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Dronedarone, a noniodinated derivative of amiodarone, is under evaluation as a potentially less toxic anti-arrhythmic alternative to amiodarone. The acute and chronic electrophysiologic effects of dronedarone and amiodarone were compared in isolated rabbit atrial muscle by microelectrode techniques. Four-week PO treatment with dronedarone or amiodarone increased action potential duration (APD90) (58 +/- 4 ms control versus 69 +/- 2 ms dronedarone, p < 0.01; 68 +/- 3 ms amiodarone, p < 0.01 for a 100-mg/kg/d dose) and effective refractory period (49 +/- 6 ms control versus 68 +/- 4 ms dronedarone, p < 0.01; 63 +/- 3 ms amiodarone, p < 0.01). The APD90 prolonged reverse rate-dependency. In contrast, acute superfusion with 10 microM dronedarone or amiodarone decreased APD90 (61 +/- 6 ms control versus 53 +/- 4 ms dronedarone, p < 0.05; 52 +/- 6 ms amiodarone, p < 0.05), effective refractory period (50 +/- 5 ms control versus 44 +/- 4 ms dronedarone, p < 0.05; 43 +/- 6 ms amiodarone, p < 0.05), and the maximum upstroke slope of the action potential (Vmax) (188 +/- 9 V/s control versus 182 +/- 11 V/s dronedarone p < 0.05; 182 +/- 11 V/s amiodarone, p < 0.05). Thus, chronic and acute electrophysiologic effects of dronedarone on rabbit atrial muscle are similar to those of amiodarone, suggesting a similar potential against atrial arrhythmias.
The total sample size was 9626 patients. Women received a higher weight-adjusted dose of digitalis compared with men (0.0027 mg/kg per day vs 0.0025 mg/kg per day; P < 0.001). Overall, 199 AEs to digitalis were diagnosed. Women were more likely than men to suffer from an AE to digitalis (odds ratio, 1.51; 95% CI, 1.12-2.02). This finding was confirmed after correction for dose of digitalis, age, physical and cognitive impairment, atrial fibrillation, chronic obstructive pulmonary disease, glomerular filtration rate, and use of amiodarone, beta-blockers, nondihydropyridine calcium channel blockers, and potassium-sparing diuretics (odds ratio, 1.58; 95% CI, 1.01-2.48).
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As the population ages, recurrent ventricular tachycardia (VT) is increasingly encountered in elderly patients with ischemic heart disease. Radiofrequency catheter ablation is useful for reducing VT therapy in patients with an implantable defibrillator. The utility of radiofrequency catheter ablation in the elderly is not well defined.
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Areas of certainty and uncertainty concerning AIT are present among expert European thyroidologists, both from a diagnostic and a therapeutic standpoint. Diagnostic criteria need to be refined in order to improve therapeutic outcome.
Pharmacological conversion to sinus rhythm is generally difficult to achieve, particularly in long-lasting persistent atrial fibrillation (AF). The purpose of this study is to compare the effectiveness of two agents, amiodarone and bepridil, in achieving conversion to sinus rhythm in patients with persistent AF.
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Subjects from a random sample of the population with abnormal results on FT4, sensitive-TSH or antithyroid autoantibodies.
The purpose of this study was to (1) determine how often implantable cardioverter-defibrillator (ICD) system modifications were needed to obtain an adequate safety margin for defibrillation, (2) identify how often and for what indications defibrillation threshold (DFT) testing was not performed, and (3) identify factors predicting the need for modification.
A case study is presented in which amiodarone (A) was given during the whole of pregnancy and during the breast feeding period. An intensive observation of thyroid tests, serum concentrations of A and its metabolite, desethylamiodarone (DEA) was undertaken. The child was observed in the same way from birth until 2 months of age. The milk was analyzed for A and DEA. As reported in other published cases, transplacental passage was found and there was a relatively high concentration of amiodarone in the milk. Our child like the other children was healthy at birth, being euthyroid and with no goiter or corneal deposits. No effect was observed of the medication on growth, thyroid tests or cornea. It is concluded that amiodarone can be given during pregnancy but it is advisable to use as low doses as possible and control the serum concentrations at regular intervals. Breast feeding need not be forbidden.
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Spontaneous conversion to sinus rhythm (SR) during amiodarone pretreatment was observed in 13 pts (19.2%). DCC was performed in 54 pts and SR was restored in 41 of the study pts (76%). Complications occurred in 3 pts, including 1 case of apparent hyperthyroidism and 2 cases of decreased TSH level, and required amiodarone withdrawal. After 12 months, 72.2% of pts maintained SR on low dose (179.2+/-42.1 mg/day) amiodarone. Spontaneous conversion to SR during amiodarone loading was significantly related to long-term SR maintenance after successful DC cardioversion (p<0.013; RR 2.01; 95% CI 1.34-3.03).
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In this prospective study, 226 consecutive adult patients (group A) who had various heart operations utilizing cardiopulmonary bypass between April and November of 1998 at the University of Miami/Jackson Memorial Hospital, were given oral amiodarone (200 mg three times a day), starting immediately after arrival in the intensive care unit until the day of hospital discharge. The incidence of new AF in this group of patients was assessed and compared with a historical group of 239 patients (group B) who had had cardiac operations with cardiopulmonary bypass in the preceding 9 months at the same institution.
SNEDDS of amiodarone (AM) and talinolol were developed. Pharmacokinetic parameters were assessed in vivo. Effect on intestinal permeability, P-gp efflux and toxicity was evaluated in vitro (Caco-2) and ex vivo (Ussing). Solubilization was assessed in vitro (Dynamic Lipolysis Model). Effect on intraenterocyte metabolism was evaluated using CYP3A4 microsomes.
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Studies have suggested that chronic amiodarone treatment (a class III antiarrhythmic) may have effects on the myocardium that resemble those of hypothyroidism. Since hypothyroidism is associated with decreased expression of Na,K-ATPase alpha 1, alpha 2 and beta 1 subunits in heart and alpha 2 subunit in skeletal muscle, we aimed to test the hypothesis that chronic in vivo administration of amiodarone would result in changes in the expression of Na,K-ATPase isoforms that resembled those seen in hypothyroid rat. Rats were treated with 40 micrograms/g body weight amiodarone for 3 and 6 weeks. Na,K-ATPase alpha 1, alpha 2, beta 1 mRNA and protein levels and beta 2 mRNA were measured in cardiac ventricle and skeletal muscle. After 3 weeks of amiodarone cardiac alpha 1, alpha 2 and beta 1 protein levels were decreased to 0.65, 0.42, and 0.54 of control, respectively. After 6 weeks of treatment, cardiac alpha 1 and beta 1 levels returned to control and alpha 2 remained depressed. At the mRNA level alpha 2 and beta 2 decreased to 0.6-fold of control after 6 weeks treatment. There was no effect of amiodarone on skeletal muscle Na,K-ATPase expression at either time point. We conclude that the effects of amiodarone on myocardial Na,K-ATPase expression are similar to those of hypothyroidism after 3 weeks of amiodarone treatment, but by 6 weeks the similarities are limited to the decrease in alpha 2 and beta 2 expression.(ABSTRACT TRUNCATED AT 250 WORDS)
Omega-3 polyunsaturated fatty acid supplementation commenced >1 month prior to electrical cardioversion and continued thereafter reduces the recurrence of persistent AF. Randomized controlled trials on long-term fish oil supplementation are needed to confirm these findings.
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Mexiletine is an antiarrhythmic agent with structural and electrophysiologic properties similar to those of lidocaine. Mexiletine decreases ventricular automaticity while shortening both action potential duration and effective refractory period. The drug may be administered orally or intravenously. Hepatic metabolism is the major route of elimination. The elimination half-life is approximately 10 hours, but longer in patients with acute myocardial infarction, chronic congestive heart failure or hepatic insufficiency. Mexiletine suppresses ventricular ectopy in the acute phase of myocardial infarction. The drug is effective for some patients in whom lidocaine has failed. It suppresses chronic ventricular ectopy and is well tolerated in approximately two-thirds of stable outpatients treated with this agent. In that population, mexiletine is comparable in efficacy to quinidine, procainamide and disopyramide. It is effective in 30-50% of patients with ventricular arrhythmias refractory to other antiarrhythmic drugs. In patients with refractory arrhythmias, the efficacy of mexiletine may be enhanced by combination with propranolol, quinidine or amiodarone. Adverse reactions limit use of mexiletine in approximately 20% of patients. Gastrointestinal and central nervous system side effects are the most common. Mexiletine does not depress myocardial function. Aggravation of arrhythmias is uncommonly observed. The usual intravenous dose of mexiletine is 150-250 mg over at least 10 minutes. Long-term oral dosages are usually 200-300 mg 3 or 4 times daily.
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Amiodarone is a widely used antiarrhythmic drug. There is also evidence that amiodarone decreases multidrug resistance in human cell lines. In this paper, we have shown that amiodarone has similar effect on yeast, Saccharomyces cerevisiae, decreasing multiple drug resistance. Amiodarone stimulates the accumulation of ethidium bromide by inhibiting its efflux from the cells. The effect of amiodarone is much stronger on wild-type cells compared to the mutant with inactivated ABC-transporters. Interestingly, the action of amiodarone is additive with the one of chloroquine, a known inhibitor of ABC-transporters. We speculate that these findings could help in the development of antifungal drug mixes.
Sudden cardiac death remains a major health issue in western countries as well as in Hong Kong. Despite increasing knowledge of the mechanisms and risk factors of sudden cardiac death, methods for identifying high-risk candidates and predicting the efficacy of measures to prevent sudden cardiac death are still inadequate. A significant proportion of patients have known heart disease but are generally considered to be at low risk for this event. More efforts are needed to improve the success rate of out-of-hospital resuscitation through better warning systems, the use of amiodarone for refractory arrhythmias, and the widespread availability of automated defibrillation devices to allow early defibrillation. It is likely that these measures could increase the number of survivors following cardiac arrest. In survivors of sudden cardiac death episodes, treatment of the underlying cardiac disease, especially early revascularisation for myocardial ischaemia, is required. In the majority of patients, implantation of an implantable cardioverter defibrillator, with or without the use of an anti-arrhythmic drug such as amiodarone, would then be used to maintain survival. Furthermore, for individuals at significant risk of sudden cardiac death, primary prevention of sudden cardiac death through the placement of an implantable cardioverter defibrillator is increasingly being used.
Radiofrequency catheter ablation is the treatment of choice in Wolff-Parkinson-White syndrome with episodes of aborted sudden death.
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We have constructed computational models of canine ventricular cells and tissues, ultimately combining detailed tissue architecture and heterogeneous transmural electrophysiology. The heterogeneity is introduced by modifying the Hund-Rudy canine cell model in order to reproduce experimentally reported electrophysiological properties of endocardial, midmyocardial (M) and epicardial cells. These models are validated against experimental data for individual ionic current and action potential characteristics, and their rate dependencies. 1D and 3D heterogeneous virtual tissues are constructed, with detailed tissue architecture (anisotropy and orthotropy, due to fibre orientation and sheet structure) of the left ventricular wall wedge extracted from a diffusion tensor imaging data set. The models are used to study the effects of tissue heterogeneity and class III drugs on transmural propagation and tissue vulnerability to re-entry. We have determined relationships between the transmural dispersion of action potential duration (APD) and the vulnerable window in the 1D virtual ventricular wall, and demonstrated how changes in the transmural heterogeneity, and hence tissue vulnerability, can lead to generation of re-entry in the 3D ventricular wedge. Two class III drugs with opposite qualitative effects on transmural APD heterogeneity are considered: d-sotalol that increases transmural APD dispersion, and amiodarone that decreases it. Simulations with the 1D virtual ventricular wall show that under d-sotalol conditions the vulnerable window is substantially wider compared to amiodarone conditions, primarily in the epicardial region where unidirectional conduction block persists until the adjacent M cells are fully repolarised. Further simulations with the 3D ventricular wedge have shown that ectopic stimulation of the epicardial region results in generation of sustained re-entry under d-sotalol conditions, but not under amiodarone conditions or in control. Again, APD increase in M cells was identified as the major contributor to tissue vulnerability--re-entry was initiated primarily due to ectopic excitation propagating around the unidirectional conduction block in the M cell region. This suggests an electrophysiological mechanism for the anti- and proarrhythmic effects of the class III drugs: the relative safety of amiodarone in comparison to d-sotalol can be explained by relatively low transmural APD dispersion, and hence, a narrow vulnerable window and low probability of re-entry in the tissue.
Knowledge about drug-drug interactions commonly arises from preclinical trials, from adverse drug reports, or based on knowledge of mechanisms of action. Our aim was to investigate whether drug-drug interactions were discoverable without prior hypotheses using data mining. We focused on warfarin-drug interactions as the prototype.
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Both groups underwent mitral valve replacement or repair (Cardioblate vs control: 16:8 vs 10:15), had similar gender (male: 33% vs 56%), age (66+/-8 years vs 68+/-9 years), additional aortic valve replacement (7 vs 6 patients), tricuspid annuloplasty (13 vs 13 patients), and CABG (10 vs 16 patients). There was 0% operative mortality, 0% postoperative cerebrovascular accidents, but 2 late deaths in the control group. At discharge, 3- and 12-month follow-up, more patients in the Cardioblate group returned to normal SR compared to control (29%, 57% and 75% vs 20%, 43% and 39%; p=0.030). Return of functional atrial contraction in patients in SR at 1 year was comparable between groups (63% vs 89%, NS), and more likely in non-rheumatic pathology and preoperative AF of shorter duration. The effectiveness of atrial contraction was 36+/-14% vs 43+/-18% of transmitral flow and there was no difference between groups. Amiodarone treatment decreased more in Cardioblate group over time (92%, 55% and 29% vs 52%, 52% and 21%; p=0.003), whereas warfarin decrease was comparable (100%, 100% and 71% vs 100%, 95% and 82%; NS).
Fifteen patients aged 59.3 +/- 11.5 years (mean +/- standard deviation [SD]) had recurrent symptomatic ventricular tachycardia (VT) refractory to at least 2 conventional antiarrhythmic drugs. All patients had organic heart disease; 4 had an acute myocardial infarction. The mean ejection fraction was 0.30 +/- 0.09. TWelve patients had overt congestive heart failure. Five had bundle branch block. Before treatment with intravenous amiodarone, the patients had had 6 to 40 episodes of symptomatic VT over 1 to 8 days of hospitalization. All patients received an initial bolus of 5 mg of amiodarone/kg over 15 minutes. Seven patients also received a continuous infusion of 600 to 1,000 mg of amiodarone over 12 to 24 hours. Additional doses depended on the patients' clinical responses. In 11 of 15 patients, antiarrhythmic drugs that had failed to suppress VT were continued during administration of amiodarone. In 12 of 15 patients acute control of VT was obtained with intravenous administration of amiodarone either alone or in combination with previously ineffective drugs. Three patients continued to have frequent episodes of VT while being treated with intravenous amiodarone. Mobitz type I atrioventricular block developed in 1 patient. No patient had high degree atrioventricular block, symptomatic hypotension, or a clinically apparent worsening of congestive heart failure. The use of intravenous amiodarone represents a significant advance in the acute treatment of frequent life-threatening VT refractory to other drugs. With appropriate monitoring, it can be used safely in patients with congestive heart failure, bundle branch block, or acute myocardial infarction.
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The LD50 of amitriptyline obtained from reference sources was confirmed by giving 100 mg/kg to 40 mice by intraperitoneal (IP) injection. The safety of the treatment dose of amiodarone was confirmed by giving 50 mg/kg by IP injection to 10 mice. One hundred and nine mice were randomized to receive pretreatment with 50 mg/kg amiodarone (n=55) or an equal volume of saline or water as a volume control (n=54). Thirty minutes after pretreatment or control injection, the mice received amitriptyline, 100 mg/kg. Outcome was defined as death or survival 3 h after amitriptyline injection.
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Arrhythmogenic right ventricular dysplasia is an inherited, progressive condition. Characterised by fatty infiltration of the right ventricle, it frequently results in life threatening cardiac arrhythmias, and is one of the important causes of sudden cardiac death in the young. There are characteristic electrocardiographic and echocardiographic features that all physicians need to be aware of if we are to reduce these occurrences of premature death. Diagnosis with magnetic resonance imaging is discussed along with current treatment options.
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Serial testing of drugs (STL) by means of programmed electric stimulation (PES) was implemented in 41 patients with relapsing monomorphic persisting ventricular tachycardia (S-KT) of varying aetiology and severity. To reduce underrating of the action of antiarrhythmics, milder criteria were used for evaluation of the short-term and long-term effectiveness of therapy. By STL a total of 137 drugs and their combinations were tested. S-KT was not induced by 60 of them (44%) and in 35 patients (85%). In the remaining 6 patients STL could not be completed because of non-adherence of the patients to the method or because of serious proarrhythmic action of therapy. In the course of long-term follow up (mean 21 months) in positive therapy an arrhythmic episode did not occur during the first year in any of the patients, in the course of two years it occurred in 14%, in three years in 29% and in the course of four years in 33% of the patients. Treatment preventing S-KT had to be abandoned because of serious side-effects in four patients. In all of these four patients later an arrhythmic episode developed. Long-term treatment with antiarrhythmics selected by means of STL by programmed stimulation is a rational approach to pharmacotherapy of serious ventricular arrhythmias. In cases leading to combined treatment with amiodarone and antiarrhythmics class I it would be, however, better in view of the high incidence of serious effects of this treatment to use implantation of a defibrillator.
Pretreatment with GH reduces the burden of ventricular arrhythmias in rats with postinfarction CHF due to acute MI. Growth hormone may be useful in the treatment of CHF and acute MI.
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We conducted a systematic review and aimed to answer the following clinical questions: What are the effects of interventions to prevent embolism, for conversion to sinus rhythm, and to control heart rate in people with recent-onset atrial fibrillation (within 7 days) who are haemodynamically stable? We searched: Medline, Embase, The Cochrane Library, and other important databases up to April 2010 (Clinical Evidence reviews are updated periodically; please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations such as the US Food and Drug Administration (FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA).