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We aimed to assess trends in the management of atrial fibrillation (AF) at various levels of medical care in Greece and to compare the treatment practices of cardiologists to those of non-cardiologists.
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This case demonstrates the efficacy of combining rhTSH and lithium to overcome amiodarone-induced low iodine-131 uptake in Graves' disease.
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Itraconazole and amiodarone coadministration can lead to serious cardiovascular adverse events in patients who are critically ill. Intensivists, pharmacists and medical physicians should be aware of the interaction of these two commonly used drugs.
All patients treated with intravenous amiodarone or procainamide during 25 consecutive months for the following mechanisms of SVT were included: orthodromic reciprocating tachycardia, intra-atrial reentrant tachycardia, and ectopic atrial tachycardia; junctional ectopic tachycardia was excluded. Treatment response was categorized as full success, partial success, or failure. Partial success was defined as clinical improvement and/or arrhythmia control but not meeting full success criteria. Adverse events were classified as major (requiring resuscitation) or minor (management changes). There were 40 episodes of SVT in 37 patients (median age, 34 days; 24 with congenital heart disease). Amiodarone was the initial therapy in 26 cases and procainamide in 14 cases. If partial and full success are combined, procainamide was successful in 71% of cases compared with 34% for amiodarone (P=0.046). If partial success is considered a treatment failure, procainamide was successful in 50% compared with 15% for amiodarone (P=0.029). Ten patients received the second medication after the first failed. Success was achieved in 5 of 8 amiodarone-to-procainamide crossovers compared with 1 of 2 procainamide-to-amiodarone crossovers. One major and 10 minor adverse events occurred in amiodarone patients versus 6 minor adverse events in procainamide patients (P=NS).
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Although synthesized as a coronary dilator for use as an antianginal agent over 20 years ago, amiodarone hydrochloride has recently drawn much attention as a potent antiarrhythmic compound for the control of a variety of cardiac dysrhythmias. The rapidly expanding clinical and experimental data continue to emphasize the unusual electrophysiologic, pharmacologic, and especially pharmacokinetic properties of this benzofuran derivative. The compound is a potent coronary dilator and has minimal negative inotropic propensity of a direct nature while exhibiting a mild degree of noncompetitive sympathetic antagonism. Pharmacokinetically, it has a long elimination half-life with a correspondingly long and variable latency of onset of therapeutic effect. Electrophysiologically, the drug has the propensity to lengthen the action potential duration and hence the voltage-dependent effective refractory period in all cardiac tissues after long-term, rather than short-term, administration. It has little effect on depolarization, conduction velocity, or the slow response. The precise ionic mechanisms mediating its effects on repolarization are not known. Clinically, the electrophysiologic effects of the drug differ significantly when it is given by mouth over a longer period and when it is given intravenously, a difference that remains to be explained in terms of mechanism. These differences, however, account for the varying spectrum of the drug's action after single intravenous doses (when its antiarrhythmic effects are essentially explained by the drug's action on the atrioventricular node and possibly its antiadrenergic actions) in comparison to long-term oral administration, which predictably suppresses ectopic activity and lengthens the effective refractory period in all cardiac tissues. These features may account for the drug's remarkable efficacy in the control of supraventricular and ventricular tachyarrhythmias. The safe and rational therapeutic uses of amiodarone as an antiarrhythmic agent presuppose detailed understanding of its manifold pharmacodynamic and pharmacokinetic properties.
Because hERG underlies native cardiac "I(Kr)" channels, hERG/I(Kr) inhibition by DEA as well as amiodarone may contribute to the overall effects of amiodarone administration on cardiac repolarization.
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EURIDIS and ADONIS were double-blind, multinational, parallel-group trials comparing the efficacy and safety of dronedarone with placebo over 12 months. This retrospective subanalysis of EURIDIS/ADONIS compared the effects of dronedarone in patients discontinuing amiodarone within 2 days before randomization ("rapid switch") with results in patients who had received no amiodarone during the 2 months preceding randomization.
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In heart failure, decreased cardiac output leads to a number of adaptive mechanisms. Among these, neuroendocrine activation including activation of the renin-angiotensin-aldosterone system, augmentation of vasopressin and endothelin release, and activation of the sympathetic nervous system occur. The increase of adrenergic drive is characterized by decreased baroreceptor sensitivity, increased plasma norepinephrine levels and cardiac norepinephrine spillover, and desensitization of postsynaptic β-adrenergic signal transduction. While increased sympathetic drive initially helps to maintain contractile performance of the damaged heart, the above changes chronically result in catecholamine refractoriness and are associated with a poor prognosis.Besides diuretics, the current therapy of heart failure includes ACE inhibitors, digitalis, and β-blockers. In addition, there is evidence that AT1 receptor antagonists might be useful, and, in the presence of arrrhythmia, amiodarone is widely used. The current review briefly summarizes how these drugs interfere with the sympathetic nervous system and speculates that antiadrenergic properties might contribute to the beneficial effects of some of these agents with respect to exercise tolerance and survival of patients with heart failure.
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The efficacy and safety of low-dose amiodarone (Cordarone; Wyeth-Ayerst, Philadelphia, PA) was assessed in 62 symptomatic patients with paroxysmal atrial fibrillation who were resistant to at least two types of IA drugs. The beneficial response to this treatment was defined as a reduction in paroxysmal atrial fibrillation of greater than or equal to 50% within 1 month. Of the 42 patients (67.7%) who were responders, 39 (62.9%) were completely free of episodes. Intolerable side effects were seen in 12 patients (19.3%). Tolerable side effects were encountered by 73% of patients. Most of the adverse effects were transient and responded to a reduction in the dose. In conclusion, (1) low-dose amiodarone produces a beneficial response in the prevention of paroxysmal atrial fibrillation, and (2) low-dose amiodarone is well tolerated.
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Extracellular matrix components play an active role in cancer progression and prognosis. Versican, a large extracellular matrix proteoglycan, can promote cancer metastasis through facilitating cell proliferation, adhesion, migration and angiogenesis. We had previously demonstrated that amiodarone caused ectopic overexpression of similar to versican b (s-vcanb), inhibited EGFR/GSK3β/Snail signaling, and enhanced Cdh5 at the heart field of zebrafish, indicating interference with epithelial-mesenchymal transition (EMT). Since S-vcanb is homologous to mammalian versican V2 isoform, we examined the effects of amiodarone on mammalian tumor proliferation, migration, invasion and metastasis in vitro and in vivo and on EMT signaling pathways. Monolayer wound assays and extracellular matrix transwell invasion assays showed reduced migration and invasion by 15 μM amiodarone treated B16OVA, JC, 4T-1, MDA-MB-231 and MCF-7 tumor cell lines. All cancer cell lines showed reduced metastatic capabilities in vivo after treatment with amiodarone in experimental animals. Western blots revealed that EMT-related transcription factors Snail and Twist were reduced and E-cadherin was enhanced in amiodarone treated cells through an EGFR/ERK/GSK3β-dependent pathway. Immunohistochemistry showed amiodarone lead to increased expression of versican V2 isoform concomitant with reduced versican V1. Our study illustrated the role of versican v2 in EMT modulation and cancer suppression by amiodarone treatment.
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Both the Naranjo and Drug Interaction Probability Scales indicated a "probable" relationship between the development of digoxin toxicity and dronedarone. Due to a p-glycoprotein-mediated interaction, dronedarone is able to decrease the renal clearance of digoxin, thus putting patients at risk for potentially fatal digoxin toxicity.
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Three patients with amiodarone induced optic neuropathy presented with mildly decreased vision, visual field defects, and bilateral optic disc swelling. Upon discontinuing the medication, visual function and optic disc swelling slowly improved in all three patients.
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Brugada syndrome predisposes individuals to ventricular arrhythmias and sudden cardiac death, in the absence of structural heart disease. The typical Brugada electrocardiogram (ECG) phenotype is often concealed in affected population, and the existing genetic testing is capable of detecting just about 20% of cases. Therefore, the diagnosis largely requires various pharmacological provocative agents like class I antiarrhythmic drugs to unmask the unique features of Brugada ECG phenotype. We report an unusual case of "unmasking" of Brugada ECG pattern with ventricular tachycardia brought out by amiodarone infusion.
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During cardiopulmonary resuscitation, no specific drug therapy has been shown to improve survival to hospital discharge after cardiac arrest, and only few drugs have a proven benefit for short-term survival. This article reviews recent experimental and clinical data about vasopressor, antiarrhythmic and thrombolytic agents.
Amiodarone produces use-dependent block of cardiac sodium channels in vitro. This study assessed whether similar use-dependent block occurred in 19 patients with coronary artery disease and inducible, sustained, monomorphic ventricular tachycardia treated with amiodarone. Beat-to-beat measurements of ventricular paced QRS durations during 12-beat trains at cycle lengths of 700, 600, 400 and 300 ms were analyzed at a baseline antiarrhythmic drug-free study and after 2 and 10 weeks of amiodarone therapy. At the drug-free study, there were no significant changes in paced QRS durations within the 12-beat trains at any pacing cycle lengths. After 2 and 10 weeks of amiodarone therapy, progressive prolongation of paced QRS durations occurred over the 12-beat trains at pacing cycle lengths of 600, 400 and 300 ms (p less than 0.05). Significant changes in QRS duration were not observed at a pacing cycle length of 700 ms. This progressive prolongation in QRS duration can be fitted as a function of beat number to a monoexponential equation and occurred with an onset time constant of 1.02 +/- 0.41 beats (306 +/- 122 ms) at a pacing cycle length of 300 ms. The magnitude of QRS prolongation increased as the pacing cycle length was shortened. The magnitudes of QRS prolongation were similar after 2 and 10 weeks of amiodarone therapy. In conclusion, use-dependent prolongation in QRS duration occurs at rapid pacing cycle lengths in humans receiving amiodarone.
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Male Sprague-Dawley rats weighing approximately 300 g were used. The animals were randomized into two groups. The intensive care group (IC) n=20 and conventional care group (CC) n=20. Experimental MI was induced by ligation of the left coronary artery producing large anterolateral MI. Animals in the IC group received isoflurane anesthesia and respiratory support postoperatively. The heart rhythm was monitored continuously and ventricular arrhythmias were treated with amiodarone and cardioversion.
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To analyse the current knowledge based on the experimental and clinical research studies focused on cardiopulmonary resuscitation.
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Because postdefibrillation bradycardia or asystole is of clinical concern in patients with implanted automatic cardioverter defibrillators, we analyzed the cardiac rhythm after 157 intraoperative defibrillations in 50 patients undergoing implantation of the device. Factors that could influence the heart rhythm immediately after defibrillation were also analyzed. The postdefibrillation heart rate and the duration of postdefibrillation asystole did not correlate with age, conduction abnormalities, type or duration of arrhythmia before defibrillation, delivered energy, lead system, or left ventricular ejection fraction, but they did correlate with the resting preoperative heart rate and the concomitant performance of coronary artery bypass surgery at the time of defibrillator implantation. Temporary pacing (for prolonged asystole) was required in only two patients, both of whom had also undergone bypass surgery. Fourteen patients being treated with amiodarone had slower resting and postdefibrillation heart rates, but the mean duration of posdefibrillation asystole was similar to that seen in patients not receiving any antiarrhythmic medication. On follow-up, 25 monitored and 178 unmonitored automatic defibrillator discharges occurred in 24 patients, without evidence of symptomatic postdefibrillation bradyarrhythmias. Thus significant postdefibrillation bradyarrhythmias were uncommon, but when such a propensity existed it could not be predicted reliably on clinical grounds alone.
Powikłania leczenia przeciwzakrzepowego można ograniczyć poprzez maksymalizację czasu przebywania pacjenta w optymalnym zakresie terapeutycznym (therapeutic range – TTR). Wciąż jednak niewiele wiadomo na temat czynników predykcyjnych leczenia przeciwzakrzepowego. Celem pracy była ocena jakości leczenia przeciwzakrzepowego u chorych przyjmujących warfarynę oraz identyfikacja czynników wpływających na jego pogorszenie.
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The effects on ventricular arrhythmias of a new class IA drug, flecainide, were compared with those of amiodarone in 10 patients with frequent, chronic, and stable ventricular ectopic beats (VEBs). The study consisted of an initial 1-week, placebo-controlled, baseline period followed by two 12-day, randomized, crossover, double-blind treatment periods with incremental dosage and 1 month of placebo between drug periods. Frequent VEBs, which were present in all 10 patients during both placebo control periods (30 or more VEBs/hour every hour, during 24-hour Holter monitoring), were markedly suppressed (reduction greater than 80%) in nine patients with both drugs (p less than 0.01). There was almost total abolition of the VEBs in six patients with flecainide, and the satisfactory results with a minimal dose in three demonstrate its fast onset of action. Side effects from either agent were infrequent and no discontinuation was necessary. We conclude from our study that flecainide is a highly effective antiarrhythmic agent.
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Mutations in ion channels are common among patients with glioblastoma multiforme (GBM) and promote cell migration and invasion. We sought to evaluate the association between the use of specific ion channel blockers such as digoxin, amiodarone, diltiazem and verapamil and GBM risk and survival.
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Current density of I(f) and the expression of HCN2 and HCN4 were decreased by amiodaron which might be the possible antiarrhythmic working mechanisms of amiodaron.
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Ectopic rhythms with impulse frequency of 60-90 per minute are referred to as "accelerated"; those with the frequency of 91-130 impulses per minute are termed "nonparoxysmal tachycardia". Forty patients (27 with nonparoxysmal tachycardia and 13 with accelerated ectopic rhythms) were under observation. Accelerated rhythms were nearly always free of clinical symptoms and did not require an anti-arrhythmia treatment. Nonparoxysmal supraventricular and ventricular tachycardia was usually accompanied by aggravation of the patient's condition. Nonparoxysmal tachycardia turned to paroxysmal one or vice versa in 7 patients. Cordarone, beta-adrenergic agents and isoptin were particularly effective in the treatment of nonparoxysmal supraventricular tachycardia, while ethmosine, cordaron and rhythmodan proved most effective against ventricular arrhythmia.
The new anti-arrhythmic agents studied in the last decade have mostly come from research orientated towards determining the compounds which block the electrical currents implicated in the process of repolarisation (class III action). To this must be added dronedarone, which is related to amiodarone and as such displays the 4 classes of anti-arrhythmic properties. Pure class III agents prolong the cardiac action potential and therefore the refractory period and QT interval. The conduction velocity is unaltered. These agents act best on re-entry arrhythmias. Dofetilide is a prototype. The class III action is linked to blockade of the Ikr current and can paradoxically lower it at increased heart rates. Dofelitide has not shown a harmful effect on the survival of high risk ischaemic patients. The conversion of atrial tachyarrhythmias into sinus rhythm can be obtained in one to two thirds of cases. As for the prevention of these arrhythmias, its success rate can exceed 60%. On the other hand, the occurrence of torsades de pointe is in the order of 3%, justifying the initiation of treatment under hospital conditions. Ibutilide acts by blocking the Ikr and INa-s currents. Used only intravenously, this agent is capable of converting back to sinus rhythm a third of atrial fibrillation episodes and two thirds of flutter. The risk of torsades de pointe is 3.5% so this treatment must also be commenced in the hospital setting. Azimilide blocks multiple Iks channels as well as Ikr, Ica and Ina. The electrophysiological effect is sustained at rapid heart rates. When evaluated in patients with paroxysmal atrial fibrillation, azimide prolonged the interval until recurrence, associated with an excellent tolerance (torsades de pointe in 0.55% of cases). In a survival study, azimide demonstrated a neutral effect in high risk subjects with diminished ejection fraction and sinusal variability. Unlike the previous agents, dronedarone is a benzofurane with a similar structure to amiodarone but without iodine. The 800 mg dose is associated with the best risk-benefit ratio. In patients with left ventricular dysfunction, the administration of this agent has been associated with excess mortality. Two recent studies on the prevention of atrial fibrillation have demonstrated that dronedarone is moderately effective with an excellent general tolerance.
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We report the cases of 2 adult patients with this combined lesion who underwent simultaneous aortic valve replacement and transpericardial bypass of the coarctation.
We determined the refractoriness and monophasic action potential duration at 90% of repolarization (MAP90), at 5 pacing cycle lengths (300 to 700 ms) and in 5 right atrial sites after internal cardioversion of persistent atrial fibrillation in 27 patients.