摘要
As arritmias na cardiopatia chagásica (CCH) são responsáveis por incapacitação física e morte em indivíduos adultos em faixa etária precoce e produtiva, decorrendo daí a necessidade de sua abordagem criteriosa e, às vezes, mais agressiva para se obter controle completo. As arritmias cardíacas mais encontradas na CCH são as bradiarritmias e as taquicardias. Entre as bradicardias estão as alterações sinoatriais e os bloqueios atrioventriculares, cujo tratamento padrão é o emprego de implante de marcapasso definitivo. Entre as taquiarritmias, encontram-se as supraventriculares extrassístoles atriais, taquicardia atrial ectópica, "flutter" atrial e fibrilação atrial que provocam morbidades como progressão para disfunção ventricular esquerda e fenômenos tromboembólicos, e as ventriculares, cujo desfecho pode ser a morte súbita instantânea. A abordagem deve ser, inicialmente, por meio de eletrocardiograma de 12 derivações, pela gravação ambulatorial (Holter), ecocardiograma, teste ergométrico, e por fim, o estudo eletrofisiológico e a ressonância nuclear magnética. O tratamento farmacológico pode ser conduzido com o uso dos fármacos existentes em nosso mercado, como amiodarona, propafenona e sotalol. O tratamento invasivo, pode consistir em ablação por cateter, embora com resultados ainda abaixo de índices confortadores, devido à possibilidade de recidivas. O uso de cardiodesfibrilador implantável é a última alternativa, que também tem suas limitações
Arrhythmias in Chagas cardiomyopathy (CCM) are responsible for physical disability and death in adults in early and productive age group, from which arises the need for a judicious and sometimes more aggressive approach to achieve the complete control. The arrhythmias most common in CCM are bradyarrhythmias and tachycardias. Among the bradycardias are the sinoatrial changes and atrioventricular blocks, whose standard treatment is the use of permanent pacemaker implantation. Among tachyarrhythmias are the supraventricular ones - atrial extrasystoles, ectopic atrial tachycardia, atrial flutter and atrial fibrillation - causing morbidity and progression of left ventricular dysfunction and thromboembolic events, and the ventricular ones, whose outcome can be the instantaneous sudden death. The approach should be initially through 12-lead electrocardiogram, by ambulatory ECG recording (Holter), echocardiogram, stress testing, and finally the electrophysiological study and magnetic resonance imaging. Pharmacological treatment can be conducted with the use of marketed drugs such as amiodarone, propafenone and sotalol. The invasive treatment may consist of catheter ablation, although the results are still below comforting rates due to the possibility of recurrence. The use of implantable cardioverter defibrillator is the last alternative, which also has its limitations
Subject(s)
Humans , Adolescent , Adult , Arrhythmias, Cardiac/physiopathology , Chagas Cardiomyopathy/rehabilitation , Ventricular Dysfunction/therapy , Sotalol/pharmacology , Propafenone/pharmacology , Echocardiography , Magnetic Resonance Spectroscopy , Electrocardiography, Ambulatory/methods , Exercise Test , Amiodarone/pharmacology摘要
The effects of the antiarrhythmic drug propafenone at c-type kv1.4 channels in Xenopus laevis oocytes were studied with the two-electrode voltage-clamp techinique. Defolliculated oocytes (stage V-VI) were injected with transcribed cRNAs of ferret Kv1.4 delta N channels. During recording, oocytes were continuously perfused with control solution or propafenone. Propafenone decreased the currents during voltage steps. The block was voltage-, use-, and concentration- dependent manners. The block was increased with positive going potentials. The voltage dependence of block could be fitted with the sum of monoexponential and a linear function. Propafenone accelerated the inactivate of current during the voltage step. The concentration of half-maximal block (IC(50)) was 121 micrometer/L. With high, normal, and low extracellular potassium concentrations, the changes of IC(50) value had no significant statistical differences. The block of propafenone was PH- dependent in high-, normal- and low- extracellular potassium concentrations. Acidification of the extracellular solution to PH 6.0 increased the IC50 values to 463 micrometer/L, alkalization to PH 8.0 reduced it to 58 micrometer/L. The results suggest that propafenone blocks the kv1.4 delta N channel in the open state and give some hints for an intracellular site of action.
Subject(s)
Animals , Anti-Arrhythmia Agents/pharmacology , Hydrogen-Ion Concentration , Inhibitory Concentration 50 , /antagonists & inhibitors , Oocytes/drug effects , Patch-Clamp Techniques , Potassium/metabolism , Potassium Channel Blockers/pharmacology , Propafenone/pharmacology , Xenopus laevis摘要
Mediante sestimulación auricular esofágica se evaluó un aspecto de la hipótesis de los receptores modulados, denominado "uso-dependencia". Esta consiste en el enlentecimiento de la conducción intraventricular, con el aumento de la frecuencia cardíaca en presencia de antiarrítmicos de clase I. Se estudiaron 15 pacientes con > 30 extrasístoles ventriculares sintomáticas/hora tratados con propafenona por vía oral. El marcapaseo auricular mostró incremento en la duración del complejo QRS con ciclos de estimulación de 600 mseg y aun con dosis de 450 mg/día. Se correlacionaron los hallazgos con la variación en la actividad ectópica observada por Holter
Subject(s)
Humans , Male , Female , Adolescent , Adult , Middle Aged , Cardiac Complexes, Premature/drug therapy , Propafenone/pharmacology , Lown-Ganong-Levine Syndrome/drug therapy , Administration, Oral , Aged, 80 and over , Analysis of Variance , Electrocardiography, Ambulatory , Heart Rate , Propafenone/administration & dosage , Reaction Time , Regression Analysis , Stimulation, Chemical摘要
Objetivo - Avaliar os efeitos agudos da propafenona sobre os períodos refratários anterógrado e retrógrado de vias anômalas (VA). Métodos - Foram estudados 40 apcientes sintomáticos. Por técnica de extra-estímulos, determinaram-se os períodos refratários anterógrado e retrógrado das VA em condiçöes de controle e após 2,0mg/Kg de propafenona IV. Os resultados foram analisados em funçäo dos períodos refratários anterógrado e retrógrado das VA><270ms no controle. Resultados - Período refratário anterógrado médio da VA no controle de 275 ñ 76ms e no pós-droga de 462 ñ 190ms (p < 0,01). Período refratário retrógrado médio da VA no controle de 264 ñ 44ms, passando no pós-droga para 438 ñ 184ms (p < 0,01). Período refratário efetivo anterógrado do nódulo AV no controle de 236 ñ 40ms, passando no pós-droga para 276 ñ 47ms (p < 0,05). Período refratário efetivo atrial no controle de 210 ñ 23ms, passando para 215 ñ 24ms (p = ns). Período refratário efetivo ventricular no controle de 240 ñ 34ms, passando no pós-droga para 250 ñ 40ms (p:ns). Notou-se o aparecimento de bloqueio completo anterógrado e retrógrado da VA no pós-droga em, respectivamente, 15 e 12(42//, 35//) pacientes. Dos 15 pacientes com bloqueio anterógrado da VA no pós-droga, 11 apresentavam período refratário anterógrado da VA>270ms (p<0,02). Dos 12 pacientes com bloqueio completo retrógrado da VA no pós-droga, 4 apresentavam período refratário retrógrado da VA > 270ms e 8,<270ms (p=ns). Conclusäo - A propafenona produziu significativo aumento dos períodos refratários efetivos anterógrado e retrógrado das VA. Observou-se tendência a uma maior açäo frente a períodos refratários efetivos anterógrdos das VA>270ms. Este padräo de resposta näo foi observado em relaçäo aos períodos refratários efetivos retrógrdos da VA
Purpose - To evaluate the electrophysialogical effects of intravenous propafenone in the anterograde and retrograde effective refractory period of the accessory pathways (AP), in patients with WolffParkinson-White syndrome. Methods - Forty symptomatic patients were studied.. All patients were undergone to electrophysiologic study at baseline and after IV propafenone (2.0mg/kg). Drug effects were analysed according to the basal state of the anterograde and retrograde effective refractory periods of the AP><270ms. Results - The mean anterograde and retrograde effective refractory periods of the AP were 275±76ms and 264±44ms at the control and 462±190ms and 438±184ms after drug respectively (p<0.01 in both situations). The mean anterograde effective refractory period of the AV node was 236±40ms (control) and 276±57ms (post-drug )- p<0.05. The mean atrial and right ventricular effective refractory period in the control were 210±23ms and 240±34ms passing to 215±24ms and 250±40ms after drug respectively (p=ns). After drug, complete anterograde and retrograde block of the AP, ocurred in 15 (42°/) and 12 (35°/) patients respectively. Out of 15 patients with complete anterograde block of the AP, 11 had anterograde effective refractory period of the AP>270ms and 4,<270ms (p<0.02). Out of 12 patients with complete retrograde block of the AP after drag, 4 had retrograde effective refractory period >270ms and 8, <270ms (p:ns). Conclusion - Propafenone caused signifcant increase in the anterograde and retrograde effective refractory periods of the AP. There was a tendency of the drug to show better effectiveness in patients with anterograde effective refractory period of the AP>270ms. This results were not seen in relation to the retrograde effective refractory peried of the AP
Subject(s)
Humans , Male , Female , Adolescent , Adult , Middle Aged , Propafenone/pharmacology , Heart Ventricles , Electrophysiology , Heart Block/chemically induced , Atrioventricular Node , Tachycardia, Paroxysmal/chemically induced , Heart Ventricles/physiopathology摘要
A comparative study between the effects of verapamil, diltiazem and propafenone [calcium channel blockers] was done on the carotid arterial blood pressure with simultaneous ECG recording as well as on the adrenaline induced arrhythmia in anesthetized intact cat. Verapamil, diltiazem and propafenone produced a dose-related decrease of the arterial blood pressure with dose related bradycardia in chloralosed anesthetized cats. The potency ratio between verapamil and diltiazem was 26 while that between verapamil and propafenone was 39. As regards the antiarrhythmic effects of these drugs, verapamil was found to increase significantly the minimal arrhythmogenic dose of adrenaline as well as diltiazem and propafenone