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Therapeutic hypothermia (TH) is a process of cooling a patient post ventricular tachycardia/ventricular fibrillation (VT/VF) cardiac arrest to 32-34 degrees C for 24 hours. This improves neurological outcome and is part of current guidelines. Hypothermia prolongs QT interval, which can precipitate torsades de pointes (TdP). We performed a retrospective review of all patients who received TH in our hospital over a period of 2 years to assess the effect of TH on the corrected OT interval (QTc) and any possible pro-arrhythmia. A total of 13 patients received TH. QTc prolonged in all patients with an average of 80.3 + 57.2 ms., and up to 109.8 + 80.4 ms in patients who received Amiodarone concurrently. No TdP was seen in any patient. We conclude that TH is safe, though careful monitoring of the OTc interval is advisable especially with concurrent use of QT prolonging drugs.
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Atrial fibrillation is the most common sustained arrhythmia in patients with rheumatic heart disease (RHD). This study was conducted to determine the maintenance of sinus rhythm with amiodarone therapy following DC cardioversion (DCCV), early after successful balloon mitral valvuloplasty (BMV).
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A 36-year-old man who experienced daily episodes of atrial fibrillation that was refractory to antiarrhythmic medication, including amiodarone, was enrolled in our focal atrial fibrillation radiofrequency catheter ablation protocol. The left superior pulmonary vein was the earliest site mapped, and radiofrequency ablation was performed. Atrial fibrillation was interrupted and sinus rhythm restored after one radiofrequency pulse inside the left superior pulmonary vein. Atrial fibrillation recurred and a new procedure was performed in an attempt to isolate (26 radiofrequency pulses around the ostium) the left superior pulmonary vein. Ten days later, the patient developed chest pain and hemoptysis related to severe left superior and inferior pulmonary veins stenosis. Balloon angioplasty of both veins was followed by complete relief of symptoms after 2 months of recurrent pulmonary symptoms. The patient has been asymptomatic for 12 months, without antiarrhythmic drugs.
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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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Demographic shifts toward an increasingly older population have resulted in a high prevalence of persons taking cardiovascular medication. Many patients on cardiovascular medications will require surgical intervention for conditions often unrelated to their cardiovascular pathology. Cardiologists and anesthesiologists alike must be knowledgeable about the potential interactions between cardiovascular drugs and anesthetics agents or adjuvant therapies administered perioperatively. Current recommendations suggest that beta blockers, calcium channel blockers, amiodarone, and alpha2 agonists should be continued throughout the perioperative period, whereas angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, and diuretics should be discontinued on the morning of surgery and resumed in the immediate postoperative period, unless contraindicated.
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Postoperative junctional ectopic tachycardia is a potentially life-threatening arrhythmia that is often resistant to conventional antiarrhythmic drugs. Amiodarone was suggested to be an adequate treatment; however, data regarding its efficacy and safety are limited. This study evaluated the efficacy of amiodarone in the first-line treatment of postoperative junctional ectopic tachycardia and assessed factors associated with failure of amiodarone therapy.
Iodine-induced thyrotoxicosis or "jodbasedow phenomenon" has been reported throughout the world since iodine has been administered to treat endemic goitre. Nowadays, iodinated radiocontrast agents and the antiarrhythmic drug amiodarone are the most common sources of excess iodine load subsequently leading to iodine-induced thyrotoxicosis, especially in elderly patients with underlying goitre. The aim of the study was to identify the number of cases of iodine-induced thyrotoxicosis among patients with thyrotoxicosis in a large urban hospital. Over an 18-month period thyrotoxicosis has been diagnosed in a total of 39 patients. Eight patients with iodine-induced thyrotoxicosis (5 female, 3 male; mean age 60.6 years) have been identified (20%). In all patients with iodine-induced thyrotoxicosis, iodine exposure with a mean iodine dose of 21.5 g was documented 2 to 16 weeks before diagnosis (iodinated radiocontrast agents in 5 patients, amiodarone in 2 patients, kelp tablets in 1 patient). Clinical features were predominantly tachyarrhythmias and heart failure, while 6 of 8 patients had goitre (thyroid volume 31 to 193 ml). Thyroid antibodies were not detected. Diagnosis was confirmed in 5 of 8 patients with increased urinary iodine concentrations (3436 to > 6000 nmol/24 h), and in 3 of 8 patients with a low tracer uptake in thyroid scintigraphy (1 to 4%). Treatment consisted of methimazole in all patients, additional tional beta-blockers and lithium in 4 patients, and prednisone in 5 patients. The mean treatment ment duration was 9.2 months, and patients became euthyroid after a mean treatment duration of 6.4 weeks. One patient (with still elevated free thyroxine levels) died of myocardial infarction 4 weeks after antithyroid drug therapy had been installed. The incidence, mechanisms and features of iodine-induced thyrotoxicosis are discussed. Iodine-induced thyrotoxicosis is a common disease, and the recognition and treatment of iodine-induced thyrotoxicosis, particularly in elderly patients and patients with goitre, are of clinical importance.
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Antiarrhythmic pharmaceutical development for the treatment of atrial fibrillation (AF) is moving in several directions. The efficacy of existing drugs, such as carvedilol, for rate control and, possibly, suppression of AF, is more appreciated. Efforts are being made to modify existing agents, such as amiodarone, in an attempt to ameliorate safety and adverse effect concerns. This has resulted in promising data from the deiodinated amiodarone analog, dronedarone, and further work with celivarone and ATI-2042. In an attempt to minimize ventricular proarrhythmia, atrial selective drugs, such as intravenous vernakalant, have demonstrated efficacy in terminating AF in addition to promising data in suppression recurrences when used orally. Several other atrial selective drugs are being developed by multiple manufacturers. Other novel therapeutic mechanisms, such as drugs that enhance GAP junction conduction, are being developed to achieve more effective drug therapy than is offered by existing compounds. Finally, nonantiarrhythmic drugs, such as angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, high-mobility group coenzyme A enzyme inhibitors and omega-3 fatty acids/fish oil, appear to have a role in suppressing AF in certain patient subtypes. Future studies will clarify the role of these drugs in treating AF.
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Out-of-hospital resuscitation protocols for patients suffering cardiac arrest have historically included cardiopulmonary resuscitation, defibrillation, and rapid transport to a hospital. For many years, use of drugs to improve myocardial perfusion or to correct arrhythmias that occur during cardiac arrest has been part of prehospital efforts to revive patients in ventricular tachycardia or ventricular fibrillation. Use of some of these drugs, however, may be based more on tradition than on well-documented evidence of efficacy. The authors reviewed pertinent data on the vasopressors epinephrine and vasopressin and the antiarrhythmics amiodarone and lidocaine to evaluate the usefulness of these drugs in cardiac arrest. They found little clinical data supporting the prehospital use of lidocaine in cardiac arrest, and despite a great deal of laboratory and clinical data addressing the efficacy of epinephrine, there is no large, randomized, controlled clinical trial supporting its use. Data on amiodarone and vasopressin support the use of these drugs in out-of-hospital resuscitation efforts.
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The implantable cardioverter defibrillator (ICD) protects patients from sudden cardiac death due to ventricular tachyarrhythmias. The capability of an improved overall survival of high-risk patients in comparison to the best pharmacologic therapy has been evaluated over the last few years in prospective randomized trials. In patients with a history of resuscitated ventricular fibrillation (VF) or unstable ventricular tachycardia (VT), the ICD was superior to therapy with amiodarone in 3 large trials involving 2,024 patients. At 2-year follow-up, ICD therapy was associated with a relative reduction in the risk of death of 20% to 30%. With respect to primary prevention of arrhythmogenic death, data are less convincing. The Multicenter Automatic Implantable Defibrillator (MADIT) study proved superiority of ICD therapy over medical treatment in coronary patients with depressed left ventricular function, nonsustained VT, and inducible but not suppressible sustained VT/VF. The second trial, the Coronary Artery Bypass Graft (CABG)-Patch trial, failed to show a similar superiority in 900 patients with an ejection fraction of < or = 35% and an abnormal signal-averaged electrocardiograph undergoing coronary artery bypass grafting. Thus, the role of device therapy for primary prevention of sudden death has not been established. Future prospective studies are needed to clarify this issue.
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Cardiovascular disease is a leading cause of death in captive chimpanzees and is often associated with myocardial fibrosis, which increases the risk of cardiac arrhythmias. In this case report, we present a 36-y-old male chimpanzee (Pan troglodytes) diagnosed with frequent ventricular premature complexes (VPC). We placed a subcutaneous implantable loop recorder for continual ECG monitoring to assess his arrhythmias without the confounding effects of anesthetics. During his initial treatment with the antiarrhythmia medication amiodarone, he developed thrombocytopenia, and the drug was discontinued. After reviewing other potential therapies for the treatment of cardiac arrhythmias, we elected to try acupuncture and laser therapy in view of the positive results and the lack of adverse side effects reported in humans. We used 2 well-known cardiac acupuncture sites on the wrist, PC6 (pericardium 6) and HT7 (heart 7), and evaluated the results of the therapy by using the ECG recordings from the implantable loop recorder. Although periodic increases in the animal's excitement level introduced confounding variables that caused some variation in the data, acupuncture and laser therapy appeared to decrease the mean number of VPC/min in this chimpanzee.
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Amiodarone and its major metabolite, desethylamiodarone, were measured in the plasma, white blood cells (WBCs) and red blood cells (RBCs) of 14 patients receiving chronic amiodarone therapy. The mean plasma concentrations (+/- standard error of the mean) of amiodarone and desethylamiodarone were 2.4 +/- 0.6 and 1.6 +/- 0.4 microgram/ml, respectively. The drug level in the WBCs was 62 +/- 12 micrograms/g protein during the early loading phase and 106 +/- 33 micrograms/g protein during maintenance phase of amiodarone therapy. Desethylamiodarone concentration in the WBCs was 42 +/- 18 and 190 +/- 33 micrograms/g protein during the loading and maintenance phases, respectively. Although a trend in WBC to plasma concentration was seen, there was no linear correlation between these levels. In 1 patient with severe neuropathy, biopsy of the nerve and muscle showed high concentrations of both amiodarone and desethylamiodarone. Although there was a decrease in tissue drug levels, proportionately high tissue:plasma drug levels were detected at the time of necropsy approximately 6.5 months after amiodarone was discontinued in this patient. Neutrophils from all patients receiving chronic amiodarone therapy showed multiple myelin-like polymorphic inclusion bodies (onionoid bodies) upon electron microscopic examination. Our observations suggest that WBC drug concentrations and electron microscopic changes may provide a means of correlating tissue concentrations and of following patients receiving chronic amiodarone therapy.