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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:

Similar Products:
Cartia Xt, Lanoxin


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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The tissue distribution and hepatic microsomal metabolism of amiodarone were studied in a hyperlipidemic rat model. Rats were rendered hyperlipidemic by the intraperitoneal injection of poloxamer 407. Other normolipidemic animals given saline in place of poloxamer 407 were used as control animals. After single intravenous injection of amiodarone HCl (25mg/kg) rats were anesthetized and plasma and tissue specimens were obtained. Liver microsomal protein was harvested and used to measure velocity of desethylamiodarone formation from amiodarone and cytochrome P450 (CYP) protein expression. Hyperlipidemia caused large increases in plasma concentrations of amiodarone. In tissues, however, concentrations of drug selectively increased, decreased or did not change. In heart, the site of action of the drug, as well as liver and spleen, amiodarone concentrations increased. In other tissues such as kidney, lung and brain, concentrations decreased. No changes were seen in fat or thyroid. Decreases were observed in liver metabolic efficiency, and expression of CYP3A1/2 and 2C11. No changes were seen in CYP2B1/2, 2C6, 2D1 or 1A2. This experimental hyperlipidemia caused a complex pattern of changes in tissue distribution of AM. In addition, there are decreases in the expression of some important rat CYP isoenzymes.

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Patients with apical hypertrophy have a natural favourable history. Non Specific Ventricular Tachycardia (NSVT) at ambulatory monitoring is more favourable if it is not associated with consciousness disorders. A high rate of NSVT episodes at Holter or the association with syncope can lead to a less favourable prognosis and therefore require pharmacological or electric treatment. The role of ET (electrophysiological test) has not yet been clearly described and is in progress. Recent studies of molecular genetics help to identify high-risk patients. Sustained monomorphic VT is not frequent but when it occurs it should be treated with BT. Patients with a light risk of VT should be treated with pharmacological therapy (white amiodarone and/or sotalol) and preferably with implantable defibrillator (ID) if VT cannot be eliminated. ID should be implanted also in the few patients surviving heart attack to avoid the risk of relapses.

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Bacillus stearothermophilus, a useful model to evaluate membrane interactions of lipophilic drugs, adapts to the presence of amiodarone in the growth medium. Drug concentrations in the range of 1-2 microM depress growth and 3 microM completely suppresses growth. Adaptation to the presence of amiodarone is reflected in lipid composition changes either in the phospholipid classes or in the acyl chain moieties. Significant changes are observed at 2 microM and expressed by a decrease of phosphatidylethanolamine (relative decrease of 23.3%) and phosphatidylglycerol (17.9%) and by the increase of phosphoglycolipid (162%). The changes in phospholipid acyl chains are expressed by a decrease of straight-chain saturated fatty acids (relative decrease of 12.2%) and anteiso-acids (22%) with a parallel increase of the iso-acids (9.8%). Consequently, the ratio straight-chain/branched iso-chain fatty acids decreases from 0. 38 (control cultures) to 0.30 (cultures adapted to 2 microM amiodarone). The physical consequences of the lipid composition changes induced by the drug were studied by fluorescence polarization of diphenylhexatriene and diphenylhexatriene-propionic acid, and by differential scanning calorimetry. The thermotropic profiles of polar lipid dispersions of amiodarone-adapted cells are more similar to control cultures (without amiodarone) than those resulting from a direct interaction of the drug with lipids, i.e., when amiodarone was added directly to liposome suspensions. It is suggested that lipid composition changes promoted by amiodarone occur as adaptations to drug tolerance, providing the membrane with physico-chemical properties compatible with membrane function, counteracting the effects of the drug.

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Prolonged periods of atrial fibrillation (AF) or high frequency atrial pacing lead to a significant shortening of atrial refractory periods. This time-dependent electric remodelling is reduced significantly by the administration of verapamil.

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The study included 40 pediatric cardiosurgical patients with postoperative junctional ectopic tachycardia. Intravenous amiodarone in 2-mg/kg boluses and, if necessary, as continuous infusion (10 to 15 mug/kg/min), were used as the first-line therapy. Restoration of sinus rhythm or slowing of junctional ectopic tachycardia to a rate that allowed atrial or atrioventricular sequential pacing was considered as efficacy of therapy.

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In the intervention group, 79.1% (n = 4076; 95% confidence interval [CI], 78.0%-80.2%) of dispensings were monitored compared with 70.2% (n = 3522; 95% CI, 68.9%-71.5%) in the usual-care group (P < .001). For example, 78.6% of amiodarone (95% CI, 73.1%-83.5%) dispensing was monitored in the intervention group vs 51.4% (95% CI, 44.4%-58.4%) in the group receiving usual care (P < .001).

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Many sinus node disease (SND) patients suffer from atrial fibrillation (AF). Anti-arrhythmic drugs (AADs) are the therapeutic mainstay for AF prophylaxis. The PITAGORA trial has a multicentre, prospective, randomized, single blind design to compare amiodarone with Class IC AADs in patients who have an AF history and are paced for SND.

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Metastatic tumors of the ventricles may cause symptomatic ventricular tachycardia such as described in this 66-year-old man, who presented with recurrent presyncope. The tumor may be readily diagnosed by 2-dimensional echocardiography, ultrafast computed tomography, or magnetic resonance imaging. Such tumors usually indicate an advanced stage of disease, and curative treatment is rarely possible. However, in this patient, effective control of the arrhythmia was achieved with a moderate dosage of oral amiodarone (600 mg daily for 4 weeks, then 400 mg daily), and he had no further episodes of presyncope. This report shows that the effectiveness of amiodarone in the control of symptomatic ventricular tachycardias may also extend to those that are probably secondary to metastatic tumors of the heart.

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An open, prospective study of 10 consecutive AIH patients without underlying thyroid abnormalities referred to a tertiary referral center, and treated with KClO4 (600 mg/day) for a period of 26+/-13 days (range, 15-45 days). An additional, historical group of 12 consecutive patients with subclinical AIH left untreated while continuing or after withdrawing amiodarone was retrospectively evaluated as to the outcome of thyroid function.

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The effects of chronic amiodarone treatment on several thyroid and cardiac function parameters were studied in 50 euthyroid patients with refractory ventricular arrhythmias, divided in responders and nonresponders according to their sensitivity to the antiarrhythmic action of the drug. No differences in the severity of cardiac disease and blood amiodarone concentrations were found in the two groups. Amiodarone induced a significant inhibition of peripheral T4 monodeiodination, more pronounced in responders compared to nonresponders. On the contrary, only in responsive patients, elevated basal and TRH-stimulated TSH levels were observed (despite serum T3 levels were not different from those in nonresponders) and the indirect indices of cardiac performance, particularly the systolic time intervals, fell in a range usually observed in the hypothyroid states. These findings suggest that amiodarone, besides the well-known inhibition of T4 to T3 conversion, also induces a partial resistance to the thyroid hormones, which is probably involved in the therapeutical effectiveness of the drug.

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Acute hepatitis is a very rare, but potentially fatal, adverse effect of intravenous amiodarone. We present a case of an 88-year-old man with history of ischemic dilated cardiomyopathy and severely depressed left ventricular function that was admitted to our coronary care unit with diagnosis of decompensated heart failure and non-sustained ventricular tachycardia. A few hours after the beginning of intravenous amiodarone he developed an acute hepatitis. There was a completely recovery within the next days after amiodarone withdrawn and other causes of acute hepatitis have been ruled out. This case highlights the need for close monitoring of hepatic function during amiodarone infusion in order to identify any potential hepatotoxicity and prevent a fatal outcome. Oral amiodarone is, apparently, a safe option in these patients.

cordarone drug information

Amiodarone (AMIO), a potent antiarrhythmic drug, is clinically widely used despite its frequent side effects after chronic administration. These side effects coincide with an intralysosomal accumulation of AMIO and its main metabolite desethylamiodarone (DEA) and may be causally related to the drug-induced intracellular storage of phospholipids (PL). Kinetics of cellular uptake and release of radiolabelled AMIO and DEA were studied following single and multiple exposures of cultured human skin fibroblasts to 5 and 10 microM drug concentrations. AMIO and DEA were efficiently taken up into cultured cells. The rate of uptake was slower than that of other cationic amphiphilic drugs. The intracellular steady state concentrations were in the millimolar range suggesting a lysosomal trapping. Repetitive exposures of cultures resulted in a cumulative and partly saturable drug uptake. The accumulation of DEA was higher than that of AMIO throughout. AMIO and DEA previously taken up into the cells during a 2 hr exposure were completely released into the washing media, suggesting an exchangeable form of the accumulated drugs. Following repetitive exposures only part of the drugs was released. Under chasing conditions using washing media containing non-labelled AMIO and DEA respectively or ammonium chloride the release of the chronically accumulated 14C-labelled drugs was increased. This suggested a drug storage in the form of complexes in acidic compartments. Phospholipid (PL) content as well as individual PL fractions were changed in whole cells and in isolated plasma membranes. PL accumulation is assumed to occur by inhibition of PL degradation due to formation of non-degradable drug-PL complexes or by inhibition of phospholipase activities. Cellular PL accumulation seemed to interfere with PL recycling. Changes in PL composition of purified plasma membranes were in part complementary to the ones in whole cells. The alterations in membrane PL composition may explain the changes in membrane fluidity and the decrease in beta-adrenoceptor density and in isoproterenol-stimulated cAMP formation. The results obtained provide an explanation for the pharmacokinetic, and possibly for the pharmacodynamic and also toxicological behaviour of AMIO and DEA in vivo.

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There was a negative chronotropic effect by both metoprolol and the metoprolol/amiodarone combination in isolated rat hearts. However, the acute effects of the metoprolol/amiodarone combination showed no myocardial contractility depression or bradycardia accentuation compared with metoprolol alone. CF increased by 9.2% at minute 1 through minute 5 (P=0.004) with the metoprolol/amiodarone combination. There was no difference in systolic pressure or myocardial contractility among the groups.

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Methods for estimating the bioavailability of drugs with long elimination half-lives are examined. Provided both absorption and disposition are linear a simple linear regression method is developed which can be used to calculate bioavailability in situations where only an incomplete estimate of the area under the curve (AUC) is available. The regression method and the traditional method of comparing the AUC following an oral dose to the AUC following an i.v. dose were applied to simulated data. It was found that the AUC ratio method works well as long as absorption is complete within the time over which the AUC is computed. The regression method is less precise than the AUC ratio method but is more accurate for drugs with long absorption half-lives. When applied to published data on a beta blocker the two methods produced comparable results. The bioavailability of amiodarone in three human subjects was calculated to be 0.20, 0.44 and 0.98 using the regression method with similar results from the ratio method. It is not possible to estimate the clearance of amiodarone from single dose data.

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This is a retrospective descriptive study.

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Three cases are reported in which resolution of severe esophagitic dyspepsia followed amiodarone therapy for cardiac arrhythmias. This effect has proved long lasting. The mechanism of amiodarone action may be related to its calcium antagonist or nitratelike properties that reduce lower esophageal sphincter tone. An alternate hypothesis calls attention to structural similarities between amiodarone and the histamine antagonist ranitidine, and suggests a previously unrecognized action of amiodarone on histamine receptors.

cordarone drug class

Fluconazole for fungal infections and amiodarone for arrhythmia are commonly prescribed medications, and coadministration of such medications is sometimes inevitable in clinical practice. However, both medications have been associated with prolonged QTc intervals and subsequent arrhythmias, which are sometimes fatal. We present the case of a 75-year-old man with sudden cardiac arrest triggered by coadministration of fluconazole and amiodarone, which raises the need for caution regarding coadministration of these medications. To our knowledge, this case has not been previously described.

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Supraventricular arrhythmias after thoracotomy for pulmonary resections are well documented. There has been considerable interest in their incidence, nature, predictability from preoperative assessment and treatment. The purpose of this study is to define prevalence, type, risk factors for post-thoracotomy supraventricular arrhythmias and to assess the efficacy of amiodarone as an antiarrhythmic drug.

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The effectiveness of amiodarone and quinidine in converting atrial fibrillation of recent onset (less than three weeks) to sinus rhythm was compared in a randomized, open-label study. Patients with signs of heart failure determining a NYHA class 3 or 4, acute myocardial infarction, unstable angina pectoris, sick sinus syndrome, Wolff-Parkinson-White syndrome, conduction disturbances, dysthyroidism, or undergoing concomitant therapy with antiarrhythmic drugs, were excluded from the study. Sixty-eight consecutive patients were randomized to receive amiodarone (group A) or quinidine (group B). Group A was treated with amiodarone intravenously as a bolus of 5 mg/Kg over a 20 min period followed by a 15 mg/Kg infusion during the first 24 hours and then orally at a dose of 0.4 g every 6 hours. Group B was treated with quinidine sulphate orally at a dose of 0.2 g every 6 hours during the first day; 0.4 g every 6 hours the second day and 0.6 g every 6 hours during the third day of therapy. Quinidine was preceded by rapid intravenous digitalization depending on the patient's clinical status so as to obtain a ventricular rate of about 100 beats/min, with subsequent oral digitalis administration in maintenance doses. Both treatments were continued until conversion or for a maximum of three days. If the sinus rhythm was not restored, patients underwent electrical cardioversion. Drug efficacy was assessed on the basis of conversion to sinus rhythm. Six patients converted to sinus rhythm with intravenous digitalization alone and were excluded from the comparison between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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Ten healthy pigs underwent implantation of transvenous pacing systems, after which sterile talc was infused into the pericardial sac via a pericardiotomy. In five animals, PBM was applied to the atrial epicardial surface just before talc infusion. Electrophysiologic evaluations were performed using the pacing system immediately after chest closure and 7 days later. Atrial histologic evaluations were performed.

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We have developed novel cocktail liposomes bearing doxorubicin in their hydrophilic cores, and amiodarone, a potent multidrug resistance inhibitor, in their lipid bilayers. The efficacy of these liposomes was studied in DU145 human prostate carcinoma cells. Intracellular calcein retention, which is inversely proportional to multidrug resistance activity, significantly increased following cell incubation with amiodarone loaded liposomes. Fluorescence confocal microscopy on cells incubated with the cocktail liposomes revealed enhanced intranuclear doxorubicin accumulation. Two liposomal drug concentration combinations were employed to assess the differential cytotoxicity of the cocktail liposomes, doxorubicin (1.4 microM)-amiodarone (15 microM) and doxorubicin 3 (microM)-amiodarone (45 microM), and two incubation times, 5 and 19 h. Cell toxicity was determined by XTT assays at 24, 48, and 72 h following incubation and was significantly enhanced for incubation with the cocktail liposomes. On the whole, we believe that these liposomes will greatly contribute to the cancer chemotherapy arena.

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This study recruited 866 patients, and oral anticoagulant therapy was monitored by the prothrombin time expressed as the international normalized ratio (INR). Genotyping of CYP2C9*2, CYP2C9*3, and VKORC1 3673 polymorphisms was performed.

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QRS duration in the surface electrocardiogram is an easily obtainable parameter with a significant prognostic impact in patients with congestive heart failure and a reduced EF. In this German subgroup of Val-HeFT patients, it was an independent predictor of all-cause mortality.

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Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is one of the most common causes of hyponatremia. The usual causes are malignancies, central nervous system, pulmonary disorders, and drugs. Amiodarone is a broad spectrum antiarrhythmic agent widely used in the management of arrhythmias. The different side effects include thyroid dysfunction, visual disturbances, pulmonary infiltrates, ataxia, cardiac conduction abnormalities, drug interactions, corneal microdeposits, skin rashes, and gastrointestinal disturbances. SIADH is a rare but lethal side effect of amiodarone. We describe a 62-year-old male who was suffering from advanced prostatic malignancy, taking amiodarone for underlying heart disease. He developed SIADH which was initially thought to be paraneoplastic in etiology, but later histopathology refuted that. This case emphasizes the importance of detailed drug history and the role of immunohistochemistry in establishing the diagnosis and management of hyponatremia due to SIADH.

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The aim of the study was to clarify whether the pharmacokinetic interaction between theophylline and mexiletine is mediated by inhibition of CYP1A2 and to assess the possible interaction potential of other antiarrhythmic drugs with drugs metabolized by CYP1A2.

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The purpose of this article is to review the literature on the efficacy of magnesium in addition to Class III antiarrhythmics, specifically amidarone, ibutilide, and dofetilide for the cardioversion of atrial fibrillation.

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The goal of this study was to evaluate the effect of amiodarone on mortality, ventricular arrhythmias and clinical complications in high risk postinfarction patients.

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Amiodarone is an anti-arrhythmic drug with a content of 39% Iodine. No adverse effects on fetal thyroid function have previously been observed with maternal ingestion of Amiodarone during pregnancy. A case of severe congenital hypothyroidism with goiter, associated with maternal ingestion of 200 mg Amiodarone daily from the 13th week of pregnancy, is described here. No other environmental causes of goiter, nor a congenital organic thyroid disorder could be demonstrated.

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cordarone tablets 200mg 2016-02-22

Amiodarone is recognized as the most effective therapy for maintaining sinus rhythm (SR) post cardioversion in patients with atrial fibrillation (AF). It is also recommended for controlling AF in patients with congestive heart failure (CHF). We buy cordarone retrospectively examined the efficacy and safety of oral amiodarone in patients with AF and CHF.

cordarone 10 mg 2015-04-21

Amiodarone is a Class III antiarrhythmic with an adverse-effect profile involving many different organ systems. buy cordarone It also has been shown to inhibit the metabolism of drugs cleared by oxidative microsomal enzymes. Clonazepam undergoes extensive hepatic metabolism, primarily by reduction and acetylation, and is therefore susceptible to altered disposition during concomitant administration of agents that inhibit hepatic microsomal enzymes. Hypothyroidism, occurring in up to 11 percent of patients treated with amiodarone, can also alter drug metabolism and sensitize the central nervous system, thus increasing the potential for toxicity. It is likely that a combination of these factors was responsible for the symptoms described in this patient.

cordarone drug 2015-03-26

Associated with amiodarone (AM) therapy is pneumonitis, which may progress to life-threatening pulmonary fibrosis. Although the etiology of amiodarone-induced pulmonary toxicity (AIPT) is unknown, a role for direct toxicity by oxidative stress has been proposed. We have used a single intratracheal administration of AM (1.8 mg (2.64 mumol)) to male golden Syrian hamsters to investigate the role of oxidative stress in AIPT. The antioxidant capacity of the lung was assessed following AM administration by buy cordarone evaluating glutathione status and antioxidant enzyme activities. The efficacy of treatment with the antioxidant agents butylated hydroxyanisole, diallyl sulfide, and N-acetylcysteine, in attenuation of AM-induced pulmonary fibrosis was also investigated. AM significantly (p < 0.05) increased the ratio of oxidized to total lung glutathione both 30 min (control, 0.93 +/- 0.23%; AM, 2.06 +/- 0.26%) and 120 min (control, 0.90 +/- 0.21%; AM, 3.58 +/- 1.34%) post administration. AM also increased activities of glutathione reductase (by 89%) 3 days post administration, and glutathione peroxidase (by 110 and 45%, respectively) and total superoxide dismutase (by 58 and 35%, respectively) both 3 and 7 days post administration. However, treatment of hamsters with butylated hydroxyanisole (150 s.c.) or diallyl sulfide (200, p.o.) for 3 days prior to AM, or treatment with N-acetylcysteine (10 mg intratracheally) 10 min prior to AM had no effect on pulmonary fibrosis 21 days post treatment, as determined by lung wet weight and hydroxyproline content, and had inconsistent effects on histologically determined disease index.(ABSTRACT TRUNCATED AT 250 WORDS)

cordarone overdose death 2016-02-10

Amiodarone has been found to decrease serum T3 by blocking peripheral T4 5'-deiodinase. This reduction in T3 levels may contribute to the effectiveness of this drug in moderating cardiac arrhythmias. To further characterize the effect of amiodarone on thyroid hormone metabolism and biological action, male Sprague-Dawley rats were thyroidectomized and then fed 500 ug T4 or 50 ug T3 and 500 mg amiodarone/kg of powdered diet for 6 to 8 weeks. Hepatic and cardiac levels of T4, T3, alpha-glycerophosphate dehydrogenase (GPD) and malic enzyme (ME) were used as indicators of thyroid hormone availability and action at the cellular level. Conversion of T4 to T3 was measured in liver homogenates. Serum TSH, T4 and T3 were also measured. Amiodarone reduced hepatic GPD and ME in thyroidectomized rats receiving dietary T4. Liver T4 levels were significantly increased by amiodarone and the T3/T4 ratio was reduced (P less than .05). Amiodarone inhibited hepatic T4 to T3 conversion and decreased serum T3. The decreased T3 action at the cellular level, indicated by the reduction in hepatic GPD and ME, is not due to pharmacologic effects of amiodarone since these enzyme levels were not affected by amiodarone in thyroidectomized buy cordarone rats replaced with T3.

cordarone loading dose 2015-09-06

Most effective improvement of outcome by prevention of full cardiorespiratory arrest. Basic life support: initially five rescue breaths, followed by chest compressions (100-120/min depth about one third of chest diameter), compression-ventilation ratio 15:2. Foreign body airway obstruction with insufficient cough: alternate back blows and chest compressions (infants), or abdominal compressions (children >1 year). Treatment of potentially reversible causes: ("4 Hs and 4 Ts") hypoxia and hypovolaemia, hypokalaemia and hyperkalaemia, hypothermia, and tension pneumothorax, tamponade, toxic/therapeutic disturbances, thrombosis (coronary/pulmonary). Advanced life support: adrenaline (epinephrine) 10 µg/kgBW i.v. or i.o. every 3-5 min. Defibrillation (4 J/kgBW buy cordarone ; monophasic or biphasic) followed by 2 min CPR, then ECG and pulse check. NEWBORNS: Initially inflate the lungs with bag-valve mask ventilation (p(AW) 20-40 cmH₂O). If heart rate remains <60/min, start chest compressions (120 chest compressions/min) and ventilation with a ratio 3:1. Maintain normothermia in preterm babies by covering them with foodgrade plastic wrap or similar. POSTRESUSCITATION PHASE: Early protocol-based intensive care stabilization; initiate mild hypothermia early regardless of initial cardiac rhythm [32-34°C for 12-24 h (adults) or 24 h (children); slow rewarming (<0.5°C/h)]. Consider percutaneous coronary intervention (PCI) in patients with presumed cardiac ischemia. Prediction of CPR outcome is not possible at the scene, determine neurological outcome <72 h after cardiac arrest with somatosensory evoked potentials, biochemical tests and neurological examination. ACUTE CORONARY SYNDROME: Even if only a weak suspicion of an acute coronary syndrome is present, record a prehospital 12-lead ECG. In parallel to pain therapy, administer aspirin (160-325 mg p.o. or i.v.) and clopidogrel (75-600 mg depending on strategy); in ST-elevation myocardial infarction (STEMI) and planned PCI also prasugrel (60 mg p.o.). Antithrombins, such as heparin (60 IU/kgBW, max. 4000 IU), enoxaparin, bivalirudin or fondaparinux depending on the diagnosis (STEMI or non-STEMI-ACS) and the planned therapeutic strategy. In STEMI define reperfusion strategy depending on duration of symptoms until PCI, age and location of infarction. TRAUMA: In severe hemorrhagic shock, definitive control of bleeding is the most important goal. For successful CPR of trauma patients a minimal intravascular volume status and management of hypoxia are essential. Aggressive fluid resuscitation, hyperventilation and excessive ventilation pressure may impair outcome in patients with severe hemorrhagic shock.

cordarone brand name 2016-10-11

Acute intravenous administration of cordarone in a dose of 5 mg/kg was demonstrated to decrease the mean values of the peak increase rate in left ventricular pressure, circulatory myocardial fiber shortening velocity, ejection fraction, and specific peripheral vascular resistance by 19.5, buy cordarone 12.3, 10.3, and 26.2%, respectively. Less marked changes occurred in stroke and cardiac outputs. The effects were more pronounced during a more rapid intravenous administration of the agent, as well as in patients with lower myocardial contractility. Chronic administration of oral cordarone in doses of 200 to 300 mg a day had a low effect on cardiac hemodynamic parameters. Sinus bradycardia was significant in reducing the cardiac output (-10.8%). All the patients displayed prolonged Q-T interval that was maximally apparent in patients with the baseline prolonged interval (+13.1%).

cordarone tablets 2015-11-20

Rat liver mitochondria, cultured rat hepatocytes, or rats were treated with these drugs, and the effects on mitochondrial respiration, beta-oxidation, reactive oxygen buy cordarone species formation, and lipid peroxidation were determined.

cordarone tab 2015-02-16

To assess the effects of propafenone and amiodarone on left atrium and left buy cordarone atrial appendage contractility.

cordarone 20 mg 2016-12-27

This case showed that thyrotoxicosis, MNG and amiodarone may contribute to thyroid carcinogenesis. Amiodarone should be carefully commenced in cases with MNG buy cordarone .

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Pacemakers were adjusted to optimize AF detection. Patients with AF burden >1% were randomized to dronedarone 400 mg twice daily (BID) or placebo. Pacemakers were interrogated after 4 and 12 weeks of treatment. The primary endpoint was the change in AF burden from buy cordarone baseline over the 12-week treatment period. Patients with permanent AF, severe/recently decompensated heart failure, and current use of antiarrhythmic drugs were excluded. AF burden was assessed by a core laboratory blinded to treatment assignment.

cordarone drug class 2015-06-07

We report the case of a heart transplant patient whose cyclosporine clearance decreased by more than 50% after the institution of amiodarone therapy. This interaction necessitated a significant dosage reduction to maintain cyclosporine concentrations within the therapeutic range. To investigate the mechanism of the interaction, a cyclosporine-lipoprotein buy cordarone -binding determination was performed. The results suggest that drug displacement from competitive lipoprotein-binding sites is not responsible for the alterations in cyclosporine pharmacokinetics. Clearance data suggests, however, that the primary mechanism for the interaction is the inhibition cyclosporine metabolism by the cytochrome P-450 system. This report emphasizes the importance of reevaluating therapeutic drug regimens when new agents are added to prevent complications caused by drug interactions. If amiodarone and cyclosporine must be used concomitantly, cyclosporine levels must be monitored frequently, in anticipation of this interaction.

cordarone 50 mg 2015-04-15

This was a prospective observational study over 9 months, set in two general medical wards. We studied consecutive patients (n = 141) who were receiving digoxin. Measurements included digitalis toxicity, defined by ECG criteria and resolution after stopping digoxin; all additional medications (including antiarrhythmics) continued. The observer was "blinded" to serum digoxin buy cordarone level and to concomitant drugs.

cordarone reviews 2016-06-28

Common control trials can be more efficient than buy cordarone other designs, but induce dependence between treatment comparisons and require cautious interpretation.

cordarone tab uses 2017-04-30

To buy cordarone report a case of amiodarone-induced thyrotoxicosis (AIT) concomitant with thyroid cancer in multinodular goiter (MNG).

cordarone dosage 2016-07-01

We have reviewed the records of 65 children with paroxysmal supraventricular tachycardia (PST) without congenital heart disease followed a mean of 4 years, with a total of 121 episodes. PST appeared before 6 months of age in 42 (64.6%) children. Thirteen patients (20%) had a present factor which might predispose to PST in 66.2% of the patients who were younger than 6 months of age, and in only 4.3% of those over 6 months. Wolff-Parkinson-White syndrome was present on surface ECG during sinus rhythm in 26.1% of children younger than 6 months, and in 39. Topamax Drug Classification 1% of those over 6 months. Digoxin was the initial treatment in 84.3% of the episodes with a success rate of 75% when were employed alone and of 84.2% when were employed in combination of quinidine. PST recurred at least once in 35 children (53.8%), the 90% within three months of the first episode. All patients were alive and 63 (96.9%) doing well. One patient developed cerebral anoxia and now has hemiparesia and another patient has incessant PST. We conclude that children with PST without congenital heart disease and without delay in diagnosis had a good outcome.

cordarone tablets dosage 2016-11-11

Atrial fibrillation (AF) usually develops within the first 72 h following cardiac surgery, and is often self-limiting. Within 48 h of acute onset of symptoms, approximately 50% of patients spontaneously convert to normal sinus rhythm. Thus, the relative risks and benefits of therapy must be carefully considered. The etiology of AF following cardiac surgery is similar to that in non-surgical patients except that pericardial inflammation and increased adrenergic tone play an increasingly important role. Further, AF after surgery may be associated with transient risk factors that resolve as the patient moves out from surgery, and the condition is less likely to recur compared to AF arising in other circumstances. Immediate heart rate control is important in preventing ischemia, tachycardia-induced cardiomyopathy, and left ventricular dilatation. At our institution, amiodarone is frequently used as a first-line drug for treating AF after cardiac surgery. Inconsistent prescribing practices, variable dosage regimens, and a lack of consensus regarding the appropriate use of amiodarone prompted the need for developing practice guidelines. Multidisciplinary collaboration between the departments of cardiac surgery Arava Generic Name , pharmacy, and anesthesiology led to the development of a protocol for postoperative AF. We review the clinical evidence from published trials and discuss our guidelines, defining amiodarone use for AF in the cardiac surgery setting.

cordarone 300 mg 2015-09-28

To examine the effects of chronic amiodarone on the electrophysiology of canine pulmonary vein (PV) sleeve preparations and left ventricular Amaryl Maximum Dose wedge preparation.

cordarone 100 mg 2016-10-12

Medicinal antiarrhythmic therapy is either used in the acute setting to convert atrial fibrillation to sinus rhythm or as chronic medication to preserve sinus rhythm if a rhythm control strategy is followed. The choice of the antiarrhythmic agent is based on the presence or absence of structural heart disease. In addition, oral anticoagulation should be established according to current guidelines. In the acute setting the armamentarium comprises flecainide, propafenone, vernakalant and amiodarone. Usually, combination therapy with an atrioventricular (AV) node slowing drug (a beta blocker or verapamil) is used. For chronic rhythm control a class IC drug, such as sotalol, dronedarone and amiodarone is given depending on the comorbidities. In the absence of structural heart disease, rare episodes of paroxysmal atrial fibrillation can be treated by a pill-in-the-pocket strategy, i.e. self-administered pharmacological cardioversion with flecainide or propafenone. Despite recent advances in catheter ablation of atrial fibrillation, medical rhythm control continues to play an important role Tablet Amaryl 3mg due to its ubiquitous availability and relatively easy use. The risk for proarrhythmia has to be evaluated in all patients.

cordarone 100 tablet 2017-07-17

Atypical manifestations of pulmonary toxicity and previously unreported autonomic nervous Flagyl S Suspension system dysfunction complicating amiodarone therapy were observed in a patient being treated for sustained ventricular tachycardia. Pulmonary and hepatic nodules on computed tomographic scan masquerading as metastatic carcinoma were initially noted. Focal infiltrates and a large left pleural effusion mimicking infection, malignant neoplasm, or collagen vascular disease became manifest at a later stage. Autonomic dysfunction presented as incapacitating orthostatic hypotension and persisted for six weeks after amiodarone withdrawal. The pleuropulmonary toxic effects were reversible on discontinuation of amiodarone therapy, and resolution was hastened by short-course steroid treatment.

cordarone mg 2015-10-27

Amiodarone is an effective anti-arrhythmic agent. However, during long-term therapy, patients can develop severe adverse pulmonary reactions that are potentially life-threatening. A case of amiodarone-induced pulmonary toxicity is presented in a 78 Tegretol Alcohol Liver -year-old woman. She developed dyspnea and a pulmonary mass with associated multiple lung nodules mimicking a lung cancer following 5 years of treatment with amiodarone for atrial fibrillation. After drug withdrawal, and without any additional treatment, clinical and radiological improvement was observed, and radiological findings resolved completely within 6 months.

cordarone generic 2017-05-24

Despite the availability and use of effective methods for limiting infarct size with thrombolytic agents and primary angioplasty, patients experiencing a myocardial infarction (MI) are at increased risk for a second cardiac event in the post-MI period (e.g., reinfarction, heart failure, and sudden death). For this reason, postinfarction risk management is crucial. An extensive data base has firmly established the efficacy of beta blockers in reducing cardiovascular risk following acute MI. The full advantages of angiotensin-converting enzyme (ACE) inhibitors have only recently begun to emerge as the result of a growing understanding of the mechanisms of adverse outcomes following MI. The importance of lipid-lowering agents, in particular the "statins," should be considered in all post-MI patients, especially since recent studies have conclusively shown improved survival and reduced rates of MI and coronary artery bypass surgery in this population with this therapy. Aspirin is now considered a standard part of the early management of Trileptal 800 Mg the acute infarct patient as well as for secondary prevention in post-MI patients. At present, chronic anticoagulation with warfarin should be reserved for selected patients. The nondihydropyridine calcium antagonists diltiazem and verapamil can be considered for post-MI use only in patients in whom beta blockers are contraindicated and who have preserved systolic function and/or those without clinical heart failure. In contrast, the dihydropyridine calcium antagonists, particularly nifedipine, have no role in secondary prevention. Although long-term benefits are minimal, nitrates continue to be useful in post-MI patients with residual ischemia (angina or silent ischemia), heart failure (systolic or diastolic), or postinfarction hypertension. Antiarrhythmic agents, except amiodarone, are relatively contraindicated in post-MI patients. Recent data show that vitamin E reduces the rate of nonfatal MI. Its role in cardiovascular death and overall mortality remains to be clarified. Despite their demonstrated value, agents used in secondary prevention generally appear to be underutilized. In addition, when pharmacologic therapies are administered for secondary prevention, they are often prescribed at lower doses than those tested and proved in trials. A greater appreciation for the efficacy and safety profiles of these agents could lead to more widespread use and more pronounced reductions in morbidity and mortality among post-MI patients.

cordarone drug interactions 2016-07-10

Choline incorporation into cardiac myocyte is altered by some antiarrhythmic drugs, suggesting this may be part of their antiarrhythmic Mestinon 90 Mg properties.

cordarone 800 mg 2015-06-13

From the population of patients who underwent ICD implantation for primary or secondary prevention of SCD in 2008-2010, we selected 376 patients with coronary artery disease or dilated cardiomyopathy (56 females, 320 males). Mean age was 66.1 ± 11.2 (range 22-89) years. ICD implantation protocols and in-hospital and outpatient records were reviewed retrospectively. We analysed the following clinical and procedural variables: age, gender, left ventricular ejection fraction (LVEF), New York Heart Association (NYHA) functional class, mean heart rate (HR), QRS width, number of antiarrhythmic ICD interventions, type of SCD prevention, ICD type, performing defibrillation threshold testing (DFT) to establish defibrillation safety margin at ICD implantation, ventricular lead location, history of cardiovascular disease and Seroquel 300 Mg arrhythmia, medications used (amiodarone, sotalol, beta-blockers, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, statins, loop diuretics, aldosterone antagonists). Date and cause of death were established by contacting patient family and/or the hospital to which the patient was admitted shortly before death or the general practitioner caring for the patient (verification of death certificates).