Quais as medicações antiarrítmicas indicadas para o tratamento da taquicardia ventricular no paciente com cardiopatia estrutural? / Which antiarrhythmic drugs are indicated for the management of ventricular tachycardia in patients with structural heart disease?

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...

[Arrhythmias in pregnancy. How and when to treat?]. / Arritmias en el embarazo Cómo y cuándo tratar?

Cardiac arrhythmias can develop during pregnancy. The risk of arrhythmias is relatively higher during labor and delivery. Potential factors that can promote arrhythmias in pregnancy or during labor and delivery, include the direct cardiac electrophysiological effects of hormones, changes in autonomic tone, hemodynamic perturbations, hypokalemia, and underlying heart disease. In this review, the basis for treatment of supraventricular and ventricular tachycardias are described. No drug therapy is usually needed for the management of supraventricular or ventricular premature beats, but potential stimulants, such as smoking, caffeine, and alcohol should be eliminated. In paroxysmal supraventricular tachycardia, vagal stimulation maneuvers should be attempted first. In pregnant women with atrial fibrillation, the goal of treatment is conversion to sinus rhythm by electrical cardioversion. Rate control can be achieved by a cardioselective beta-adrenergic blocker drug and/ or digoxin. Ventricular arrhythmias may occur in the pregnant women, specially when cardiomyopathy, congenital heart disease, valvular heart disease, or mitral valve prolapse exists. Electrical cardioversion or treatment with sotalol may be used (amiodarone is not safe for the fetus). Finally, in women with congenital long QT syndrome, beta-blocker therapy must be continued during pregnancy and postpartum period.

Arritmias en el embarazo: cómo y cuándo tratar? / Arrhythmias in pregnancy: how and when to treat?

Cardiac arrhythmias can develop during pregnancy. The risk of arrhythmias is relatively higher during labor and delivery. Potential factors that can promote arrhythmias in pregnancy or during labor and delivery, include the direct cardiac electrophysiological effects of hormones, changes in autonomic tone, hemodynamic perturbations, hypokalemia, and underlying heart disease. In this review, the basis for treatment of supraventricular and ventricular tachycardias are described. No drug therapy is usually needed for the management of supraventricular or ventricular premature beats, but potential stimulants, such as smoking, caffeine, and alcohol should be eliminated. In paroxysmal supraventricular tachycardia, vagal stimulation maneuvers should be attempted first. In pregnant women with atrial fibrillation, the goal of treatment is conversion to sinus rhythm by electrical cardioversion. Rate control can be achieved by a cardioselective beta-adrenergic blocker drug and/ or digoxin. Ventricular arrhythmias may occur in the pregnant women, specially when cardiomyopathy, congenital heart disease, valvular heart disease, or mitral valve prolapse exists. Electrical cardioversion or treatment with sotalol may be used (amiodarone is not safe for the fetus). Finally, in women with congenital long QT syndrome, beta-blocker therapy must be continued during pregnancy and postpartum period.

Efficacy and safety of sotalol versus quinidine for the maintenance of sinus rhythm after conversion of atrial fibrillation. SOCESP Investigators. The Cardiology Society of São Paulo.

To compare the efficacy and safety of sotalol and quinidine after conversion of atrial fibrillation (AF) of <6 months, a prospective multicenter trial enrolled 121 patients who were randomized to receive dl-sotalol (160 to 320 mg/day, 58 patients) or quinidine sulfate (600 to 800 mg/day, 63 patients). Patients with left ventricular ejection fraction of <0.40 or left atrial diameter >5.2 cm were excluded. After 6 months of follow-up, using the Kaplan-Meier method, the probabilities of success were comparable between sotalol (74%) and quinidine (68%), but recurrences occurred later with sotalol than with quinidine (69 vs 10 days, p <0.05). Four patients developed proarrhythmic events, 3 (5%) with sotalol and 1 (2%) with quinidine, which were all associated with diuretic therapy. In patients converted from recent-onset AF (< or = 72 hours), sotalol was more effective than quinidine (93% vs 64%, p = 0.01), whereas in chronic AF (> 72 hours), quinidine was more effective than sotalol (68% vs 33%, p <0.05). During recurrences, the ventricular rate was significantly reduced in patients taking sotalol (98 to 82 beats/min, p <0.05). Independent predictors of therapeutic success were recent-onset AF in the sotalol group (p <0.001) and absence of hypertension in the quinidine group (p <0.05). In conclusion, sotalol and quinidine have comparable efficacy and safety for the maintenance of sinus rhythm in the overall group. In recent-onset AF, sotalol was more effective, whereas in chronic AF, quinidine had a better result. Recurrences occurred later with sotalol when compared with quinidine. Because of proarrhythmia, these drugs should be used judiciously in patients on diuretic therapy.

[The effectiveness and safety of d,l-sotalol in the ambulatory treatment of atrial fibrillation and flutter]. / Eficacia y seguridad del d,l sotalol en el tratamiento ambulatorio de pacientes con fibrilación y flutter atriales.

Data on short and long term efficacy and safety of d,l sotalol in patients with atrial fibrillation or atrial flutter is limited. The aims of this study were to (1) assess the antiarrhythmic efficacy of d,l sotalol maintaining normal sinus rhythm in patients with refractory atrial fibrillation or flutter, (2) evaluate the efficacy of d,l sotalol in preventing recurrences of paroxysmal atrial fibrillation or flutter, (3) evaluate the control of ventricular rate in patients with paroxysmal or refractory atrial fibrillation or flutter unsuccessfully treated with other antiarrhythmic agents, (4) determine predictors of efficacy (5) assess the safety of d,l sotalol in this setting. Two hundred patients with chronic or paroxysmal atrial fibrillation or atrial flutter or both, who had failed one to six previous antiarrhythmic drug trials were treated with d,l sotalol 80 to 440 mg/day orally. Fifty four percent was female, age 47 +/- 16 years (range 7-79), follow up period 7 +/- 7 months (range 1 to 14 months), 79% of patients had the arrhythmia for more than one year. The atrial fibrillation in 37.5% of patients was chronic and paroxysmal in 23.5. The atrial flutter was chronic in 31% of patients and paroxysmal in 8%. Eighty two percent of patients was in functional class I (NYHA) and 82% had cardiac heart disease: left atrial (LA) size 44 +/- 10 mm, right atrial (RA) size 37 +/- 7 mm and left ventricular ejection fraction (LVEF) 58 +/- 8%. Total success was achieved in 58% of patients (atrial fibrillation 40% and 18% in atrial flutter), partial success in 38% (atrial fibrillation in 18% and 20% in atrial flutter) and 4% of patients failure. It was p < 0.07 when compared total success vs partial success among atrial fibrillation and atrial flutter groups. Patients with cardiac heart disease responded worst (p = 0.10) to the drug than those without it, specially if the heart was dilated. We concluded that d,l sotalol has moderate efficacy to convert and maintain normal sinus rhythm, as well as it acts controlling paroxysmal relapses and ventricular heart rate.

Metabolic responses to catecholamines.

Isoproterenol and propranolol, in a single dose, caused hyperglycemia after 15 and 30 min, either in the conscious rat or in the anesthetized dog. In this latter species no modifications of the serum potassium were observed. Adrenaline, 5 microgram/kg, iv provoked hyperglycemia at the same intervals and hyperkalemia at min 1st and 2nd with further hypokalemia until 90 min. The beta-adrenergic blocker, sotalol, 5 mg/kg, iv, administered prior to adrenaline suppressed the increase in glycemia and the late decrease in serum potassium, but not the early hyperkalemia. In the isolated hind limb of the dog the intra femoral artery administration of adrenaline, 3 microgram/kg, produced similar hyperglycemia either in the artery or in the femoral vein, starting from the 15 min. Contrarily, the serum concentration of potassium was significantly less in the vein than in the artery at the 1st min. These findings suggest that different receptors are involved in the glucose and potassium response to adrenaline, and the skeletal muscle plays an important role in the regulation of the early hyperkalemia.