BACKGROUND AND OBJECTIVES: Extracorporeal membrane oxygenation (ECMO) support is increasingly used in primary percutaneous coronary intervention (PCI) during cardiopulmonary resuscitation (CPR) to treat acute myocardial infarction (AMI) patients who experienced cardiogenic shock. However, to date, there have been no studies on the relationship between clinical outcomes and CPR time in such patients with AMI treated by ECMO-assisted primary PCI. METHODS: From July 2008 to March 2016, we analyzed data from 42 AMI with cardiogenic shock patients who underwent CPR and were treated by ECMO-assisted primary PCI. The primary outcome was 30-day in-hospital mortality after primary PCI. The predictors of mortality were determined using a Cox proportional hazards model. RESULTS: Thirty-day in-hospital mortality was observed for 33 patients (78.6%). The mean CPR time was 37.0±37.3 minutes. The best cut-off CPR time value associated with clinical outcome was calculated to be 12.5 minutes using receiver operating characteristic curve analysis. Multivariate analysis revealed that CPR time of > 12.5 minutes was an independent predictor of 30-day mortality (adjusted hazard ratio, 4.71; 95% confidence interval, 1.30–17.406; p=0.018). CONCLUSIONS: Despite ECMO support, the clinical outcomes of AMI patients with a complication of cardiogenic shock remain poor. Prolonged CPR time is associated with a poor prognosis in patients with AMI treated by ECMO-assisted primary PCI.
Cardiopulmonary Resuscitation ; Extracorporeal Membrane Oxygenation ; Hospital Mortality ; Humans ; Membranes ; Mortality ; Multivariate Analysis ; Myocardial Infarction ; Percutaneous Coronary Intervention ; Prognosis ; Proportional Hazards Models ; ROC Curve ; Shock, Cardiogenic

BACKGROUND AND OBJECTIVES: Extracorporeal membrane oxygenation (ECMO) support is increasingly used in primary percutaneous coronary intervention (PCI) during cardiopulmonary resuscitation (CPR) to treat acute myocardial infarction (AMI) patients who experienced cardiogenic shock. However, to date, there have been no studies on the relationship between clinical outcomes and CPR time in such patients with AMI treated by ECMO-assisted primary PCI. METHODS: From July 2008 to March 2016, we analyzed data from 42 AMI with cardiogenic shock patients who underwent CPR and were treated by ECMO-assisted primary PCI. The primary outcome was 30-day in-hospital mortality after primary PCI. The predictors of mortality were determined using a Cox proportional hazards model. RESULTS: Thirty-day in-hospital mortality was observed for 33 patients (78.6%). The mean CPR time was 37.0±37.3 minutes. The best cut-off CPR time value associated with clinical outcome was calculated to be 12.5 minutes using receiver operating characteristic curve analysis. Multivariate analysis revealed that CPR time of > 12.5 minutes was an independent predictor of 30-day mortality (adjusted hazard ratio, 4.71; 95% confidence interval, 1.30–17.406; p=0.018). CONCLUSIONS Despite ECMO support, the clinical outcomes of AMI patients with a complication of cardiogenic shock remain poor. Prolonged CPR time is associated with a poor prognosis in patients with AMI treated by ECMO-assisted primary PCI.

Although the majority of patients with schizophrenia are not actually violent, an increased tendency toward violent behaviors is known to be associated with schizophrenia. There are several factors to consider when identifying the subgroup of patients with schizophrenia who may commit violent or aggressive acts. Comorbidity with substance abuse is the most important clinical indicator of increased aggressive behaviors and crime rates in patients with schizophrenia. Genetic studies have proposed that polymorphisms in the promoter region of the serotonin transporter gene and in the catechol-O-methyltransferase gene are related to aggression. Neuroimaging studies have suggested that fronto-limbic dysfunction may be related to aggression or violence. By identifying specific risk factors, a more efficient treatment plan to prevent violent behavior in schizophrenia will be possible. Management of comorbid substance use disorder may help prevent violent events and overall aggression. Currently, clozapine may be the only effective antipsychotic medication to repress aggressive behavior. With the current medical field moving toward tailored medicine, it is important to identify vulnerable schizophrenia populations and provide efficient treatment.
Aggression ; Antipsychotic Agents ; Catechol O-Methyltransferase ; Clozapine ; Comorbidity ; Crime ; Humans ; Neuroimaging ; Promoter Regions, Genetic ; Risk Factors ; Schizophrenia ; Serotonin Plasma Membrane Transport Proteins ; Substance-Related Disorders ; Violence

L-type Ca2+ channels play an important role in regulating cytosolic Ca2+ and thereby regulating hormone secretions in neuroendocrine cells. Since hormone secretions are also regulated by various kinds of protein kinases, we investigated the role of some kinase activators and inhibitors in the regulation of the L-type Ca2+ channel currents in rat pituitary GH3 cells using the patch-clamp technique. Phorbol 12,13-dibutyrate (PDBu), a protein kinase C (PKC) activator, and vanadate, a protein tyrosine phosphatase (PTP) inhibitor, increased the Ba2+ current through the L-type Ca2+ channels. In contrast, bisindolylmaleimide I (BIM I), a PKC inhibitor, and genistein, a protein tyrosine kinase (PTK) inhibitor, suppressed the Ba2+ currents. Forskolin, an adenylate cyclase activator, and isobutyl methylxanthine (IBMX), a non-specific phosphodiesterase inhibitor, reduced Ba2+ currents. The above results show that the L-type Ca2+ channels are activated by PKC and PTK, and inhibited by elevation of cyclic nucleotides such as cAMP. From these results, it is suggested that the regulation of hormone secretion by various kinase activity in GH3 cells may be attributable, at least in part, to their effect on L-type Ca2+ channels.
Adenylyl Cyclases ; Animals ; Cell Line* ; Colforsin ; Cytosol ; Genistein ; Neuroendocrine Cells ; Nucleotides, Cyclic ; Patch-Clamp Techniques ; Phorbol 12,13-Dibutyrate ; Phosphotransferases ; Protein Kinase C ; Protein Kinases* ; Protein Tyrosine Phosphatases ; Protein-Tyrosine Kinases ; Rats* ; Vanadates