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Cordarone (Amiodarone)

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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:
Amidrone, Amiobal, Amiocar, Amiodacore, Amiodar, Amiodarex, Amiodaron, Amiodarona, Amiodaronum, Amiodura, Amiogamma, Amiohexal, Amiokordin, Amiorit, Amiotach, Amirone, Ancaron, Ancoron, Angoron, Angoten, Aratac, Arycor, Asulblan, Atlansil, Braxan, Cardilor, Cardiodarone, Cardiron, Cor mio, Coradona, Corbionax, Cordalin, Cordan, Cordarex, Cornaron, Coronal, Coronax, Coronovo, Daritmin, Daronal, Diarona, Escodaron, Eudarona, Eurythmic, Hexarone, Kendaron, Keritmon, Miocor, Miodar, Miodrone, Mioritmin, Miotenk, Nexterone, Nodis, Novarona, Opacorden, Pacerone, Pacet, Procor, Rhythmiodarone, Rithmik, Ritmocardyl, Rivodaron, Rivodarone, Sedacoron, Tiaryt, Trangorex

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Also known as:  Amiodarone.


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.


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.


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


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.


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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This review evaluates the efficacy, safety, tolerability and side effects of dronedarone in the treatment of AF. In particular, the review includes studies comparing: dronedarone and placebo (ANDROMEDA, ATHENA, DAFNE, ERATO, EURIDIS/ADONIS, HESTIA, PALLAS trials), dronedarone and amiodarone (DIONYSOS trial), ranolazine and dronedarone given alone and in combination (HARMONY trial).

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Randomized clinical trial results suggest that the current cardiopulmonary resuscitation and advanced cardiac life support guidelines may need to be modified. Early defibrillation during the electrical phase of cardiac arrest remains the most crucial intervention, but performing cardiopulmonary resuscitation before defibrillation may be more effective, as compared with immediate defibrillation, during the circulatory phase of cardiac arrest. Biphasic waveforms are superior to monophasic damped sine waveforms in achieving defibrillation. Novel cardiopulmonary resuscitation methods that increase negative intrathoracic pressure promote an increase in blood flow return to the heart. These devices have been correlated with improved short-term survival rates during the circulatory phase of cardiac arrest. Vasopressin administration, given alone or in combination with epinephrine, should be considered during the circulatory phase of out-of-hospital cardiac arrest, particularly in patients presenting with asystole as the initial rhythm. Induction of hypothermia during the metabolic phase in cardiac arrest survivors improves 6-month survival rates and neurologic outcomes.

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Of 122,465 patients (353,168 person-years of follow-up, age 72.1 ± 10.3 years, 98.4% males), amiodarone was prescribed in 11,655 (9.5%). Cumulative, unadjusted mortality rates were higher for amiodarone recipients than for nonrecipients (87 vs 73 per 1,000 person-years, P < .001). However, in multivariate and propensity-matched survival analyses, there was no significant difference in mortality (multivariate hazard ratio 1.01, 95% CI 0.97-1.05, P = .51, and propensity-matched hazard ratio 1.02, 95% CI 0.97-1.07, P = .45). The hazard of death was not modified by age, sex, heart failure, kidney function, β-blocker use, or warfarin use, but there was evidence of effect modification among patients diagnosed with AF as an inpatient versus outpatient.

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Inflammatory thyroid disorders encompass a broad spectrum of diseases that are generally self-limited, and relatively easy to diagnose and manage. Autoimmune subtypes are by far the most commonly encountered diagnoses and create the most confusion because of simultaneous overlap and the potential for interconversion among the subtypes. The otolaryngologist will frequently see these disorders and provide valued consultative care and surgical intervention as needed.

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Use of molecular pharmacology to reprofile older drugs discovered before the advent of recombinant technologies is a fruitful method to elucidate mechanisms of drug action, expand understanding of structure-activity relationships between drugs and receptors, and in some cases, repurpose approved drugs. The H3 histamine receptor is a G-protein-coupled receptor (GPCR) primarily expressed in the central nervous system where among many things it modulates cognitive processes, nociception, feeding and drinking behavior, and sleep/wakefulness. In binding assays and functional screens of the H3 histamine receptor, the antiarrhythmic drugs lorcainide and amiodarone were identified as potent, selective antagonists/inverse agonists of human and rat H3 histamine receptors, with relatively little or no activity at over 20 other monoamine GPCRs, including H1, H2, and H4 receptors. Potent antagonism of H3 receptors was unique to amiodarone and lorcainide of 20 antiarrhythmic drugs tested, representing six pharmacological classes. These results expand the pharmacophore of H3 histamine receptor antagonist/inverse agonists and may explain, in part, the effects of lorcainide on sleep in humans.

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Electrical storm can be acutely treated with the combination of a class III and a class Ic antiarrhythmic agent when a class III agent alone is insufficient and when radiofrequency ablation is not an option. Patients receiving this drug combination can be discharged from the hospital only if they have an ICD.

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 CRT with (atrial transseptal) endocardial LV lead placement is associated with repolarization characteristics that are considered to be less arrhythmogenic than those generated by CS (epicardial) LV lead placement. Further work is needed to determine whether these changes translate to a reduction in proarrhythmia.

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Pulmonary toxicity, including fibrosis, is a serious adverse effect associated with the antidysrhythmic drug amiodarone (AM). We tested the potential usefulness of pirfenidone against AM-induced pulmonary toxicity in the hamster model. Intratracheal AM administration resulted in pulmonary fibrosis 21 days posttreatment, as evidenced by an increased hydroxyproline content and histological damage. Dietary pirfenidone administration (0.5% w/w in chow), for 3 days prior to and continuously after AM, prevented fibrosis and suppressed elevation of pulmonary transforming growth factor (TGF)-beta1 mRNA content at 7 and 21 days post-AM. Protection against AM-induced lung damage was not observed when supplementation with pirfenidone was delayed until 7 days following AM administration, suggesting that alteration of early events in AM lung toxicity is necessary for the protective effect of pirfenidone. Both AM and bleomycin, another pulmonary fibrogen, caused inflammation 24 h after intratracheal dosing, measured as increased lactate dehydrogenase activity, protein content, and cellular alterations in bronchoalveolar lavage fluid, with the response to AM markedly greater than that to bleomycin. Administration of AM, but not bleomycin, also caused whole lung mitochondrial dysfunction, alveolar macrophage death, and an influx of eosinophils into the lung, of which pirfenidone was able to decrease only the latter. We conclude that: (1) AM induces alveolar macrophage death and severe, acute pulmonary inflammation with associated eosinophilia following intratracheal administration; (2) mitochondrial dysfunction may play an early role in AM pulmonary injury; and (3) pirfenidone decreases AM-induced pulmonary fibrosis in the hamster, probably through suppression of TGF-beta1 gene expression.

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Ophthalmological examination revealed unilateral optic disc edema with relatively well-preserved visual acuity. In routine tests, results of complete blood count, erythrocyte sedimentation rate, liver and kidney function tests, chest x-ray, Goldmann visual field examination, and brain computed tomography scan were normal. Orbital ultrasonography revealed optic disc edema with prominent optic nerve head and without orbital pathology.

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Between May and December, 1991, the clinical records of 59 patients with auricular fibrillation was checked.

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The lung hydroxyproline content was higher in the treated groups (CTL: 0.35 ± 0.017, AT: 0.38 ± 0.012, AMI: 0.375 ± 0.018 and AMI + AT: 0.38 ± 0.012 unit/mg protein), but did not reach significance when compared with the CTL (p = 0.56). Amiodarone administration significantly increased the score of pulmonary fibrosis (0.5) in comparison with the AT (0.125) and CTL (0) (p < 0.5). The combination of amiodarone and atorvastatin exacerbated the pulmonary fibrosis (1.5; p < 0.01) compared to the AMI (0.5; p < 0.001), AT (0.125) and CTL (0).

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This article is a review of the most recent findings in resuscitation techniques in advanced cardiac life support. The article focuses particularly on the period after July 1, 2003, but relevant new findings before this period are also included.

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Hypertrophy of the myocardium occurring in hypertrophic cardiomyopathy (HCM) may affect different locations of the left ventricle. If the hypertrophy is sited in the region of the basal septum, obstruction of the left ventricular outflow tract (hypertrophic obstructive cardiomyopathy [HOCM]) occurs. characteristic of left ventricular function in HCM is hypercontractility and disordered diastolic relaxation.

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Amiodarone has a high incidence of side effects, but few pro-arrhythmic effects. We report a case of amiodarone-induced torsade de pointes in a child aged 10 years. The patient had severe dilated cardiomyopathy, and even though he was treated with low oral doses of amiodarone, without dosage increments and electrolyte imbalance, he developed torsade de pointes at nights, after T-wave modification and increases of the corrected QT interval (QTc, 20%), QT dispersion (QTd, 175%) and QTcd (116%). The arrhythmic events were preceded by sinus bradycardia at Holter monitoring. Amiodarone therapy was discontinued. Intravenous magnesium administration was not effective in the suppression of torsade de pointes. High-rate atrial pacing prevented recurrences of the arrhythmias and reduced the QTc interval by 20%, QTd by 50%, and QTcd by 70%; QTd and QTcd returned below normal limits. This case underscores the need of careful electrocardiographic monitoring during amiodarone therapy.

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In this non-randomised retrospective study of 139 consecutive patients all patients had inducible ventricular tachycardia at baseline electrophysiological studies. Before the availability of ATPICD, 22 patients were treated with sotalol as part of a randomised study comparing the efficacy of sotalol to amiodarone. After ATPICD became available sotalol was used in 49 patients in whom intravenous testing predicted sotalol to be effective and ATPICD were implanted in 68 patients in whom sotalol was predicted to be ineffective at electrophysiological testing. Thus, 68 patients were treated with an ATPICD and 71 with sotalol.

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cordarone 150 mg iv 2016-10-01

We determined the incidence of stroke or peripheral or pulmonary embolism in patients with no history of atrial fibrillation (n=2114), predictors of thromboembolism and the relationship to left ventricular ejection fraction. Median follow-up was 45.5 months. Kaplan-Meier estimates (95% CIs) for the incidence of thromboembolism by 4 years were 4.0% (3.0% to 4.9%), with 2.6% (1.1% to 4.1%) in patients randomized to amiodarone, 3.2% (1 Abilify Maintena Dose .8% to 4.7%) in patients randomized to ICD, and 6.0% (4.0% to 8.0%) in patients randomized to placebo (approximate rates of 0.7%, 0.8%, and 1.5% per year, respectively). By multivariable analysis, hypertension (P=0.021) and decreasing left ventricular ejection fraction (P=0.023) were significant predictors of thromboembolism; treatment with amiodarone or ICD treatment was a significant predictor of thromboembolism-free survival (P=0.014 for treatment effect; hazard ratio [95% CI] versus placebo, 0.57 [0.33 to 0.99] for ICD; 0.44 [0.24 to 0.80] for amiodarone). Inclusion of atrial fibrillation during follow-up in the multivariable model did not affect the significance of treatment assignment as a predictor of thromboembolism.

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In patients with symptomatic AF, QOL improves after treatment, independent of the specific drug used for treatment. This is especially true for patients in whom treatment prevents Zocor Cold Medicine AF recurrence.

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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 Cymbalta Dosage Sweating , 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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To determine the incidence of postoperative junctional ectopic tachycardia (JET), we reviewed 343 consecutive patients undergoing surgery between 1997 and 1999. The impact of this arrhythmia on in-hospital morbidity Augmentin Weight Based Dosing and our protocol for treatment were assessed.

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We performed a retrospective analysis of nine infants (median Geodon Recommended Dosage age 2 months) who received combined flecainide and amiodarone therapy for attempted control of refractory tachyarrhythmias. Trough serum drug levels of flecainide were monitored, and 24-h ambulatory electrocardiographic monitoring was used to determine efficacy of therapy.

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Perioperative atrial arrhythmias (PAAs) in noncardiothoracic Motrin 300 Dosage patients have poorly defined risk factors and management.

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7 controlled studies were identified (n=117) testing 6 combinations of resuscitative medications. ROSC rates for treatment versus control groups were as Highest Dosage Of Effexor Xr follows: amiodarone (6% vs. 18%, p=0.6, n=34), bretylium (35% vs. 35%, p=1.0, n=40), intermediate- and high-dose epinephrine (adrenaline) (36% vs. 27%, p=1.0, n=22), vasopressin (60% vs. 0%, p<0.0001, n=39), vasopressin and amiodarone (0% vs. 0%, p=NS, n=11), low-dose epinephrine and amiodarone (91% vs. 30%, p=0.0075, n=21). Cumulatively, among all studies administering vasopressors, the rate of ROSC was 62% in treatment groups contrasted to 17% in control groups (p<0.0001, n=77).

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To investigate the feasibility and effectiveness of radiofrequency catheter ablation (RFCA) to treat per-manent atrial fibrillation (AF) under the guidance of Benicar Max Dose Carto-Merge technique.

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Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, and is associated with a significantly increased risk of thromboembolic events and mortality. From the age of 50 years, prevalence of AF doubles every 10 years, being more common in males and reaching 5.9% in patients 65 years and older. The treatment of AF has as first objective the restoration and maintenance of sinus rhythm. The drugs used to date present several limitations in terms of side and pro-arrhythmic effects, associated with a limited antiarrhythmic effect. Recent European guidelines for the management of AF have pointed out that the pharmacological antiarrhythmic Betnovate 1 Mg Cream therapy to maintain sinus rhythm is helpful for symptoms related to the arrhythmia. Amiodarone is the drug with the greatest potential for maintenance of sinus rhythm in the older population as well. Other drugs currently in use are flecainide, propafenone, sotalol, and more recently introduced dronedarone and vernakalant. To date, there is no consensus among scientific societies on the management of AF: for elderly patients, who account for the majority of patients with AF, a strictly individualized evaluation is mandatory.

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The aims of this review paper are: (1) to identify the pharmacological basis of interference of a variety of Glucophage 500 Mg Weight Loss substances with MIBG uptake; and (2) to update the list of drugs that definitely interfere with MIBG on the grounds of evidence in the literature.