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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.
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.
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.
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.
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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.
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.
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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.
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.