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37 patients were identified with AIT (mean age 65, range 20-86 years). In 30 patients in whom AIT persisted, 25 underwent CFDS.
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It is very important to diagnose correctly the etiology of thyrotoxicosis, because the course and treatment of thyrotoxicosis with low radioactive iodine uptake differ significantly from that of hyperthyroidism due to Graves' disease or toxic nodular goiter. Many causes of subacute thyroiditis have been identified producing a characteristic course of transient hyperthyroidism, followed by hypothyroidism, and usually recovery. Ectopic hyperthyroidism includes factitious thyroid hormone ingestion, struma ovarii, and, rarely, large deposits of functioning thyroid cancer metastases. Iodine-induced hyperthyroidism may be associated with low radioiodine uptakes. Amiodarone-associated hyperthyroidism may be the result of subacute thyroiditis or iodine-induced hyperthyroidism; assessment and treatment can be quite challenging.
One hundred and eighty-four diabetic patients were enrolled in the three trials. Overall, the study population averaged 66.9 +/- 7.3 years of age, 71.7% were male, 7.1% underwent valve surgery, 4.9% had prior AF, 17.9% had heart failure and 84.2% and 41.8% received postoperative beta-blockade and prophylactic amiodarone, respectively. Forty patients (21.7%) received a preoperative TZD and 144 (78.3%) did not. In total, 66 patients (35.9%) developed post-CTS AF. Upon multivariate logistic regression, the preoperative use of TZDs was found to be associated with a 20% non-statistically significant reduction in post-CTS AF (adjusted odds ratio; 0.80, 95% CI 0.32-1.99; p = 0.63).
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In the present manuscript we critically review the available evidence for pleiotropic effects of dronedarone in settings of myocardial and cerebral ischemia/reperfusion, both from experimental and clinical data.
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Successful pharmacological cardioversion of atrial fibrillation causes the left atrium and left atrial appendage contractility impairment similar to that observed with other methods of the sinus rhythm restoration. Following the AF cardioversion the level of left atrial stunning is higher in the patients treated with propafenone than in subjects receiving amiodarone.
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A 68-year-old male was admitted because of progressive dyspnea and tachyarrhythmia. Symptoms of thyrotoxicosis, including agitation, sleep disturbances, and palpitations, had developed 14 days earlier and the patient's condition had worsened despite initiation of antithyroid treatment.
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Class III antiarrhythmic drugs, especially amiodarone (a broad-spectrum antiarrhythmic agent), have gained popularity for use in clinical practice in recent years. Other class III antiarrhythmic drugs include bretylium, dofetilide, ibutilide and sotalol. These agents are effective for the management of various types of cardiac arrhythmias both atrial and ventricular in origin. Class III antiarrhythmic drugs may interact with other drugs by two major processes: pharmacodynamic and pharmacokinetic interactions. The pharmacodynamic interaction occurs when the pharmacological effects of the object drug are stimulated or inhibited by the precipitant drug. Pharmacokinetic interactions can result from the interference of drug absorption, metabolism and/or elimination of the object drug by the precipitant drug. Among the class III antiarrhythmic drugs, amiodarone has been reported to be involved in a significant number of drug interactions. It is mainly metabolised by cytochrome P450 (CYP)3A4 and it is a potent inhibitor of CYP1A2, 2C9, 2D6 and 3A4. In addition, amiodarone may interact with other drugs (such as digoxin) via the inhibition of the P-glycoprotein membrane transporter system, a recently described pharmacokinetic mechanism of drug interactions. Bretylium is not metabolised; it is excreted unchanged in the urine. Therefore the interactions between bretylium and other drugs (including other antiarrhythmic drugs) is primarily through the pharmacodynamic mechanism. Dofetilide is metabolised by CYP3A4 and excreted by the renal cation transport system. Drugs that inhibit CYP3A4 (such as erythromycin) and/or the renal transport system (such as triamterene) may interact with dofetilide. It appears that the potential for pharmacokinetic interactions between ibutilide and other drugs is low. This is because ibutilide is not metabolised by CYP3A4 or CYP2D6. However, ibutilide may significantly interact with other drugs by a pharmacodynamic mechanism. Sotalol is primarily excreted unchanged in the urine. The potential for drug interactions due to hepatic enzyme induction or inhibition appears to be less likely. However, a number of drugs (such as digoxin) have been reported to interact with sotalol pharmacodynamically. If concurrent use of a class III antiarrhythmic agent and another drug cannot be avoided or no published studies for that particular drug interaction are available, caution should be exercised and close monitoring of the patient should be performed in order to avoid or minimise the risks associated with a possible adverse drug interaction.
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The objective of this study was to assess the effectiveness of pre-emptive dexmedetomidine versus amiodarone in preventing junctional ectopic tachycardia (JET) in pediatric cardiac surgery.
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TriService Research Facility.
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Sudden death accounts for a significant proportion of all death in patients with heart failure. Of currently available therapy, amiodarone and the implantable defibrillator (ICD) appear to have the greatest potential to reduce sudden death in heart failure. In this paper, the currently available information on the relative role of amiodarone and implantable defibrillators (ICD) in heart failure is reviewed.
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Intravenous amiodarone can cause severe and refractory hypotension.
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In the evaluation of patients with ventricular arrhythmias, those patients with asymptomatic ventricular arrhythmias, who usually comprise a low-risk population, have to be differentiated from patients with symptomatic ventricular arrhythmias (presyncopal symptoms, syncope, cardiac arrest). In general, patients with asymptomatic ventricular arrhythmias should not be treated with antiarrhythmic drugs; however, patients with recent myocardial infarction and asymptomatic ventricular arrhythmias, which may indicate an increased risk of sudden death, should undergo further risk stratification, since some of them might benefit from preventive antiarrhythmic therapy with a beta-blocking agent of amiodarone. In contrast to asymptomatic patients, patients with symptomatic ventricular arrhythmias are at high risk for sudden death, and, if functional status does not mandate against active therapy, these patients should undergo coronary angiography and electrophysiologic evaluation. Revascularization procedures and specific antiarrhythmic measures such as antiarrhythmic drug therapy, ablative therapy (surgical resection or transcatheter radiofrequency ablation of the arrhythmogenic focus) or the implantation of a cardioverterdefibrillator (ICD) are frequently needed in such patients. Consequently, in this high-risk population, early referral to a cardiac center with an electrophysiologic laboratory is recommended, whereas it should be strongly mandated against empirical antiarrhythmic drug therapy.
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Blood lipid levels were measured in 23 patients with amiodarone associated hypothyroidism (most of them had ischemic heart disease). Abnormalities of lipid spectrum were found in 12 of these patients. All 12 patients were subjected to replacement therapy with l-thyroxine. Compensation of thyroid status was associated with average 12.6 and 12.3% lowering of total and low density lipoprotein cholesterol, respectively. However target levels of low density lipoprotein cholesterol were achieved only in 1 patient. There were no significant changes of high density lipoprotein cholesterol and triglycerides.
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Fibrillatory waves of surface ECG lead V1 closely reflect right atrial, and, to a lesser degree, left atrial activity. Time-frequency analysis allows noninvasive monitoring of antiarrhythmic drug effects on fibrillatory rate and waveform.
Oral amiodarone is a potent antiarrhythmic agent with a slow onset of action. Its electrophysiologic properties following chronic administration are well known, but its acute electrophysiologic actions are poorly defined. The objectives of the present study were to correlate the electrophysiologic actions of intravenous amiodarone in humans with the acute and chronic effects of the drug relative to plasma and tissue concentrations of the drug. In humans (n = 10), 5 mg/kg intravenous amiodarone (serum concentration 6.50 +/- 3.34 micrograms/ml at 10 minutes; 2.13 +/- 0.71 micrograms/ml at 20 minutes, n = 7) increased the AH interval by 16.4% (p less than 0.005), the antegrade effective refractory period (ERP) of the atrioventricular (AV) node by 14.4% (p less than 0.025), and the functional refractory period (FRP) of the AV node by 15.5% (p less than 0.005). The ERP or FRP of the atrium of the right ventricle was not significantly changed; there was no effect on the HV interval or the QT and R-R intervals of the ECG. In rabbits (n = 11) given 10 mg/kg intravenous amiodarone (mean +/- SD serum concentration 0.49 +/- 0.17 micrograms/ml; mean myocardial concentration 7.0 +/- 1.9 micrograms/gm, n = 3), there were no significant effects on the ECG intervals. In isolated rabbit sinoatrial (SA) node, atria, and AV node (three preparations) superfused with 5 X 10(-6)M amiodarone (3.41 micrograms/ml), there was no effect on the action potential duration (APD) or other parameters of the transmembrane potential.(ABSTRACT TRUNCATED AT 250 WORDS)
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Estimates generated using NONMEM indicated that the clearance of AMD was influenced by BMI, age and daily dosage of AMD. The final pharmacokinetic model was CL (L/h) = 0*16 * TBW * 0.53(AGE >or= 65 ) * 0*78(BMI >or= 25) * DD(0.51), V(d) (L) = 10*2 * TBW, where CL is total body clearance, TBW is total body weight (kg), DD (mg/kg/day) is daily dosage of AMD, AGE (years) >or=65 = 1 for patient was 65 years old or over and 0 otherwise, BMI (kg/m(2)) >or=25 = 1 for patient was 25 kg/m(2) or over and 0 otherwise and V(d) is apparent volume of distribution. The clearance of AMD decreased significantly by 22.3% with a BMI higher than 25 kg/m(2). The clearance of AMD also decreased significantly by 46.9% when patient age was more than 65 years.
Atrial tachyarrhythmias (AT) are the most common cardiac rhythm disturbance. In the present study, we analyzed the cholinergic-adrenergic interaction in the in vitro induction of cholinergic-dependent tachyarrhythmia by high-frequency electric stimulation. Tachyarrhythmia was evoked in isolated rat right atria by trains of electric stimuli. Atrial response was expressed as the tachyarrhythmia induction index (ATI, i.e. the fraction of applied trains that resulted in arrhythmia induction). ATI was reversibly increased by 0.6 microM carbachol (CCh), which also decreased atrial spontaneous rate (ASR). In contrast, 10 nM isoproterenol (ISO), 100 microM tyramine and the phosphodiesterase inhibitor isobutyl-methylxanthine (IBMX, 100 microM) increased ASR and decreased ATI. Amiodarone (AMI, 10 microM) reduced ATI in the presence and absence of CCh. Further CCh addition restored ATI in atria treated with either IBMX or AMI, but not when both compounds were present. Increase in ATI by CCh in atria pretreated with IBMX plus ISO was significantly attenuated by 3 mM NaF. The antagonism between cholinergic muscarinic and beta-adrenergic receptor stimulation (the former facilitating and the latter inhibiting tachyarrhythmia installation) possibly involves regulation of the phosphorylation status of adenosine cyclic 3'-5'-monophosphate (cAMP)-dependent protein kinase substrates. Additionally, cAMP-independent, AMI-sensitive mechanism stimulated by CCh (possibly muscarinic-dependent K(+) current activation) seems to contribute to AT facilitation.
Both drugs were equally effective in restoring SR, though procainamide acts quicker in the loading phase. Both medications are safe and side effects develop only in the maintenance phase.
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Of the 48,612 patients who accessed the pharmacy in this VA medical center, 17,760 (36.5%) had an active order for simvastatin 40 mg or 80 mg per day, and 92 of these patients (0.52%) also had an active order for amiodarone. These patients were prescribed simvastatin primarily for secondary prevention (88 [95.7%] with coronary artery disease [CAD] as the indication for statin therapy), and were highly controlled with mean (SD) baseline LDL-C of 71 (21) mg per deciliter. The mean (median) duration of therapy on the combination of amiodarone plus simvastatin 40 mg or more per day was 43 (37) months. Of the 92 patients, 26 (28.3%), 35 (38.0%), and 18 (19.6%) patients had 1, 2, or 3 or more additional risk factors for myopathy, respectively. 16 patients were not converted per protocol to an alternate statin (4 were taken off amiodarone, 2 were taken off statin therapy, 6 had the simvastatin dose reduced to 20 mg per day or less, and 4 were converted to an alternate statin off-protocol), and 14 patients did not have follow-up laboratory values. For the 62 patients converted per protocol and with follow-up laboratory values, there were no statistically significant changes in mean lipid or aminotransferase values after conversion. One patient reported symptoms of myalgia after conversion to rosuvastatin; however, the conversion protocol did not require obtaining creatine kinase values.
From 16,164 out-of-hospital cardiac arrest cases, 500 adult patients using a single antiarrhythmic drug for shock-resistant VT/VF were enrolled and categorized into 4 groups (73 LID, 47 NIF, 173 AMD-≤150, and 207 AMD-300). Multivariate analyses evaluated the outcomes of NIF, AMD-≤150, or AMD-300 groups versus LID group. Odds ratios (ORs) for survival to admission were 3.21 [95% confidence interval (CI): 1.38-7.44, P < 0.01] in NIF and 3.09 (95% CI: 1.55-6.16, P < 0.01) in AMD-≤150 groups and significantly higher than those of the LID group. However, the OR was 1.78 (95% CI: 0.90-3.51, P = 0.10) in AMD-300 group and was not significant than LID group. ORs for 24-hour survival were 6.68 in NIF, 4.86 in AMD-≤150, and 2.97 in AMD-300, being significantly higher in these groups.
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A 62 year old man developed a neuropathy after several months of treatment with amiodarone. The clinical picture was atypical in that it associated a polyradiculoneuritis with cell-protein dissociation and an axial and peripheral cerebellar syndrome. Pathology of muscle and nerve showed dense inclusions in Schwann cell cytoplasm and in pericytes, highly suggestive of fat inclusions. Discontinuation of amiodarone therapy resulted in a slow regression of disorders. Diabetes mellitus developed. Several pathogenic hypotheses are proposed.
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Atrial fibrillation is a common occurrence after cardiac surgery and the source of financial expenditure and complications. A critical literature review was undertaken to examine the use of amiodarone therapy to prevent or manage atrial fibrillation after cardiac surgery. Evidence strongly suggests that perioperative treatment of cardiac patients with amiodarone may reduce the incidence of atrial fibrillation with minimal adverse effects. Further study is warranted to determine the optimal timing and dosing, for the drug's most cost-effective use.
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Amiodarone is a widely used agent for life-threatening arrhythmias. Although amiodarone-induced thyrotoxicosis (AIT) is a major adverse effect that can cause recurrence of arrhythmias and exacerbation of heart failure, risk factors for AIT among amiodarone-treated Japanese patients have not been elucidated. Here, we investigated the prevalence and predictive factors for AIT. The study subjects were 225 patients treated with amiodarone between 2008 and 2012, who were euthyroid before amiodarone therapy. All patients with AIT were diagnosed by measurement of thyroid hormones and ultrasonography. Among the 225 subjects, 13 patients (5.8%) developed AIT and all the patients were classified as Type 2 AIT. Baseline features of patients with AIT were not different from those who did not develop AIT, except for age (AIT, 55.1 ± 13.8, non-AIT, 68.1 ± 12.0 years, P < 0.001). Multivariate analyses using the Cox proportional hazard model identified age as the sole determinant of AIT (hazard ratio: 0.927, 95% confidence interval: 0.891-0.964). Receiver operating characteristic curve analysis identified age of 63.5 years as the cutoff value for AIT with sensitivity of 70.3% and specificity of 69.2%. In summary, this study showed that the prevalence of AIT is 5.8% in Japanese patients treated with amiodarone and that young age is a risk factor for AIT.