ABSTRACT
The difficulty in swallowing is a frequent problem when oral solid dosage forms (conventional tablets or capsules) are administered to paediatric population or patients with dysphagia. An interesting alternative to overcome these problems are non-conventional formulations like chewable gels, commonly known as 'gummies'. Therefore, this work addresses the design, development and characterization of gummies using gelatine and pectin, for the vehiculization of the antiarrhythmic amiodarone (AMIO). Applying a Design of Experiments (DoE) approach, four gelatine (GG1-GG4) and eight pectin formulations (PG1-PG8) were developed. Considering the obtained results for responses during DoE evaluation (i.e., volume, syneresis, hardness, and gumminess), GG3 and PG8 were selected for complete characterization. Water activity, pH, drug content, texture parameters (adhesiveness, springiness, cohesiveness, and fracturability), disintegration time, in vitro dissolution, and microbiological features were evaluated. The obtained results were within the expected values for this type of formulation. The dissolution profiles showed a 94 % - 99 % of the AMIO content released for GG3 and PG8, respectively, so they could be considered suitable as immediate release dosage forms. In conclusion, the chewable gels were successfully developed and characterised, suggesting a potential means to accomplish a final prototype for the improvement of congenital cardiopathies treatment.
Subject(s)
Amiodarone , Anti-Arrhythmia Agents , Gels , Heart Defects, Congenital , Pectins , Amiodarone/administration & dosage , Amiodarone/chemistry , Humans , Pectins/chemistry , Anti-Arrhythmia Agents/administration & dosage , Anti-Arrhythmia Agents/chemistry , Heart Defects, Congenital/drug therapy , Gelatin/chemistry , Animals , Child , Administration, Oral , Drug Liberation , Drug Compounding/methods , Solubility , Chemistry, Pharmaceutical/methodsABSTRACT
Resumen: Antecedentes: La prevalencia del síndrome del QT largo (SQTL) producido por medicamentos es una de las reacciones adversas que en el último tiempo ha aumentado en prevalencia y mortalidad. No solamente ocurre con el uso de medicamentos para el tratamiento de cardiopatías, sino también en medicamentos con otra acción terapéutica. Objetivo: Evaluar la prevalencia del síndrome del SQTL inducido por medicamentos en salas de cardiología de un hospital de alta complejidad. Métodos: Estudio prospectivo, de tipo descriptivo y de corte transversal en 36 pacientes cardiópatas, que consistió en evaluar la frecuencia del uso de medicamentos que son capaces de producir un SQTL y la prevalencia de este efecto adverso. Los datos clínicos se recolectaron de la ficha clínica y de entrevistas con los pacientes. Se efectuó un seguimiento para detectar la aparición de prolongación del intervalo QT. Los resultados obtenidos fueron presentados por medio de estadística descriptiva (programa estadístico Statgraphics Centurion, versión XVI). No hubo estadística inferencial dada la ausencia de un grupo control. Resultados: 41,7%, de los 36 pacientes presentaron SQTL que en 86,7% de ellos fue asociado a un medicamento. Los medicamentos más frecuentemente asociados a este efecto adverso fueron Amiodarona (38,5%) y Ondansetrón (23,1%), y el factor de riesgo mayormente involucrado fue el sexo femenino (61,5%). Conclusión: Existió una alta prevalencia del uso de medicamentos que producen un SQTL, destacándose que existen medicamentos utilizados para otras patologías que también pueden producirlo.
Abstract: Background: The prevalence of the Long QT interval syndrome (LQTS) associated to drugs has increased en the last decades along with an increased mortality due to this condition. It occurs not only with drugs used to treat cardiac disease but also to other drugs. Aim: To evaluate the prevalence of drug induced LQTS in cardiology wards of a high complexity hospital. Method: This is a prospective, descriptive and cross sectional study in 36 patients with heart disease. The use of drugs known to affect the QT interval along with the frequency of LGTS were evaluated. Clincal data was obtained from clinical records and personal interviews. Patients were followed for the appearance of LQTS. Descriptive were used to present the results. No inferential statistics were used as no control group was involved (Statgraphics Centurion, version XVI). Results: 41.7% of the 36 patients developed LQTS and the association with drugs was present in 86.7% of them. The drugs most commonly identified were amiodarone (38.5%) and ondansetron (23.1%) of patients. Female geneder was the most common associated condition (61.5%). Conclusion: There was a frequent use of drugs known to produce LQTS, but other drugs may also be associated int this group of patients with heart disease admitted to intensive or intermediate care facilities.
Subject(s)
Humans , Male , Female , Aged , Aged, 80 and over , Long QT Syndrome/chemically induced , Long QT Syndrome/epidemiology , Electrocardiography , Amiodarone/adverse effects , Prospective Studies , Amiodarone/administration & dosageABSTRACT
A cardiomiopatia arritmogênica do ventrículo direito é uma desordem hereditária caracterizada pela substituição fibrogordurosa do músculo cardíaco. O manejo clínico busca reduzir os riscos de morte súbita e melhorar a qualidade de vida, aliviando os sintomas arrítmicos e de insuficiência cardíaca. O ecocardiograma é o exame inicial para a investigação da cardiomiopatia arritmogênica do ventrículo direito, podendo apresentar dilatação das câmaras direitas e disfunção sistólica do ventrículo direito. Este relato chama atenção por envolver o diagnóstico de cardiomiopatia arritmogênica do ventrículo direito em paciente atleta. Mulher, 47 anos, maratonista, sem história familiar de morte súbita cardíaca, deu entrada na emergência com palpitação associada à pré-síncope. O eletrocardiograma da admissão mostrava taquicardia ventricular. O ecocardiograma revelou aumento de câmaras cardíacas direitas e disfunção sistólica do ventrículo direito. O cateterismo cardíaco não evidenciou doença coronária obstrutiva. A paciente foi orientada acerca da necessidade de suspensão de atividades físicas, porém, 3 meses depois, foi readmitida com instabilidade hemodinâmica por nova taquicardia ventricular, tendo sido cardiovertida. Realizou ressonância cardíaca, que evidenciou áreas de discinesia e formação de microaneurismas em ventrículo direito. Foi diagnosticada com cardiomiopatia arritmogênica do ventrículo direito, tendo sido com cardioversor desfibrilador implantável, amiodarona e betabloqueador. A diferenciação entre a cardiomiopatia arritmogênica do ventrículo direito e o coração do atleta representa um desafio, devido à sobreposição de alterações estruturais que coexistem nessas entidades, daí a importância da análise integrada de fatores clínicos, eletrocardiográficos e morfofuncionais.(AU)
Subject(s)
Humans , Female , Middle Aged , Death, Sudden, Cardiac , Tachycardia, Ventricular/diagnosis , Arrhythmogenic Right Ventricular Dysplasia/genetics , Arrhythmogenic Right Ventricular Dysplasia/mortality , Heart Failure , Genetic Diseases, Inborn , Electric Countershock/methods , Echocardiography/methods , Magnetic Resonance Spectroscopy/methods , Electrocardiography, Ambulatory/methods , Heart Transplantation/methods , Defibrillators, Implantable , Catheter Ablation/methods , Electrocardiography/methods , Amiodarone/administration & dosage , Anti-Arrhythmia Agents/therapeutic useABSTRACT
Amiodarone, considered a potent antiarrhythmic, is known to cause pulmonary toxicity. Chronic interstitial pneumonitis is the most common presentation. However, acute pulmonary toxicity is rare and has a higher case fatality rate. We present a 61-year-old patient with persistent atrial fibrillation who, after a one-month treatment with oral amiodarone at a low dose impregnation of 400 mg/day, develops acute pulmonary toxicity, with radiographic and tomographic resolution after antiarrhythmic suspension and steroid treatment.
Se sabe que la amiodarona, un potente antiarrítmico, causa toxicidad pulmonar. La neumonitis intersticial crónica es la presentación más común. Sin embargo, la toxicidad pulmonar aguda es rara y provoca una mayor mortalidad. Se presenta un paciente de 61 años con fibrilación auricular persistente que, tras tratamiento por un mes con amiodarona vía oral a dosis baja de impregnación de 400 miligramos al día, desarrolló toxicidad pulmonar aguda secundaria al antiarrítmico confirmada por radiografía y tomografía. Su caso tuvo resolución después de la suspensión del fármaco y tratamiento con esteroides.
Subject(s)
Amiodarone/adverse effects , Anti-Arrhythmia Agents/adverse effects , Lung Diseases/chemically induced , Acute Disease , Amiodarone/administration & dosage , Anti-Arrhythmia Agents/administration & dosage , Atrial Fibrillation/drug therapy , Dose-Response Relationship, Drug , Humans , Male , Middle AgedABSTRACT
AIMS: Amiodarone (AMIO) is currently used in medical practice to reverse ventricular tachycardia. Here we determine the effects of AMIO in the electromechanical properties of isolated left ventricle myocyte (LVM) from mice and guinea pig and in a cellular model of Long QT Syndrome Type 3 (LQTS-3) using anemone neurotoxin 2 (ATX II), which induces increase of late sodium current in LVM. MAIN METHODS AND KEY FINDINGS: Using patch-clamp technique, fluorescence imaging to detect cellular Ca2+ transient and sarcomere detection systems we evaluate the effect of AMIO in healthy LVM. AMIO produced a significant reduction in the percentage of sarcomere shortening (0.1, 1 and 10 µM) in a range of pacing frequencies, however, without significant attenuation of Ca2+ transient. Also, 10 µM of AMIO caused the opposite effect on action potential repolarization of mouse and guinea pig LVM. When LVM from mouse and guinea pig were paced in a range of pacing frequencies and exposed to ATX (10 nM), AMIO (10 µM) was only able to abrogate electromechanical arrhythmias in LVM from guinea pig at lower pacing frequency. SIGNIFICANCE: AMIO has negative inotropic effect with opposite effect on action potential waveform in mouse and guinea pig LVM. Furthermore, the antiarrhythmic action of AMIO in LQTS-3 is species and frequency-dependent, which indicates that AMIO may be beneficial for some types of arrhythmias related to late sodium current.
Subject(s)
Amiodarone/pharmacology , Anti-Arrhythmia Agents/pharmacology , Cardiac Conduction System Disease/drug therapy , Long QT Syndrome/drug therapy , Myocytes, Cardiac/drug effects , Amiodarone/administration & dosage , Animals , Anti-Arrhythmia Agents/administration & dosage , Cardiac Conduction System Disease/physiopathology , Dose-Response Relationship, Drug , Guinea Pigs , Heart Ventricles/cytology , Long QT Syndrome/physiopathology , Male , Mice , Mice, Inbred C57BL , Myocytes, Cardiac/metabolism , Patch-Clamp Techniques , Sarcomeres/drug effects , Sarcomeres/metabolism , Sodium Channels/drug effects , Sodium Channels/metabolism , Species SpecificityABSTRACT
Chronic Chagas heart disease has different clinical manifestations including arrhythmias, heart failure, and stroke. Chest pain is one of the most common symptoms and when associated with changes in the electrocardiogram, such as T-wave changes, electrically inactive areas, and segmental wall motion abnormalities, may lead to a misdiagnosis of acute coronary syndrome (ACS). Here, we describe two patients with Chagas heart disease and syncope due to sustained ventricular tachycardia who were misdiagnosed with ACS, and discuss the role of novel imaging modalities in the differential diagnosis and risk stratification.
Subject(s)
Arrhythmias, Cardiac/etiology , Chagas Cardiomyopathy/complications , Aged , Amiodarone/administration & dosage , Amiodarone/therapeutic use , Anti-Arrhythmia Agents/administration & dosage , Anti-Arrhythmia Agents/therapeutic use , Clopidogrel/administration & dosage , Clopidogrel/therapeutic use , Defibrillators, Implantable , Diagnosis, Differential , Female , Humans , Male , Middle Aged , Platelet Aggregation Inhibitors/administration & dosage , Platelet Aggregation Inhibitors/therapeutic useABSTRACT
Se sabe que la amiodarona, un potente antiarrítmico, causa toxicidad pulmonar. La neumonitis intersticial crónica es la presentación más común. Sin embargo, la toxicidad pulmonar aguda es rara y provoca una mayor mortalidad. Se presenta un paciente de 61 años con fibrilación auricular persistente que, tras tratamiento por un mes con amiodarona vía oral a dosis baja de impregnación de 400 miligramos al día, desarrolló toxicidad pulmonar aguda secundaria al antiarrítmico confirmada por radiografía y tomografía. Su caso tuvo resolución después de la suspensión del fármaco y tratamiento con esteroides.
Amiodarone, considered a potent antiarrhythmic, is known to cause pulmonary toxicity. Chronic interstitial pneumonitis is the most common presentation. However, acute pulmonary toxicity is rare and has a higher case fatality rate. We present a 61-year-old patient with persistent atrial fibrillation who, after a one-month treatment with oral amiodarone at a low dose impregnation of 400 mg/day, develops acute pulmonary toxicity, with radiographic and tomographic resolution after antiarrhythmic suspension and steroid treatment.
Subject(s)
Humans , Male , Middle Aged , Amiodarone/adverse effects , Lung Diseases/chemically induced , Anti-Arrhythmia Agents/adverse effects , Atrial Fibrillation/drug therapy , Acute Disease , Dose-Response Relationship, Drug , Amiodarone/administration & dosage , Anti-Arrhythmia Agents/administration & dosageABSTRACT
INTRODUCTION: Approximately seven to eight million people worldwide have Chagas disease. In Brazil, benznidazole is the most commonly used active drug against Trypanosoma cruzi; however, its efficacy is limited, and side effects are frequent. Recent studies suggest that amiodarone may be beneficial in the treatment of this disease, by exerting anti-T. cruzi action. This study evaluated changes in T. cruzi cell count in in vitro cultures subjected to different doses of benznidazole, amiodarone, and their combination. METHODS: T. cruzi (Y strain) cultures containing approximately 100,000 cells were treated with either 100mg, 50mg, 25mg, 12.5mg, or 10mg of benznidazole, amiodarone, or their combination. On the 4th day, cell count was compared to the baseline data. RESULTS: On the 4th day, no parasites were observed in any of the treated cultures. CONCLUSIONS: Benznidazole and amiodarone were equally effective in eliminating T. cruzi in culture. The combination of the two drugs was also equally effective, but our data cannot demonstrate synergism, as similar results were obtained when the drugs were tested individually or in combination. It is suggested that this study be repeated with other T. cruzi strains to determine whether similar results can be obtained again.
Subject(s)
Amiodarone/pharmacology , Nitroimidazoles/pharmacology , Trypanocidal Agents/pharmacology , Trypanosoma cruzi/drug effects , Amiodarone/administration & dosage , Animals , Dose-Response Relationship, Drug , Drug Combinations , Mice , Nitroimidazoles/administration & dosage , Parasitic Sensitivity Tests , Trypanocidal Agents/administration & dosageABSTRACT
Abstract INTRODUCTION: Approximately seven to eight million people worldwide have Chagas disease. In Brazil, benznidazole is the most commonly used active drug against Trypanosoma cruzi; however, its efficacy is limited, and side effects are frequent. Recent studies suggest that amiodarone may be beneficial in the treatment of this disease, by exerting anti-T. cruzi action. This study evaluated changes in T. cruzi cell count in in vitro cultures subjected to different doses of benznidazole, amiodarone, and their combination. METHODS: T. cruzi (Y strain) cultures containing approximately 100,000 cells were treated with either 100mg, 50mg, 25mg, 12.5mg, or 10mg of benznidazole, amiodarone, or their combination. On the 4th day, cell count was compared to the baseline data. RESULTS: On the 4th day, no parasites were observed in any of the treated cultures. CONCLUSIONS: Benznidazole and amiodarone were equally effective in eliminating T. cruzi in culture. The combination of the two drugs was also equally effective, but our data cannot demonstrate synergism, as similar results were obtained when the drugs were tested individually or in combination. It is suggested that this study be repeated with other T. cruzi strains to determine whether similar results can be obtained again.
Subject(s)
Animals , Trypanocidal Agents/pharmacology , Trypanosoma cruzi/drug effects , Parasitic Sensitivity Tests , Amiodarone/pharmacology , Nitroimidazoles/pharmacology , Trypanocidal Agents/administration & dosage , Dose-Response Relationship, Drug , Drug Combinations , Amiodarone/administration & dosage , Mice , Nitroimidazoles/administration & dosageABSTRACT
A miocardiopatia não compactada (MNC) é uma cardiopatia rara e congênita. Sua origem, possivelmente, ocorre durante o desenvolvimento embrionário, devido às alterações genéticas, cursando com insuficiência cardíaca, arritmia, precordialgia e tromboembolismo venoso. Nesse estudo, descreve-se o caso de uma mulher de 34 anos de idade, diagnosticada com MNC e em acompanhamento em hospital terciário, no oeste do interior paulista, junto ao departamento de Cardiologia. Inicialmente, a paciente apresentou sintomas arrítmicos associados à precordialgia, refratários ao tratamento antiarrítmico. O quadro progrediu, havendo dispneia e sudorese. Diante disso, iniciou-se investigação aprofundada, cogitando-se MNC. Objetivou-se demonstrar o quadro clínico inicial, a progressão da sintomatologia e a eficácia do seguimento realizado pelos profissionais que a assistem
Noncompaction cardiomyopathy (NCC) is a rare congenital heart disease possibly originating during embryonic development due to genetic changes, and resulting in heart failure, arrhythmia, precordialgia and venous thromboembolism. This study describes the case of a 34-year-old woman, diagnosed with NCC in follow-up with the Cardiology Department at a tertiary hospital in the west of the state of São Paulo. Initially, the patient presented arrhythmic symptoms associated with precordialgia, refractory to antiarrhythmic treatment; the symptoms progressed, with dyspnea and excessive sweating. Therefore, an in-depth investigation was initiated, considering NCC. The objective was to demonstrate the initial clinical symptoms, progression of the symptomatology, and the effectiveness of the follow-up performed by the attending professionals
Subject(s)
Humans , Female , Adult , Tertiary Healthcare , Cardiomyopathy, Dilated/diagnosis , Cardiomyopathy, Dilated/therapy , Tertiary Care Centers , Arrhythmias, Cardiac , Prognosis , Thromboembolism/diagnosis , Thromboembolism/therapy , Magnetic Resonance Spectroscopy/methods , Echocardiography, Doppler/methods , Electrocardiography, Ambulatory/methods , Heart Failure/diagnosis , Heart Failure/therapy , Amiodarone/administration & dosageABSTRACT
Relatamos o caso de paciente do sexo masculino, com 23 anos de idade, portador de miocárdio não compactado e taquicardia ventricular monomórfica sustentada. O paciente foi submetido a implante de cardiodesfibrilador implantável após diagnóstico confirmado por meio de ressonância nuclear magnética cardíaca e mantido em tratamento clínico com medicação antiarrítmica, sem recorrência de arritmia ventricular no acompanhamento ambulatorial
We report the case of a 23-year-old male patient with noncompacted myocardium and sustained monomorphic ventricular tachycardia. The patient was submitted to mplantable cardioverter defibrillator after diagnosis confirmed by cardiac magnetic resonance imaging and was kept on clinical treatment with antiarrhythmic medication without the recurrence of ventricular arrhythmia in the outpatient follow-up
Subject(s)
Humans , Male , Adult , Cardiomyopathy, Dilated/complications , Cardiomyopathy, Dilated/diagnosis , Isolated Noncompaction of the Ventricular Myocardium/diagnosis , Tachycardia, Ventricular/diagnosis , Amiodarone/administration & dosage , Death, Sudden , Echocardiography/methods , Electrocardiography/methods , Heart Defects, Congenital , Heart Rate , Metoprolol/administration & dosageABSTRACT
Evaluar la presencia de disfunción tiroidea en pacientes con arritmias cardíacas tratados con Amiodarona (AMD) Métodos: se realizó el estudio en 24 pacientes que presentaron arritmias supraventriculares o ventriculares tratados con AMD, atendidos en el Servicio de Medicina Interna de la Ciudad Hospitalaria "Dr. Enrique Tejera" durante el período julio 2015 abril 2016. Se les determinaron T3L, T4L y TSH a manera de tamizaje previo a la administración de AMD y fueron citados y divididos en 3 grupos de 3, 6 y 12 meses de tratmiento de AMD con determinación del perfil tiroideo en la consulta. Resultados: El hipotiroidismo inducido por AMD (HIA) se presentó en 20,83% (n=5), siendo más frecuente en aquellos pacientes asculinos que tenían 3 meses de tratamiento y que recibían una dosis de 1400 mg/semanal. La tirotoxicosis inducida por AMD (TIA) se presentó en 8,33% (n=2) ambos masculinos con dosis de 1400 mg/semanal. No se encontró asociación entre HIA y TIA con el tiempo, dosis, grupo etario ni género (P>0,05). T3L, T4L y TSH registraron el mayor y menor promedio a los 12 y 3 meses (P < 0,05); 12 y 6 meses; 3 y 12 meses respectivamente. Conclusión: La frecuencia de HIA fue de 20,83 % y TIA de 8,33 %. No hubo asociación estadísticamente significativa entre la HIA o TIA con la duración de consumo, dosis, grupo etario ni género. La TSH presentó el mayor promedio a los 3 meses, la T3L y T4L a los 12 meses (AU)
to evaluate the presence of thyroid dysfunction in patients with cardiac arrhythmia who were treated with Amiodarone (AMD). Methods: the study was done in 24 patients who were treated for supraventricular or ventricular arrhythmia at the Department of Internal Medicine of Hospital "Dr. Enrique Tejera" in Valencia, Venezuela from July 2015 to April 2016. FT3, FT4 and TSH were measured to the administration of AMD. The patients were divided in 3 groups according to time of use of the drug as follows: 3, 6 and 12 months, and their thyroid function was measured at each of these periods. Results: 20.83 % (n=5) presented Amiodarone induced hypothyroidism (AIH), which was more frequent in males at 3 months of treatment and who received 1400 mg weekly. Amiodarone induced thyrotoxicosis (AIT) was found in 8.33% (n=2) also in male patients using 1400mg weekly. There was no association between AIH or AIT and duration, dose of AMD, age or gender. (p>0.05) FT3, FT4 and TSH registered their higher and lower averages on 12 and 3 months (P < 0,05); 12 and 6 months; 3 and 12 months respectively. Conclusion: AIH's frequency was 20.83 % and 8.33% for AIT. There was no statistically significant association between AIH or AIT and duration, dose of AMD, age or gender TSH average measure was higher at 3 months and the FT3 and FT4 at 12 months(AU)
Subject(s)
Humans , Male , Female , Adult , Middle Aged , Aged , Arrhythmias, Cardiac/drug therapy , Thyroid Diseases/etiology , Amiodarone/administration & dosage , Amiodarone/adverse effects , Internal MedicineABSTRACT
Relato de 5 casos de pacientes com fibrilação atrial persistente de longa duração refratários ao tratamento com fármacos antiarrítmicos e submetidos a ablação da fibrilação atrial por cateter há pelo menos 12 meses. Os pacientes apresentavam as mesmas queixas, estavam utilizando os mesmos medicamentos, eram portadores de hipertensão resistente e de outras comorbidades, e voltaram a apresentar fibrilação atrial persistente de longa duração. Todos foram submetidos a denervação renal simpática associada a reisolamento das veias pulmonares e passaram a apresentar redução significativa da pressão arterial, tanto sistólica como diastólica, aferida no consultório e por monitorização ambulatorial da pressão arterial de 24 horas após o procedimento. Mesmo após o imediato sucesso do procedimento, com recuperação do ritmo sinusal, em menos de 12 meses os pacientes tiveram recorrência de fibrilação atrial persistente. Observou-se, porém, redução do volume do átrio esquerdo 12 meses após o procedimento. Conclui-se que a denervação renal simpática foi eficaz no controle da pressão arterial, com consequente redução do volume do átrio esquerdo
Case report of 5 patients with persistent long-standing atrial fibrillation refractory to treatment with antiarrhythmic drugs undergoing atrial fibrillation ablation by catheter for at least 12 months. Patients had the same complaints, were using the same drugs, were carriers of resistant hypertension and other comorbidities and resumed persistent long-standing atrial fibrillation. All of them were submitted to renal sympathetic denervation combined to re-isolation of the pulmonary veins and had a significant systolic and diastolic blood pressure reduction, measured at the clinic and by 24-hour outpatient monitoring after the procedure. Even after the immediate success of the procedure, with the recovery of sinus rhythm, in less than 12 months patients had a recurrence of persistent atrial fibrillation. However, a reduction in the volume of the left atrium was observed 12 months after the procedure. It is concluded that sympathetic renal denervation was effective in blood pressure control with consequent reduction of left atrial volume
Subject(s)
Humans , Male , Adult , Middle Aged , Arterial Pressure , Atrial Fibrillation/drug therapy , Hypertension , Pulmonary Veins , Sympathectomy/methods , Age Factors , Amiodarone/administration & dosage , Analysis of Variance , Catheter Ablation/methods , Drug Therapy/methods , Heparin/administration & dosage , Treatment OutcomeSubject(s)
Male , Female , Humans , Tachycardia, Ventricular/etiology , Tachycardia, Ventricular/physiopathology , Electrocardiography , Echocardiography , Magnetic Resonance Spectroscopy , Catheter Ablation/methods , Atenolol/administration & dosage , Metoprolol/administration & dosage , Amiodarone/administration & dosageABSTRACT
As taquicardias ventriculares são as arritmias cardíacas com maior potencial de instabilidade clínica e mortalidade cardíaca. Embora possam ocorrer no contexto de pacientes sem cardiopatia estrutural demonstrável, quase sempre ocorrem em coração estruturalmente alterado, com substrato anatômico para reentradas. As alterações cardíacas podem ser isquêmicas e não isquêmica. A distinção entre as etiologias é importante por terem diferentes mecanismos e origens de taquicardia ventricular, que irá determinar a escolha do tratamento adequado das arritmias ventriculares e prevenção de morte súbita. Os principais objetivos no manejo destes pacientes são: a reversão imediata da taquicardia, a prevençãode recorrências e a redução da mortalidade cardiovascular. Atualmente os fármacos com eficácia e perfil de segurança mais utilizados para tratamento de taquicardia ventricular em pacientes com cardiopatia estrutural são os betabloqueadores, amiodarona e sotalol. Com exceção dos betabloqueadores, os antiarrítmicos não possuem a eficácia em manejo primário ou na prevenção de morte súbita demonstrada em estudos clínicos randomizados atuais de forma consistente. Em portadores de cardiodesfibrilador implantável, os antiarrítmicos podem atuar na supressão das taquicardias ventriculares não sustentadas e sustentadas, na lentificação das taquicardias ventriculares com intuito de facilitar a reversão por antitachycardia pacing e prevenir sincopes, além de controlas as taquicardias supraventriculares. Devido aos efeitos colaterais e potencial efeito pró-arrítmico, devem ser utilizados com precaução e com controle adequado...
Ventricular tachycardia is the cardiac arrhythmia with the most potential to result in clinical instability and cardiac mortality. Although it can occur in patients without structural heart disease, it tends to occur where there is underlying heart disease, with anatomical substrate for reentry. It can be subdivided into ischemic and non-ischemic. This is an important distinction, because the mechanisms and origins of ventricular tachycardia may differ between the two, which will determine the choice of treatment for the ventricular arrhythmia and help prevent sudden death. The objective in clinical management of these patients includes: immediate reversal of tachycardia, prevention of relapses, and reducing cardiovascular mortality. The beta-blockers amiodarone and sotalol are currently the most commonly used antiarrhythmic agents, with the best efficacy and safety profile for treating ventricular tachycardia in patients with structural heart disease. With the exception of beta-blockers, currently available antiarrhythmic drugs have not been shown, in randomized clinical trials, to be effective in the primary management of patients with life-threatening ventricular arrhythmias or in the prevention of sudden cardiac death. Inpatients with implantable cardioverter-defibrillators, the potential beneficial effects of antiarrhythmic drugs may be the suppression of non-sustained and sustained ventricular tachycardias, slowing of ventricular tachycardia rate to facilitate pace termination or prevent syncope, and control of atrial tachyarrhythmias. Due to potential adverse effects of antiarrhythmic drugs and the risk of proarrhythmia, close monitoring of the patient is recommended...
Subject(s)
Humans , Anti-Arrhythmia Agents/administration & dosage , Anti-Arrhythmia Agents/therapeutic use , Myocardial Ischemia , Patients , Tachycardia, Ventricular/etiology , Tachycardia, Ventricular/therapy , Amiodarone/administration & dosage , Amiodarone/therapeutic use , Arrhythmias, Cardiac/diagnosis , Arrhythmias, Cardiac/therapy , Cardiomyopathies/diagnosis , Cardiomyopathies/therapy , Drug Therapy/methods , Sotalol/adverse effects , Sotalol/therapeutic use , Heart VentriclesABSTRACT
Background: Tilmicosin is widely used in veterinary medicine and its accidental overdose by injection may cause death viacausing negative inotropy and positive chronotropy in both the treated animal and the veterinarian. In addition, there is noany antidote against to tilmicosin-caused death. Amiodarone blocks some channels in the heart, but it has much complexeffect including vagotonic, bradycardic etc on the heart. Considering vagotonic and bradycardic effects of amiodarone, ithas been hypothesised that amiodarone may prevent tilmicosin-caused death. The aim of this study was to determine theeffect of amiodarone on the survival rate of rats in tilmicosin-caused lethal toxicity.Materials, Methods & Results: Twenty female Wistar rats (body weight: 288 ± 33.8 g, age: 7-8 months) were used in thisstudy. The study protocol was approved by the Ethical Committee. Rats received food and water ad libitum. The rats weredivided into two groups containing 10 rats each. Rats in Group 1 were administered 360 mg/kg of tilmicosin in a singlesubcutaneous injection. Rats in Group 2 were administered 25 mg/kg of amiodarone via the tail vein at 8. min after thesingle subcutaneous injection of tilmicosin in a dose of 360 mg/kg. After the injections, deaths were recorded at 0, 2, 6, 10,12 and 24 h. At the end of the 24-h period, survival/death ratio was analysed by the Chi-square test. The level of statisticalsignifi cance was set at P < 0.05. The survival rate of Group 2 (40%) was statistically signifi cantly (P < 0.025) higher thanthat of Group 1 (0.0%). In control group all rats died at 10 h after subcutaneously tilmicosin injection. In Group 2 wereadministered 25 mg/kg of amiodarone (intravenously) at 8 min after the single subcutaneous injection of tilmicosin in adose of 360 mg/kg, and 2 rats died at 2 h and 4...
Subject(s)
Animals , Rats , Amiodarone/administration & dosage , Amiodarone/therapeutic use , Cardiotoxins/antagonists & inhibitors , Macrolides/toxicity , Drug Overdose/veterinaryABSTRACT
BACKGROUND: Amiodarone is an effective medication in preventing atrial fibrillation (AF), but it interferes with the metabolism of warfarin. OBJECTIVES: This study sought to examine the association of major thrombotic clinical events and bleeding with the use of amiodarone in the ARISTOTLE (Apixaban for Reduction in Stroke and Other Thromboembolic Events in Atrial Fibrillation) trial. METHODS: Baseline characteristics of patients who received amiodarone at randomization were compared with those who did not receive amiodarone. The interaction between randomized treatment and amiodarone was tested using a Cox model, with main effects for randomized treatment and amiodarone and their interaction. Matching on the basis of a propensity score was used to compare patients who received and who did not receive amiodarone at the time of randomization. RESULTS: In ARISTOTLE, 2,051 (11.4%) patients received amiodarone at randomization. Patients on warfarin and amiodarone had time in the therapeutic range that was lower than patients not on amiodarone (56.5% vs. 63.0%; p < 0.0001). More amiodarone-treated patients had a stroke or a systemic embolism (1.58%/year vs. 1.19%/year; adjusted hazard ratio [HR]: 1.47, 95% confidence interval [CI]: 1.03 to 2.10; p = 0.0322). Overall mortality and major bleeding rates were elevated, but were not significantly different in amiodarone-treated patients and patients not on amiodarone. When comparing apixaban with warfarin, patients who received amiodarone had a stroke or a systemic embolism rate of 1.24%/year versus 1.85%/year (HR: 0.68, 95% CI: 0.40 to 1.15), death of 4.15%/year versus 5.65%/year (HR: 0.74, 95% CI: 0.55 to 0.98), and major bleeding of 1.86%/year versus 3.06%/year (HR: 0.61, 95% CI: 0.39 to 0.96). In patients who did not receive amiodarone, the stroke or systemic embolism rate was 1.29%/year versus 1.57%/year (HR: 0.82, 95% CI: 0.68 to 1.00), death was 3.43%/year versus 3.68%/year (HR: 0.93, 95% CI: 0.83 to 1.05), and major bleeding was 2.18%/year versus 3.03%/year (HR: 0.72, 95% CI: 0.62 to 0.84). The interaction p values for amiodarone use by apixaban treatment effects were not significant. CONCLUSIONS: Amiodarone use was associated with significantly increased stroke and systemic embolism risk and a lower time in the therapeutic range when used with warfarin. Apixaban consistently reduced the rate of stroke and systemic embolism, death, and major bleeding compared with warfarin in amiodarone-treated patients and patients who were not on amiodarone.
Subject(s)
Amiodarone/administration & dosage , Anticoagulants/administration & dosage , Atrial Fibrillation/drug therapy , Aged , Anti-Arrhythmia Agents/administration & dosage , Atrial Fibrillation/physiopathology , Brazil/epidemiology , Cause of Death/trends , Dose-Response Relationship, Drug , Drug Administration Schedule , Drug Therapy, Combination , Electrocardiography , Europe/epidemiology , Factor Xa Inhibitors/administration & dosage , Female , Follow-Up Studies , Humans , Incidence , Male , Middle Aged , Ontario/epidemiology , Pyrazoles/administration & dosage , Pyridones/administration & dosage , Stroke/epidemiology , Stroke/etiology , Stroke/prevention & control , Survival Rate/trends , Thromboembolism/complications , Thromboembolism/epidemiology , Thromboembolism/prevention & control , Treatment Outcome , United States/epidemiology , Warfarin/administration & dosageABSTRACT
Relata-se o caso de paciente do sexo masculino portador de síndrome de Wolff-Parkinson-White,hipertrofia ventricular e doença do sistema de condução, que apresentou duas paradas cardiorrespiratórias,insuficiência cardíaca congestiva e uma nova variação no gene PRKAG2.
We report the case of a male patient suffering from Wolff-Parkinson-White syndrome, ventricularhypertrophy, cardiac conduction system disease, who presented two cardiorespiratory arrests, congestive heartfailure and a new variation in the PRKAG2 gene.