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[PMID]:29245231
[Au] Autor:Iguchi S; Yamaguchi N; Takami H; Komatsu T; Ookubo H; Sekii H; Inoue K; Okazaki S; Okai I; Maruyama S; Nomura T; Sugita M
[Ad] Endereço:aDepartment of Emergency and Critical Care MedicinebDepartment of Cardiology, Juntendo University Nerima HospitalcDepartment of Infectious Diseases, Tokyo Women's Medical University, Tokyo, Japan.
[Ti] Título:Higher efficacy of direct hemoperfusion using coated activated-charcoal column for disopyramide poisoning: A case report.
[So] Source:Medicine (Baltimore);96(49):e8755, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Cases of severe disopyramide poisoning are rare and few have been reported. We report a case in which activated-charcoal column hemoperfusion was dramatically effective for life-threatening disopyramide poisoning. PATIENT CONCERNS: A teenage girl who had overdosed on disopyramide (total dose, 4950 mg) was brought to our hospital. She was resuscitated from short period cardiopulmonary arrest and subsequently showed severe cardiogenic shock and ventricular arrhythmia. DIAGNOSES: Disopyramide poisoning (self-evident). INTERVENTIONS: As hemodynamics remained unstable after providing percutaneous cardiopulmonary support and intra-aortic balloon pumping, we attempted direct hemoperfusion using a coated activated-charcoal hemoperfusion column. OUTCOMES: Hemodynamics including electrocardiography and serum disopyramide concentration were dramatically improved, and the patient was ambulatory by hospital day 14. LESSONS: Because disopyramide has low molecular weight and a small distribution volume, blood purification is considered to be the most effective therapy. We selected direct hemoperfusion for relatively high protein-binding rate. In fact, clinical status was dramatically improved, and the calculated half-life of the direct hemoperfusion phase was the shortest of all phases. In cases of severe or life-threatening disopyramide poisoning, blood purification therapy including direct hemoperfusion using a coated activated-charcoal column should be performed.
[Mh] Termos MeSH primário: Antiarrítmicos/envenenamento
Disopiramida/envenenamento
Overdose de Drogas/terapia
Hemoperfusão/métodos
[Mh] Termos MeSH secundário: Adolescente
Antídotos/uso terapêutico
Carvão Vegetal/uso terapêutico
Feminino
Seres Humanos
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 0 (Antidotes); 16291-96-6 (Charcoal); GFO928U8MQ (Disopyramide)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171222
[Lr] Data última revisão:
171222
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171217
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008755


  2 / 1570 MEDLINE  
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[PMID]:28632743
[Au] Autor:Luo C; Wang K; Zhang H
[Ad] Endereço:School of Computer Science and Technology, Harbin Institute of Technology (HIT), Harbin, China.
[Ti] Título:In silico assessment of the effects of quinidine, disopyramide and E-4031 on short QT syndrome variant 1 in the human ventricles.
[So] Source:PLoS One;12(6):e0179515, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIMS: Short QT syndrome (SQTS) is an inherited disorder associated with abnormally abbreviated QT intervals and an increased incidence of atrial and ventricular arrhythmias. SQT1 variant (linked to the rapid delayed rectifier potassium channel current, IKr) of SQTS, results from an inactivation-attenuated, gain-of-function mutation (N588K) in the KCNH2-encoded potassium channels. Pro-arrhythmogenic effects of SQT1 have been well characterized, but less is known about the possible pharmacological antiarrhythmic treatment of SQT1. Therefore, this study aimed to assess the potential effects of E-4031, disopyramide and quinidine on SQT1 using a mathematical model of human ventricular electrophysiology. METHODS: The ten Tusscher et al. biophysically detailed model of the human ventricular action potential (AP) was modified to incorporate IKr Markov chain (MC) formulations based on experimental data of the kinetics of the N588K mutation of the KCNH2-encoded subunit of the IKr channels. The modified ventricular cell model was then integrated into one-dimensional (1D) strand, 2D regular and realistic tissues with transmural heterogeneities. The channel-blocking effect of the drugs on ion currents in healthy and SQT1 cells was modeled using half-maximal inhibitory concentration (IC50) and Hill coefficient (nH) values from literatures. Effects of drugs on cell AP duration (APD), effective refractory period (ERP) and pseudo-ECG traces were calculated. Effects of drugs on the ventricular temporal and spatial vulnerability to re-entrant excitation waves were measured. Re-entry was simulated in both 2D regular and realistic ventricular tissue. RESULTS: At the single cell level, the drugs E-4031 and disopyramide had hardly noticeable effects on the ventricular cell APD at 90% repolarization (APD90), whereas quinidine caused a significant prolongation of APD90. Quinidine prolonged and decreased the maximal transmural AP heterogeneity (δV); this led to the decreased transmural heterogeneity of APD across the 1D strand. Quinidine caused QT prolongation and a decrease in the T-wave amplitude, and increased ERP and decreased temporal susceptibility of the tissue to the initiation of re-entry and increased the minimum substrate size necessary to prevent re-entry in the 2D regular model, and further terminated re-entrant waves in the 2D realistic model. Quinidine exhibited significantly better therapeutic effects on SQT1 than E-4031 and disopyramide. CONCLUSIONS: The simulated pharmacological actions of quinidine exhibited antiarrhythmic effects on SQT1. This study substantiates a causal link between quinidine and QT interval prolongation in SQT1 and suggests that quinidine may be a potential pharmacological agent for treating SQT1 patients.
[Mh] Termos MeSH primário: Potenciais de Ação/efeitos dos fármacos
Disopiramida/farmacologia
Piperidinas/farmacologia
Piridinas/farmacologia
Quinidina/farmacologia
[Mh] Termos MeSH secundário: Arritmias Cardíacas/tratamento farmacológico
Arritmias Cardíacas/genética
Arritmias Cardíacas/patologia
Linhagem Celular
Disopiramida/uso terapêutico
Canal de Potássio ERG1/genética
Eletrocardiografia
Ventrículos do Coração/efeitos dos fármacos
Ventrículos do Coração/fisiopatologia
Seres Humanos
Modelos Biológicos
Piperidinas/uso terapêutico
Polimorfismo de Nucleotídeo Único
Piridinas/uso terapêutico
Quinidina/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ERG1 Potassium Channel); 0 (KCNH2 protein, human); 0 (Piperidines); 0 (Pyridines); 113558-89-7 (E 4031); GFO928U8MQ (Disopyramide); ITX08688JL (Quinidine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170621
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179515


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[PMID]:27567136
[Au] Autor:Kehl DW; Rader F; Pollick C; Trento A; Siegel RJ
[Ad] Endereço:Cedars-Sinai Heart Institute, Los Angeles, California. Electronic address: devinwkehl@gmail.com.
[Ti] Título:Medical Management (ß Blocker ± Disopyramide) of Left Ventricular Outflow Gradient Secondary to Systolic Anterior Motion of the Mitral Valve After Repair.
[So] Source:Am J Cardiol;118(7):1053-6, 2016 Oct 01.
[Is] ISSN:1879-1913
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Systolic anterior motion of the mitral valve (SAM) occurs intraoperatively after mitral valve repair (MVRr) in up to 14% of cases and typically resolves in the operating room with conservative measures. Less commonly SAM may also occur in the early or late postoperative period. The clinical course and optimal management of such cases is poorly defined, but reoperation is common. We describe our experience using disopyramide to successfully treat postoperative SAM refractory to beta blockade. Seven patients were retrospectively identified with mitral valve prolapse who underwent MVRr from 2003 to 2015 and were found during follow-up to have severe SAM with a left ventricular outflow tract (LVOT) gradient not observed intraoperatively. All 7 patients were successfully managed medically. In 5 cases, SAM persisted even after maximization of beta blockade, and the addition of disopyramide led to significant improvement or resolution of SAM, the LVOT gradient, and mitral regurgitation. The postoperative LVOT gradient initially exceeded 30 mm Hg in 6 of 7 patients. In 2 patients, the LVOT gradient exceeded 100 mm Hg, and both were managed medically with disopyramide with complete resolution of SAM. In conclusion, SAM after MVRr typically follows a benign clinical course and can be managed medically in most cases. When an initial treatment strategy of beta blockade is insufficient, the addition of disopyramide can effectively alleviate and terminate this condition and should be considered before reoperation.
[Mh] Termos MeSH primário: Antagonistas Adrenérgicos beta/uso terapêutico
Disopiramida/uso terapêutico
Anuloplastia da Valva Mitral
Insuficiência da Valva Mitral/tratamento farmacológico
Prolapso da Valva Mitral/cirurgia
Complicações Pós-Operatórias/tratamento farmacológico
Bloqueadores do Canal de Sódio Disparado por Voltagem/uso terapêutico
[Mh] Termos MeSH secundário: Idoso
Ecocardiografia Doppler em Cores
Feminino
Doenças das Valvas Cardíacas/diagnóstico por imagem
Doenças das Valvas Cardíacas/tratamento farmacológico
Seres Humanos
Masculino
Meia-Idade
Valva Mitral
Insuficiência da Valva Mitral/diagnóstico por imagem
Complicações Pós-Operatórias/diagnóstico por imagem
Estudos Retrospectivos
Sístole
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Adrenergic beta-Antagonists); 0 (Voltage-Gated Sodium Channel Blockers); GFO928U8MQ (Disopyramide)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170524
[Lr] Data última revisão:
170524
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160828
[St] Status:MEDLINE


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[PMID]:26818487
[Au] Autor:Sherrid MV
[Ad] Endereço:New York University Langone Medical Center, 530 First Avenue, NYC, NY 10016, USA. mark.sherrid@nyumc.org.
[Ti] Título:Drug Therapy for Hypertrophic Cardiomypathy: Physiology and Practice.
[So] Source:Curr Cardiol Rev;12(1):52-65, 2016.
[Is] ISSN:1875-6557
[Cp] País de publicação:United Arab Emirates
[La] Idioma:eng
[Ab] Resumo:HCM is the most common inherited heart condition occurring in 1:500 individuals in the general population. Left ventricular outflow obstruction at rest or after provocation occurs in 2/3 of HCM patients and is a frequent cause of limiting symptoms. Pharmacologic therapy is the first-line treatment for obstruction, and should be aggressively pursued before application of invasive therapy. Beta-blockade is given first, and up-titrated to decrease resting heart rate to between 50 and 60 beats per minute. However, beta-blockade is not expected to decrease resting gradients; its effect rests on decreasing the rise in gradient that accompanies exercise. For patients who fail beta-blockade the addition of oral disopyramide in adequate dose often will decrease resting gradients and offer meaningful relief of symptoms. Disopyramide vagolytic side effects, if they occur, can be greatly mitigated by simultaneous administration of oral pyridostigmine. This combination allows adequate dosing of disopyramide to achieve therapeutic goals. Verapamil utility in obstructive HCM with high resting gradients is limited by its vasodilating effects that can, infrequently, worsen gradient and symptoms. As such, we tend to avoid it in patients with high gradients and limiting heart failure symptoms. In a head-to-head comparison of intravenous drug administration in individual obstructive HCM patients the relative efficacy for lowering gradient was disopyramide > beta-blockade > verapamil. Severe symptoms in non-obstructive HCM are caused by fibrosis or severe myocyte disarray, and often by very small LV chamber size. Severe symptoms caused by these anatomic and histologic abnormalities, in the absence of obstruction, are less amenable to current pharmacotherapy. New pharmacotherapeutic approaches to HCM are on the horizon, that are to be evaluated in formal therapeutic trials.
[Mh] Termos MeSH primário: Cardiomiopatia Hipertrófica/tratamento farmacológico
Cardiomiopatia Hipertrófica/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Cardiomiopatia Hipertrófica/etiologia
Disopiramida/uso terapêutico
Eletrocardiografia
Seres Humanos
Hipertensão/complicações
Obstrução do Fluxo Ventricular Externo/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
GFO928U8MQ (Disopyramide)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:170201
[Lr] Data última revisão:
170201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160129
[St] Status:MEDLINE


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[PMID]:26441377
[Au] Autor:Król M; Ufnal M; Szulczyk B; Podsadni P; Drapala A; Turlo J; Dawidowski M
[Ad] Endereço:Department of Drug Technology and Pharmaceutical Biotechnology, Medical University of Warsaw, Banacha 1, 02-097 Warsaw, Poland.
[Ti] Título:Characterization of Disopyramide derivative ADD424042 as a non-cardiotoxic neuronal sodium channel blocker with broad-spectrum anticonvulsant activity in rodent seizure models.
[So] Source:Eur J Pharm Sci;81:42-51, 2016 Jan 01.
[Is] ISSN:1879-0720
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:It was reported that antiarrhythmic drugs (AADs) can be useful in controlling refractory seizures in humans or in enhancing the action of antiepileptic drugs (AEDs) in animal models. Disopyramide phosphate (DISO) is an AAD that blocks sodium channels in cardiac myocytes. We evaluated a DISO derivative, 2-(2-chlorophenyl)-2-(pyridin-2-yl)acetamide (ADD424042) for its anticonvulsant activity in a battery of rodent models of epileptic seizures. The compound displayed a broad spectrum of activity in the 'classical' models as well as in the models of pharmacoresistant seizures. Furthermore, ADD424042 showed good therapeutic indices between the anticonvulsant activity and the motor impairment. On the contrary, no anticonvulsant effects but severe lethality were observed in the primary anticonvulsant testing of the parent DISO. By performing the whole-cell voltage-clamp experiments in dispersed cortical neurons we demonstrated that ADD424042 decreased the maximal amplitude of voltage-gated sodium channels with an IC50 value in nM range. Moreover, the compound enhanced use-dependent block and decreased excitability in pyramidal neurons in the current-clamp experiments in cortical slices. Importantly, we found that ADD424042 possessed either no, or very small cardiotoxic effect. In contrast to DISO, ADD424042 did not produce any apparent changes in electrocardiogram (ECG) and arterial blood pressure recordings. ADD424042 had no effect on QT and corrected QT intervals, at a dose which was 15 times higher than ED50 for the anticonvulsant effect in the MES model. Taken together, these data suggest that ADD424042 has the potential to become a lead structure for novel broadly acting AEDs with wide margin of cardiac safety.
[Mh] Termos MeSH primário: Antiarrítmicos/uso terapêutico
Anticonvulsivantes/uso terapêutico
Disopiramida/análogos & derivados
Convulsões/tratamento farmacológico
Bloqueadores dos Canais de Sódio/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Disopiramida/uso terapêutico
Eletrocardiografia
Masculino
Camundongos
Ratos Sprague-Dawley
Ratos Wistar
Convulsões/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-(2-chlorophenyl)-2-(pyridin-2-yl)acetamide); 0 (Anti-Arrhythmia Agents); 0 (Anticonvulsants); 0 (Sodium Channel Blockers); GFO928U8MQ (Disopyramide)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151007
[St] Status:MEDLINE


  6 / 1570 MEDLINE  
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[PMID]:26684556
[Au] Autor:Verlinden NJ; Coons JC
[Ad] Endereço:Department of Pharmacy, Allegheny General Hospital, Pittsburgh, Pennsylvania.
[Ti] Título:Disopyramide for Hypertrophic Cardiomyopathy: A Pragmatic Reappraisal of an Old Drug.
[So] Source:Pharmacotherapy;35(12):1164-72, 2015 Dec.
[Is] ISSN:1875-9114
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hypertrophic cardiomyopathy (HCM) is a genetic cardiac disorder characterized by unexplained left ventricular hypertrophy in the absence of other cardiac or systemic etiologies. Approximately two-thirds of patients with HCM develop left ventricular outflow tract (LVOT) obstruction with or without provocation, whereas nearly half develop heart failure with preserved ejection fraction. Medical management of heart failure with preserved ejection fraction is based on the presence of symptoms and LVOT obstruction and frequently includes ß-blockers or verapamil. Disopyramide is a class Ia antiarrhythmic that historically was used for the treatment of arrhythmias; however, its contemporary use is often reserved for patients with HCM who are persistently symptomatic despite ß-blockers or verapamil and have evidence of LVOT obstruction. The pharmacologic rationale for use of disopyramide is largely based on its strong negative inotropic property. Three clinical studies have showed significant improvements in heart failure symptoms and a reduction in the need for invasive therapy in patients treated with disopyramide. Appropriate dosing and monitoring of disopyramide are important to mitigate the potential for anticholinergic adverse events and proarrhythmias. Disopyramide is a safe and effective medication that reduces heart failure symptoms and LVOT gradient and delays the need for invasive therapy in patients with obstructive HCM.
[Mh] Termos MeSH primário: Antiarrítmicos/uso terapêutico
Cardiomiopatia Hipertrófica/tratamento farmacológico
Disopiramida/uso terapêutico
[Mh] Termos MeSH secundário: Antiarrítmicos/administração & dosagem
Disopiramida/administração & dosagem
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); GFO928U8MQ (Disopyramide)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:151219
[Lr] Data última revisão:
151219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151220
[St] Status:MEDLINE
[do] DOI:10.1002/phar.1664


  7 / 1570 MEDLINE  
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[PMID]:26348084
[Au] Autor:Yasuda C; Yasuda S; Yamashita H; Okada J; Hisada T; Sugiura S
[Ad] Endereço:Department of Human and Engineered Environmental Studies, Graduate School of Frontier Sciences, The University of Tokyo, Chiba, Japan.
[Ti] Título:The human ether-a-go-go-related gene (hERG) current inhibition selectively prolongs action potential of midmyocardial cells to augment transmural dispersion.
[So] Source:J Physiol Pharmacol;66(4):599-607, 2015 Aug.
[Is] ISSN:1899-1505
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:The majority of drug induced arrhythmias are related to the prolongation of action potential duration following inhibition of rapidly activating delayed rectifier potassium current (I(Kr)) mediated by the hERG channel. However, for arrhythmias to develop and be sustained, not only the prolongation of action potential duration but also its transmural dispersion are required. Herein, we evaluated the effect of hERG inhibition on transmural dispersion of action potential duration using the action potential clamp technique that combined an in silico myocyte model with the actual I(Kr) measurement. Whole cell I(Kr) current was measured in Chinese hamster ovary cells stably expressing the hERG channel. The measured current was coupled with models of ventricular endocardial, M-, and epicardial cells to calculate the action potentials. Action potentials were evaluated under control condition and in the presence of 1, 10, or 100 µM disopyramide, an hERG inhibitor. Disopyramide dose-dependently increased the action potential durations of the three cell types. However, action potential duration of M-cells increased disproportionately at higher doses, and was significantly different from that of epicardial and endocardial cells (dispersion of repolarization). By contrast, the effects of disopyramide on peak I(Kr) and instantaneous current-voltage relation were similar in all cell types. Simulation study suggested that the reduced repolarization reserve of M-cell with smaller amount of slowly activating delayed rectifier potassium current levels off at longer action potential duration to make such differences. The action potential clamp technique is useful for studying the mechanism of arrhythmogenesis by hERG inhibition through the transmural dispersion of repolarization.
[Mh] Termos MeSH primário: Canais de Potássio Éter-A-Go-Go/genética
Coração/efeitos dos fármacos
Miócitos Cardíacos/efeitos dos fármacos
Bloqueadores dos Canais de Potássio/farmacologia
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Animais
Antiarrítmicos/farmacologia
Células CHO
Cricetinae
Cricetulus
Disopiramida/farmacologia
Relação Dose-Resposta a Droga
Canal de Potássio ERG1
Endocárdio/citologia
Endocárdio/efeitos dos fármacos
Canais de Potássio Éter-A-Go-Go/efeitos dos fármacos
Seres Humanos
Técnicas de Patch-Clamp
Pericárdio/citologia
Pericárdio/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 0 (ERG1 Potassium Channel); 0 (Ether-A-Go-Go Potassium Channels); 0 (KCNH2 protein, human); 0 (Potassium Channel Blockers); GFO928U8MQ (Disopyramide)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150909
[St] Status:MEDLINE


  8 / 1570 MEDLINE  
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[PMID]:26084458
[Au] Autor:Fujino T; Yamazaki Y; Tsubota T; Ikeda T
[Ad] Endereço:Department of Cardiovascular Medicine, Toho University Faculty of Medicine.
[Ti] Título:Early-Morning Type Ventricular Fibrillation With J Wave.
[So] Source:Int Heart J;56(4):459-61, 2015.
[Is] ISSN:1349-3299
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:A 67-year-old man who had cardiopulmonary arrest (CPA) at home was admitted to our institution. His spontaneous circulation was restored by bystander cardiopulmonary resuscitation (CPR) performed by his wife and an automated external defibrillator (AED). J waves were observed in the inferior leads of an electrocardiogram. We performed an implantable cardioverter defibrillator (ICD) implantation. After the ICD implantation, appropriate shocks due to ventricular fibrillation (VF) were observed on interrogation of the ICD at a frequency of twice a month. Most VF events occurred in the early morning between 1:00 to 6:00, and ventricular premature contractions (VPCs) were detected just before the occurrence of VF. Since the VF events always occurred in the early morning, we started long-acting disopyramide (150 mg/day, before bedtime), which has a muscarinic receptor blocking action. As a result, he has not received any appropriate ICD shocks for more than two years.
[Mh] Termos MeSH primário: Disopiramida/administração & dosagem
Cardioversão Elétrica/métodos
Parada Cardíaca
Fibrilação Ventricular
[Mh] Termos MeSH secundário: Idoso
Antiarrítmicos/administração & dosagem
Reanimação Cardiopulmonar/métodos
Desfibriladores Implantáveis
Cardioversão Elétrica/instrumentação
Eletrocardiografia/métodos
Parada Cardíaca/etiologia
Parada Cardíaca/terapia
Seres Humanos
Masculino
Periodicidade
Recidiva
Resultado do Tratamento
Fibrilação Ventricular/complicações
Fibrilação Ventricular/diagnóstico
Fibrilação Ventricular/fisiopatologia
Fibrilação Ventricular/terapia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); GFO928U8MQ (Disopyramide)
[Em] Mês de entrada:1509
[Cu] Atualização por classe:150713
[Lr] Data última revisão:
150713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150619
[St] Status:MEDLINE
[do] DOI:10.1536/ihj.14-394


  9 / 1570 MEDLINE  
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[PMID]:24917414
[Au] Autor:Haruki S; Minami Y; Suzuki A; Hagiwara N
[Ad] Endereço:Department of Cardiology, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo, 162-8666, Japan.
[Ti] Título:Effects of flecainide on left ventricular pressure gradient and symptoms in obstructive hypertrophic cardiomyopathy: a comparison of flecainide and disopyramide.
[So] Source:Heart Vessels;30(5):604-10, 2015 Sep.
[Is] ISSN:1615-2573
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:It remains unclear whether flecainide, a Class I antiarrhythmic drug, improves left ventricular pressure gradient (LVPG) or symptoms in patients with obstructive hypertrophic cardiomyopathy (HCM). Our study evaluated the long-term efficacy of flecainide, compared to disopyramide, when administered orally, on LVPG and symptoms in obstructive HCM patients. Among 164 obstructive HCM patients, 15 were administered oral flecainide therapy and 33 administered oral disopyramide therapy. LVPG declined from 79.8 ± 36.6 to 39.2 ± 36.7 mmHg (p = 0.003) after flecainide therapy and from 74.5 ± 26.4 to 31.4 ± 24.8 mmHg (p < 0.001) after disopyramide therapy. The percent reduction in LVPG was -47.9 ± 43.2 % in patients treated with flecainide, comparable to the results for those treated with disopyramide (-57.1 ± 33.0 %; p = 0.425). We found no significant differences in improvement in NYHA functional class between patients treated with flecainide and those treated with disopyramide (p = 0.331). Patients treated with flecainide exhibited no significant adverse side effects, and there was no need for myectomy or alcohol septal ablation to reduce LVPG and symptoms. Improvements in LVPG and symptoms were similar in patients treated with flecainide and patients treated with disopyramide, suggesting that flecainide is a potentially useful alternative for symptomatic obstructive HCM patients, particularly those with disopyramide-induced vagolytic side effects, narrow angle glaucoma, or prostatic hyperplasia and pre-existing urination difficulties. Our data must be viewed with caution, however, in view of the small number of study patients. Flecainide therapy will require further proof of safety before it can be routinely recommended in patients with symptomatic obstructive HCM.
[Mh] Termos MeSH primário: Cardiomiopatia Hipertrófica/tratamento farmacológico
Disopiramida/administração & dosagem
Flecainida/administração & dosagem
Ventrículos do Coração/fisiopatologia
Obstrução do Fluxo Ventricular Externo/tratamento farmacológico
Pressão Ventricular/efeitos dos fármacos
[Mh] Termos MeSH secundário: Administração Oral
Antiarrítmicos/administração & dosagem
Cardiomiopatia Hipertrófica/etiologia
Cardiomiopatia Hipertrófica/fisiopatologia
Relação Dose-Resposta a Droga
Ecocardiografia
Feminino
Seguimentos
Ventrículos do Coração/diagnóstico por imagem
Seres Humanos
Masculino
Meia-Idade
Estudos Retrospectivos
Fatores de Tempo
Resultado do Tratamento
Obstrução do Fluxo Ventricular Externo/complicações
Obstrução do Fluxo Ventricular Externo/fisiopatologia
Pressão Ventricular/fisiologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); GFO928U8MQ (Disopyramide); K94FTS1806 (Flecainide)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:171014
[Lr] Data última revisão:
171014
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140612
[St] Status:MEDLINE
[do] DOI:10.1007/s00380-014-0534-3


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[PMID]:24735741
[Au] Autor:Hamada M; Ikeda S; Shigematsu Y
[Ad] Endereço:Division of Cardiology, Uwajima City Hospital, 1-1 Goten-machi, Uwajima, Ehime 798-8510, Japan. Electronic address: mhamada@uwajima-mh.jp.
[Ti] Título:Advances in medical treatment of hypertrophic cardiomyopathy.
[So] Source:J Cardiol;64(1):1-10, 2014 Jul.
[Is] ISSN:1876-4738
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:We reviewed the natural history of patients with hypertrophic cardiomyopathy (HCM). The effect of medical treatments on natural history, left ventricular (LV) functions and LV remodeling was also evaluated. Sudden cardiac death and end-stage heart failure are the most serious complications of HCM. Age <30 years and a family history of sudden premature death are risk factors for sudden cardiac death in HCM patients. End-stage heart failure is not a specific additional phenomenon observed in patients with HCM, but is the natural course of the disease in most of those patients. After the occurrence of heart failure, the progression to cardiac death is very rapid. Young age at diagnosis, a family history of HCM, and greater wall thickness are associated with a greater likelihood of developing end-stage heart failure. Neither beta-blockers nor calcium antagonists can prevent this transition. The class Ia antiarrhythmic drugs, disopyramide and cibenzoline are useful for the reduction of LV pressure gradient. Unlike disopyramide, cibenzoline has little anticholinergic activity; therefore, this drug can be easily adapted to long-term use. In addition to the reduction in LV pressure gradient, cibenzoline can improve LV diastolic dysfunction, and induce regression of LV hypertrophy in patients with HCM. A decrease in intracellular Ca(2+) concentration through the activation of the Na(+)/Ca(2+) exchanger associated with cibenzoline therapy is likely to be closely related with the improvement in HCM-related disorders. It is possible that cibenzoline can prevent the progression from typical HCM to end-stage heart failure.
[Mh] Termos MeSH primário: Cardiomiopatia Hipertrófica Familiar/tratamento farmacológico
[Mh] Termos MeSH secundário: Adolescente
Antagonistas Adrenérgicos beta/uso terapêutico
Adulto
Idoso
Antiarrítmicos/uso terapêutico
Bloqueadores dos Canais de Cálcio/uso terapêutico
Cardiomiopatia Hipertrófica Familiar/complicações
Morte Súbita Cardíaca/etiologia
Morte Súbita Cardíaca/prevenção & controle
Diástole
Progressão da Doença
Disopiramida/uso terapêutico
Feminino
Insuficiência Cardíaca/etiologia
Insuficiência Cardíaca/prevenção & controle
Seres Humanos
Imidazóis/uso terapêutico
Masculino
Meia-Idade
Sístole
Disfunção Ventricular Esquerda/tratamento farmacológico
Disfunção Ventricular Esquerda/etiologia
Remodelação Ventricular
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Adrenergic beta-Antagonists); 0 (Anti-Arrhythmia Agents); 0 (Calcium Channel Blockers); 0 (Imidazoles); GFO928U8MQ (Disopyramide); Z7489237QT (cifenline)
[Em] Mês de entrada:1504
[Cu] Atualização por classe:150512
[Lr] Data última revisão:
150512
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140417
[St] Status:MEDLINE



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