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Fifty-three white rat males were divided into 4 groups: intact, with arrhythmia, with arrhythmia treated with cordaron, with arrhythmia treated with cardiotron. The rats' diet was enriched with animal fats. Anesthesia was made with uretan (1,0-1,2 g/kg, i.p.). Arrhythmia was induced with akonitine (30-40 mg/kg, i.v.). The drugs were administered 12 and 25 days before arrhythmia induction which was registered on ECG at min 3, 5, 15 and 25 in 1, 11 and 111 standard leads. Total lipid fatty acids (TLFA) of plasma were detected in heart inflowing and outflowing blood with gas chromatography. Arrhythmia drastically changes qualitative characteristics of arterio-venous difference for fatty acids. Cordaron and cardiotron prevented arrhythmia in 63-75% cases. TLFA arterio-venous difference recovered by 55-69%. Cordaron and cardiotron may have a mediating mechanism of action on fatty acid absorption by the heart in normalization of normal heart rate in experimental arrhythmia.
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This study was designed to assess the effects of a perioperative dosing regimen of amiodarone administration, high thoracic epidural anesthesia (TEA), or a combination of the 2 regimens on atrial fibrillation (AF) after coronary artery bypass grafting (CABG).
The survival rate of patients undergoing cardiopulmonary resuscitation is 5 to 15%. New cardiopulmonary resuscitation treatment approaches under investigation include the use of vasopressin as a vasopressor, amiodarone for the treatment of ventricular tachyarrhythmias, and adenosine antagonists (i.e., theophylline) for bradyasystolic rhythms. More innovative approaches include the use of thyroid hormone and endothelin.
In AF, there was a higher risk of severe bleeding in smokers, mainly in those treated with VKAs.
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Hypertrophic cardiomyopathy (HCM) is an inherited cardiac disease characterized by unexplained left ventricular hypertrophy, typically involving the interventricular septum. Hypertrophy may be present in infants, but commonly develops during childhood and adolescence. Management of children with HCM aims to provide symptomatic relief and prevention of sudden death, which is the primary cause of death. Unfortunately, no randomized comparative trials to date have assessed different treatment options in HCM. Medical treatment with negative inotropic agents (beta-adrenoceptor antagonists [beta-blockers], verapamil) is the first therapeutic choice in all symptomatic patients. Beta-blockers also appear to have prognostic merit in children. Surgical myectomy is effective in reducing symptoms in children with left ventricular (LV) obstruction who are unresponsive to medical treatment, although a repeat operation may be needed in a substantial proportion of patients due to relapse of LV obstruction. The recently introduced percutaneous septal ablation can also be regarded as a feasible alternative in this cohort. Technical limitations of both invasive therapeutic options should be carefully considered, preferably in experienced centers. Results of recent randomized trials indicate that dual chamber pacing, once considered a therapeutic option for patients with HCM, should only be used as treatment for conduction abnormalities. Regular clinical risk stratification for sudden death is of vital importance for the prevention of sudden death in young patients. Familial history of sudden death at a young age, LV hypertrophy >3 cm, unexplained syncope, nonsustained ventricular tachycardia in Holter monitoring, and abnormal blood pressure response during exercise are currently considered clinical risk factors for sudden death. Each factor has a low positive predictive accuracy, but patients having two or more of these risk factors are deemed as high risk. Secondary prevention of sudden death in patients successfully resuscitated from cardiac arrest and/or sustained ventricular tachycardia warrants treatment with an implantable cardioverter defibrillator (ICD). Primary prevention of sudden death in patients considered to be at high risk should aim at the management of obvious arrhythmogenic mechanisms (paroxysmal atrial fibrillation, sustained monomorphic ventricular tachycardia, conduction system disease, accessory pathway, myocardial ischemia), and the prevention and/or management of ventricular tachyarrhythmias with amiodarone and/or ICD implantation, respectively. The choice of treatment in children is greatly influenced by technical aspects, such as adverse effects of amiodarone, and ICD implantation difficulties or complications. Amiodarone could also be used as a bridge in children at high risk, until they reach adulthood, possibly achieving a lower risk status, or until their physical growth permits ICD implantation as long-term therapy.
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Preoperative characteristics and operative variables of the patients were similar in both groups. Incidence of new-onset atrial fibrillation and maximal ventricular rate response were recorded. The incidence of new-onset atrial fibrillation (11.8% versus 26.5%) (P = .025) and maximal ventricular rate response (109 +/- 13.8 beats/min versus 124.5 +/- 13.9 beats/min) (P = .011) were significantly lower in the amiodarone group. Duration of atrial fibrillation was 17.5 +/- 8.1 hours for the amiodarone group compared with 32.7 +/- 12 hours for the control group (P = .002).
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The study examined the effects of amiodarone on SAECG in relation to the results of programmed ventricular stimulation in 68 patients with old myocardial infarction, spontaneous and inducible sustained ventricular tachycardia (VT).
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Idiopathic verapamil-responsive left ventricular tachycardia is an uncommon arrhythmia in childhood. Although this tachycardia is usually responsive to verapamil, non-pharmacologic therapy may be necessary in the long-term follow-up. We report a thirty-four month old child with incessant left ventricular tachycardia refractory to digoxin and amiodarone. The diagnosis was confirmed by electrophysiologic study. Intravenous verapamil successfully controlled the arrhythmia. On oral verapamil, the patient remains asymptomatic over a follow up period of 7 years and 10 months.
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Twenty pigs were intubated and instrumented to measure aortic pressures and central venous pressures (CVP). After allowing the animals to stabilize for 60 minutes, amiodarone overdose (1 mg/kg/min) was initiated for a maximum of 20 minutes. Afterwards, the animals were randomized into 2 groups. Group A (n = 10) received 0.9% Normal Saline (NS) and Group B (n = 10) received 20% Intralipid® (ILE). A bolus dose of 2 ml/kg in over 2 min time was initially administered in both groups followed by a 45 min infusion (0.2 ml/kg/min) of either NS or ILE.
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Class III antiarrhythmic agents are used for conversion to and maintenance of sinus rhythm from arrhythmias of atrial or ventricular origin. Monotherapy can be limited by adverse events or recurrent arrhythmias. Sotalol, dofetilide, and ibutilide may induce torsade de pointes in 2-8% of patients, whereas amiodarone induces torsade de pointes in less than 1%. We reviewed the literature regarding the possible combination of class III antiarrhythmics and risk for inducing torsade de pointes. Animal studies using amiodarone plus sotalol or d-sotalol suggest that these drug combinations prolong the QTc interval but do not induce torsade de pointes. Similar data extracted from human studies of ibutilide in patients also receiving amiodarone or sotalol showed greater efficacy with combination therapy than with monotherapy, without increased torsade de pointes induction. Reduced transmural dispersion of repolarization with amiodarone and sotalol combination therapy may serve as a mechanism for reducing the risk of torsade de pointes compared with sotalol monotherapy.
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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Cases series. The clinical and biochemical response to medical and surgical management of five consecutive Tasmanian patients presenting with severe type-II amiodarone-associated thyrotoxicosis was reviewed.
According to the update of the Finnish guidelines for management of patients with atrial fibrillation (AF) dronedarone should be used only in patients with non-permanent AF as a second line medication. It is recommended to monitor the patients regularly and stop dronedarone if permanent AF, heart failure or other adverse events are detected. Dabigatran and rivaroxaban can be used as an alternative to warfarin in patients requiring oral anticoagulation therapy. The selection between warfarin and the new anticoagulants should be based on careful evaluation of the benefits and disadvantages of the drugs in a given patient.
We compared the ability of a new amiodarone-like agent, SR 33589, with that of amiodarone, D,L-sotalol, and lignocaine to reduce the incidence of ventricular fibrillation (VF) and associated arrhythmias caused by acute coronary artery occlusion in anesthetized pigs. Ischemia was induced by occlusion of the left coronary descending artery (LAD) for 30 min. Premature ventricular complexes (PVCs), ventricular tachycardia (VT), and ventricular fibrillation (VF) were recorded during coronary occlusion. SR 33589 (1.25, 2.50, and 5 mg/kg intravenously, i.v.) markedly reduced the occurrence of ventricular arrhythmias during ischemia. The incidence of VF was reduced from 90% in the control group to 30% (p < 0.05) with 1.25 mg/kg, to 10% (p < 0.001) with 2.50 mg/kg, and to 20% (p < 0.01) with 5 mg/kg. In addition, SR 33589, especially at the two higher doses, caused a sustained reduction in both the incidence of VT and the number of PVCs per minute. In comparison, amiodarone 10 and 20 mg/kg i.v. reduced the incidence of VF (40 and 50%, respectively), but these reductions never reached a level of statistical significance. The incidence of VT and the number of PVCs per minute were also decreased significantly by amiodarone. D,L-sotalol 3 mg/kg i.v. exerted significant anti-arrhythmic activity; the incidence of VF was reduced 20% (p < 0.01), and both the incidence of VT and number of PVC per minute were also reduced. In contrast, lignocaine given as a 2-mg/kg bolus followed by an infusion at 70 micrograms/kg/min had no antiarrhythmic or antifibrillatory activity in this preparation.(ABSTRACT TRUNCATED AT 250 WORDS)
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Number of shocks per patient per 30 days predicts outcome in Chagas' disease patients treated with ICD.
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In patients with ICDs, beta-blockers had a favorable effect on survival. Sotalol and amiodarone had a neutral effect on survival. There was a trend toward a deleterious effect with digoxin use. These findings suggest a need for further investigation addressing survival effects of antiarrhythmic drugs when given concomitantly in patients with ICDs.
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The anaesthetic management of a patient with a phaeochromocytoma and cardiomyopathy is described. The control of dysrhythmias was the major problem. Ventricular dysrhythmias were treated with lignocaine, and intravenous amiodarone was used to control the supraventricular rhythm disturbances.
Chagas disease is caused by the protozoan Trypanosoma cruzi and is characterized by heart failure and sudden death. Identifying which factors are involved in evolution and treatment response is actually challenging. Thus, the aim of this work was to determine the Th1/Th17 (IL-6, IL-2, TNF, IL-17 and IFN-γ) and Th2 (IL-4 and IL-10) serum profile in Venezuelan Chagasic patients stratified according amiodarone treatment, hypertension and arrhythmias.
We describe a patient who was treated with amiodarone for ventricular arrhythmia based on arrhythmogenic right ventricular dysplasia and who subsequently developed severe amiodarone-induced thyrotoxicosis. Discontinuation of amiodarone resulted in sustained ventricular tachycardia, which was successfully treated with a DC electrical shock, and subsequently atrial fibrillation, leading to brain embolism due to occlusion of the left middle cerebral artery. Combination treatment with amiodarone and prednisolone was effective both in reducing the serum concentration of thyroid hormones and in improving the patient's general condition. As the use of amiodarone becomes more widespread, treatment with prednisolone for this kind of thyrotoxicosis, which is resistant to conventional treatment, will be required increasingly frequently because iodine overload of the thyroid gland persists for some time after discontinuation of amiodarone treatment.
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It is known proved that amiodarone, in chronic therapy, can cause side effects in several organs. The drug, because of its molecular structure and because of its iodine content, interferes with thyroid function and may produce ipo and hyperthyroidism. This should be related to the functional situation and to the autoregulatory mechanisms of the gland and to the iodine amount in the environment. Concerning the pathogenesis of these alterations, a controversy arose about autoimmune mechanisms and the significance which can be ascribed to the presence of circulatory antithyroid antibodies in amiodarone treated patients. In the present work the amount of antithyroid antibodies in a number of amiodarone treated patients has been related to the functional situation of the gland and to the period of treatment. The authors have studied 51 patients under short and long term therapy in comparison with a control group of 36 subjects. All the subjects under consideration live in Northwest Tuscany, an area where iodine intake is moderately low, therefore dysthyroidism and endemic goitre are rather frequent. No significant differences have been found about the amount of circulating antithyroid antibodies in the three groups under consideration.
DAFNE established an effective dose to be 400 mg b.i.d. ADONIS and EURIDIS showed significant prevention of AF/AFL recurrence hazard ratio (HR 0.78 and 0.73) compared to placebo. In ATHENA, cardiovascular death/hospitalization was significantly reduced (HR 0.76) in patients with AF and additional risk factors. ANDROMEDA was stopped because dronedarone increased early mortality (HR 2.13) in advanced heart failure (HF). ERATO found that dronedarone significantly reduced heart rate compared to placebo in patients with AF. DIONYSOS showed that amiodarone was superior to dronedarone to maintain sinus rhythm in patients with AF/AFL.
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We describe a patient with asymptomatic apical hypertrophic cardiomyopathy (AHCM) who later developed cardiac arrhythmias, and briefly discuss the diagnostic modalities, differential diagnosis and treatment option for this condition. AHCM is a rare form of hypertrophic cardiomyopathy which classically involves the apex of the left ventricle. AHCM can be an incidental finding, or patients may present with chest pain, palpitations, dyspnea, syncope, atrial fibrillation, myocardial infarction, embolic events, ventricular fibrillation and congestive heart failure. AHCM is frequently sporadic, but autosomal dominant inheritance has been reported in few families. The most frequent and classic electrocardiogram findings are giant negative T-waves in the precordial leads which are found in the majority of the patients followed by left ventricular (LV) hypertrophy. A transthoracic echocardiogram is the initial diagnostic tool in the evaluation of AHCM and shows hypertrophy of the LV apex. AHCM may mimic other conditions such as LV apical cardiac tumors, LV apical thrombus, isolated ventricular non-compaction, endomyocardial fibrosis and coronary artery disease. Other modalities, including left ventriculography, multislice spiral computed tomography, and cardiac magnetic resonance imagings are also valuable tools and are frequently used to differentiate AHCH from other conditions. Medications used to treat symptomatic patients with AHCM include verapamil, beta-blockers and antiarrhythmic agents such as amiodarone and procainamide. An implantable cardioverter defibrillator is recommended for high risk patients.
Intravenous antidysrhythmic drug; Comparator: Intravenous lidocaine or amiodarone;
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Meta-analysis showed amiodarone to be associated with an increased risk of developing bradycardia and hypotension when used for the prophylaxis of postoperative atrial fibrillation. The greatest risk in the occurrence of these adverse events arose when using regimens containing i.v. amiodarone, initiating prophylaxis during the postoperative period, and using regimens with average daily doses exceeding 1 g.