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Cordarone (Amiodarone)
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Cordarone

Cordarone is used to treat a variety of different types of fast, abnormal heart rhythms (these are known as tachyarrhythmias). It is used for severe rhythm disorders when other treatments are not effective or cannot be used.

Other names for this medication:

Similar Products:
Cartia Xt, Lanoxin

 

Also known as:  Amiodarone.

Description

Cordarone is an antiarrhythmic. It works by stabilizing the heart rhythm in conditions in which the heart is beating too fast or in an irregular rhythm.

Generic name of Cordarone is Amiodarone.

Cordarone is also known as Amiodarone, Pacerone.

Brand name of Cordarone is Cordarone.

Dosage

Cordarone is best taken with food. However, it is more important to take it consistently with regard to meals. If you take it with food, try to always take it with food to improve absorption of this medicine. If you prefer to take it on an empty stomach, then always try to take it on an empty stomach.

If you want to achieve most effective results do not stop taking Cordarone suddenly.

Overdose

If you overdose Cordarone and you don't feel good you should visit your doctor or health care provider immediately.

Storage

Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F) away from moisture, light and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Cordarone are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Cordarone if you are allergic to Cordarone components.

Do not take Cordarone if you're pregnant or you plan to have a baby, or you are a nursing mother.

Do not take Cordarone if you have complete, second degree, third degree, or severe sinoatrial heart block, an abnormally slow heartbeat, or shock due to serious heart problems, or if you have had fainting due to slow heartbeat (except if you have a pacemaker).

Do not take Cordarone if you are taking cisapride, dofetilide, an H1 antagonist (eg, astemizole, loratadine, terfenadine), an HIV protease inhibitor (eg, ritonavir), a phosphodiesterase type 5 inhibitors (eg, vardenafil), or a streptogramin (eg, dalfopristin, quinupristin).

Lab tests, including electrocardiogram (ECG), chest x-rays, lung tests, liver tests, thyroid tests, and eye exams, may be performed to monitor your progress.

Be careful with Cordarone if you have allergies to medicines, foods, or other substances.

Use Cordarone with great care in case you want to undergo an operation (dental or any other).

Avoid alcohol.

Avoid machine driving.

Try to protect your skin from the sunlight.

Do not stop taking Cordarone suddenly.

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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.

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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.

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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.

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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.

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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.

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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)

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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.

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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.

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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.

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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).

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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.

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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).

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cordarone 60 mg 2016-08-27

Effects of chronic amiodarone therapy on the circadian rhythmicity and buy cordarone power spectral changes of heart rate and QT intervals from Holter recordings were evaluated in three groups of patients: group 1 baseline (n = 10); group 2, treated for 3 to 6 months (n = 11); and group 3, treated for > 1 year (n = 13). Amiodarone reduced heart rate, which reached steady state at 3 to 6 months; bradycardia was evident during the entire 24 hours. The corrected QT (QTc) interval increased as a function of treatment duration. It was 457 +/- 39, 530 +/- 28 (p < 0.001), and 581 +/- 36 (p < 0.0002) msec for groups 1, 2, and 3, after 6 months, respectively. The circadian rhythmicity of QTc was abolished in group 3. Power spectral analysis showed a tendency for amiodarone to reduce both R-R and QT interval variabilities, suggesting inhibition of autonomic control on the heart by the drug. The effectiveness of amiodarone against ventricular arrhythmias may result in part from the sustained bradycardia in concert with continuous uniform prolongation of myocardial repolarization.

cordarone 400 mg 2015-01-14

From a population of 4,039 buy cordarone outpatients referred for evaluation of acute (n = 96) and chronic (n = 3,943) liver disease over a 10-year period, we reviewed the records of those patients diagnosed with acute bona fide drug-induced hepatitis.

cordarone online 2016-09-21

Association of autonomic status and efficacy of therapy with amiodarone was studied in 90 patients with paroxysmal atrial fibrillation of ischemic (n=45, mean age 62 years) and nonischemic (n=45, mean age 38 years) origin buy cordarone . Autonomic status was assessed by measurement of heart rate variability. Electrophysiological and echocardiographical studies were also conducted before and after 4 weeks of amiodarone therapy. Treatment with amiodarone was accompanied by substantial lowering of the tone of autonomic nervous system in patients with adrenergic type of paroxysmal atrial fibrillation while there was no dynamics of parasympathetic tone in patients with vagal or mixed types. Positive association between amiodarone therapy and decrease of left atrial dimension and improvement of left ventricular contractility was also observed. It was concluded that the use of amiodarone was justified in adrenergic but not in vagal or mixed variants of paroxysmal atrial fibrillation.

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Cytochrome P450 2C8 is one of the primary enzymes responsible for the metabolism of a wide range of drugs such as paclitaxel, cerivastatin, and amiodarone. We have sequenced the CYP2C8 gene from 201 Japanese subjects and found five novel nonsynonymous single nucleotide polymorphisms (SNPs): 511G>A (G171S), 556C>T (R186X; X represents the translational stop codon), 556C>G (R186G), 740A>G (K247R), and 1149G>T (K383N), with the allele frequency of 0.0025. The CYP2C8 variants were heterologously buy cordarone expressed in COS-1 cells and functionally characterized in terms of expression level, paclitaxel 6alpha-hydroxylase activity, and intracellular localization. The prematurely terminated R186X variant was undetectable by Western blotting and inactive toward paclitaxel 6alpha-hydroxylation. The G171S, K247R, and K383N variants exhibited properties similar to those of the wild-type CYP2C8. Paclitaxel 6alpha-hydroxylase activity of the R186G transfectant was only 10 to 20% that of wild-type CYP2C8. Furthermore, the R186G variant displayed a lower level of protein expression in comparison to the wild type, which was restored by the addition of a proteasome inhibitor (MG-132; Z-Leu-Leu-Leu-aldehyde). The reduced CO-difference spectral analysis using recombinant proteins from an insect cell/baculovirus system revealed that the R186G variant has a minor peak at 420 nm in addition to the characteristic Soret peak at 450 nm, suggesting the existence of improperly folded protein. These results indicate that the novel CYP2C8 SNPs, 556C>T (R186X) and 556C>G (R186G), could influence the metabolism of CYP2C8 substrates such as paclitaxel and cerivastatin.

cordarone iv dosage 2015-10-09

Patient 1, a 72-year-old man, was admitted with a history of flu-like symptoms and dry cough for three weeks and exertional dyspnea. Prophylactic antibiotic treatment with nitrofurantoin (100 mg/day) had been given for one year for renal calculi. Patient 2, a 64-year-old man, was admitted with increasing buy cordarone dyspnea at rest. He was known to have several cardiological disorders, including episodes of ventricular tachycardia, for which he had been on amiodarone (200 mg/d) for 8 years. Both patients were in reduced general state of health.

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Amiodarone has been used in cardiology for more than 20 years as an anti-angina and anti-arrhythmia agent. In the seventies, variations in thyroid hormone and TSH concentrations buy cordarone were described in treated patients. Only recently, however the pathogenic mechanisms leading to dysthyroidism in long-term treatment have been described. Today, the gravity of amiodarone-induced hyperthyroidism has been greatly reduced due to a better understanding of the underlying mechanisms and better surveillance of thyroid function. In clinical practice, the following attitude can be proposed. Thyroid exploration should be completed before prescribing amiodarone: clinical examination should emphasize personal or familial history in search of dysthyroidism or goitre; hormone assays (TSH, free T4) are needed to eliminate any latent thyroid dysfunction, particularly hyperthyroidism with little or no clinical manifestation but sometimes the causal factor in cardiac symptomatology; search for a significant level of anti-thyroperoxidase antibodies can reveal underlying chronic thyroiditis. After prescription, clinical surveillance and TSH assay should be performed at 3 months then every 6 months during treatment. After withdrawal, surveillance should be continued with check-ups at 6 and 12 months.

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Incidence of JET was 27% possibly due to the large number of Fallot repair and Senning operation. Longer CPB and ACC times buy cordarone are risk factors for JET.

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Action potential duration at 90% buy cordarone repolarization (APD(90)) was not affected by sildenafil in the therapeutic ranges (< or =1 microM), but shortened by higher concentration (> or =10 microM) in both guinea pig papillary muscles and canine Purkinje fibers. D-Sotalol prolonged APD(90) in the same preparations with concentrations > or =1 microM in a reverse frequency-dependent manner. Co-administration of sildenafil (10 and 30 microM) abolished the APD-prolonging effects of D-sotalol (30 microM) and amiodarone (100 microM). Sildenafil, with concentrations up to 30 microM, had no significant effect on both the rapid (I(Kr)) and the slow (I(Ks)) components of the delayed rectifier potassium currents in guinea pig ventricular myocytes. Sildenafil dose-dependently blocked L-type Ca(2+) current (I(Ca,L)), but had no effect on persistent Na(+) current in guinea pig ventricular myocytes. ECG recordings in intact guinea pigs revealed significant shortening of QTc interval by sildenafil (10 and 30 mg/kg orally). The QT-prolonging effects by D,L-sotalol (50 mg/kg) and amiodarone (100 mg/kg) were abolished by sildenafil (30 mg/kg).

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Concomitant administration of grapefruit juice can increase the plasma concentration of numerous drugs in humans and decrease the concentration of a few others. Such elevations of drug plasma concentrations have, on occasion, resulted in adverse clinical effects. Increased concentrations are primarily mediated by chemicals in grapefruit juice, which inhibit the CYP 3A4 drug-metabolizing enzyme in the small intestines. This inhibition decreases the first-pass metabolism of drugs using the CYP 3A4 intestinal system and increases the bioavailability and maximal plasma drug concentrations (Cmax) of the CYP 3A4 substrates. The effect of grapefruit juice on drug metabolism is most pronounced in drugs with a high first-pass metabolism (eg, felodipine, amiodarone), in which it inhibits the first-pass metabolism of the CYP 3A4 substrates leading to an increase in Cmax and area under the concentration time curve (AUC). The use of grapefruit juice with a few specific drugs (eg, fexofenadine, digoxin) may lower plasma drug concentrations by inhibiting buy cordarone drug absorption catalyzed by the organic anion transporting polypeptide (OATP).

cordarone 800 mg 2017-04-21

Five hundred and four amiodarone-naïve patients were randomized to receive dronedarone 400 mg bid (n = 249) or amiodarone 600 mg qd for 28 days then 200 mg qd (n = 255) for at least 6 months. Primary composite endpoint was recurrence of AF (including unsuccessful electrical cardioversion, no spontaneous conversion and no electrical cardioversion) or premature study discontinuation. Main safety endpoint (MSE) was occurrence of thyroid-, hepatic-, pulmonary-, neurologic-, skin-, eye-, or gastrointestinal-specific events, or premature study drug discontinuation following an adverse buy cordarone event.

cordarone generic name 2015-12-18

Amiodarone- (AM-) induced pulmonary toxicity (AIPT) is still a matter of research and is poorly understood. In attempting to resolve this issue, we treated Sprague-Dawley rats with AM doses of 80 mg/kg/day/i.p. for one, two, three, and four weeks. The rats were weighed at days 7, 14, 21, and 28 and bronchoalveolar lavages (BAL) were obtained to determine total leukocyte count (TLC). For each group, lung weighing, histopathology, and homogenization were performed. Fresh homogenates were used for determination of ATP content, lipid peroxides, GSH, catalase, SOD, GPx, GR activities, NO, and hydroxyproline levels. The results showed a significant decrease in body weight and GSH depletion together with an increase in both lung weight and buy cordarone lung/body weight coefficient in the first week. Considerable increases in lung hydroxyproline level with some histopathological alterations were apparent. Treatment for two weeks produced a significant increase in BAL fluid, TLC, GR activity, and NO level in lung homogenate. The loss of cellular ATP and inhibition of most antioxidative protective enzymatic system appeared along with alteration in SOD activity following daily treatment for three weeks, while, in rats treated with AM for four weeks, more severe toxicity was apparent. Histopathological diagnosis was mostly granulomatous inflammation and interstitial pneumonitis in rats treated for three and four weeks, respectively. As shown, it is obvious that slow oedema formation is the only initiating factor of AIPT; all other mechanisms may occur as a consequence.

cordarone 20 mg 2016-07-09

The aim of this study was to evaluate the safety and efficacy of ambulatory external cardioversion (EC) by means of monophasic and biphasic shock in patients with persistent atrial buy cordarone fibrillation (AF).

cordarone dosage 2015-08-10

We performed an eye examination of 22 patients buy cordarone with long-term amiodarone medication. In addition to corrected visual acuity, colour vision was studied with the Standard Pseudoisochromatic Plates part 2 and Farnsworth-Munself 100 hue test. Contrast sensitivity was examined with the Pelli-Robson chart. Visual fields were tested by Goldmann and Friedmann perimetry.

cordarone 50 mg 2016-07-06

Postoperative AF incidence was 25, 15,4, and 17,9% in groups IV, III, and II, respectively, whereas it was 5% in group I which was lower than all other groups, but the difference was only significant between groups I buy cordarone and IV (P=0.012).

cordarone tablet dose 2017-10-27

To review the common corneal manifestations Effexor Best Dosage of systemic medications in order to describe the characteristic clinical features associated with particular systemic drugs, the indications for drug cessation, and the risks for irreversible ocular toxicity.

cordarone 10 mg 2016-08-11

to estimate the prevalence of elderly who had used PIM before being admitted to hospital admission and to identify the risk factors and Allegra Dosage Instructions the hospitalizations related to ADR arising from PIM.

cordarone drug information 2016-06-12

Junctional ectopic tachycardia is common after pediatric heart surgery. After tetralogy of Fallot repair, the incidence of junctional ectopic tachycardia may be as high as 15% to 20%. We introduced prophylactic amiodarone for tetralogy repair. This study was conducted to evaluate Levitra 5mg Online the effectiveness of the prophylactic amiodarone.

cordarone oral dose 2017-09-22

Sustained ventricular tachycardia (VT) in coronary heart disease (CHD) represents a major risk factor for sudden death. The Authors evaluated the prophylactic efficacy of the chronic administration of amiodarone (A) on this arrhythmia and simultaneously the trend of ventricular extrasystole during the antiarrhythmic treatment. Twenty-three patients were examined, 17 with post-infarction cardiopathy and 6 with mixed angina. They showed either 1 or more episodes (2 patients) of sustained VT involving hemodynamic difficulties. The ejection fraction (EF) ranged between 20 and 45% average (35.2 +/- 9). All patients underwent a basal 24 hour ECG 3 days after the VT cardioversion, and every 6 months. All subjects took A orally for a period ranging from 7 to 67 months (average 23.04 +/- 14) at the dose of 800 mg/day 7 for days, and then 200 or 400 mg/day according to the presence or absence of ventricular extrasystoles (VE) greater than or equal to 30/hr and/or Lown's class (L) greater than or equal to 3. No patients died suddenly during the follow-up; 6 of them died for causes other than arrhythmia. Four of them showed only 1 sustained VT relapse after a period of 6 to 11 months. Two of these 4 patients showed a persistent increase of the number of VE and Naprosyn Prescription Dose L-class while, in the remaining 2 patients, the number of VE remained substantially unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

cordarone 100 mg 2015-03-28

Survival rates after out-of-hospital-cardiac-arrest (OHCA) differ widely between EMS systems. Since hypertonic saline appears to improve long-term outcome after OHCA, some local EMS systems have included it in their treatment protocols for OHCA. Our first aim was to give a quality review of one of these protocols. Our second aim was to assess whether short-term survival improves when hypertonic saline is used in resuscitation after Voltaren Xr Medication OHCA.

cordarone tab 2016-03-29

In hearts in which late INa is augmented to mimic congenital Starlix Generic or acquired pathological conditions, amiodarone has a concentration-dependent biphasic effect to induce and then suppress arrhythmic activity, secondary to inhibition of HERG K+ and late Na+ currents. This is the first preclinical model demonstrating the potential for amiodarone to induce TdP.

cordarone overdose 2015-12-12

Clinical trials have reported a low time in therapeutic range (TTR) in patients with atrial fibrillation treated with both warfarin andamiodarone. These trials included centers and countries with both high and low TTRs. What is the impact of amiodarone on the TTR in a single, high-quality anticoagulation clinic? TTR was assessed in amiodarone and nonamiodarone-treated patients from a University anticoagulation clinic. Baseline characteristics between patients ever-taking or never-taking amiodarone were similar, except more amiodarone patients were smokers (19.5 vs. 6.1%, P = 0.0031). The TTR calculated from 8901international normalized ratios (INRs) in 249 nonamiodarone patients with a mean follow-up of 34 ± 20 months (mean INR 36 ± 18) was 66 ± 16.6% compared with 61.3 ± 16.2% (P = 0.111) from 1455 INRs in 41 amiodarone-treated patients with a mean follow-up of 28 ± 20 months (mean INR 35 ± 22). Factors associated with a low TTR were male sex (P = 0.0013), smoker (P = 0.0048), and amiodarone use (P = 0.0374). A second on-treatment analysis, in which the TTR was calculated only during amiodarone therapy, resulted in similar findings; however, amiodarone did not emerge as a predictor of a low TTR. In 11 patients, the TTR prior to amiodarone (54.5 ± 22.2%) was not significantly different in the first 3 months (54.6 ± 33.4%) or after 3 months (67.2 ± 33.7%) of amiodarone. In a single high-quality anticoagulation center, anticoagulation quality, as measured by the TTR, can be comparable in amiodarone and nonamiodarone-treated patients.

cordarone tablets dosage 2017-11-28

In recent years a number of trends in the pharmacologic management of cardiac arrest have developed. Interventions that should be considered, especially for patients with refractory ventricular fibrillation, are high-dose epinephrine and additional antifibrillatory therapies, such as amiodarone and magnesium sulfate. Other advances in the management of refractory ventricular fibrillation include an improved understanding of the mechanism of action of epinephrine and other pressor agents in the arrested heart, and refined indications and recommendations for the use of sodium bicarbonate, lidocaine, bretylium and beta-blocking agents.

cordarone generic 2016-09-26

One hundred six consecutive patients with heart transplants.

cordarone brand name 2015-04-13

There is controversy over whether therapy to prevent ventricular tachyarrhythmias should be selected noninvasively (by trying drugs and monitoring the patient electrocardiographically) or invasively (by selecting a drug that prevents induction of the arrhythmia by programmed stimulation). We randomly assigned 57 patients with symptomatic and demonstrable ventricular tachyarrhythmias to therapy selected either noninvasively or invasively. The tachyarrhythmias involved were sustained ventricular tachycardia (35 patients), nonsustained ventricular tachycardia with hypotension (15 patients), and ventricular fibrillation (7 patients). The noninvasive approach sought reduction of ventricular premature beats by more than 80 percent and of couplets by more than 90 percent, with elimination of three or more successive ventricular beats on ambulatory monitoring and exercise testing. The invasive approach sought to prevent the induction of five or more repetitive beats by programmed stimulation. The noninvasive approach required fewer drug trials (3.2 +/- 1.8 [mean +/- SD] vs. 5.5 +/- 2.8, P less than 0.001) and fewer hospital days (20 +/- 15 vs. 33 +/- 24, P = 0.01) and identified a therapy predicted to be effective for more patients than did the invasive approach (29 of 29 vs. 15 of 28, P less than 0.001). When a predicted effective therapy was not found, amiodarone was prescribed despite persisting inducibility of ventricular tachycardia. Patients randomly assigned to the noninvasive approach had more symptomatic recurrences of tachyarrhythmia than those treated by the invasive approach (two-year actuarial probabilities of 0.50 +/- 0.10 vs. 0.20 +/- 0.08, P = 0.02). Similar differences were observed when amiodarone recipients were excluded. There were only three deaths from recurrent ventricular tachyarrhythmias--two in the group whose treatment was selected noninvasively and one in the group whose treatment was selected invasively (not significant). We conclude that therapy selected by the invasive approach prevents recurrences of ventricular tachyarrhythmias better than that selected by the noninvasive approach.