Sammanfattning Bakgrund: Hjärtinfarkt är ett akut tillstånd och är den vanligaste enskilda orsaken till dödsfall i Sverige. Vid en hjärtinfarkt uppstår en syrebrist i hjärtmuskeln och omedelbar behandling krävs dock väljer många patienter att inte söka akut vård i tid. Kvinnors får atypiska symtom vilket kan bidra till en fördröjd vård.  Syfte: Syftet med denna litteraturstudie var att beskriva kvinnors upplevelse att drabbas av hjärtinfarkt. Metod: Beskrivande litteraturstudie. Tio vetenskapliga artiklar med kvalitativ ansats användes i resultatet.  Huvudresultat: Resultatet visade att kvinnor ofta upplever diffusa och atypiska symtom, vilket ledde till en svårighet att associera symtomen till en hjärtinfarkt. Kvinnorna förminskade ofta symtomen i hopp om att dessa skulle försvinna och utövade många copingstrategier för att hantera symtomen. Kvinnorna väntade med att söka vård tills symtomen blev outhärdliga och blev då ofta uppmanade av anhöriga att söka vård. Många kvinnor upplevde en rädsla för att bli kallad hypokondriker vid uppsökande av vård. Resultatet beskrevs i fyra teman: Kvinnors upplevelse av symtom vid hjärtinfarkt, Kvinnors upplevelse av förnekelse/förminskning av symtomen vid hjärtinfarkt, Kvinnors upplevelse av oro och rädsla i samband med hjärtinfarkt och Kvinnors upplevelser och copingstategier som bidrog till en fördröjd vård. Slutsats: Kvinnor upplevde en svårighet att associera sina symtom till en hjärtinfarkt. Kvinnornas diffusa och otydliga symtom bidrog till en fördröjd vård. Kvinnorna upplevde en rädsla och oro att bli ignorerad och inte bli tagen på allvar av sjukvården i samband med hjärtinfarkten.    Nyckelord: Hjärtinfarkt, kvinnor, upplevelser. / Abstract Background: Myocardial infarction is an acute condition and the most common single cause of death in Sweden. In the event of a myocardial infarction, a lack of oxygen occurs in the heart muscle and immediate treatment is required, however, many patients choose not to seek emergency care in time. Women get atypical symptoms, which can contribute to delayed treatment. Aim: The aim of this literature study was to describe women's experience of suffering a myocardial infarction.Method: Descriptive literature study. Ten scientific articles with a qualitative approach were used in the result. Main Results: The result showed that women often experience diffuse and atypical symptoms, which led to a difficulty in associating the symptoms with a myocardial infarction. The women often downplayed the symptoms in the hope that they would go away and used many coping strategies to deal with the symptoms. The women waited to seek care until the symptoms became unbearable and were then often urged by relatives to seek medical care. Many women experienced a fear of being called a hypochondriac when seeking care. The results were described in four themes: Women's experience of symptoms during a myocardial infarction, Women's experience of denial/reduction of symptoms during a myocardial infarction, Women's experience of anxiety and fear associated with myocardial infarction and Women's experiences and copingstategies that contributed to delayed care.  Conclusion: Women experienced a difficulty in associating their symptoms with a myocardial infarction. The women's diffuse and unclear symptoms contributed to delayed care. The women experienced a fear and worry of being ignored and not being taken seriously by the healthcare system in connection with the myocardial infarction.     Keywords: Experiences, myocardial infarction, women

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<p>Background: Genome wide association studies (GWAS) performed in Caucasian populations have identified several single nucleotide polymorphisms (SNPs) associated with coronary artery disease (CAD), although their cumulative impact in other ethnicities is unknown. Using a genetic risk score (GRS), we examined the impact of CAD related SNPs on myocardial infarction (MI) in a multi-ethnic population.</p> <p>Methods: We included 4083 MI cases and 4473 controls from the INTERHEART case: control study, stratified by six ethnic groups: European, South Asian, other Asian, Arab, Latin American, and African. We created a GRS comprised of 25 SNPS, and tested its association with MI in individual ethnicities using logistic regression, and across ethnic groups through meta-analyses. Results were adjusted for age, sex, and modifiable risk factors.</p> <p>Results: The GRS was significantly associated with MI in Europeans (odds ratio [OR] = 1.08, 95% confidence interval [CI] 1.04-1.12 per risk allele), South Asians (OR = 1.09, 95% CI 1.05-1.14), other Asians (OR = 1.09, 95% CI 1.04-1.15), and Arabs (OR = 1.07, 95% CI 1.03-1.12). In Latin Americans and Africans the GRS was not significant. Meta-analysis of ethnic groups demonstrated a 1.06 (95% CI 1.03-1.09) increase in the odds of MI with the GRS per risk allele. Significant heterogeneity was observed, which was reduced by exclusion of Latin Americans (I2=63% to 0%). Above clinical risk factors, the GRS modestly increased population attributable risk (PAR) (0.92 to 0.94), concordance statistic (0.73 to 0.74), net reclassification improvement (0.14), and integrated discriminatory improvement (0.007).</p> <p>Conclusions:<strong> </strong>The GRS was associated with a significant increase in the odds of MI in multiple ethnic groups. Improvements in PAR, discrimination and reclassification were modest above clinical factors.</p> / Master of Science (MSc)

Neutrophils are thought to orchestrate myocardial remodeling during the early progression to cardiac failure through the release of reactive oxygen species, antimicrobial peptides, and proteases. Although neutrophil activation may be beneficial at early stages of disease, excessive neutrophil infiltration detrimentally leads to cardiomyocyte death and tissue damage. The neutrophil-derived serine protease cathepsin G (CG) has been shown to induce neonatal rat cardiomyocyte detachment and apoptosis by anoikis1. However the role of inflammatory serine proteases in cardiac remodeling and cardiac regeneration in-vivo is still unknown. We showed that cardiac injection of neutrophil derived protease led to early cardiac dilatation and dysfunction characterized by an increase in matrix metalloprotease (MMP) activation and extracellular matrix degradation along with an increase in myocyte death by apoptosis. To assess the role of these serine proteases, we used mice lacking dipeptidyl peptidase I (DPPI), an enzyme involved in major inflammatory protease activation. DPPI deficient mice demonstrated a more robust functional recovery after ischemia reperfusion (IR) and myocardial infarction (MI) injury, as well as significantly reduced myocyte apoptosis, cardiac dilatation, infarct size and mortality rate. Meanwhile, our data showed increased groups of cardiac stem cells and proliferating cardiac cells in the MI 7-days DPPI knockout mice. We also found enhanced DPPI expression in response to pathological stress stimuli in mice. These findings reveal an unrecognized role of DPPI as a key mediator of post-ischemia cardiac injury and show that inflammatory derived proteases may contribute to the pathological cardiac remodeling and cardiac regeneration, and may be considered as novel target for future therapies. / Physiology

Rationale: Autologous bone marrow- or cardiac-derived stem cell therapy for heart disease has demonstrated safety and efficacy in clinical trials but has only offered limited functional improvements. Finding the optimal stem cell type best suited for cardiac regeneration remains a key goal toward improving clinical outcomes. Objective: To determine the mechanism by which novel bone-derived stem cells support the injured heart. Methods and Results: Cortical bone stem cells (CBSCs) and cardiac-derived stem cells (CDCs) were isolated from EGFP+ transgenic mice and were shown to express c-kit and Sca-1 as well as 8 paracrine factors involved in cardioprotection, angiogenesis and stem cell function. Wild-type C57BL/6 mice underwent sham operation (n=21) or myocardial infarction (MI) with injection of CBSCs (n=57), CDCs (n=31) or saline (n=57). Cardiac function was monitored using echocardiography with strain analysis. EGFP+ CBSCs in vivo were shown to express only 2/8 factors tested (basic fibroblast growth factor and vascular endothelial growth factor) and this expression was associated with increased neovascularization of the infarct border zone. CBSC and CDC therapy improved survival, cardiac function, attenuated adverse remodeling, and decreased infarct size relative to saline-treated MI controls. CBSC treated animals showed the most pronounced improvements in all parameters. By 6 weeks post-MI, EGFP+ cardiomyocytes, vascular smooth muscle cells and endothelial cells could be identified on histology in CBSC-treated animals but not in CDC-treated animals. EGFP+ myocytes isolated from CBSC-treated animals were smaller, more frequently mononucleated, and demonstrated fractional shortening and calcium currents indistinguishable from EGFP- myocytes from the same hearts. Conclusions: CBSCs improve survival, cardiac function, and attenuate remodeling more so than CDCs and this occurs through two mechanisms: 1) secretion of the proangiogenic factors bFGF and VEGF (which stimulates endogenous neovascularization), and 2) differentiation into functional adult myocytes and vascular cells. / Physiology

In cellular MRI, micrometer-sized iron oxide particles (MPIO) are a more sensitive contrast agent for tracking inflammatory-cell migration compared to ultra-small superparamagnetic iron oxide particles (USPIO). Inflammation, which promotes adverse tissue remodeling, is known to occur in the viable myocardium adjacent to the necrosed area after a myocardial infarction (MI). This study investigated the temporal relationship between inflammatory cell infiltration and cardiac function during tissue remodeling post-MI using MPIO-enhanced MRI. The MPIO were injected into 7 C57Bl/6 mice (MI+MPIO group) via intravenous administration. The MI was induced 7 days post-MPIO injection. As control groups, 7 mice (Sham+MPIO group) underwent sham-operated surgery without myocardial injury post-MPIO injection and another 6 mice (MI-MPIO group) underwent MI surgery without MPIO injection. MRIs performed post-MI showed a significant signal attenuation at the MI zone in the MI+MPIO group compared to the control groups. The findings suggested that the inflammatory cells containing MPIO infiltrated into the myocardial injury site. Cardiac function was also measured and correlated with the labeled-cell infiltration at the MI site. This study demonstrated a noninvasive technique for monitoring inflammatory cell migration using the MPIO contrast agent. This MPIO-enhanced MRI technique could provide additional insight concerning cardiac disease progression that would improve therapeutic treatment for MI patients.