OBJECTIVES: The goal of this study was to investigate trends in admission to the emergency department and the use of invasive or surgical procedures during hospitalization for acute myocardial infarction (AMI) in Korea. METHODS: The National Health Insurance (NHI) claims database between 2007 and 2011 was used. We identified all admission claims that included codes from the tenth revision of the International Classification of Diseases beginning with I21 as the primary or secondary diagnosis. Information about the admission route, admission date, discharge date, and whether coronary artery angiography, angioplasty, or bypass surgery was performed was also obtained from the NHI database. RESULTS: Of the 513,886 relevant admission claims over the five years encompassed by this study, 295,001 discrete episodes of admission for AMI were identified by analyzing the date and length of each admission and the interval between admissions. The number of AMI admissions gradually decreased from 66,883 in 2007 to 47,656 in 2011. The number and proportion of admissions through the emergency department also decreased from 38,118 (57.0%) in 2007 to 24,001 (50.4%) in 2011. However, during the same period, admissions in which invasive or surgical procedures were performed increased from 15,342 (22.9%) to 17,505 (36.7%). CONCLUSIONS: The reported numbers of emergency department visits and admissions for AMI decreased from 2007 to 2011. However, only a small portion of the patients underwent invasive or surgical procedures during hospitalization, although the number of admissions involving invasive or surgical procedures has increased. These findings suggest that simply counting the number of admission claims cannot provide valid information on trends in AMI occurrence.
Angiography ; Angioplasty ; Coronary Vessels ; Diagnosis ; Emergency Service, Hospital ; Hospitalization* ; Humans ; International Classification of Diseases ; Korea ; Myocardial Infarction* ; National Health Programs* ; Vascular Surgical Procedures

We demonstrated previously that Coptidis rhizoma extract (CRE) prevented S-nitroso-N-acetylpenicillamine-induced apoptotic cell death via the inhibition of mitochondrial membrane potential disruption and cytochrome c release in RINm5F (RIN) rat insulinoma cells. In this study, the preventive effects of CRE against cytokine-induced beta-cell death was assessed. Cytokines generated by immune cells infiltrating pancreatic islets are crucial mediators of beta-cell destruction in insulin-dependent diabetes mellitus. The treatment of RIN cells with IL-1beta and IFN-gamma resulted in a reduction of cell viability. CRE completely protected IL-1beta and IFN-gamma-mediated cell death in a concentration-dependent manner. Incubation with CRE induced a significant suppression of IL-1beta and IFN-gamma-induced nitric oxide (NO) production, a finding which correlated well with reduced levels of the iNOS mRNA and protein. The molecular mechanism by which CRE inhibited iNOS gene expression appeared to involve the inhibition of NF-kappa B activation. The IL-1beta and IFN-gamma-stimulated RIN cells showed increases in NF-kappa B binding activity and p65 subunit levels in nucleus, and IkappaBalpha degradation in cytosol compared to unstimulated cells. Furthermore, the protective effects of CRE were verified via the observation of reduced NO generation and iNOS expression, and normal insulin-secretion responses to glucose in IL-1beta and IFN-gamma-treated islets.
Animals ; Cell Death/drug effects ; Cell Line ; Cell Nucleus/metabolism ; Cell Survival/drug effects ; Drugs, Chinese Herbal/*pharmacology ; Gene Expression Regulation, Enzymologic/drug effects ; Glucose/pharmacology ; I-kappa B Proteins/metabolism ; Insulin/secretion ; Insulin-Secreting Cells/*cytology/*drug effects/enzymology ; Interferon-gamma/*pharmacology ; Interleukin-1beta/*pharmacology ; Male ; NF-kappa B/*metabolism ; Nitric Oxide/biosynthesis ; Nitric Oxide Synthase Type II/genetics/metabolism ; Protein Transport/drug effects ; RNA, Messenger/genetics/metabolism ; Rats ; Rats, Sprague-Dawley