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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Having observed 18 cases, the authors describe a syndrome of recurrent paroxysmal atrial arrhythmia which was very homogeneous from the clinical and ECG point of view. It was usually found in middle aged males, with no demonstrable underlying heart disease, whose disorder of intra-atrial conduction occurred during sinus rhythm. The condition developed slowly over the course of years towards a maximum incidence of several short daily attacks of an arrhythmia which alternated between an atrial fibrillation and atrial flutter. Vagal overactivity is the precipitating cause of these attacks which are usually not completely nocturnal. The condition never progressed to sino-atrial block nor to permanent fibrillation. The beginning of each attack, often heralded by atrial coupling with a long enough interval to cause re-entry, is accompanied by slowing of the sinus rate down to the threshold level. The vagal effect of shortening the action potential and refractory period is recognised to be non-homogeneous in the atrial wall, and suggests a re-entry mechanism rather than hyper-excitability. This would explain the usual resistance of atrial arrhythmias of vagal origin to digitalis, beta blockers and quinidine. Amiodarone alone is usually effective because of the prolongation of the action potential which it causes. In 5 particularly resistant cases a good clinical result was obtained by the insertion of an atrial pacemaker with a fairly rapid rate.
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PMID:[The atrial arrhythmia syndrome of vagal origin]. 2 9

Without treatment, about 60% of atrial arrhythmia patients suffer a relapse within 3 months and 70% within one year. Antiarrhythmic treatment intended to reduce this percentage is therefore justified, on condition that it is well tolerated. Several preliminary questions have to be settled before this medical prophylaxis: 1) Justification of antiarrhythmic treatment (sometimes pointless to deal with very occasional episodes); 2) Treatment of the underlying heart disease (valve disease, cardiothyrotoxicosis, etc.) or promoting factors (potassium depletion etc.); 3) Accurate assessment of any associated conduction abnormalities, which may constitute a contraindication to antiarrhythmic treatment (WPW syndrome in the case of verapamil and the digitalis-like drugs) or require additional treatment (pacemaker); 4) Definition of the mechanism (vagal or sympathotonic) inducing arrhythmia; 5) Evaluation of the hemodynamic parameters of the underlying heart disease (size of the atria, ventricular function, coronary or valvular lesions) which may limit the efficacy of the treatment. Once these parameters have been identified, the primary treatment should be type la or lb antiarrhythmics, which have been shown to be effective, despite the fact that they are not without arrhythmic risks (the Ib antiarrhythmics are less effective and have a poor safety profile). The beta-blockers have preferential indications (hypersympatheticotonia, hyperthyroidism, hypertrophic myocardiopathy, mitral prolapse, angina etc.) and can be replaced by verapamil or bepridil if there are non-cardiac contraindications (ulcers, asthma, diabetes). Amiodarone is extremely effective, but its poor extracardiac safety restricts its long-term use. Complementary treatments (digitalis-like, anticoagulants or anti-PAF and cardiostimulant drugs) should be added if necessary. Recurrences (to be confirmed by ECG or Holter) should lead to rigorous confirmation of therapeutic compliance and observance of simple hygienic and dietary measures (no excessive exertion, elimination of stimulants etc.). With strict clinical and ECG monitoring, it would then be possible either to increase the dose levels (accompanied by plasma determinations if possible) or to switch to a treatment with more effective, but more aggressive drugs (amiodarone, flecainide) or to use drug associations (la and lb, la and II etc.). Repeated failure of such attempts should lead to a non-medical approach to treatment.
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PMID:[Preventive drug therapy of recurrence of atrial fibrillation]. 129 92

Flecainide (100 mg twice daily) was used for prevention of paroxysmal atrial fibrillation (PAF) in 52 patients with frequent symptomatic attacks that were resistant or intolerant to quinidine (600-900 mg/day). Underlying heart disease was present in only 8 cases and left ventricular ejection fraction was always greater than 30%. No patient had had a myocardial infarction. Vagally induced PAF was clinically documented in 35 patients. Amiodarone, previously used and ineffective, was combined with flecainide in 33 patients. After 1-5.8 years of follow-up, complete disappearance of PAF was observed in 38 patients (73%). The success rate was slightly higher in patients with vagally induced PAF (p = 0.07). Extracardiac side effects necessitated withdrawal in only 3 cases. Permanent pacemaker was needed in 7 patients on amiodarone and flecainide because of excessive sinus bradycardia. Two patients, with previously documented atrial flutter, experienced presyncopal episodes of atrial flutter with 1:1 atrioventricular (AV) conduction and wide QRS complex. No death occurred during the follow-up. In this series, quinidine proved to be unsuccessful in 46 patients and it was withdrawn in 6. We concluded that flecainide is efficient and well tolerated for long-term prevention of PAF in patients resistant to quinidine. The possibility of 1:1 AV conduction during atrial flutter may suggest the use of verapamil or beta blockers in combination with flecainide in patients with previously documented atrial flutter.
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PMID:Flecainide in quinidine-resistant atrial fibrillation. 151 1

Antiarrhythmic drugs of type I to IV (Vaughan Williams) are generally used for the treatment of ventricular tachycardia, especially in patients with symptomatic and hemodynamically not tolerated arrhythmias; however, randomized controlled studies revealed a beneficial effect on sudden cardiac death only for type-II (beta-blocking agents) and type-III (Amiodarone) antiarrhythmic drugs. These drugs are, therefore, the antiarrhythmic agents of first choice; but, in addition, underlying heart disease, triggering factors and heart-rate dependency should be considered.
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PMID:[Drug prevention and therapy of ventricular tachycardia]. 151 83

In view of their potentially dangerous proarrhythmic effects, antiarrhythmic drugs should only be prescribed for patients with poorly tolerated symptomatic supraventricular arrhythmias. The choice of a suitable preparation depends not only on the type of arrhythmia, but also on the underlying heart disease and left-ventricular function. Digoxin, verapamil, sotalol and quinidine remain first-line drugs, while in view of recent trials the type-1c antiarrhythmics (flecainide) should only be given in cases resistant to other agents. Amiodarone is also an important and efficacious "reserve" antiarrhythmic, which has to be utilized at low doses to avoid its well-known side effects.
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PMID:[Drug therapy in supraventricular arrhythmia]. 159 45

The aim of this study was to investigate the efficacy and the side effects of a long-term treatment with amiodarone. We analyzed the data of 41 patients in whom amiodarone therapy had been initiated between 1974 and 1984. Twenty-one patients had dilative cardiomyopathy, 14 patients had chronic myocardial infarction, four patients suffered from WPW syndrome with intermittent atrial fibrillation, one patient had aortic valve surgery, whereas in one patient there was no clinical evidence of a heart disease. All patients had salvos of ventricular extrasystoles, ventricular tachycardia or documented intermittent ventricular fibrillation. There have been seven drop-outs up to the present time. In each patient, the lowest antiarrhythmically effective dose was applied, which was generally higher in patients with low ejection fraction. Effective treatment of the ventricular tachycardia was achieved in 55-92% of patients and did not depend on the duration of treatment. In 10 patients in whom amiodarone therapy had to be stopped for various reasons. Sudden cardiac death was slightly more frequent than in the 24 patients treated with amiodarone, though the difference was not significant. In cases with a history of syncope the prognosis was poor, even with amiodarone therapy. Due to side effects, a dosage reduction or discontinuation of amiodarone treatment became necessary in 14 patients. Amiodarone proved to be an effective drug also for the long-term treatment of ventricular tachycardia, and possibly for the prevention of sudden cardiac death. With the exception of blue skin color, there was no accumulation of side effects, even during long-term treatment of several years.
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PMID:[Long-term treatment with amiodarone]. 171 39

A case of exercise-induced cardiac arrest secondary to catecholamine-sensitive right ventricular tachycardia in the absence of apparent structural heart disease is presented. Amiodarone therapy prevented tachycardia induction, symptoms and clinical events despite a return to vigorous exercise.
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PMID:Catecholamine-sensitive right ventricular tachycardia in the absence of structural heart disease: a mechanism of exercise-induced cardiac arrest. 176 39

Atrial fibrillation (AF) is defined as idiopathic when no one heart disease can be documented by clinical examination or by laboratory investigations. Epidemiological studies have shown that almost one third of all the cases of AF are idiopathic and that their incidence increases with age. Idiopathic AF may have different clinical manifestations: the paroxysmal form, characterised by long-lasting episodes, the transient recurrent form, characterised by frequent self-terminating episodes, or, less commonly, the chronic form. According to the literature, the risk of thromboembolic complications in idiopathic AF is not elevated and certainly lower than in AF associated with heart disease. By a clinical evaluation patients in whom an electrical cardioversion is necessary for reestablishing the sinus rhythm can be identified, considering that definite contraindications to electrical cardioversion exist. For prophylaxis of recurrences of AF the classical treatment with class 1A antiarrhythmic drugs (disopyramide or quinidine) is not very effective and not well tolerated; recently class 1C antiarrhythmic drugs have been employed with better results. In patients without heart failure their employment appears sufficiently safe. Amiodarone is certainly very effective but considering the serious side effects, its use must be limited to selected cases. Moreover non-pharmacological treatments (catheter ablation and surgery) have been developed recently for selected cases of AF refractory to antiarrhythmic drugs.
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PMID:[Idiopathic atrial fibrillation: clinical and therapeutic problems]. 181 66

Amiodarone, an anti-ischaemic and anti-arrhythmic drug, has been the object of numerous studies and seems to be highly effective in the treatment of severe ventricular arrhythmias on dilated cardiomyopathies, as well as of hypertrophic or ischaemic heart diseases. Some studies have shown a decrease in the incidence of sudden death in patients under amiodarone, but most of these studies were conducted on limited series with an insufficiently strict methodology. Contrary to other antiarrhythmic agents, amiodarone seems to be devoid of significant proarrhythmic effect and of depressant effect on cardiac function. Its anti-ischaemic activity has been demonstrated in exercise-induced and spastic angina. The side-effects of amiodarone are mainly extracardiac, and they may be a source of concern when they produce dysthyroidism or pulmonary pathology; however, they can be detected, or even prevented, by careful monitoring. Owing to its mechanism of action and its potential effectiveness, amiodarone deserves to be studied in patients at high risk of sudden death, especially those who suffer from severe ventricular arrhythmia on ischaemic cardiopathy with or without ventricular dysfunction. Three extensive clinical trials have been devised to determine with accuracy the effect of amiodarone on the mortality of patients who have survived a myocardial infarction or present with heart failure. At the end of these trials, it will perhaps be possible to evaluate the influence of a long-term amiodarone treatment on the mortality of patients whose life expectancy is shortened. The results obtained will be weighed against the side-effects of the treatment to obtain a benefit/risk ratio which, for the time being, is imperfectly known.
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PMID:[Does amiodarone have a benefit effect on mortality?]. 183 37

The incidence and clinical predictors of amiodarone pulmonary toxicity were examined in 573 patients treated with amiodarone for recurrent ventricular (456 patients) or supraventricular (117 patients) tachyarrhythmias. Amiodarone pulmonary toxicity was diagnosed in 33 of the 573 patients (5.8%), based on symptoms and new chest radiographic abnormalities (32 of 33 patients) and supported by abnormal pulmonary biopsy (13 of 14 patients), low pulmonary diffusion capacity (DLCO) (nine of 13 patients), and/or abnormal gallium lung scan (11 of 16 patients). Toxicity occurred between 6 days and 60 months of treatment for a cumulative risk of 9.1%, with the highest incidence occurring during the first 12 months (18 of 33 patients). Older patients developed it more frequently (62.7 +/- 1.7 versus 57.4 +/- 0.5 years, p = 0.018), with no cases diagnosed in patients who started therapy at less than 40 years of age. Gender, underlying heart disease, arrhythmia, and pretreatment chest radiographic, spirometric, or lung volume abnormalities did not predict development of amiodarone pulmonary toxicity, whereas pretreatment DLCO was lower in the group developing it (76.0 +/- 5.5% versus 90.4 +/- 1.4%, p = 0.01). There was a higher mean daily amiodarone maintenance dose in the pulmonary toxicity group (517 +/- 25 versus 409 +/- 6 mg, p less than 0.001) but no difference in loading dose. No patient receiving a mean daily maintenance dose less than 305 mg developed pulmonary toxicity. Patients who developed toxicity had higher plasma desethylamiodarone (2.34 +/- 0.18 versus 1.92 +/- 0.04 micrograms/ml, p = 0.009) but not amiodarone concentrations during maintenance therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical features of amiodarone-induced pulmonary toxicity. 236 24


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