BACKGROUND/AIMS: The risk factors and clinical outcome of infective endocarditis (IE) have changed over the past few decades. Recently, the incidence of Staphylococcus aureus IE (SAIE) has increased. We investigated the clinical and microbiological characteristics and clinical outcomes of SAIE. METHODS: All patient cases that were diagnosed as IE according to the modified Duke criteria in Samsung Medical Center during the period of January 1995 to December 2006 were reviewed retrospectively. The clinical and microbiological characteristics of patients with SAIE were compared to those of non-SAIE patients with IE. RESULTS: We enrolled 304 patients with IE. Of these, 240 cases were IE culture-positive, including 73 cases of SAIE. The mean age of patients with SAIE was 48.15+/-19.87 years, with male patients accounting for 71.2% of our study group. Congenital heart disease (8.2%) was less common among SAIE patients. Hospital-acquired IE was significantly more common in SAIE than in non-SAIE cohorts (p<0.05). Surgical treatment was performed in 33 cases (45.2%). Valvular regurgitation with heart failure was the most frequent cause of surgery (39.3%). Twenty-three cases exhibited complications, including extra cardiac embolization (16.4%) and heart failure (5.6%). Fever persisting for a period longer than seven days was more common among those in the SAIE group. Twelve patients (16.4%) died and four patients (5.4%) were discharged without hope of improvement. The in-hospital mortality rate was higher among SAIE patients (17.3%) compared to that among non-SAIE patients (11%), although this comparison was not statistically distinct (p> 0.05). Methicillin resistance and non-surgical treatment were significant risk factors for in-hospital mortality. CONCLUSIONS: SAIE is more strongly associated with systemic embolization, persistent fever, and longer hospital stays compared to non-SAIE. Further studies are warranted to evaluate adequate treatment and to improve the outcome of patients with SAIE.
Accounting ; Cohort Studies ; Endocarditis ; Fever ; Heart Diseases ; Heart Failure ; Hospital Mortality ; Humans ; Incidence ; Length of Stay ; Male ; Methicillin Resistance ; Retrospective Studies ; Risk Factors ; Staphylococcus ; Staphylococcus aureus

Essential thrombocythemia (ET) is a clonal disorder of myeloid stem cells that causes thrombocytosis. As a result, ET can lead to vascular thrombosis and tissue ischemia; the association of coronary artery abnormalities such as myocardial infarction or unstable angina is rare. Here we describe a 45-year-old male patient with essential thrombocythemia who presented with unstable angina. Elective coronary angiography showed total occlusion of mid right coronary artery and mid left anterior descending coronary artery. ET was confirmed by a bone marrow biopsy; treatment was started with antiplatelet therapy including aspirin and clopidogrel along with cytostatic therapy with hydroxyurea and anagrelide. After the initiation of the treatment, the platelet count decreased to 20 s 10(4)/microliter. In addition, percutaneous coronary angioplasty was successfully performed with stent placement at the right coronary artery without hemorrhagic or thrombotic complications.
Thrombocythemia, Hemorrhagic/complications/*drug therapy ; *Stents ; Quinazolinesherapeutic use ; Middle Aged ; Male ; Hydroxyureaherapeutic use ; Humans ; *Angioplasty, Transluminal, Percutaneous Coronary ; Angina, Unstable/etiology/*therapy

BACKGROUND: Pulmonary artery banding (PAB)in the functional univentricular heart (UVH)is a palliative procedure for staging toward the Fontan procedure;however,it is known to be a risk factor. MATERIALS AND METHOD: The records of all 37 patients with functional UVHs who underwent surgical palliation using PAB between September 1989 and August 1999 were reviewed retrospectively.We investigated the aortic arch obstruction,the development and progression of subaortic stenosis after PAB,and risk factor of mortality according to surgical method. RESULT: In 37 neonates and infants with single ventricular physiology,aortic arch obstruction was combined in 7.There were 6 early deaths (16.2%)after PAB and 3 late deaths (8.1%)after Fontan operation.The actuarial overall survival including early mortality at 3 and 5 years were 8 0 .7+/-6.6%,72.2 +/-8.2% respectively. Among 31 patients who survived PAB,27 patients (87.1%)could become candidates for Fontan operation;22 patients(71.0%)completed Fontan operation with 3 deaths and 5 were waiting bidirectional cavopulmonary shunt(BCPS)or Fontan operation (follow-up mean 4.5 year,minimal 2 year). Subaortic stenosis developed in 8 patients after PAB (8/29,27.6%);3 cases in the patients without arch anomaly (3/22,13.6%)and 5 in those with arch anomal y (5/7,71.4%).The subaortic stenosis was managed with Damus-Kaye-Stansel procedure (DKS)in 6 patients without operative mortality and conal septum resection in 2 without long-term survivor. Analysis of risk factors established that aortic arch obstruction was strongly associated with subaortic stenosis (p<0.001).The only risk factor of late mortality was Fontan procedure without staged palliation by BCPS (p=0.001). CONCLUSION: PAB is effective as an initial palliative step in functional UVH.And the high risk group of patients with aortic obstruction can undergo effective short-term PAB as an initial palliative step,with subsequent DKS for subaortic stenosis.This strategy,initial PAB and careful surveillance,and early relief of subaortic stenosis can maintain acceptable anatomy and hemodynamics for later Fontan procedures.
Aorta, Thoracic ; Constriction, Pathologic ; Fontan Procedure ; Heart* ; Hemodynamics ; Humans ; Infant ; Infant, Newborn ; Mortality ; Pulmonary Artery* ; Risk Factors ; Survivors

BACKGROUND: To know whether the laryngeal mask airway (LMA) triggers a pharyngo-esophago- gastric reflex during general anesthesia, we compared the esophageal motility of patients with an LMA or endotracheal tube (ETT) in place. METHODS: Fifty patients (ASA I or II) scheduled for elective orthopedic surgery with general anesthesia were randomly allocated into LMA (n = 30) or ETT (n = 20) groups. The esophageal manometric inputs were recorded continuously using an ambulatory esophageal manometric recorder and divided into five perioperative phases (preanaesthesia, induction, operation, LMA or ETT rejection, and arousal phase). RESULTS: The peristaltic percent and number of contractions per minute were significantly decreased during induction, operation, LMA or ETT rejection and arousal phases compared with preanesthetic phases in both the LMA and ETT groups. However, there were no significant group differences in any corresponding perioperative phases. CONCLUSIONS: We suggest that during general anesthesia the use of a LMA does not provoke significantly different esophageal peristalsis compared with an ETT. Thus, the LMA is unlikely to potentiate gastric regurgitation and reflux during general anesthesia by stimulating the pharyngo-esophago-gastric reflex.
Anesthesia, General* ; Arousal ; Humans ; Laryngeal Masks* ; Laryngopharyngeal Reflux ; Orthopedics ; Peristalsis ; Reflex

BACKGROUND: Propofol and lidocaine have been purported to attenuate bronchoconstriction induced by fentanyl administration during induction of anesthesia. The purpose of the present study was to study the synergic bronchodilation effect of propofol mixed with lidocaine. METHODS: Two hundred and thirty four patients were randomly allocated to five groups: Group 1 (n = 60, normal saline 0.25 ml/kg followed by fentanyl 3ng/kg), Group 2 (n = 30, propofol 2 mg/kg mixed with normal saline 0.05 ml/kg followed by normal saline 0.06 ml/kg), Group 3 (n = 50, propofol 2 mg/kg mixed with normal saline 0.05 ml/kg followed by fentanyl 3ng/kg), Group 4 (n = 33, propofol 2 mg/kg mixed with lidocaine 1 mg/kg followed by normal saline 0.06 ml/kg) and Group 5 (n = 61, propofol 2 mg/kg mixed with lidocaine 1 mg/kg followed by fentanyl 3ng/kg). All patients were injected with fentanyl or normal saline two minutes after administration of propofol premixed with lidocaine or normal saline, respectively. We checked the cough reflex, injection pain, oxygen desaturation and chest wall rigidity. RESULTS: There was a significant difference in the incidence of cough reflex between group 1 and 3 or 5. The incidience of group 5 was significantly lower than in group 3. CONCLUSIONS: This study suggests that a propofol-lidocaine mixture should be considered when patients require bronchodilation during induction of anesthesia.
Anesthesia ; Bronchoconstriction ; Cough* ; Fentanyl* ; Humans ; Incidence ; Lidocaine* ; Oxygen ; Propofol* ; Reflex* ; Thoracic Wall

BACKGROUND: The effect of opioids on nitric oxide (NO)- and peroxynitrite-induced neuronal cell death is largely unknown. In the present study, we examined the effect of morphine on NO- and peroxynitrite-induced cell death using a human neuroblastoma SH-SY5Y cell line, which abundantly expresses micro, delta, kappa-opioid receptors. METHODS: The cultured cells were pretreated with morphine and exposed to 3-morpholinosydnonimine (SIN-1) that simultaneously generates NO and superoxide, thus possibly forming peroxynitrite. The cell damage was assessed by using MTT assay and crystal violet staining. Morphological nuclear changes and enzymatic evidences of apoptosis of the cells after exposure to SIN-1 for 24 hours were evaluated by using 4', 6-diamidino-2-phenylindole (DAPI) staining and the measurement of pro-apoptotic protease (caspase-3) activity, respectively. Levels of reduced glutathion (GSH) were measured by monochloronimane (MCB) assay. RESULTS: Pretreatment of SH-SY5Y with morphine significantly inhibited the apoptotic cell death. Morphine also inhibited SIN-1-induced caspase-3 (pro-apoptotic protease) activity in a dose-dependent manner. However, naloxone (20 microM) could not antagonize completely the effect of morphine in SIN- 1-induced cell death. Pre-administered GSH and N-acetylcysteine (NAC) have been found to protect SIN-induced apoptosis, and the neuroblastoma cells treated with morphine had significantly elevated the levels of GSH. CONCLUSIONS: The present study shows that morphine protects the human neuroblastoma cell line SH- SY5Y from peroxynitrite-induced apoptotic cell death through elevated GSH levels. The protective actionof morphine seems to be associated with inhibition of the apoptotic pathway. However, it is suggested that morphine protects the cells possibly via other unknown mechanisms in addition to the activation of opioid receptors.
Acetylcysteine ; Analgesics, Opioid ; Apoptosis* ; Caspase 3 ; Cell Death ; Cell Line ; Cells, Cultured ; Gentian Violet ; Humans* ; Morphine* ; Naloxone ; Neuroblastoma* ; Neurons ; Nitric Oxide ; Peroxynitrous Acid ; Receptors, Opioid ; Superoxides

BACKGROUND: Astrocytes, representing a major non-neuronal cell population in the central nervous system (CNS), contain opioid receptors and are actively involved in several brain functions. This study is designed to evaluate the effects by which morphine contributes to cytotoxicity of nitric oxide (NO) species including NO and peroxynitrite (ONOO(-)) in primary astrocytes isolated from the cerebral cortexes of 1 - 2 day Sprague-Dawley rats. METHODS: The cultured cells were pretreated with morphine and exposed to 3-morpholinosydnonimine (SIN-1) which simultaneously generates NO and superoxide, thus possibly forming peroxynitrite. The cell damage was assessed by using an MTT (methylthizol-2-yl-2, 5-diphenyl, tetrazolium bromide) assay. Morphological nuclear changes of the cells after exposure to SIN-1 for 24 hours was evaluated by using 4', 6-diamidino-2-phenylindole (DAPI) staining. RESULTS: Morphine significantly protected primary rat astrocytes in a dose-dependent manner from the death mediated by sodium nitroprusside (SNP), a donor of nitric oxide, and SIN-1. Moreover, it was found that naloxone antagonized the protective effect of morphine on SIN-1-induced cell death, revealed as apoptosis by the occurrence of morphological nuclear changes characteristic of apoptosis. Morphine also inhibited the nuclear condensation of SIN-1-treated cells, however the action of morphine was antagonized by pretreatment of naloxone. The protective role of morphine on SIN-1-induced cytotoxicity was inhibited by DL-Buthionine-[S, R]-sulfoximine (BSO). Furthermore, the effects of morphine on SIN-1-induced cytotoxicity were blocked by pretreatment of Gi protein inhibitor, pertussis toxin, and phosphoinositide 3-kinase (PI3 kinase) inhibitors, Wortmannin and LY294002. CONCLUSIONS: These results suggest that morphine may protect primary rat astrocytes from NO species via the signaling cascades involving G-protein and PI3-kinase, and possibly regulates the anti-oxidant, glutathione (GSH).
Animals ; Apoptosis ; Astrocytes* ; Brain ; Cell Death* ; Cells, Cultured ; Central Nervous System ; Cerebral Cortex ; Glutathione ; GTP-Binding Proteins ; Humans ; Morphine* ; Naloxone ; Nitric Oxide ; Nitroprusside ; Peroxynitrous Acid ; Pertussis Toxin ; Phosphatidylinositol 3-Kinases ; Rats* ; Rats, Sprague-Dawley ; Receptors, Opioid ; Superoxides ; Tissue Donors

BACKGROUND: In the present study, we examined the effect of morphine on NO- and peroxynitrite-induced cell death using a human neuroblastoma SH-SY5Y cell line which abundantly expresses micro, delta and K-opioid receptors. METHODS: The cultured cells were pretreated with morphine (100 micrometer) and exposed to 3-morpholinosydnonimine (SIN-1, 1mM). Agarose gel electrophoresis of DNA was done with the extracts from SH-SY5Y cells. The cells were treated with selective ligands for opioid receptor subtypes and with PI3-kinase inhibitors. Cell damage was assessed by using an MTT assay. Spectrophotometric absorption spectra were measured from the mixture of morphine (100 micrometer) plus peroxynitrite (1 mM) at room temperature. RESULTS: SIN-1 treated cells showed the occurrence of a specific form of chromosomal DNA fragmentation which pretreatment with morphine inhibited. The selective ligands for opioid receptor subtypes, [D-Ala2, N-Me-Phe4, Gly-ol5]enkephalin (DAMGO, micro-opioid receptor agonist), [D-Pen2,5] enkephalin (DPDPE, delta-opioid receptor agonist) and U-69593 (K-opioid receptor agonist) at a concentration of 10 micrometer did not prevent the cell death induced by SIN-1. Naloxone (20 micrometer) hardly antagonized the effect of morphine in SIN-1-induced cell death. The PI3-kinase inhibitors Wortmannin and LY294002 did not inhibit the action of morphine on apoptotic cell death. In the measurements of spectrophotometric absorption spectra, the peak of the absorbance of the mixture of morphine plus peroxynitrite at 295 300 nm disappeared three minutes after mixing. CONCLUSIONS: The present study showed that morphine protected the human neuroblastoma cell line,SH-SY5Y, from peroxynitrite-induced apoptotic cell death. However, it is suggested that the protective action of morphine is not via the activation of opioid receptors and/or the PI3-kinase pathway but possibly via direct chemical reaction.
Absorption ; Cell Death ; Cell Line ; Cells, Cultured ; DNA ; DNA Fragmentation ; Electrophoresis, Agar Gel ; Enkephalins ; Humans* ; Ligands ; Morphine* ; Naloxone ; Neuroblastoma* ; Peroxynitrous Acid ; Phosphatidylinositol 3-Kinases ; Receptors, Opioid

BACKGROUND: Antihypertensive agents such as verapamil and esmolol are well known for their effects of hemodynamic stabilization on tracheal intubation. However, our previous study, Verapamil and esmolol did not attenuate heart rate and blood pressure. The aim of the present study was to evaluate the efficacy of combined administration of these drugs for controlling hemodynamic responses to tracheal intubation. METHODS: Forty-eight patients, ASA physical status I or II, were randomly assigned to one of four groups (n = 12 each):normal saline (control), verapamil 0.1 mg/kg, esmolol 1 mg/kg, and verapamil 0.05 mg/kg mixed with esmolol 0.5 mg/kg. Anesthesia was induced with thiopental 5 mg/kg intravenously, and then saline, verapamil, esmolol or the mixed drugs were administered as an intravenous bolus, and immediately followed by succinylcholine 1.5 mg/kg. Tracheal intubation was performed 90 s after intravenous injection of experimental drugs. Systolic and diastolic blood pressure and heart rate were measured before induction and every minute for 5 minutes after tracheal intubation. RESULTS: There was a significant attenuation in systolic blood pressure after tracheal intubation in the verapamil and mixed groups compared to the control and esmolol groups. Heart rates were significantly lower in the esmolol and mixed groups than in the verapamil groups after tracheal intubation. CONCLUSIONS: Combined administration of Verapamil 0.05 mg/kg with esmolol 0.5 mg/kg attenuated increases in blood pressure and heart rate after tracheal intubation.
Anesthesia ; Antihypertensive Agents ; Blood Pressure* ; Heart Rate* ; Heart* ; Hemodynamics ; Humans ; Injections, Intravenous ; Intubation* ; Succinylcholine ; Thiopental ; Verapamil*