss. (sammanfattning) Umeå : Umeå universitet, 2006. / Härtill 5 uppsatser.

Thesis (Th. M.)--Calvin Theological Seminary, 1994. / Abstract. Includes bibliographical references (leaves [60-61]).

Thesis (M.S.)--California Polytechnic State University, 2009. / Title from PDF title page; viewed on September 23, 2009. Major professor: Robert Crockett, Ph.D. "Presented to the faculty of California Polytechnic State University, San Luis Obispo." "In partial fulfillment of the requirements for the degree [of] Master of Science in Engineering, with Specializations in Biomedical Engineering." "June, 2009." Includes bibliographical references (p. 54-55). Also available on microfiche.