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This review evaluates the efficacy, safety, tolerability and side effects of dronedarone in the treatment of AF. In particular, the review includes studies comparing: dronedarone and placebo (ANDROMEDA, ATHENA, DAFNE, ERATO, EURIDIS/ADONIS, HESTIA, PALLAS trials), dronedarone and amiodarone (DIONYSOS trial), ranolazine and dronedarone given alone and in combination (HARMONY trial).
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Randomized clinical trial results suggest that the current cardiopulmonary resuscitation and advanced cardiac life support guidelines may need to be modified. Early defibrillation during the electrical phase of cardiac arrest remains the most crucial intervention, but performing cardiopulmonary resuscitation before defibrillation may be more effective, as compared with immediate defibrillation, during the circulatory phase of cardiac arrest. Biphasic waveforms are superior to monophasic damped sine waveforms in achieving defibrillation. Novel cardiopulmonary resuscitation methods that increase negative intrathoracic pressure promote an increase in blood flow return to the heart. These devices have been correlated with improved short-term survival rates during the circulatory phase of cardiac arrest. Vasopressin administration, given alone or in combination with epinephrine, should be considered during the circulatory phase of out-of-hospital cardiac arrest, particularly in patients presenting with asystole as the initial rhythm. Induction of hypothermia during the metabolic phase in cardiac arrest survivors improves 6-month survival rates and neurologic outcomes.
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Of 122,465 patients (353,168 person-years of follow-up, age 72.1 ± 10.3 years, 98.4% males), amiodarone was prescribed in 11,655 (9.5%). Cumulative, unadjusted mortality rates were higher for amiodarone recipients than for nonrecipients (87 vs 73 per 1,000 person-years, P < .001). However, in multivariate and propensity-matched survival analyses, there was no significant difference in mortality (multivariate hazard ratio 1.01, 95% CI 0.97-1.05, P = .51, and propensity-matched hazard ratio 1.02, 95% CI 0.97-1.07, P = .45). The hazard of death was not modified by age, sex, heart failure, kidney function, β-blocker use, or warfarin use, but there was evidence of effect modification among patients diagnosed with AF as an inpatient versus outpatient.
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Inflammatory thyroid disorders encompass a broad spectrum of diseases that are generally self-limited, and relatively easy to diagnose and manage. Autoimmune subtypes are by far the most commonly encountered diagnoses and create the most confusion because of simultaneous overlap and the potential for interconversion among the subtypes. The otolaryngologist will frequently see these disorders and provide valued consultative care and surgical intervention as needed.
Use of molecular pharmacology to reprofile older drugs discovered before the advent of recombinant technologies is a fruitful method to elucidate mechanisms of drug action, expand understanding of structure-activity relationships between drugs and receptors, and in some cases, repurpose approved drugs. The H3 histamine receptor is a G-protein-coupled receptor (GPCR) primarily expressed in the central nervous system where among many things it modulates cognitive processes, nociception, feeding and drinking behavior, and sleep/wakefulness. In binding assays and functional screens of the H3 histamine receptor, the antiarrhythmic drugs lorcainide and amiodarone were identified as potent, selective antagonists/inverse agonists of human and rat H3 histamine receptors, with relatively little or no activity at over 20 other monoamine GPCRs, including H1, H2, and H4 receptors. Potent antagonism of H3 receptors was unique to amiodarone and lorcainide of 20 antiarrhythmic drugs tested, representing six pharmacological classes. These results expand the pharmacophore of H3 histamine receptor antagonist/inverse agonists and may explain, in part, the effects of lorcainide on sleep in humans.
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Electrical storm can be acutely treated with the combination of a class III and a class Ic antiarrhythmic agent when a class III agent alone is insufficient and when radiofrequency ablation is not an option. Patients receiving this drug combination can be discharged from the hospital only if they have an ICD.
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CRT with (atrial transseptal) endocardial LV lead placement is associated with repolarization characteristics that are considered to be less arrhythmogenic than those generated by CS (epicardial) LV lead placement. Further work is needed to determine whether these changes translate to a reduction in proarrhythmia.
Pulmonary toxicity, including fibrosis, is a serious adverse effect associated with the antidysrhythmic drug amiodarone (AM). We tested the potential usefulness of pirfenidone against AM-induced pulmonary toxicity in the hamster model. Intratracheal AM administration resulted in pulmonary fibrosis 21 days posttreatment, as evidenced by an increased hydroxyproline content and histological damage. Dietary pirfenidone administration (0.5% w/w in chow), for 3 days prior to and continuously after AM, prevented fibrosis and suppressed elevation of pulmonary transforming growth factor (TGF)-beta1 mRNA content at 7 and 21 days post-AM. Protection against AM-induced lung damage was not observed when supplementation with pirfenidone was delayed until 7 days following AM administration, suggesting that alteration of early events in AM lung toxicity is necessary for the protective effect of pirfenidone. Both AM and bleomycin, another pulmonary fibrogen, caused inflammation 24 h after intratracheal dosing, measured as increased lactate dehydrogenase activity, protein content, and cellular alterations in bronchoalveolar lavage fluid, with the response to AM markedly greater than that to bleomycin. Administration of AM, but not bleomycin, also caused whole lung mitochondrial dysfunction, alveolar macrophage death, and an influx of eosinophils into the lung, of which pirfenidone was able to decrease only the latter. We conclude that: (1) AM induces alveolar macrophage death and severe, acute pulmonary inflammation with associated eosinophilia following intratracheal administration; (2) mitochondrial dysfunction may play an early role in AM pulmonary injury; and (3) pirfenidone decreases AM-induced pulmonary fibrosis in the hamster, probably through suppression of TGF-beta1 gene expression.
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Ophthalmological examination revealed unilateral optic disc edema with relatively well-preserved visual acuity. In routine tests, results of complete blood count, erythrocyte sedimentation rate, liver and kidney function tests, chest x-ray, Goldmann visual field examination, and brain computed tomography scan were normal. Orbital ultrasonography revealed optic disc edema with prominent optic nerve head and without orbital pathology.
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Between May and December, 1991, the clinical records of 59 patients with auricular fibrillation was checked.
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The lung hydroxyproline content was higher in the treated groups (CTL: 0.35 ± 0.017, AT: 0.38 ± 0.012, AMI: 0.375 ± 0.018 and AMI + AT: 0.38 ± 0.012 unit/mg protein), but did not reach significance when compared with the CTL (p = 0.56). Amiodarone administration significantly increased the score of pulmonary fibrosis (0.5) in comparison with the AT (0.125) and CTL (0) (p < 0.5). The combination of amiodarone and atorvastatin exacerbated the pulmonary fibrosis (1.5; p < 0.01) compared to the AMI (0.5; p < 0.001), AT (0.125) and CTL (0).
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This article is a review of the most recent findings in resuscitation techniques in advanced cardiac life support. The article focuses particularly on the period after July 1, 2003, but relevant new findings before this period are also included.
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Hypertrophy of the myocardium occurring in hypertrophic cardiomyopathy (HCM) may affect different locations of the left ventricle. If the hypertrophy is sited in the region of the basal septum, obstruction of the left ventricular outflow tract (hypertrophic obstructive cardiomyopathy [HOCM]) occurs. characteristic of left ventricular function in HCM is hypercontractility and disordered diastolic relaxation.
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Amiodarone has a high incidence of side effects, but few pro-arrhythmic effects. We report a case of amiodarone-induced torsade de pointes in a child aged 10 years. The patient had severe dilated cardiomyopathy, and even though he was treated with low oral doses of amiodarone, without dosage increments and electrolyte imbalance, he developed torsade de pointes at nights, after T-wave modification and increases of the corrected QT interval (QTc, 20%), QT dispersion (QTd, 175%) and QTcd (116%). The arrhythmic events were preceded by sinus bradycardia at Holter monitoring. Amiodarone therapy was discontinued. Intravenous magnesium administration was not effective in the suppression of torsade de pointes. High-rate atrial pacing prevented recurrences of the arrhythmias and reduced the QTc interval by 20%, QTd by 50%, and QTcd by 70%; QTd and QTcd returned below normal limits. This case underscores the need of careful electrocardiographic monitoring during amiodarone therapy.
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In this non-randomised retrospective study of 139 consecutive patients all patients had inducible ventricular tachycardia at baseline electrophysiological studies. Before the availability of ATPICD, 22 patients were treated with sotalol as part of a randomised study comparing the efficacy of sotalol to amiodarone. After ATPICD became available sotalol was used in 49 patients in whom intravenous testing predicted sotalol to be effective and ATPICD were implanted in 68 patients in whom sotalol was predicted to be ineffective at electrophysiological testing. Thus, 68 patients were treated with an ATPICD and 71 with sotalol.