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We evaluated the effects of amiodarone in 45 patients with recurrent ventricular tachycardia or ventricular fibrillation. At a mean follow-up time of 12.7 +/- 8.8 months (range, three to 36), amiodarone was successful in nine of 16 patients with recurrent ventricular fibrillation and 21 of 29 with recurrent ventricular tachycardia. During amiodarone therapy, ventricular tachycardia could be induced in 18 of 19 patients in whom it had been induced before therapy, but only six of these 19 had spontaneous recurrence during follow-up. Side effects included corneal microdeposits, hyperthyroidism, blue skin, nausea, and symptomatic bradycardia. Pulmonary fibrosis occurred in three patients. Doses of up to 2000 mg a day did not produce cardiac toxicity, but neurologic side effects precluded long-term therapy at this dose. We conclude that amiodarone is effective for long-term therapy of recurrent ventricular tachyarrhythmias, that induction of arrhythmia during therapy does not always predict efficacy, and that side effects are frequent but do not usually limit therapy.
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PMID:Clinical efficacy and electrophysiology during long-term therapy for recurrent ventricular tachycardia or ventricular fibrillation. 678 1

In outlining the pathology of various electrolyte metabolism abnormalities in cancer patients we considered the main clinical points between pathologies and emergency treatment. In regard to sodium (Na+) metabolism, one pathologic state that requires our attention is hypernatremia. Hypernatremia is accompanied with dehydration and is due to water loss, vomiting, diarrhea and renal insufficiency. One of the major causes of this condition is lack of the antidiuretic hormone due to intracranial metastasis of the tumor. When hypernatremia becomes severe, it is accompanied with circulatory failure, muscular asthenia, disorientation, convulsions, coma and other cerebral symptoms. Treatment consists of replenishing the water content by infusion of electrolyte solutions which should be carefully conducted after complete diagnose of the severity of the patient's pathological condition. Hyponatremia, like sick cell syndrome, is observed relatively frequently in cancer patients. When the serum Na level falls markedly, it induces cerebral edema and causes disorders of consciousness. The major treatment consists of providing both water and sodium supplements. Hyperkalemia is observed at the time of renal insufficiency, tissue lesions, vomiting, and diarrhea. When serum potassium level rises, it causes bradycardia, ventricular fibrillation, or cardiac arrest. It is important to diagnostically apprehend the severity of this condition using EKG and determining the serum K1+ level. For emergency treatment injection of calcium gluconate is very effective. Hypokalemia is often manifested by the loss of intestinal fluids due to diarrhea or during administration of diuretic agents. Clinical symptoms include neural paralysis but emergencies occur relatively infrequently. K C1 injections are used in treating this condition. Hypercalcemia is manifested in cancer patients during hyperparathyroidism. Its clinical symptoms include lassitude, tachycardia, nausea, vomiting, and renal dys-function, leading to neural symptoms in severe cases. The main treatment consists of injection of physiological saline solution and administration of calcitonin, mithramycin. Hypocalemia is manifested during renal insufficiency, lack of vitamin D, and hypothyroidism. In classic cases it causes tetanic spasms. Injection of calcium is an effective treatment but since during tetanic spasms alcalosis may easily occur, treatment should only be provided after obtaining a complete understanding of the patient's condition. The pathological conditions described above can not be said to specific to cancer but it should be kept in mind that one of their main causative factors is the involvement of mechanism which produces ectopic hormones from cancerous tissues.
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PMID:[Electrolyte metabolism and emergency]. 688 72

In a group of 95 patients having cardiac operations with extracorporeal circulation, intravenous (IV) amiodarone, administered in doses of 2.5 to 5 mg/kg, was used in the treatment of various perioperative arrhythmias. Conversion to sinus rhythm was achieved in 55 (61%) of 90 patients with supraventricular arrhythmias, the other patients showing a satisfactory slowing of their heart rate. Total suppression and control was obtained in 18 patients with persistent ventricular extrasystoles associated with various supraventricular arrhythmias. Amiodarone was administered in five patients with life-threatening ventricular arrhythmias resistant to other antiarrhythmic agents: Suppression was obtained in one of two patients with recurrent ventricular tachycardias and control was achieved in three patients with repetitive ventricular tachycardia and ventricular fibrillation, allowing the effective use of intra-aortic balloon counterpulsation (IABP) needed for hemodynamic support. Seven patients experienced minor side effects such as nausea or flushing. No complete atrioventricular (AV) block was noted. Significant hypotension occurred at the end of the IV injection in 17 (18%) patients. In all but five patients, hypotenion was transient, without clinical complications. In the five others, adrenergic drugs in four cases and IABP in one case were necessary. Those five patients had marked cardiomegaly with poor myocardial contractility. IV bolus injection of amiodarone seems prohibited in such patients; constant infusion would be preferable.
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PMID:Intravenous amiodarone in the treatment of various arrhythmias following cardiac operations. 745 41

We report the case of a 42-year-old female, affected by mitral valve prolapse and ventricular arrhythmias, who died suddenly from ventricular fibrillation recorded during Holter monitoring. The lethal arrhythmia initiated with late diastolic couplets followed by a ventricular tachycardia that eventually degenerated into ventricular fibrillation. The patient had experienced four orthostatic and stress-related syncopal episodes, associated with nausea and diaphoresis, and a positive tilt test. Holter monitoring documented ventricular arrhythmias, consisting of both isolated monomorphic and sporadic repetitive beats. Her standard ECG and exercise test were normal, but signal-averaged study findings were significantly positive. QT prolongation in the absence of arrhythmias was observed during the Valsalva manoeuvre and isoproterenol infusion. 2D echo showed a remarkable mitral valve prolapse without regurgitation and localized structural abnormalities of the right ventricle. Postmortem study confirmed mitral valve prolapse, and also disclosed pulmonary infundibulum dilatation, massive adipose infiltration of the right ventricular free wall, patchy fibrosis and scattered myocardial inflammatory infiltrates in the left ventricle; these features are all consistent with arrhythmogenic right ventricular cardiomyopathy.
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PMID:Sudden death in mitral valve prolapse with Holter monitoring-documented ventricular fibrillation: evidence of coexisting arrhythmogenic right ventricular cardiomyopathy. 764 75

We reported a case of opsoclonus-myoclonus syndrome. A 63-year-old man was admitted to Kenwakai Hospital with rapidly progressing symptoms, including lumbago, whole body pain, vertigo, nausea, and anorexia. He became bed-ridden because of severe vertigo and truncal ataxia. Five days after admission, he developed opsoclonus followed by myoclonus and mild disturbance of consciousness, but he showed no appendicular ataxia or pyramidal tract sign. He was treated with prednisolone, 40 mg/day, which was effective for disturbance of consciousness, but opsoclonus and myoclonus persisted. He died of liver dysfunction and ventricular fibrillation 3 weeks after onset. Blood examination revealed high LDH (1,106 IU/l), Al-P, and gamma-GTP titers. Tumor markers were normal except for increase NSE activity (129 ng/ml). The cerebrospinal fluid showed normal cell count, 63.9 mg/dl of protein, 7.3 mg/dl of IgG, and normal glucose. A cranial CT scan showed an old lacune only. Chest rentgenogram and CT scan revealed mediastinal and hilar lymph node enlargement. An abdominal CT scan showed multiple low density masses in the liver. Small cell lung cancer associated with opsoclonus-myoclonus syndrome was suspected. Western blot analysis revealed that his serum reacted with protein in the cerebellum, cerebrum, and dorsal root ganglion with a molecular weight of 77 kDa. This is the first time such an antibody was ever been detected in patients with opsoclonus-myoclonus syndrome. The molecular weights of the antigens previously found by the serum of patients with this syndrome, were 55 kDa and 80 kDa in patients with breast cancer, and 210 kDa in patients with neuroblastoma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of opsoclonus-myoclonus syndrome associated with anti-central nervous system antibody]. 782 Sep 64

The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage of sotalol hydrochloride are reviewed. The chemical name of sotalol hydrochloride is 4'-[1-hydroxy-2-(isopropylamino)ethyl]methanesulfonanilide monohydrochloride. Sotalol is a class III antiarrhythmic that prolongs the action potential and refractoriness of cardiac tissue and has potent nonselective beta-blocking activity. Sotalol is well absorbed after oral administration. The pharmacokinetics of sotalol can be described by an open, linear, two-compartment model. The drug is eliminated primarily by the kidneys; mean elimination half-life is 12 hours. Sotalol has been found to be effective in controlling life-threatening ventricular arrhythmias, including sustained ventricular tachycardia, ventricular fibrillation, and premature ventricular complexes. Although sotalol has FDA-approved labeling for use in the treatment of ventricular arrhythmias only, it is also effective against a variety of supraventricular arrhythmias. Noncardiac adverse effects include fatigue, impotence, depression, headache, nausea, diarrhea, and increased triglyceride levels. Cardiovascular adverse effects include atrioventricular block, bradycardia, hypotension, exacerbation of heart failure, and polymorphic ventricular tachycardia. Overall, 11-21% of patients experience adverse effects; 6-18% of these patients have reactions serious enough to warrant the discontinuation of sotalol therapy. The initial dosage of oral sotalol hydrochloride in adults is 80 mg twice daily or 160 mg once daily; the dosage can be increased every three to four days in increments of 40-160 mg/day to a maximum of 480 mg/day. Sotalol is useful in the control of intractable, life-threatening ventricular arrhythmias, as well as a variety of supraventricular arrhythmias, in patients who do not respond to or are intolerant of more conventional antiarrhythmics.
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PMID:Sotalol: a new class III antiarrhythmic agent. 813 5

The use of dobutamine stress echocardiography for the evaluation of coronary artery disease is rapidly expanding. Despite its widespread use, the feasibility and safety of dobutamine stress echocardiography has not been sufficiently documented. Between November 1992 and June 1995, we performed 1000 dobutamine stress echocardiographies. There were 744 men and 256 women with a mean age of 59 +/- 11 years. Anti anginal medication was not routinely withdrawn before the test. The mean maximal dobutamine dose was 41,4 +/- 10 mu g/kg center dot min(-1). Atropine was given additionally in 440 patients, with a mean dose of 0.5 mg. In patients receiving beta-blockers additional atropine was more often necessary as compared to those not receiving beta-blockers (278/457 = 61% versus 162/543 = 30 %, p < 0.0001). Reasons for discontinuing dobutamine infusion were achievement of target heart rate (64 % of cases) and maximal dose (12 % of cases). In 791 (79,1 %) patients no side-effects of dobutamine stress echocardiography were noticed. Termination of the study because of adverse side-effects occurred in 6.6 %. A total of 103 (10,3 %) noncardiac side-effects were observed: dizziness or nausea 6.4 %, headache 1.7 %. In one patient a focal cerebral seizure occurred. 156 cardiac side-effects occurred: blood pressure decrease of more than 20 mm Hg in 25 patients, extreme palpitations in 16 patients and pulmonary edema in one case. Most common cardiac side-effects consisted of arrhythmias (11.4 %): 9.1 % ventricular and 2.3 % supraventricular arrhythmias. Most ventricular arrhythmias were less severe (uniform and multiform premature ventricular beats, ventricular bigeminy or couplets in 71 patients). Nonsustained ventricular tachycardia, with a maximum duration of 20 s, occurred in 18 patients. In one patient sustained ventricular tachycardia developed and progressed towards ventricular fibrillation. This patient could be successfully defibrillated. Supraventricular arrhythmias presented as new atrial fibrillation in 10 patients, supraventricular tachycardia in three patients, junctional rhythm with a short decline in heart rate in nine patients and a second-degree AV block in another case. Dobutamine stress echocardiography has proven to be a safe and feasible method in the diagnosis of coronary heart disease. Minor side-effects are common and sometimes unpleasant for the patient, but do not often require termination of the study. Severe side-effects are seldom (< 1 %), but nevertheless, adequate medical and technical (defibrillator) support should be rapidly available.
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PMID:[Feasibility and safety of dobutamine stress echocardiography: experiences with 1,000 studies]. 871 45

The toad possesses several toxic substances. Toad toxin poisoning manifests itself primarily with digitalis-like, cardioactive effects which results in bradycardia, varying degrees of atrio-ventricular block, ventricular tachycardia, ventricular fibrillation and sudden death. We report a cluster poisoning in a family who became intoxicated after ingestion of cooked toad soup for a skin problem. The youngest one (15 months old) died of refractory bradydyarrhythmias soon after arriving at our hospital. A second child (20 months old), who survived, arrived in shock with hyperkalemia (potassium 7.3 mEq/ L) and varying degrees of atrio-ventricular block. She was successfully treated with atropine, lidocaine, and cardioversion, and had a transvenous temporary pacemaker implanted for 1 day. The third boy (16 years old) had hyperkalemia (potassium 6.3 mEq/L) and bradycardia. The remaining three adults had only mild symptoms of nausea, vomiting, watery diarrhea and a sensation of numbness over their oral mucosa. We found that the level of serum potassium had prognostic implications in toad intoxication. Determination of serum potassium level is readily available in almost every hospital and is therefore more convenient to measure than serum digoxin level. We conclude that if hyperkalemia develops, the treatment of toad intoxication must be more aggressive to prevent mortality.
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PMID:Prognostic implications of hyperkalemia in toad toxin intoxication. 968 59

Paroxysmal supraventricular tachycardia (SVT) may have numerous electro-physiologic mechanisms. The most common type of SVT is AV-nodal reentry tachycardia (60%) followed by the bypass tract-mediated SVT (preexcitation. 30%) and a smaller group (10%) comprising paroxysmal atrial flutter or fibrillation and atrial ectopic tachycardia. In persons with otherwise normal hearts symptoms are usually mild and include palpitations or an uneasy feeling in the chest. But some describe precordial pain. Weakness, dizziness, nausea, vomiting, and even syncope. Whenever possible a 12-lead-ECG during an episode of SVT should be obtained. If not possible the use of several Holter-ECG or of an event-recorder may be helpful. Conversion of a SVT can be accomplished by vagal maneuvers or intravenous adenosine (6-18 mg bolus injection). Further diagnostic procedures should prove or rule out a significant structural heart disease. Therapeutic options (expectative, pharmacological prophylaxis, invasive electrophysiologic testing and catheter-mediated modification or ablation) are chosen according to the objective threat (e.g. ventricular fibrillation due to 1:1 conducted atrial fibrillation in a preexcitation syndrome) and the subjective complaints. Definitive healing of the AV-nodal reentry tachycardia and the bypass tract-mediated SVT can be achieved by use of catheter-mediated modification or ablation in 95 to nearly 100%.
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PMID:[Modern therapy of paroxysmal supraventricular tachycardia]. 1009 47

The patient was a 53 year-old male who had 3 syncopal episodes over a 6-month period. In the electrophysiological study, ventricular fibrillation (VF) was repeatedly induced by the ventricular extrastimulus method. Intravenous pilsicainide was administered, and the J-point and ST-segment in the right precordial leads became slightly elevated just following drug administration. Five min later, the patient experienced severe nausea and then vomited twice, at which point the electrocardiogram (ECG) showed increased elevation of the J-point and ST-segment. These ECG changes recovered to normal 30 min later. The cause of his syncope was strongly suspected to be related to the VF associated with Brugada syndrome. An interesting aspect of this case was the particular type of J-point and ST-segment elevation that was induced when the patient experienced nausea and vomiting. It is proposed that this phenomenon originated from the vagal stimulation associated with the nausea and vomiting.
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PMID:Brugada syndrome-like ST-segment elevation increase exacerbated by vomiting. 1522 39


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