Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to assess efficacy, safety, and long-term tolerance of flecainide for the prevention of paroxysmal atrial fibrillation (PAF), 944 patients (555 male) were enrolled in an open multicenter study. All patients had had greater than or equal to 1 episodes of atrial fibrillation and were in sinus rhythm at the time of entry. The mean age was 65.3 +/- 11 years, and 43% of patients had no detectable heart disease. The mean daily dose of flecainide was 190 +/- 34 mg. Clinical examination, electrocardiogram (ECG) and 24-hour Holter monitoring were performed at entry into the study and on months 3, 6, and 9. Of the patients, 189 were lost to follow-up. Of the remaining 755 patients, 562 (74%) continued the treatment during the 9-month period and 193 (26%) dropped out. A total of 84 adverse effects were reported in 7.6% enrolled patients and in 9% of patients during follow-up, with treatment interruption in 50% of the cases. There were only 3 minor cardiovascular side effects, all leading to treatment discontinuation. No deaths in patients with recurrent PAF and no proarrhythmic events were reported. Flecainide appears to be effective in preventing PAF, with 65% of patients being arrhythmia-free after 9 months of treatment at a mean daily dose of 200 mg. Side effects were common, but clinically significant adverse events were infrequent.
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PMID:Flecainide acetate in the prevention of paroxysmal atrial fibrillation: a nine-month follow-up of more than 500 patients. 150 98

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

Flecainide acetate was administered at a dose of 100 mg twice daily to 15 patients with drug-resistant ventricular ectopy. Eleven patients had evidence of organic heart disease. Left ventricular function was normal in 13 patients, and 2 patients had mild and moderate left ventricular dysfunction respectively. All patients underwent a control (off drugs) and a flecainide Holter ECG. Flecainide suppressed ventricular ectopy by greater than 70% in 13 patients (86.6%), suppressed bigeminal beats by greater than 90% in 13 (86.6%), suppressed ventricular couplets by greater than 90% in 12 of 14 patients (85.7%), and completely suppressed runs of nonsustained ventricular tachycardia in 6 of 9 patients (66.6%). In only one patient who showed a 69% suppression of ventricular ectopy did ventricular couplets increase. No side effects of the drug were noted. We conclude that flecainide at a dose of 100 mg twice daily is highly effective in suppressing ventricular ectopy that is resistant to other anti-arrhythmic agents.
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PMID:Oral flecainide for the treatment of drug-resistant ventricular ectopy. 169 48

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

We studied 20 patients with a confirmed diagnosis of Chagas heart disease. Clinical and electrocardiography examinations at baseline documented that all patients had chronic PVC's and that 40% of them also had supraventricular extrasystoles. Also 80% of the patients had RBBB's, 70% had LBBB's and 35% had 1st. degree AV blocks. Flecainide (F) completely suppressed the arrhythmias in 85% of the patients and did partially so in 98% of the patients. Flecainide did not affect sinus node function except in one patient who developed a sinus node atrial block. PR and QRS intervals were prolonged after F but there no 2nd or 3rd degree AV blocks. Flecainide demonstrated to be highly effective with a comfortable margin of safety in the management of these patients with marked alterations of their pace-making and conduction functions.
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PMID:[Electrophysiological changes of the excitoconduction system in patients with Chagas cardiomyopathy and their modification by flecainide]. 245 50

Our study group included 12 patients (4 males, 8 females), mean age 60 yr, with symptomatic or threatening tachyarrhythmias (Lown classes IV A, B, V); 2 patients were suffering from mitral valve prolapse syndrome, 2 from ischemic heart disease; 4 from cardiac insufficiency caused by hypertensive or ischemic heart disease; 4 had no evident clinical signs of cardiopathy. Patients suffering from: cardiac insufficiency (F.C. III e IV NYHA); II and III degree BAV; atrial flutter and fibrillation; long QT syndrome; acute ischemic heart disease were excluded from the study. During short-term treatment, patients received placebo for four days and subsequently flecainide 200 mg daily for four days. During medium-term treatment patients received flecainide 200 mg daily (for six months). Several Holter/24-hour monitorings were performed for evaluation of therapy. No significant reduction in the number of ectopic ventricular beats (B.E.V.) was found with placebo whereas reductions of B.E.V. number (97% and 95%, respectively) were found during short and medium-term treatment with flecainide. Flecainide produced: changes in Lown class: from IV A, B and V to II and I; a marked reduction of subjective symptoms (dyspnea, giddiness syncope, precordial pain); ECG changes: increases in: PR: 5-25%; QRS: 11-12%; QT: 11-22%. Flecainide produced no pro-arrhythmic effects or changes in echocardiographic ventricular function index. Flecainide can be considered one of the most effective new antiarrhythmic drugs.
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PMID:[Short- and medium-term treatment of ventricular hyperkinetic arrhythmia with flecainide]. 252 12

Ventricular tachyarrhythmias and severe bradycardia, flecainide acetate's most serious side effects, occur in patients with chronic heart disease or in healthy persons after frank overdose. Toxic effects appear to correlate closely with drug levels in plasma. The surface electrocardiogram can indicate toxicity by demonstrating this drug's electrophysiologic potency to depress all major cardiac conduction pathways with marked prolongation of the PR and QRS intervals. We report the clinical course of a young, healthy person who developed polymorphous ventricular tachycardia after taking a 3800-mg dose of flecainide acetate. Sinus rhythm was restored without pacing or cardioversion after infusion of a beta-sympathomimetic agent, physostigmine, and a sodium load. The initial flecainide serum levels were five times greater than the usual upper therapeutic level. Electrocardiography showed that the lengthened electrocardiographic time intervals decreased in correlation with falling drug levels. Flecainide-associated life-threatening arrhythmias and available therapeutic interventions are discussed.
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PMID:Life-threatening flecainide toxicity. A pharmacodynamic approach. 310 47

Flecainide and encainide (class IC) are presently under clinical evaluation in Italy. They prolong the duration of the QRS but not the period of ventricular repolarisation: the prolongation of QT is due solely to the prolongation of the Q-J. Flecainide and encainide are extremely powerful and are suitable for the treatment of reciprocating supraventricular paroxysmal tachycardia and of persistent reciprocating tachycardia, the prophylaxis of WPW atrial fibrillation including cases with a short anterograde refractory period of the anomalous pathway and the treatment of ventricular ectopic beats and ventricular tachycardia. Both drugs are probably effective for the treatment of atrial fibrillation. However, in the case of atrial flutter they are of little effect of sinus rhythm cardioversion; on the other hand they significantly prolong the duration of the A-A interval, with variable results on ventricular rate. Flecainide and encainide have 'parodoxical' arrhythmogenic effects, related to administration dosages, severity of the arrhythmia and seriousness of cardiopathy. Encainide shows peculiar pharmacokinetics due to hepatic oxidating metabolisation and to production of metabolites; among these the O-demethylencainide and the 3-methoxy-O-demethylencainide have an antiarrhythmic activity, which is probably more important than the encainide parent and is longer-lasting. There are 'extensive', 'poor' and 'non-metaboliser' subjects. This results in wide pharmacokinetic inter- and intraindividual variability which must be taken into account during clinical treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Flecainide and encainide. 310 89

The clinical efficacy, adverse effects and pharmacokinetics of flecainide were evaluated in 16 pediatric and young adult patients with supraventricular tachycardia (SVT). Patients had received an average of 2.8 drugs before flecainide was tried. The following mechanisms of supraventricular arrhythmias were determined in patients by intracardiac electrophysiologic studies: atrioventricular node reentry, 4; reentry through an accessory connection, 7; atrial automatic focus, 2; atrial flutter, 3. Twelve patients had normal cardiac anatomy and 4 had congenital heart disease. Each patient received 2.8 mg/kg/day of flecainide divided into 2 doses 12 hours apart. After 3 days, the dose was increased to 5.6 mg/kg/day if necessary. In 14 patients, serum flecainide concentrations measured 3 to 4 days after beginning therapy ranged from 0.1 to 0.8 micrograms/ml (mean 0.40). Flecainide successfully controlled SVT in 8 of 16 patients. SVT in 3 of 7 patients with accessory connections and in 3 of 4 patients with atrioventricular node reentry was successfully controlled. In 1 of 2 patients with atrial automatic tachycardia, SVT had been completely controlled over 16 months. Only 1 of 3 patients treated for atrial flutter responded. Follow-up for successfully treated patients ranged from 4 to 16 months (median 9). Seven patients continue to take flecainide. None of the patients had clinical congestive heart failure. No drug-related adverse effects were noted on the resting surface electrocardiogram. Flecainide rarely produced proarrhythmic effects in this series. The 2 that were observed were mild and caused no clinical problems. Noncardiovascular side effects also occurred infrequently.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Flecainide for supraventricular tachycardia in children. 313 35

We treated 22 children, aged 3 days to 16 years 6 months (median 11 years 1 month), with flecainide for a variety of arrhythmias where a Class I agent was indicated. In 16, conventional antiarrhythmic treatment had failed. Structural heart disease was present in nine. The arrhythmia was paroxysmal re-entry atrioventricular tachycardia in nine; paroxysmal atrial tachycardia, flutter or fibrillation in five; paroxysmal ventricular tachycardia in five and frequent ventricular extrasystoles (with couplets) in three. Sinus rhythm was achieved in all four children who received flecainide during tachycardia (three received intravenous flecainide, one oral). During follow-up of 3-24 months (median 12 months), arrhythmia control was obtained in 13 children (59%). Combination therapy was used in seven of these; with digoxin in four and a beta blocker in three. Flecainide doses used in this study ranged from 1-11 mg kg-1 day-1 (median 4 mg kg-1 day-1), 25-297 mg m-2 day-1 (median 113 mg m-2 day-1). The median, pre-dose flecainide concentration in those responding to therapy was 225 micrograms l-1 and in those failing to respond was 417 micrograms l-1. An arrhythmogenic effect occurred in one child.
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PMID:Experience with flecainide for the treatment of cardiac arrhythmias in children. 314 91


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