Atrial fibrillation is the most common of the serious cardiac rhythm disturbances and is responsible for substantial morbidity and mortality. Amiodarone is currently one of the most widely used and most effective antiarrhythmic agents for atrial fibrillation. But during chronic usage amiodarone can cause some serious extra cardiac adverse effects, including effects on the thyroid. Dronedarone is a newer therapeutic agent with a structural resemblance to amiodarone, with two molecular changes, and with a better side effect profile. Dronedarone is a multichannel blocker and, like amiodarone, possesses both a rhythm and a rate control property in atrial fibrillation. The US Food and Drug Administration approved dronedarone for atrial fibrillation on July 2, 2009. In this review, we discuss the role of dronedarone in atrial fibrillation.
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The Multicenter Automatic Defibrillator Implantation Trial (MADIT) and the Coronary Artery Bypass Graft (CABG)-Patch study were the first 2 randomized trials investigating the usefulness of the implanted cardioverter defibrillator (ICD) for primary prevention of sudden death. Patients enrolled in MADIT and CABG-Patch had never experienced a sustained ventricular tachycardia (VT) but were thought to be at high risk of sudden death. All patients had coronary artery disease and severely suppressed left ventricular ejection fraction. CABG-Patch patients received their ICD during CABG surgery. Most MADIT patients already had received CABG or percutaneous transluminal coronary angiography and had no indication for revascularization procedures at study entry. MADIT patients had nonsustained spontaneous VT and inducible, nonsuppressible VT; CABG-Patch patients had only an abnormal signal-averaged electrocardiogram as an indicator of their arrhythmic risk. CABG-Patch patients did not benefit from ICD implantation, presumably due to the influence of revascularization on ischemia and left ventricular function. In contrast, MADIT patients showed an improved survival by the ICD. MADIT patients had no need for revascularization and, presumably, their risk indicator for arrhythmic events was stronger than the one used in CABG-Patch. MADIT criteria have become a class I indication for ICD implantation and, in the absence of testing for suppressibility of induced VTs, a class IIb criterion for ICD implantation. Screening for MADIT patients is expensive, as only relatively few patients after myocardial infarction fulfill the criteria. Nevertheless, in comparison with amiodarone, treatment of MADIT patients with ICDs seems to be cost-effective, especially if ICDs are implanted transvenously and have the improved battery longevity of the current devices.
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The cases presented demonstrate that rescue VT ablation of drug-refractory electrical storm is possible by a substrate-orientated ablation approach even in patients with complex chronic infarction and various VTs.
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Amiodarone is superior to placebo for cardioversion of AF, and even though the onset of conversion is delayed, its efficacy is similar at 24 h compared with class Ic drugs. These results favor amiodarone as a reasonable alternative for patients with recent AF in whom class Ic and other, more rapidly acting antiarrhythmic drugs cannot be used.
Administration of oral azithromycin, in addition to previously well-tolerated long-term amiodarone therapy, was associated with a marked prolongation of QT interval and increased QT dispersion, both substrates for life-threatening ventricular tachyarrhythmia and torsades de pointes. This is a report of QT prolongation and increased QT dispersion associated with the use of azithromycin. The report assumes an added significance, in view of widespread empirical use of this antibiotic for the treatment of lower respiratory infections and belief of its safety in patients with cardiac diseases. Based on the authors' experience, they would like to emphasize that the combination of azithromycin with other drugs known to prolong QT or causing torsades de pointes be used with caution until the question of the proarrhythmic effect of azithromycin is resolved by further studies.
The objective of this prospective study was to identify factors affecting the response to glucocorticoids in a large cohort of patients with type 2 AIT followed prospectively.
Restoration of SR was achieved in 36 of 39 dogs (92.3%). Presence of heart disease or atrial enlargement had no effect on cardioversion characteristics or ability to restore SR. Median duration of SR following cardioversion and treatment with amiodarone was 120 days. Dogs with lone AF remained in SR longer than those with heart disease.
To evaluate the utility of color-flow Doppler sonography (CFDS) in the differential diagnosis and management of AIT.
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A cohort of 1073 patients admitted to the CCU within 24 h of the onset of symptoms of an acute myocardial infarction and heart failure (Killip and Kimball A-B) were randomized to receive amiodarone (n=542) or placebo (n=531) for 6 months. Because of the higher mortality, on an interim analysis, from a 'high dose' of amiodarone or placebo (516 patients) the protocol was changed to a 'low dose' or placebo (557 patients). Mortality with high doses of amiodarone was 16.30% vs 10.16% in the placebo group (P=0.04), whereas mortality with low doses was 6.61% vs 9.47% in the control group (P=0.20). Several non-fatal adverse effects were observed in 108 and 73 patients treated with amiodarone and placebo, respectively.
There were no differences between groups regarding to age, gender and delay from symptoms initiation and medical assistance. Conversion to sinus rhythm occurred, in QG-71.4% cases; PG-47.8% and AG-50% (p > 0.05). Time delay in minutes to conversion were, respectively (media +/- SD): QG-112 +/- 43; PG-44.1 +/- 28; AG-20 +/- 13, significantly lower in PG and AG related to QG (p = 0.001). Although not significant, side effects were observed mostly in PG.
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Retrospective case series of consecutive emergency admissions with haemodynamically-tolerated sustained monomorphic VT administered bolus dose intravenous amiodarone 300 mg, according to current UK advanced life support practice guidelines.
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Amiodarone's role as a cause of toxic optic neuropathy is based on case reports. Annual frequency estimates of 0.36% to 2.0%, which have been made without reference to the dose or duration of treatment, are 12 to 200 times higher than those for idiopathic nonarteritic anterior ischemic neuropathy. The object of this study was to determine the incidence, dose, and time until onset of bilateral vision loss from amiodarone as a secondary end point in an investigation of amiodarone's role in preventing sudden death.
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Several medications have been associated with the development of the BOOP lesion. Often, symptoms include nonproductive cough and shortness of breath with bilateral crackles by examination. Occasionally, there is fever and rash, and, rarely, eosinophilia. The chest radiograph usually shows bilateral patchy infiltrates. In rare situations, the outcome is fatal, although cessation of the medication or treatment with corticosteroid therapy results in resolution of symptoms and radiographic abnormalities for most patients.
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A combined mexiletine and amiodarone treatment was applied in nine cases with recurrent refractory ventricular tachycardia. During the first two days of treatment, mexiletine and amiodarone were perfused intravenously at a dose of 1,000 mg. and 1,500 mg. per 24 hours, respectively. Simultaneously amiodarone was also given orally at a dose of 600 mg. per 24 hours. From the third day onwards, the intravenous administration was interrupted and both drugs were continued orally at a dose of 600 mg. daily. The first three patients were very critically ill and had had at least five episodes of ventricular tachycardia per 24 hours during the last 10 days in the intensive care unit. The treatment resulted in total suppression of the tachycardic episodes within three days after initiation of therapy. In the remaining six cases, ventricular tachycardia was easily initiated by programmed electrical stimulation of the heart. No arrhythmia could be elicited by repeated testing on the seventh day of treatment. The mean follow-up period was 6 months. Two patients with poor left ventricular function died in intractable heart failure. Another one died suddenly 4-1/2 months after his release from the hospital. He had a large aneurysm and whether he continued his treatment is unknown. A fourth patient had an aneurysmectomy; he suffered a recurrence, and died at his second operation. All the others presently remain asymptomatic. The association of a class I (mexiletine) with a class III (amiodarone) agent is theoretically attractive for the treatment of refractory ventricular arrhythmias. The present findings corroborate this hypothesis, but show that this association is not able to protect individuals with severe underlying myocardial damage.
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Dispersion of ventricular repolarization, assessed as QT dispersion in the ECG or by multiple monophasic action potential (MAP) recordings, is defined as the difference between the earliest and latest repolarization. It is thus measured in the time domain. However, myocardial refractoriness is primarily a function of the membrane potential during phase 3 repolarization. The purpose of this study, therefore, was to measure dispersion of ventricular repolarization in the voltage domain and to study its relation to VF inducibility. To further validate this concept, the effect of chronic amiodarone treatment on the voltage dispersion were assessed. MAPs were recorded simultaneously at 10 epicardial and endocardial sites in isolated rabbit hearts, both under baseline conditions (n = 8) and after chronic amiodarone treatment (n = 8). Repolarization dispersion in the voltage domain was calculated as the difference between the highest and lowest repolarization level of all 10 MAPs at 10-ms steps, starting from the MAP plateau level to complete repolarization. Plotting these voltage differences along the time axis resulted in a dispersion curve, which rose during early repolarization, reached a peak during phase 3 repolarization, and thereafter declined toward zero. There was a close correlation between VF vulnerability in response to electrical field stimuli and the time during which voltage dispersion was maximal (r = 0.828, P < 0.0001). Amiodarone caused a right-ward shift of both the dispersion curve (P = 0.007) and VF vulnerability (P = 0.025), but did not change the magnitude nor the shape of the voltage dispersion curve and its relation to VF vulnerability. Repolarization dispersion in the voltage domain describes an alternate approach for evaluating the heterogeneity of ventricular repolarization and may help to characterize arrhythmia susceptibility under experimental conditions.
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A randomized trial of 209 ambulatory patients with recurrent symptomatic persistent atrial fibrillation, conducted from December 2002 through March 2007 at 7 Dutch medical centers.
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A 70-year-old woman suffering from atrial fibrillation was treated with amiodarone, but developed acute respiratory failure necessitating mechanical ventilation for four weeks. Pulmonary function remained restrictively impaired after weaning from the ventilation, due to pulmonary fibrosis. Pulmonary toxicity is a well-known adverse reaction to amiodarone, but it rarely requires mechanical ventilation. The Netherlands Centre for Monitoring of Adverse Reactions to Drugs received II reports of this life-threatening reaction since 1976.
Sequential usage of up to 3 antiarrhythmic drugs of different classes of action provides almost complete success in conversion of recent-onset AF in patients refractory to short-term conversion attempt in the emergency room.
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High uptake and retention of MIBI in thyroid tissue is characteristic in Type I AIT, while in sharp contrast, low uptake of MIBI in the thyroid tissue was observed in Type II AIT. Mixed-type AIT shows uptake value between Types I and II. MIBI imaging outperforms other methods with a lower misdiagnosis rate.
Recent demonstration that the level of sympathetic nervous drive to the failing heart in patients with severe heart failure is a major determinant of prognosis, and that mortality in heart failure is reduced by beta-adrenergic blockade, indicate the clinical relevance of heart failure neuroscience research. The cardiac sympathetic nerves are preferentially stimulated in severe heart failure, with the application of isotope dilution methods for measuring cardiac norepinephrine release to plasma indicating that in untreated patients cardiac norepinephrine spillover is increased as much as 50-fold, similar to levels of release seen in the healthy heart during near maximal exercise. This preferential activation of the cardiac sympathetic outflow contributes to arrhythmia development and to progressive deterioration of the myocardium, and has been linked to mortality in both mild and severe cardiac failure. Although the central nervous system mechanisms involved in the sympathetic nervous activation at present remain uncertain, increased intracardiac diastolic pressure seems to be one peripheral reflex stimulus, and increased forebrain norepinephrine turnover an important central mechanism.Additional neurophysiological abnormalities present in the failing human heart include release of the sympathetic cotransmitters, epinephrine and neuropeptide Y, at high levels more typical of their release during exercise in healthy subjects, and the possible presynaptic augmentation of norepinephrine release from the cardiac sympathetic nerves by the regionally released epinephrine. Following on the demonstrable benefit of beta-adrenergic blockade in heart failure, additional antiadrenergic measures (central suppression of sympathetic outflow with imidazoline binding agents such as clonidine, blocking of norepinephrine synthesis by dopamine-beta-hydroxylase inhibition, antagonism of neuropeptide Y) are now under active investigation.
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Tremendous strides have been made in recent years in the treatment and prevention of sudden cardiac death. Large scale trials have now established several interventions that may improve survival in patients susceptible to sudden cardiac death. In patients who have had a sustained ventricular tachyarrhythmia, the current therapy of choice is an implantable cardioverter defibrillator. For prophylaxis of sudden cardiac death in patients without a previous event, several approaches should be considered. Beta-Adrenergic blocking agents are an effective pharmacologic therapy in patients following myocardial infarction, and their efficacy has also most recently been demonstrated in patients with congestive heart failure. There is no Vaughan Williams class I or III antiarrhythmic drug that has demonstrated efficacy as a prophylactic agent to reduce mortality in these populations, with the possible exception of amiodarone. The best therapeutic approach for prophylactic therapy to prevent sudden cardiac death appears to be the implantable cardioverter defibrillator; however, its use can be justified only in patients at high risk for developing sudden cardiac death. Further work is needed to identify the high risk populations in which this therapy is warranted.
Pediatric resuscitation is a constantly evolving subject that is on the mind of anyone taking care of sick children. Clinicians are continually searching for the most effective methods to resuscitate children in terms of short- and long-term outcomes. It is important to be familiar with not only the agents being used but also the optimal way to use them.
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A total of 3978 episodes of venous catheterization were prospectively included from September 2002 to December 2007. A catheter management protocol was implemented during this period of time. The incidence and variables associated to the occurrence of PPIVC were determined.
One-thousand four hundred and thirty-five acute medical admissions, of whom 40 patients (2.8%) had AF.
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Serum concentrations of total T4 significantly increased in the last 3 days of the study (ANOVA, P = 0.0002). However, serum total T3 progressively and significantly decreased throughout the study (ANOVA, P < 0.0001). Serum free thyroid hormone concentrations (free T3 and free T4) did not significantly change during the study. Serum rT3 (ANOVA, P < 0.0001) and TSH (ANOVA, P = 0.0009) rapidly and progressively increased throughout the study. Starting from the first 24 h, serum concentrations of T3 sulphate (T3-S) significantly and progressively increased from (mean +/- SD) 0.057 +/- 0.029 nmol/l under basal conditions to 0.089 +/- 0.036 nmol/l after 5 days of amiodarone therapy (ANOVA, P = 0.0011). Since total T3 levels progressively decreased throughout the study, the ratio of the T3-S and total T3 values progressively increased from 4.8 +/- 2.7% under basal conditions to 10.6 +/- 7.3% after 5 days of amiodarone therapy (ANOVA, repeated measures, P < 0.0001). Basal serum concentrations of sulphate metabolites of T2 (T2-S, 2.22 +/- 1.7 nmol/l) and T1 (T1-S, 1.29 +/- 0.74 nmol/l) did not significantly change throughout the study.
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In this new era of managed care, the emphasis has been on the reduction of intensive-care stay after coronary artery bypass surgery. "Fast-track" or rapid weaning protocols have become increasingly popular due to evidence that shows their cost-effectiveness and safety. With new advances in surgical and anesthetic techniques, the goal is often to have patients extubated within 4 to 6 hours upon arrival in the intensive-care unit. Patients who are not candidates for the fast-track protocol are often those who either have poor respiratory function and a large A-a gradient or those who have hemodynamic instability from poor cardiac function after bypass. These patients need more intensive care and more traditional weaning from mechanical ventilation. Those that are not able to wean from the mechanical ventilator within a few weeks are candidates for tracheostomy in order to avoid complications from prolonged endotracheal intubation and to improve pulmonary toilet. The treatment of perioperative low cardiac output syndrome is another goal after bypass surgery. Poor cardiac function can be managed with a variety of vasopressor and inotropic agents based on what the suspected derangement is from clinical examination and hemodynamic measurements (eg, low preload, low cardiac index, high or low systemic vascular resistance). Another modality that has been shown to have benefit on reducing hospital stay and costs is prophylaxis for atrial fibrillation, which may occur in 40% of patients who undergo bypass surgery and in 60% of those who undergo valve replacement surgery. Beta-blockers and amiodarone have both been found to be effective as prophylaxis against postoperative atrial fibrillation.
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Postoperative atrial fibrillation is the most frequent complication arising after cardiac surgery, occurring in 40% of cases. The treatment of postoperative atrial fibrillation with epicardial amiodarone/corticosteroid hydrogel delivery can increase efficacy and reduce side effects. To further evaluate whether amiodarone hydrogel is superior to corticosteroid hydrogel or placebo, we performed a randomized prospective study in 150 patients with coronary artery bypass grafting to compare the effectiveness with different epicardial drug approaches in the postoperative period.
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Atrial fibrillation is the most common cardiac rhythm disorder associated with hospitalization. Two therapeutic options have been available: antiarrhythmic drug therapy, and external or internal electrical cardioversion. Electrical cardioversion of atrial fibrillation remains one of the most widely used and effective treatments for the restoration of normal sinus rhythm. However, many patients continue to receive an antiarrhythmic drug before and after cardioversion in an attempt either to cardiovert the arrhythmia chemically or to maintain sinus rhythm after successful cardioversion. Because some pharmacological agents can affect the cardioversion procedure for atrial fibrillation or flutter, and because many patients with such arrhythmias may require electrical cardioversion when they are taking antiarrhythmic drugs, the question of a possible effect of drug therapy on the efficacy and safety of electrical cardioversion of atrial fibrillation arises. Early reports of direct current cardioversion provoking potentially lethal ventricular arrhythmias raised suspicions of an arrhythmogenic role for digoxin antiarrhythmic therapy, and it is customary to withhold these drugs for 24 to 48 h before cardioversion is attempted. However, this complication is likely to arise only in patients who are close to, or actually manifesting, signs of drug toxicity. On the other hand, treatment with therapeutic concentrations of antiarrhythmic drugs before cardioversion may in some cases be associated with a significant reduction in the number of shocks and decreased energy required to restore sinus rhythm, a lower incidence of postshock arrhythmias and a reduced risk of early recurrence of atrial fibrillation.
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To estimate cost-effectiveness of dronedarone versus amiodarone, propafenone, and sotalol in patients with atrial fibrillation (AF).
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Amiodarone is used in treatment of cardiac arrhythmias. Therapeutic use of amiodarone is limited by its side effects, including pulmonary toxicity. Human Placenta Extract (HPE) contains a variety of bio-active substances. Thus, the present study aimed to quantitatively evaluate the protective effects of HPE on the structural lung changes induced by amiodarone using stereological methods. Sprague-Dawley male rats were divided into four groups. The first, second, and third groups received no treatment, amiodarone (100 mg/kg, i.p.), and HPE (500 µL/kg, i.p.), respectively. The fourth group was treated with amiodarone + HPE. The animals' lungs were removed after 10 days. The lung volume was estimated using the Cavalieri principle on the embedded and cut tissue and corrected for shrinkage. The volume density of the parenchyma, alveolar space, and septa were estimated using point-counting method. The surface area of the alveoli, the volume-weighted means alveoli volume, and mean septum thickness were also estimated in all groups. The total volume and thickness of the alveolar septum were increased by 40 % and 28 %, respectively. However, the total volume of the alveolar space was decreased by 31 % in the amiodarone treated-rats. The mean alveolar volume was decreased by 64 % on the average in the amiodarone treated group. Yet, these changes were not detected in the amiodarone+HPE group. Moreover, RBC accumulation in the alveolar space and septa was ameliorated after HPE treatment. HPE can protect the lung tissue from the structural changes induced by amiodarone.