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[PMID]:21416822
[Au] Autor:D'Este D; Sorbo MD
[Ad] Endereço:U.O.C. di Cardiologia, Ospedale di Dolo (VE). daniele.deste@ulss13mirano.ven.it
[Ti] Título:[When and how to treat ventricular ectopic beats].
[Ti] Título:L'extrasistolia ventricolare isolata: quando e come trattarla..
[So] Source:G Ital Cardiol (Rome);11(10 Suppl 1):21S-26S, 2010 Oct.
[Is] ISSN:1827-6806
[Cp] País de publicação:Italy
[La] Idioma:ita
[Ab] Resumo:Ventricular ectopic beats are commonly observed in daily clinical practice, either in symptomatic or asymptomatic subjects. In many subjects these arrhythmias are casually detected during a screening visit. Their occurrence is usually associated with no clinical significance. However, in some cases the presence of ventricular ectopic beats indicates susceptibility towards life-threatening arrhythmias or ventricular dysfunction. Appropriate ECG analysis and clinical evaluation are important to detect subjects in whom effective treatment is necessary.
[Mh] Termos MeSH primário: Complexos Ventriculares Prematuros/terapia
[Mh] Termos MeSH secundário: Antiarrítmicos/administração & dosagem
Antiarrítmicos/uso terapêutico
Arritmias Cardíacas/diagnóstico
Eletrocardiografia
Encainida/administração & dosagem
Encainida/uso terapêutico
Teste de Esforço
Seres Humanos
Incidência
Prevalência
Prognóstico
Propafenona/administração & dosagem
Propafenona/uso terapêutico
Ensaios Clínicos Controlados Aleatórios como Assunto
Bloqueadores dos Canais de Sódio/administração & dosagem
Bloqueadores dos Canais de Sódio/uso terapêutico
Esportes
Complexos Ventriculares Prematuros/diagnóstico
Complexos Ventriculares Prematuros/tratamento farmacológico
Complexos Ventriculares Prematuros/epidemiologia
Complexos Ventriculares Prematuros/mortalidade
[Pt] Tipo de publicação:COMPARATIVE STUDY; ENGLISH ABSTRACT; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 0 (Sodium Channel Blockers); 68IQX3T69U (Propafenone); SY3J0147NB (Encainide)
[Em] Mês de entrada:1105
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110323
[St] Status:MEDLINE


  2 / 340 MEDLINE  
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[PMID]:12380159
[Ti] Título:[Caution in therapy of ventricular extrasystole. Staying safe with electrolytes].
[Ti] Título:Bei der Therapie ventrikulärer Extrasystolen ist Vorsicht angesagt. Mit Elektrolyten auf der sicheren Seite..
[So] Source:MMW Fortschr Med;144(33-34):62, 2002 Aug 22.
[Is] ISSN:1438-3276
[Cp] País de publicação:Germany
[La] Idioma:ger
[Mh] Termos MeSH primário: Antiarrítmicos/efeitos adversos
Ácido Aspártico/administração & dosagem
Complexos Cardíacos Prematuros/tratamento farmacológico
Encainida/efeitos adversos
Flecainida/efeitos adversos
Infarto do Miocárdio/tratamento farmacológico
Potássio/administração & dosagem
[Mh] Termos MeSH secundário: Antiarrítmicos/administração & dosagem
Complexos Cardíacos Prematuros/mortalidade
Causas de Morte
Combinação de Medicamentos
Encainida/uso terapêutico
Flecainida/uso terapêutico
Seres Humanos
Infarto do Miocárdio/mortalidade
Ensaios Clínicos Controlados Aleatórios como Assunto
Taxa de Sobrevida
Resultado do Tratamento
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 0 (Drug Combinations); 30KYC7MIAI (Aspartic Acid); K94FTS1806 (Flecainide); RWP5GA015D (Potassium); SY3J0147NB (Encainide)
[Em] Mês de entrada:0212
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:021017
[St] Status:MEDLINE


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[PMID]:12176090
[Au] Autor:Dorne JL; Walton K; Slob W; Renwick AG
[Ad] Endereço:Clinical Pharmacology Group, University of Southampton, Biomedical Sciences Building, Bassett Crescent East, Southampton SO16 7PX, UK.
[Ti] Título:Human variability in polymorphic CYP2D6 metabolism: is the kinetic default uncertainty factor adequate?
[So] Source:Food Chem Toxicol;40(11):1633-56, 2002 Nov.
[Is] ISSN:0278-6915
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Human variability in the kinetics of CYP2D6 substrates has been quantified using a database of compounds metabolised extensively (>60%) by this polymorphic enzyme. Published pharmacokinetic studies (after oral and intravenous dosing) in non-phenotyped healthy adults, and phenotyped extensive (EMs), intermediate or slow-extensive (SEMs) and poor metabolisers (PMs) have been analysed using data for parameters that relate primarily to chronic exposure (metabolic and total clearances, area under the plasma concentration time-curve) and primarily to acute exposure (peak concentration). Similar analyses were performed with the available data for subgroups of the population (age, ethnicity and disease). Interindividual differences in kinetics for markers of oral exposure were large for non-phenotyped individuals and for EMs (coefficients of variation were 67-71% for clearances and 54-63% for C(max)), whereas the intravenous data indicated a lower variability (34-38%). Comparisons between EMs, SEMs and PMs revealed an increase in oral internal dose for SEMs and PMs (ratio compared to EMs=3 and 9-12, respectively) associated with lower variability than that for non-phenotyped individuals (coefficients of variation were 32-38% and 30% for SEMs and PMs, respectively). In relation to the uncertainty factors used for risk assessment, most subgroups would not be covered by the kinetic default of 3.16. CYP2D6-related factors necessary to cover 95-99% of each subpopulation ranged from 2.7 to 4.1 in non-phenotyped healthy adults and EMs to 15-18 in PMs and 22-45 in children. An exponential relationship (R(2)=0.8) was found between the extent of CYP2D6 metabolism and the uncertainty factors. The extent of CYP2D6 involvement in the metabolism of a substrate is critical in the estimation of the CYP2D6-related factor. The 3.16 kinetic default factor would cover PMs for substrates for which CYP2D6 was responsible for up to 25% of the metabolism in EMs.
[Mh] Termos MeSH primário: Citocromo P-450 CYP2D6/genética
Citocromo P-450 CYP2D6/metabolismo
Variação Genética
Fenilpropanolamina
Polimorfismo Genético
[Mh] Termos MeSH secundário: Adulto
Idoso
Envelhecimento
Compostos Benzidrílicos/metabolismo
Cresóis/metabolismo
Cicloexanóis/metabolismo
Debrisoquina/metabolismo
Desipramina/metabolismo
Encainida/metabolismo
Grupos Étnicos
Seres Humanos
Hidroxilação
Lactente
Recém-Nascido
Nefropatias/enzimologia
Cinética
Hepatopatias/enzimologia
Taxa de Depuração Metabólica
Metoprolol/metabolismo
Propafenona/metabolismo
Especificidade por Substrato
Tartarato de Tolterodina
Cloridrato de Venlafaxina
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzhydryl Compounds); 0 (Cresols); 0 (Cyclohexanols); 33RU150WUN (Phenylpropanolamine); 5T619TQR3R (Tolterodine Tartrate); 68IQX3T69U (Propafenone); 7D7RX5A8MO (Venlafaxine Hydrochloride); EC 1.14.14.1 (Cytochrome P-450 CYP2D6); GEB06NHM23 (Metoprolol); SY3J0147NB (Encainide); TG537D343B (Desipramine); X31CDK040E (Debrisoquin)
[Em] Mês de entrada:0210
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:020815
[St] Status:MEDLINE


  4 / 340 MEDLINE  
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[PMID]:9835260
[Au] Autor:Krishnan SC; Josephson ME
[Ad] Endereço:Harvard-Thorndike Electrophysiology Institute, Beth Israel Deaconess Hospital, Boston, Massachusetts 02215, USA.
[Ti] Título:ST segment elevation induced by class IC antiarrhythmic agents: underlying electrophysiologic mechanisms and insights into drug-induced proarrhythmia.
[So] Source:J Cardiovasc Electrophysiol;9(11):1167-72, 1998 Nov.
[Is] ISSN:1045-3873
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Three patients in whom Class IC sodium channel blockers induced ST segment elevation in leads V1 through V3 are described. The underlying electrophysiologic mechanism, implications for drug-induced proarrhythmia, and the relationship of the finding to the Brugada syndrome type of idiopathic ventricular fibrillation are discussed.
[Mh] Termos MeSH primário: Antiarrítmicos/farmacologia
Arritmias Cardíacas/induzido quimicamente
Eletrocardiografia/efeitos dos fármacos
[Mh] Termos MeSH secundário: Arritmias Cardíacas/fisiopatologia
Fibrilação Atrial/fisiopatologia
Cardiomiopatia Dilatada/fisiopatologia
Eletrofisiologia
Encainida/farmacologia
Flecainida/farmacologia
Seres Humanos
Masculino
Meia-Idade
Bloqueadores dos Canais de Sódio
Fibrilação Ventricular/fisiopatologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 0 (Sodium Channel Blockers); K94FTS1806 (Flecainide); SY3J0147NB (Encainide)
[Em] Mês de entrada:9902
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:981203
[St] Status:MEDLINE


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[PMID]:9024734
[Au] Autor:Anderson JL; Pratt CM; Waldo AL; Karagounis LA
[Ad] Endereço:University of Utah, Salt Lake City 84143, USA.
[Ti] Título:Impact of the Food and Drug Administration approval of flecainide and encainide on coronary artery disease mortality: putting "Deadly Medicine" to the test.
[So] Source:Am J Cardiol;79(1):43-7, 1997 Jan 01.
[Is] ISSN:0002-9149
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In his book Deadly Medicine and on television, Thomas Moore impugns the process of antiarrhythmic drug approval in the 1980s, alleging that the new generation of drugs had flooded the marketplace and had caused deaths in numbers comparable to lives lost during war. To assess these important public health allegations, we evaluated annual coronary artery disease death rates in relation to antiarrhythmic drug sales (2 independent marketing surveys). Predicted mortality rates were modeled using linear regression analysis for 1982 through 1991. Deviations from predicted linearity were sought in relation to rising and falling class IC and overall class I antiarrhythmic drug use. Flecainide came to market in 1986 and encainide in 1987. Combined class IC sales peaked in 1987 and 1988 (maximum market penetration, 20%, first quarter 1989). Results of the Cardiac Arrhythmia Suppression Trial (CAST) were disclosed in April 1989. Overall annual class I antiarrhythmic prescription sales actually fell slightly (-3% to -4%/yr) in the 2 years before CAST and then more abruptly (- 12%) in the year after CAST (1990). Sales of class IC drugs fell dramatically after CAST (by 75%). Coronary death rates (age adjusted) fell in a linear fashion during the decade of 1982 through 1991. No deviation from predicted rates was observed during the introduction, rise, and fall in class IC (and other class I) sales: rates were 126/100,000 in 1985 (before flecainide), 114 and 110 in 1987 and 1988 (maximum sales), and 103 in 1990 (after CAST). Deviations in death rates in the postulated range of 6,000 to 25,000 per year were shown to be excluded easily by the 95% confidence intervals about the predicted rates. Entry of new antiarrhythmic drugs in the 1980s did not lead to overall market expansion and had no adverse impact on coronary artery disease death rates, which fell progressively. Thus, the allegations in Deadly Medicine could not be confirmed.
[Mh] Termos MeSH primário: Antiarrítmicos/uso terapêutico
Doença das Coronárias/mortalidade
Aprovação de Drogas
Encainida/uso terapêutico
Flecainida/uso terapêutico
Complexos Ventriculares Prematuros/tratamento farmacológico
[Mh] Termos MeSH secundário: Doença das Coronárias/complicações
Uso de Medicamentos
Estudos de Avaliação como Assunto
Seres Humanos
Modelos Lineares
Padrões de Prática Médica
Análise de Sobrevida
Estados Unidos
United States Food and Drug Administration
Complexos Ventriculares Prematuros/complicações
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); K94FTS1806 (Flecainide); SY3J0147NB (Encainide)
[Em] Mês de entrada:9703
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:970101
[St] Status:MEDLINE


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[PMID]:8848377
[Au] Autor:Sweeney RJ; Gill RM; Steinberg MI; Reid PR
[Ad] Endereço:Department of Electrophysiology Research, Lilly Research Laboratories Division, Eli Lilly and Company, Indianapolis, Indiana, USA.
[Ti] Título:Effects of flecainide, encainide, and clofilium on ventricular refractory period extension by transcardiac shocks.
[So] Source:Pacing Clin Electrophysiol;19(1):50-60, 1996 Jan.
[Is] ISSN:0147-8389
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The mechanisms by which pharmacological agents alter electrical defibrillation are not fully understood. It has been proposed that, in addition to directly stimulating tissue, defibrillation may involve refractory period extension (RPE) produced by the shock. Accordingly, pharmacological agents might modulate defibrillation by altering RPE. This study examined the effect of Class I and Class III antiarrhythmic agents on RPE by transcardiac shocks. METHODS: In four groups of pentobarbital anesthetized dogs, RPE was measured during rapid ventricular pacing before and after administration of either the Class I agents flecainide (n = 7) or encainide (n = 7), the Class III agent clofilium (n = 7), or vehicle (n = 5). Measurements included QRS duration during sinus rhythm and a conduction time, QTC interval and refractory period, and RPE for 4- to 10-V/cm shocks delivered 20-80 ms before the end of the tissue absolute refractory period. For the 6-V/cm shocks, the interval after the shock during which tissue remained refractory (RIAS) was also computed. RESULTS: Drugs affected QRS duration, conduction time, QTC, and refractory period ( without shocks) in accordance with their anticipated Class I and Class III actions. Without drugs, significant RPE was observed in all animals for all shocks delivered 40 ms or less before the end of the refractory period. Clofilium, encainide, and flecainide had a tendency to increase RPE but only clofilium produced a significant increase. For 6-V/cm shocks with different timings, the minimum RIAS was found to be approximately 43 ms, and occurred for shocks given 20-30 ms before the end of the refractory period. CONCLUSIONS: At drug dosages that produced moderate Class III ( approximately equal to 15%) or strong Class I (approximately equal to 35%) effects, only the Class III agent significantly increased RPE and RIAS. Thus, in addition to altering tissue excitability, the effect of antiarrhythmic agents to increase RPE and the minimum RIAS may help explain their influence on defibrillation threshold.
[Mh] Termos MeSH primário: Antiarrítmicos/farmacologia
Cardioversão Elétrica
Sistema de Condução Cardíaco/efeitos dos fármacos
Fibrilação Ventricular/terapia
Função Ventricular/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Estimulação Cardíaca Artificial
Cães
Encainida/farmacologia
Flecainida/farmacologia
Sistema de Condução Cardíaco/fisiologia
Compostos de Amônio Quaternário/farmacologia
Período Refratário Eletrofisiológico/efeitos dos fármacos
Fatores de Tempo
Fibrilação Ventricular/fisiopatologia
Função Ventricular/fisiologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 0 (Quaternary Ammonium Compounds); 847G178BMC (clofilium); K94FTS1806 (Flecainide); SY3J0147NB (Encainide)
[Em] Mês de entrada:9610
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:960101
[St] Status:MEDLINE


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[PMID]:8775589
[Au] Autor:Obias-Manno D; Friedmann E; Brooks MM; Thomas SA; Haakenson C; Morris M; Wimbush F; Somelofski C; Goldner F
[Ad] Endereço:Washington Hospital Center, Washington, DC, USA.
[Ti] Título:Adherence and arrhythmic mortality in the cardiac arrhythmia suppression trial (CAST).
[So] Source:Ann Epidemiol;6(2):93-101, 1996 Mar.
[Is] ISSN:1047-2797
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Patient adherence to therapy is essential to assess treatment efficacy, particularly in clinical trials. Active treatment usually is expected to benefit patients. The healthy adherer effect, the association or greater adherence to all health-promoting behaviors, including medication and overall concern for health, explains the improved survival of more adherent patients in both active and placebo medication groups of several clinical trials. The Cardiac Arrhythmia Suppression Trial (CAST), a placebo-controlled double-blind clinical trial of post-myocardial infarction (MI) patients with asymptomatic ventricular arrhythmias, in which active medication (encainide or flecainide) led to increased mortality, provided an opportunity to examine the relationship of adherence to survival from a different perspective. We consider whether adherence to active treatment was related to arrhythmic mortality and whether a healthy adherer effect might counteract the effect of treatment on mortality among patients taking active medication. Adherence (average pill count) at the first follow-up visit did not differ in the active treatment (92.2%, standard deviation (SD) = 11.97, n = 574) and placebo (90.8%, SD = 13.66, n = 579) groups. In a Cox proportional hazard regression model, medication adherence predicted arrhythmic mortality among the active (P < 0.0062) but not the placebo medication group. The effect of adherence on arrhythmic mortality was significant beyond the effects of ejection fraction, race, spouse, smoking status, diuretic medication, and history of MI. A 10% increase in adherence led to more than a threefold increase of risk of arrhythmic death. The design of the CAST, which included a titration phase, may have tended to select relatively adherent patients since only those whose arrhythmias were suppressed with active medication were randomized into the trial. The data do not support a strong healthy adherer effect in the CAST. There was no evidence in this study that a healthy adherer effect counterbalanced the effect of the active medication.
[Mh] Termos MeSH primário: Arritmias Cardíacas/mortalidade
Comportamentos Relacionados com a Saúde
Cooperação do Paciente
[Mh] Termos MeSH secundário: Antiarrítmicos/efeitos adversos
Arritmias Cardíacas/tratamento farmacológico
Encainida/efeitos adversos
Feminino
Flecainida/efeitos adversos
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); K94FTS1806 (Flecainide); SY3J0147NB (Encainide)
[Em] Mês de entrada:9612
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:960301
[St] Status:MEDLINE


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[PMID]:8680488
[Au] Autor:Kellen JC; Ettinger A; Todd L; Brezsnyak ML; Campion J; McBride R; Thomas S; Corum J; Schron E
[Ad] Endereço:University of Calgary, Alberta.
[Ti] Título:The Cardiac Arrhythmia Suppression Trial: Implications for nursing practice.
[So] Source:Am J Crit Care;5(1):19-25, 1996 Jan.
[Is] ISSN:1062-3264
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Care of patients with ventricular arrhythmia after myocardial infarction requires careful nursing management, including assisting with arrhythmia monitoring and testing. Because ventricular premature depolarization is a known risk factor for sudden cardiac death, it was hypothesized that the suppression of asymptomatic or mildly symptomatic ventricular premature depolarization would improve survival in these patients. OBJECTIVE: To review the Cardiac Arrhythmia Suppression Trial findings and provide implications for nursing practice for patients after myocardial infarction. METHODS: The Cardiac Arrhythmia Suppression Trial was a multicenter, randomized, placebo-controlled trial designed to determine whether the suppression of ventricular premature depolarizations in postmyocardial infarction patients would improve survival. Three class I antiarrhythmic drugs were used: encainide, flecainide, or moricizine. Patients for whom the drug suppressed their arrhythmia 80% or more were randomly assigned to that drug and dose or its matching placebo and were followed every 4 months (main study). Patients with 1% to 79% suppression were randomly assigned to the drug or its placebo that best treated their arrhythmia and followed every 4 months. RESULTS: Suppression of asymptomatic or mildly symptomatic ventricular premature depolarization in patients using encainide, flecainide, or moricizine failed to improve patient survival and was even harmful in some cases. CONCLUSIONS: Our results showed that in the absence of effective antiarrhythmic drug therapy, supportive nursing care and arrhythmia monitoring is important until appropriate therapy for the management of these arrhythmias in patients who have had a myocardial infarction can be found. Clinical trials are essential to provide an evaluation of therapies and direction for further studies, as well as a basis for practicing clinicians.
[Mh] Termos MeSH primário: Antiarrítmicos/uso terapêutico
Cuidados Críticos
Infarto do Miocárdio/enfermagem
Complexos Ventriculares Prematuros/tratamento farmacológico
[Mh] Termos MeSH secundário: Idoso
Morte Súbita Cardíaca/prevenção & controle
Encainida/uso terapêutico
Feminino
Flecainida/uso terapêutico
Seres Humanos
Masculino
Meia-Idade
Monitorização Fisiológica
Moricizina/uso terapêutico
Infarto do Miocárdio/fisiopatologia
Avaliação em Enfermagem
Taxa de Sobrevida
Complexos Ventriculares Prematuros/enfermagem
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 2GT1D0TMX1 (Moricizine); K94FTS1806 (Flecainide); SY3J0147NB (Encainide)
[Em] Mês de entrada:9608
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM; N
[Da] Data de entrada para processamento:960101
[St] Status:MEDLINE


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PubMed Central Texto completo
[PMID]:8541168
[Au] Autor:Greenberg HM; Dwyer EM; Hochman JS; Steinberg JS; Echt DS; Peters RW
[Ad] Endereço:Division of Cardiology, St Luke's/Roosevelt Hospital, New York, NY 10019, USA.
[Ti] Título:Interaction of ischaemia and encainide/flecainide treatment: a proposed mechanism for the increased mortality in CAST I.
[So] Source:Br Heart J;74(6):631-5, 1995 Dec.
[Is] ISSN:0007-0769
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To determine whether an interaction between encainide or flecainide and intercurrent ischaemia could account for the observed increase in cardiac and sudden deaths in the study group in the Cardiac Arrhythmia Suppression Trial (CAST) I. DESIGN: CAST I was a randomised, double blind, placebo controlled study in which patients received the drug which suppressed at least 6 premature ventricular contractions per minute by 80% or episodes of non-sustained ventricular tachycardia by 90%. Arrhythmic sudden death or aborted sudden death were the study end points. Measured secondary end points included recurrent myocardial infarction, new or increasing angina pectoris, congestive heart failure, and syncope. The CAST I database was analysed to determine which of three end points occurred first--cardiac death or cardiac arrest, angina pectoris, or non-fatal recurrent infarction. They were regarded as mutually exclusive end points. The triad of cardiac or sudden arrhythmic death plus congestive heart failure and syncope was similarly analysed. RESULTS: It was assumed that recurrent non-fatal infarction and new or increasing angina pectoris were ischaemic in origin. The sum of these non-fatal ischaemic end points and sudden death were nearly identical in the placebo group (N = 129) and the treatment group (N = 131). The one year event rate in each group was 21%. However, the treatment group had a much greater fatality rate (55 v 17; P < 0.0001) than the placebo group. The same relation was found when the data were examined on the basis of drug exposure rather than intention to treat. The temporal and circadian events were similar in each group and were consistent with an ischaemic pattern. No such patterns emerged from analysis of the presumed non-ischaemic end points of congestive heart failure and syncope. CONCLUSIONS: These data suggest that the interaction between active ischaemia and treatment with encainide or flecainide may have been responsible for the increased mortality seen in the treatment group in CAST I. This conversion of a non-fatal to a fatal event emphasises the need for future antiarrhythmic drugs to be screened in ischaemic models.
[Mh] Termos MeSH primário: Antiarrítmicos/efeitos adversos
Encainida/efeitos adversos
Flecainida/efeitos adversos
Isquemia Miocárdica/induzido quimicamente
[Mh] Termos MeSH secundário: Angina Pectoris/induzido quimicamente
Angina Pectoris/mortalidade
Bases de Dados Factuais
Morte Súbita Cardíaca/etiologia
Interações Medicamentosas
Insuficiência Cardíaca/induzido quimicamente
Insuficiência Cardíaca/mortalidade
Seres Humanos
Infarto do Miocárdio/induzido quimicamente
Infarto do Miocárdio/mortalidade
Isquemia Miocárdica/mortalidade
Estudos Retrospectivos
Síncope/induzido quimicamente
Síncope/mortalidade
Estados Unidos
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); K94FTS1806 (Flecainide); SY3J0147NB (Encainide)
[Em] Mês de entrada:9602
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:951201
[St] Status:MEDLINE


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[PMID]:7805221
[Au] Autor:Goldstein S; Brooks MM; Ledingham R; Kennedy HL; Epstein AE; Pawitan Y; Bigger JT
[Ad] Endereço:Heart and Vascular Institute, Henry Ford Hospital, Detroit, MI 48202.
[Ti] Título:Association between ease of suppression of ventricular arrhythmia and survival.
[So] Source:Circulation;91(1):79-83, 1995 Jan 01.
[Is] ISSN:0009-7322
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: We tested the hypothesis that patients whose ventricular arrhythmias are easy to suppress have a lower rate of arrhythmic death, defined as arrhythmic death and nonfatal cardiac arrest, the primary end point in the Cardiac Arrhythmia Suppression Trials (CAST-I and CAST-II), than patients whose ventricular arrhythmias are hard to suppress. In addition, we evaluated the association between ease of suppression of ventricular arrhythmias and mortality of all causes. METHODS AND RESULTS: CAST-I investigated the effect on arrhythmic death of ventricular premature depolarization (VPD) suppression achieved by three drugs, encainide, flecainide, and moricizine, at two different dose levels; CAST-II investigated the same effect, using moricizine alone at three dose levels. If suppression was achieved, patients were randomized to the effective active drug or corresponding placebo. To examine the independence of easily suppressed ventricular arrhythmias as a predictor of arrhythmic death, we adjusted statistically for other variables that were related both to ease of suppression and arrhythmic death. Patients with ventricular arrhythmias (n = 1778) that were easy to suppress had fewer arrhythmic deaths during follow-up than those with ventricular arrhythmias that were hard to suppress (n = 1173) (relative risk, .59; P = .003). Patients whose VPDs were easily suppressed were older and had a lower frequency of prior history of heart failure and myocardial infarction. They also had a higher incidence of anterior myocardial infarction, VPD frequency, and average ejection fraction. After adjusting for these variables, we found that easily suppressed ventricular arrhythmias were still significant predictors of arrhythmic death (relative risk, .66; P = .013). CONCLUSIONS: This study shows that the ease of VPD suppression identifies a subgroup of postmyocardial infarction patients who have low risk of arrhythmic death.
[Mh] Termos MeSH primário: Encainida/uso terapêutico
Flecainida/uso terapêutico
Moricizina/uso terapêutico
Fibrilação Ventricular/tratamento farmacológico
[Mh] Termos MeSH secundário: Idoso
Estudos Cross-Over
Seguimentos
Seres Humanos
Meia-Idade
Fatores de Risco
Fibrilação Ventricular/mortalidade
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
2GT1D0TMX1 (Moricizine); K94FTS1806 (Flecainide); SY3J0147NB (Encainide)
[Em] Mês de entrada:9502
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:950101
[St] Status:MEDLINE



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