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Rhythm control therapy improves the quality of life in properly selected patients with atrial fibrillation (AF). Sodium channel blockers are recommended as a first-line therapy for lone paroxysmal AF. Pilsicainide, a pure sodium channel blocker is the most frequently used drug in Japan. In addition to amiodarone, several reports performed in Japan described defibrillating effect of bepridil. These two drugs are considered as first choice for rhythm control treatment to lone persistent AF. Since sodium channel blockers increase mortality in patients with reduced cardiac function, amiodarone or bepridil are recommended for rhythm control in AF accompanied with structural heart disease. However, sufficient treatment for underlying heart disease is required prior to administration of antiarrhythmic drugs.
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Amiodarone (AM) is a potent antidysrhythmic agent that is limited in clinical use by its adverse effects, including potentially life-threatening AM-induced pulmonary toxicity (AIPT). The present study tested the ability of dietary supplementation with vitamin E (500 IU d,1-alpha-tocopherol acetate/kg chow) to protect against pulmonary damage following intratracheal administration of AM (1.83 micromol) to the male golden Syrian hamster. At 21 days post-dosing, animals treated with AM had increased lung hydroxyproline content and histological disease index values compared to control (P < 0.05), which were indicative of fibrosis. Dietary vitamin E supplementation for 6 weeks resulted in a 234% increase in lung vitamin E content at the time of AM dosing, and maintenance on the diet prevented AM-induced elevation of hydroxyproline content and disease index 21 days post-dosing. Dietary vitamin E supplementation also decreased hydroxyproline content and disease index values in hamsters treated intratracheally with distilled water, the AM vehicle. These results demonstrate a protective role for vitamin E in an in vivo model of AIPT, and suggest that this antioxidant may have non-specific antifibrotic effects in the lung.
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Three emergency medical services systems serving the Minneapolis-St. Paul metro area participated in the protocol. Inclusion criteria included age 18 to 75 years, body habitus accommodating automated Lund University Cardiac Arrest System (LUCAS) cardiopulmonary resuscitation (CPR), and estimated transfer time from the scene to the cardiac catheterization laboratory of ≤30 minutes. Exclusion criteria included known terminal illness, Do Not Resuscitate/Do Not Intubate status, traumatic arrest, and significant bleeding. Refractory VF/VT arrest was defined as failure to achieve sustained return of spontaneous circulation after treatment with 3 direct current shocks and administration of 300 mg of intravenous/intraosseous amiodarone. Patients were transported to the University of Minnesota, where emergent advanced perfusion strategies (extracorporeal membrane oxygenation; ECMO), followed by coronary angiography and primary coronary intervention (PCI), were performed, when appropriate. Over the first 3 months of the protocol, 27 patients were transported with ongoing mechanical CPR. Of these, 18 patients met the inclusion and exclusion criteria. ECMO was placed in 83%. Seventy-eight percent of patients had significant coronary artery disease with a high degree of complexity and 67% received PCI. Seventy-eight percent of patients survived to hospital admission and 55% (10 of 18) survived to hospital discharge, with 50% (9 of 18) achieving good neurological function (cerebral performance categories 1 and 2). No significant ECMO-related complications were encountered.
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To evaluate the effect of acidosis on rectifier potassium current (Ikr) blockers, the human ether-a-go-go-related gene (HERG), which encodes IKr, was expressed in Xenopus laevis oocytes. The two electrodes voltage clamp technique was used and the experiments were performed at room temperature.
Atrial fibrillation developed in 28 patients in group 1A, whereas it developed in 12 in group 1B (P=0.005). Atrial flutter developed in 10 patients in group 1A but in 3 patients in group 1B (P=0.045). Multifocal atrial tachycardia developed in 13 patients in group 1A and in 4 in group 1B (P=0.022). Multivariate analysis identified ejection fraction (P<0.002, odds ratio (OR) 0.93), inotropy requirement (P<0.001, OR 3.98) amiodarone (P<0.001, OR 0.18), and FEV(1)<75% of predicted value (P<0.048, OR 1.84) as predictor of SVT. There were statistically significant differences between A and B subgroups of group 1 for hospital (P<0.001) and intensive care unit (ICU) stay (P<0.001). There was also statistically significant difference between groups 1A and 2 comparison for ICU (P<0.001; 6.4+/-3.4 versus 1.4+/-0.6 days) and hospital stay (P<0.001; 17.6+/-8.2 versus 6.9+/-0.6 days).
Baseline serum thyroid hormone concentrations and thyroid volume help identify patients with type 2 AIT at risk of a delayed response to glucocorticoids.
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Observational study over a 10-year period. Seventy-one out of 2651 patients (2,885 procedures, 2,106 bypass procedures) received amiodarone therapy for newly detected postoperative tachyarrhythmias. All patients received catecholamine infusions as standard post-op therapy to support cardiac function and output. In most cases a loading dose of amiodarone was given over 1-4 h followed by a continuous infusion. Catecholamine infusion dose requirements were monitored as was heart rate, blood pressure, central venous pressure, and sedation dose requirements pre treatment and at 0.5, 1, 2, 4, 8, 12 and 24 h after the begin of the amiodarone administration.
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Practice guidelines have expanded to include a new Class IIa recommendation for implantable cardiac defibrillator (ICD) use in patients post-myocardial infarction (MI) with a left ventricular ejection fraction (LVEF) =30% on the basis of the results of the Multicenter Automatic Defibrillator Implantation Trial II (MADIT II). Given that over 3 million patients in North America meet these criteria and over 400,000 additional patients will meet these criteria every year, the potential costs to the healthcare system are substantial and possibly prohibitive. The results of MADIT II must be interpreted in the context of other studies. The benefits of ICD therapy may vary substantially across subgroups of MADIT II patients. Studies of amiodarone suggest that it may be useful if used in addition to beta-blockers, and the relative value of this therapy compared to ICD therapy remains to be elucidated. Subgroups of MADIT II patients with QRS duration >0.12 seconds or LVEF =25% appear to derive the greatest benefit from ICD therapy. Cost-effectiveness depends on the magnitude of benefit expected and will differ across subgroups of patients with different levels of risk. Better risk stratification strategies are needed to predict which patients will benefit most. Results of ongoing studies will be crucial in determining the relative effectiveness of ICD compared to optimal medical therapy including the use of amiodarone and beta-blockers. Predictors of subsets of MADIT II patients most likely to benefit from ICD therapy are urgently needed in order to prioritize allocation of healthcare resources.
UV photography demonstrates subclinical corneal iron, confirming its deposition in an integrated HS line/vortex pattern. Coincident iron and amiodarone deposition occurs in amiodarone keratopathy.
Negative tracheal pressure (NTP) during tracheal obstruction in obstructive apnea increases vagal tone and causes pronounced shortening of the atrial effective refractory period (AERP), thereby perpetuating atrial fibrillation (AF). The role of different atrial potassium channels under those conditions has not been investigated.
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Dronedarone is recommended as the successor drug to amiodarone because a faster onset of effects and less side effects are to be expected. This review describes the pharmacological properties of this multi-channel blocker and summarizes the results from recent studies proving successful antiarrhythmic therapy using dronedarone in patients with atrial fibrillation.
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Amiodarone causes phospholipid storage in the lysosomes of various types of lung cell in animals and man. It has been proposed that this is due to its ability to inhibit lysosomal phospholipase A. To investigate this further, a crude lysosomal fraction from rat lung was prepared and phospholipase A was isolated and its positional specificity was determined. Analysis of the products formed after incubation with 2-[1-14C]oleoylphosphatidylcholine showed that only phospholipase A1 activity is present. This soluble preparation of lung lysosomal phospholipase A1 was used to study inhibition by amiodarone and desethylamiodarone, in vitro. Both were extremely potent inhibitors of the lung acid phospholipase A1. To evaluate the levels of amiodarone in lung lysosomes, rats were treated with the agent for 3 days and the combined mitochondrial/lysosomal fraction of lung tissue was prepared by differential centrifugation. This fraction had been shown previously to be highly enriched in amiodarone. Purified mitochondria and lysosomes were isolated from the combined mitochondrial/lysosomal fraction with Percoll gradients and analyzed for their drug content by HPLC. Amiodarone and desethylamiodarone were present in roughly equal amounts, relative to protein, in mitochondria and lysosomes, respectively. Amiodarone appears to differ from other cationic amphiphilic drugs which cause lipidosis because the latter are more highly lysosomotropic. Although amiodarone does not appear to be highly lysosomotropic in lung, it causes lysosomal phospholipid storage because of its ability to concentrate in lung and because it inhibits lysosomal phospholipase A to a much greater extent than other cationic amphiphiles such as diethylaminoethoxyhexestrol, chloroquine and chlorphentermine.
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Medications prescribed for elderly outpatients (≥ 65 years) in Primorsko-Goranska County, Croatia, who received five or more different drugs simultaneously in 2010, were analyzed. The prevalence of potentially inappropriate drugs prescribed to the elderly was assessed using the new comprehensive protocol developed by authors Mimica Matanović and Vlahović-Palčevski.
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ICDs decreased deaths during the 5 years from 37.0% to 29.7% at a net cost of euro26,222 to euro20,008 per patient, yielding cost-benefit ratios of 0.17 (UK) and 0.14 (France)-more than a 5 to 1 return on investment. Sensitivity analyses showed ICDs represent value for money whenever a life is valued at least at euro274,000.
Atrial fibrillation (AF) is common in ICU patients and is associated with a two- to fivefold increase in mortality. This paper provides a reappraisal of the management of AF with a special focus on critically ill patients with haemodynamic instability. AF can cause hypotension and heart failure with subsequent organ dysfunction. The underlying mechanisms are the loss of atrial contraction and the high ventricular rate. In unstable patients, sinus rhythm must be rapidly restored by synchronised electrical cardioversion (ECV). If pharmacological treatment is indicated, clinicians can choose between the rate control and the rhythm control strategy. The optimal substance should be selected depending on its potential adverse effects. A beta-1 antagonist with a very short half-life (e.g., esmolol) is an advantage for ICU patients because the effect of beta-blockade on cardiovascular stability is unpredictable in those patients. Amiodarone is commonly used in the ICU setting but has potentially severe cardiac and noncardiac side effects. Digoxin controls the ventricular response at rest, but its benefit decreases in the presence of adrenergic stress. Vernakalant converts new-onset AF to sinus rhythm in approximately 50% of patients, but data on its efficacy and safety in critically ill patients are lacking.
Several liver diseases that are characterized by chronic steatosis lead to steatohepatitis lesions in some susceptible subjects. We tested the hypothesis that acute or chronic steatosis may lead to lipid peroxidation.
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The total atrial conduction time (TACT) is an important electrophysiological parameter. We developed a new transthoracic echocardiographic tool (PA-TDI). The PA-TDI interval is a reflection of the TACT. In the present study, we evaluated the clinical and echocardiographic correlates of intra-atrial conduction delay.
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It has been reported that hyperthyroidism is associated with an altered endothelial function and increased risk of arterial thromboembolism. The aim of our study was to estimate chosen markers of endothelial dysfunction in iodine-induced thyrotoxicosis (IIT).
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We investigated whether defibrillation thresholds (DFTs) could be measured more safely during defibrillator implantation by measuring the upper limit of vulnerability (ULV) without using any special equipment. Nonthoracotomy ICD implantation with endocardial leads was performed in 13 patients, and through the use of the ICD function itself, ULV and DFT were measured using the delayed four-episode up-down algorithm. Myocardial injures caused by high-energy current were assessed by electrocardiograms and serial CPK-MB. ULV was confirmed in all cases, and it strongly correlated with DFT. The average ULV was 5.9 +/- 3.3 J, while the average DFT was 7.9 +/- 4.3 J (r = 0.89, p < 0.0001, DFT = 1.20+1.14x ULV). The average ULV was thus significantly lower (p < 0.01). Although six patients were on amiodarone therapy, the strong correlation between ULV and DFT was also maintained (r = 0.97), p < 0.01) in these patients. In all cases, the CPK-MB failed to increase, and no myocardial injuries were detectable on electrocardiograms. We confirmed that ULV could be easily and safety measured during ICD implantation, and that ULV could be used instead of DFT.
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Serum determinations of total T4, total T3, reverse T3, free T3 index, free T4, free T4 index, TBG, T4/TBG ratio, TSH and cholesterol were carried out on 18 euthyroid patients with coronary heart disease. Serum samples were obtained before treatment and after 15 days, 2, 4, 6, 8, 10, 12, 14 and 16 months of treatment with amiodarone (400 mg/day). Patients were divided into two groups, according to patterns of TSH response to thyrotrophin-releasing hormone (TRH): (I) patients with normal responses (n = 12), and (II) patients with subnormal responses (n = 6). Patients of group I showed total T4, free T4 and reverse T3 increments and total T3 and free T3 index decreases, whereas patients of group II were distinguished by the absence of T3 decreases and a rise in free T4 levels that showed a significant correlation with a drop in serum cholesterol (r = -0.767; p. less than 0.001). No patient of either group showed clinical signs of thyroid dysfunction. These results show that the appearance of hormonal patterns of hyperthyroidism is unpredictable and very frequent in patients with no previous thyroid abnormalities undergoing long-term treatment with the drug.
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Amiodarone, a complex compound with variegated electropharmacologic and pharmacokinetic properties and an equally complex side-effect profile, continues to have a critical role in the control of ventricular and supraventricular tachyarrhythmias as the use of class I agents has declined. Such is also the case with sotalol. Unlike other so-called class III agents, amiodarone non-competitively blocks sympathetic stimulation, and its effects on repolarization are not associated with reverse use dependency. Rarely does it produce torsades de pointes despite its propensity to induce significant bradycardia and marked prolongation of the QT interval. During long-term therapy with the drug, there is no impairment of ventricular function; in fact, there are significant increases in the left ventricular ejection fraction during protracted amiodarone therapy in patients with heart failure. Long-term amiodarone administration consistently demonstrates marked efficacy in a wide spectrum of arrhythmias. The major limitation of amiodarone during long-term therapy is its unusual side-effect profile, although the increasing trend for low-dose drug therapy has demonstrated a major decline in the overall incidence of serious adverse reactions. Amiodarone is effective in controlling symptomatic ventricular tachycardia and fibrillation (VT/VF) in > 60-70% of patients when conventional agents (especially class I) are ineffective or not well tolerated. The efficacy of amiodarone compared with that of an implantable cardioverter-defibrillator in patients with VT/VF and in survivors of cardiac arrest remains uncertain when total mortality is used as the primary endpoint of comparison. Amiodarone suppresses ventricular ectopy and markedly suppresses nonsustained VT. It prevents inducible VT/VF in a small number of patients, but slows VT rate in a larger number. The role of the drug in prolonging survival in the postmyocardial infarction patient is unclear, although preliminary data from blinded studies suggest that the drug decreases arrhythmia-related mortality. Similarly, in heart failure, amiodarone has the potential to reduce total mortality but appears to be selectively effective in nonischemic rather than in ischemic cardiomyopathy. Intravenous amiodarone was recently introduced in the United States for the control of recurrent destabilizing VT or VF resistant to conventional therapy. There is also evolving data indicating that the drug might be the most potent agent in maintaining sinus rhythm in patients with atrial fibrillation or flutter converted chemically or electrically to sinus rhythm. However, blinded controlled comparative studies involving sotalol, quinidine, or pure class III drugs have not been carried out. The available data nevertheless suggest that, barring its side-effect profile, amiodarone is a desirable prototype of a broad-spectrum antifibrillatory and antiarrhythmic compound.