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

The pharmacologic treatment of atrial fibrillation (AF) is aimed at controlling the ventricular response, restoring sinus rhythm, and preventing or delaying relapses. In the control of ventricular response, digitalis maintains a primary role when the arrhythmia is accompanied by heart failure. In ischemic, hypertensive, and degenerative (whose number is increasing at present) cardiopathies without evident ventricular dilatation, treatments with calcium antagonists (such as verapamil, gallopamil, or diltiazem) or beta-blocking agents must be preferred. In order to control the ventricular response in patients with chronic AF during physical activity, the association of digitalis with beta-blocking agents or calcium antagonists seems to provide satisfactory results. The drugs of the IC class, especially flecainide, represent a certain therapeutical progress in the restoration of sinus rhythm in the treatment of paroxysmal atrial fibrillation affecting subjects without evident alterations of ventricular function, particularly in subjects with Wolff-Parkinson-White syndrome, with forms of vagal origin, or with atrial fibrillation alone. A therapeutic combination of digitalis and quinidine may produce resolution of the arrhythmia in the presence of altered ventricular function or when AF is of an uncertain onset. In patients with hypertensive, ischemic, and/or degenerative cardiopathy without evident ventricular or advanced heart failure, the verapamil-quinidine association may also be effective and even quicker. The combination of drugs of the I and III class for restoration of the sinus rhythm in particularly resistant forms of AF without evident structural heart alterations is promising but must be verified in a greater number of patients. In the prevention of relapses amiodarone appears to have the widest spectrum of advantages from an electrophysiologic point of view; however, because of its many side effects, amiodarone represents a late therapeutical choice. The promising results obtained with flecainide are disputed by the results of the CAST, which limit the possibilities of using this drug to a low number of cases (W.P.W. syndrome, AF of vagal origin, atrial fibrillation alone). In the past, quinidine and disopyramide have been the drugs most widely used in the prophylaxis of AF. These drugs have a similar efficacy, and both of them provided some positive results. However, because of untoward side effects (especially for quinidine) during chronic treatment, the use of these drugs has been questioned. Perhaps in the majority of patients, the less dangerous therapeutic choice after the termination of the fibrillation is a combination of drugs slowly down AV node activity (digitalis or calcium antagonists and beta blockers) with class IA antiarrhythmics.
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PMID:The pharmacologic treatment of atrial fibrillation. 167 64

Antiarrhythmic treatment is based on the hypothesis that ventricular premature beats (VPBs), in the presence of underlying cardiac disease and impaired ventricular function, may predispose to sudden cardiac death. The effectiveness of treatment, however, has not been proven. For acute treatment of paroxysmal ventricular tachycardia, on comparison of the effectiveness of lidocaine and ajmaline, some new aspects have been rendered. VENTRICULAR PREMATURE BEATS (VPB): Isolated VPBs can be found in 40 to 75% of healthy subjects; if their number is substantial, investigation is warranted. For VPBs with subjective symptoms, beta-receptor blockers or specific antiarrhythmic agents, if necessary in combination, may be given. In several studies it has been shown that the prognosis of patients with frequent and complex VPBs, that is couplets and salvos, without heart disease is not compromised. In one long-term study over an average of 6.5 years, sudden death was observed in only one of 70 subjects who had 566 VPBs/24 hours, 60% additionally couplets and 26% salvos in the Holter ECG. Accordingly, treatment for the sake of prognosis is not warranted. For patients with mitral valve prolapse or only mildly impaired ventricular function and asymptomatic arrhythmias, treatment is not necessary since it has not been shown to be beneficial. Coronary artery disease is the most frequent cause of ventricular arrhythmias and sudden death. In numerous studies in patients after myocardial infarction, a relationship has been recognized between frequent and complex VPBs and overall mortality as well as sudden death. Particularly at risk are patients with very frequent and complex VPBs with additional impairment of ejection fraction to less than 30 to 40% but this group only accounts for 10% of patients after infarction. Only in one interventional study, carried out with aprindine, there was a significant reduction in overall mortality from 12.5 to 7.8% with an adverse reaction rate, however, of 21%. In high-risk patients with a low ejection fraction and numerous, complex VPBs as well, in a further study with aprindine, after one year, there was no decrease in overall mortality as compared with the placebo group. The cause for the insufficient effectiveness of the antiarrhythmic agents in various interventional studies has been attributed to a limited number of patients, rigid dosing regimens, inadequate suppression of VPBs and a high incidence of adverse reactions. In the multicenter, randomized, placebo-controlled CAST study with newer substances, a total of 2309 patients with essentially asymptomatic VPBs at a rate of more than 6/hour and an ejection fraction less than 55% or 40% admitted more than 90 days after infarction, respectively, were followed from six days to two years after myocardial infarction to determine if the significant suppression of VPBs in patients with coronary artery disease with antiarrhythmic agents leads to a reduction in arrhythmia-associated deaths. Flecainide, encainide and moricizine led to a significant suppression of VPBs in 75% of the patients. After an average of ten months, the rate of arrhythmia-induced deaths of 4.5% in those treated with encainide or flecainide was significantly higher than the 1.2% observed in the placebo group. These results appear attributable to a proarrhythmic effect of the class IC drugs during long-term treatment.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:New aspects of the clinical use of anti-arrhythmia agents with special reference to acute therapy of ventricular tachycardia (lidocaine vs. ajmaline). 218 94

Sudden cardiac death is defined as death due to a primary cardiac cause or mechanism, occurring within one hour of the onset of acute illness in a person thought to be free of, or with symptomatically mild, heart disease, or simply prehospital death. Of persons dying suddenly, 90% have coronary artery disease, less commonly, dilated cardiomyopathy or hypertrophic cardiomyopathy, preexcitation syndrome, long QT-syndrome, conduction disturbances, congenital or valvular heart disease as well as cardiac tamponade are responsible. In the USA, the incidence of sudden cardiac death is approximately 450,000 per year, in the Federal Republic of Germany the number lies at about 70,000 to 80,000. The most important risk factors for sudden cardiac death are impaired left ventricular ejection fraction, myocardial ischemia and arrhythmias. In general, sudden cardiac death is caused by ventricular fibrillation which arises mainly by degeneration of ventricular tachycardia (VT). The terminal arrhythmia, it is assumed, is precipitated by premature ventricular beats originating in an arrhythmogenic substrate. MEDICAL ANTIARRHYTHMIC TREATMENT IN PATIENTS WITH CORONARY ARTERY DISEASE AFTER MYOCARDIAL INFARCTION: STUDIES WITH CLASS I DRUGS: The results of nine large, randomized , controlled studies are available in which the mortality of patients on antiarrhythmic treatment has been studied (Table 1). Two studies each were carried out with aprindine, phenytoin, mexiletine and tocainide as well as one study with endainide, flecainide or morizicine. With the exception of the CAST study, no study showed a significant difference between treated patients and the control group with respect to mortality or incidence of sudden cardiac death. The CAST study was terminated after ten months because the administration of flecainide and encainide led to overall mortality of 7.7% vs. 3.0% in the control group and the rate of sudden cardiac death at 4.5% was significantly higher in the treatment group than the 1.2% incidence found in controls (Table 2). For nearly all of the studies described, the patient groups were not sufficiently large and subgrouping according to patient characteristics was not carried out such that possibly, inhomogeneity of the entire collective may not have been recognized precluding identification of some individuals who may have shown benefit from antiarrhythmic treatment. The necessity for treatment in many of those receiving drugs is questionable since generally the rhythm profile of the patients was not taken into consideration for the decision to treat. Proarrhythmic effects, accordingly, were also not assessed. Individual treatment and dosage adjustment by monitoring with effectiveness criteria was carried out in one study only in which, even here, criteria for effectiveness were arbitrarily capable of eliciting antiarrhythmic actions. Calculation of mortality rates was carried out on the basis of the total number of deaths in the respective groups without taking into consideration that by the end of the study, in the treatment group the medication had been discontinued in up to 40% of the patients. STUDIES WITH CLASS II DRUGS: For treatment with beta-receptor blockers there are 15 large, controlled, randomized, long-term studies available in which total mortality and the incidence of sudden cardiac death were studied.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Can sudden cardiac death be prevented by treatment with anti-arrhythmia drugs?]. 218 95

The Cardiac Arrhythmia Suppression Trial II (CAST II) was a double-masked placebo-controlled randomized trial that compared the survival effects of moricizine to placebo in postmyocardial infarction arrhythmia patients. The quality-of-life outcome measures were designed prospectively for CAST and were previously shown to have high reliability and clinical discriminative validity. The CAST quality-of-life instrument detected significant differences between moricizine and placebo. In particular, moricizine was most strongly associated with inferior social activity and satisfaction scores (p = .014) and lower scores for overall contentment with life (p = .007). Moreover, the quality-of-life measures improved significantly for both the moricizine and placebo treatment groups after entry into the clinical trial. These results indicate that the CAST quality-of-life instrument is sensitive for assessing pharmacological therapies in the treatment of heart disease.
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PMID:Moricizine and quality of life in the Cardiac Arrhythmia Suppression Trial II (CAST II). 785 Nov 6

After a brief classification of antiarrhythmic drugs and their mode of action, ventricular dysrhythmias are defined and characterized with respect to underlying causes. A short chapter is dedicated to the treatment of acute ventricular tachycardia, a longer one to the prophylaxis of ventricular dysrhythmias, based on our knowledge in the "post CAST Study era' (CAST = Cardiac Arrhythmia Suppression Trial). A special interest is dedicated to patients commonly encountered in daily practise: patients with coronary artery disease, patients with chronic heart failure, and patients without underlying heart disease. Then a separate assessment is made of the proarrhythmic effects of antiarrhythmic drugs.
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PMID:[Ventricular arrhythmias: diagnosis and drug therapy]. 868 56

The last decade has seen considerable changes in both attitude and approach to the management of arrhythmia. Much of this has resulted from trials such as the CAST (Cardiac Arrhythmia Suppression Trial) and the CASH (Cardiac Arrhythmia Study Hamburg), which demonstrated the potentially lethal consequences of using class I sodium channel blockers in patients with structural heart disease. The subsequent popularity of the class III agents and recognition that they are the best available therapy has led to the popularity of amiodarone and sotalol in the treatment of arrhythmia. Although these agents can achieve good efficacy in the suppression of atrial fibrillation their use is not without problems. Sotalol requires careful patient selection due to the risk of proarrhythmia and although cardiac effects are rare with amiodarone therapy, potentially serious non-cardiac adverse effects can limit the long-term use of this agent. Although treatment guidelines have helped to clarify our current knowledge and outline appropriate clinical application of antiarrhythmic agents, the need for antiarrhythmic agents which marry efficacy with improved safety and clinical applicability is apparent.
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PMID:The role of class III antiarrhythmic agents in maintaining sinus rhythm. 1122 May 19