BACKGROUND: Recently, the amiodarone has emerged as a promising antiarrhythmic agent and its efficacy and safety has been widely accepted with many literatures. But there was no general agreement regarding the dosage and indication of intravenous (IV) amiodarone in acute myocardial infarction with life-threatening refractory ventricular tachyarrhythmias. METHOD: From October 1995 through October 1997, we recruited retrospectively 9 patients of acute myocardial infarction who had received IV amiodarone for life-threatening refractory ventricular tachyarrhythmias and analyzed the initial response, adverse effect, and loading dose. RESULTS: 1) Acute efficacy:Eight of 9 patients promptly restored normal sinus rhythm immediately after intravenous amiodarone administration. 2) In-Hospital Mortality:One patients died due to ventricular tachyarrhythmias refractory to aggressive management and 5 in 8 patients who had responded promptly with IV amiodarone discharged alive and other 3 patients died due to cardiogenic shock with normal sinus rhythm. 3) Immediate adverse effects:Five patients experienced immediate adverse effects after IV amiodarone; 3 patients of hypotension, 1 patient of first degree AV block, and the other of Morbitz type 2 AV block. 4) Long term follow-up:Among 5 patients discharged alive, one died as unexpected consequence. Other 4 patients have been still alive without maintenance medication. CONCLUSION: The IV amiodarone for suppression of life-threatening ventricular tachyarrhythmias in patients with acute myocardial infarction seemed to be an effective second-line therapeutic drug and have acceptable adverse effects. In the future, the large scale study regarding the dosage and indication might be warrented.
Amiodarone* ; Atrioventricular Block ; Humans ; Hypotension ; Myocardial Infarction* ; Retrospective Studies ; Shock, Cardiogenic ; Tachycardia*

BACKGROUND AND OBJECTIVES: Some patients with Kawasaki disease (KD) present with fever and cervical lymphadenopathy alone. The purpose of this study was to characterize the clinical features of these unusual KD patients and determine whether this is a severe form of KD associated with increased risks of intravenous immunoglobulin (IVIG) resistance and coronary artery lesions (CALs). SUBJECTS AND METHODS: A total of 146 children with KD were reviewed retrospectively, and classified into two groups according to initial clinical features. Those presenting with only fever and cervical lymphadenopathy (LKD) were classified as LKD patients. Other-KD patients included all except the LKD patients. RESULTS: Among 146 KD patients, 13 (8.9%) were classified as LKD patients. The LKD patients were significantly older and admitted earlier. The duration between fever onset and KD diagnosis was significantly longer in the LKD patients (5.9 days vs. 4.9 days, p=0.023). The frequency of IVIG resistance was not different between the two groups., In the LKD patients, the incidence of CALs was significantly higher in the acute phase, and without significant difference in the convalescent phase. The percentage of neutrophils and C-reactive protein, albumin, and total bilirubin levels were significantly higher in LKD patients. CONCLUSION: Even though LKD patients were older, admitted earlier, and had higher inflammatory marker levels, they did not have a greater risk of CALs or IVIG resistance. However, echocardiography may be helpful in the acute stage if patients have only fever and cervical lymphadenopathy and are unresponsive to empirical antibiotics.
Anti-Bacterial Agents ; Bilirubin ; C-Reactive Protein ; Child ; Coronary Vessels ; Diagnosis ; Echocardiography ; Fever* ; Humans ; Immunoglobulins ; Immunoglobulins, Intravenous ; Incidence ; Lymphatic Diseases* ; Mucocutaneous Lymph Node Syndrome* ; Neck ; Neutrophils ; Retrospective Studies

BACKGROUND: The purpose of this study was to investigate the pharmacokinetics of amikacin in critically ill patients undergoing continuous venovenous hemodiafiltration (CVVHDF). METHODS: Pharmacokinetic parameters in each of six renal failure patients were estimated by measurement of amikacin levels in serum and effluent samples. RESULTS: Average clearance of amikacin by CV VHDF was 28.5+/-4.6 mL/min (mean+/-standard deviation). The sieving coefficient was 0.62+/-0.2 in the hemodiafiltration system of Gambro AN69 membrane set. Volume of distribution of amikacin was estimated to be 0.47+/-0.08 L/kg lean body weight. The half-life of amikacin was significantly reduced by hemodiafiltration to 11.4+/-1.6 hr. 40% of the administered amikacin was removed by CVVHDF over the 24 hour study period. CONCLUSION: We recommend that 10 mg/kg of amikacin should be given i.v. every 48 hours to critically ill patients during CVVHDF. However, individualized approach based on therapeutic drug monitoring of plasma amikacin concentration is necessary for optimum amikacin therapy during CVVHDF due to the varying nature of critically ill patients.
Amikacin* ; Body Weight ; Critical Illness ; Drug Monitoring ; Half-Life ; Hemodiafiltration* ; Humans ; Membranes ; Pharmacokinetics ; Plasma ; Renal Insufficiency

Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disorder that is associated with repetitive head injury and has distinctive neuropathological features that differentiate this disease from other neurodegenerative diseases. Intraneuronal tau aggregates, although they occur in different patterns, are diagnostic neuropathological features of CTE, but the precise mechanism of tauopathy is not known in CTE. We performed whole RNA sequencing analysis of post-mortem brain tissue from patients with CTE and compared the results to normal controls to determine the transcriptome signature changes associated with CTE. The results showed that the genes related to the MAP kinase and calcium-signaling pathways were significantly downregulated in CTE. The altered expression of protein phosphatases (PPs) in these networks further suggested that the tauopathy observed in CTE involves common pathological mechanisms similar to Alzheimer's disease (AD). Using cell lines and animal models, we also showed that reduced PPP3CA/PP2B phosphatase activity is directly associated with increases in phosphorylated (p)-tau proteins. These findings provide important insights into PP-dependent neurodegeneration and may lead to novel therapeutic approaches to reduce the tauopathy associated with CTE.
Alzheimer Disease ; Brain ; Brain Injury, Chronic* ; Cell Line ; Craniocerebral Trauma ; Gene Expression Profiling* ; Humans ; Models, Animal ; Neurodegenerative Diseases ; Phosphoprotein Phosphatases ; Phosphotransferases ; Sequence Analysis, RNA ; Tauopathies* ; Transcriptome*