Drug-resistant Tachyarrhythmias Research Articles

Amiodarone used alone or in combination with propranolol: a very effective therapy for tachyarrhythmias in infants and children.

The aim of the study was to evaluate the efficacy of amiodarone used alone or in combination with propranolol in infants and children affected by life-threatening or drug-resistant tachyarrhythmias. The study included 27 children (median age 3 months), affected by life-threatening and/or drug-resistant supraventricular or ventricular tachyarrhythmias. The loading dose of amiodarone was 10-20 mg/kg/day and the maintenance dose ranged between 3 and 20 mg/kg/day. When amiodarone was ineffective, propranolol was added at a dosage of 2-4 mg/kg/day. The study population was divided into two groups: group A was composed of patients <1 year and group B of patients >1 year. The effectiveness of the therapy was assessed by clinical evaluation, Holter monitoring, exercise testing, and, in patients with reentry tachycardias, electrophysiological testing. Amiodarone used alone was effective or partially effective in 4/14 (28%) patients in group A and in 11/13 (85%) patients in group B (p < 0.006). Among amiodarone-resistant patients, the combined therapy with propranolol was effective in 8/10 patients in group A and 2/2 patients in group B. Therefore, amiodarone used alone or in combination with propranolol was effective in 25/27 (93%) patients. During the follow-up (20.5 +/- 13 months) there were no arrhythmic effects but side effects were noted in 5/27 (18.5%) patients. Amiodarone seems to be an effective drug in the control of the life-threatening and/or drug-resistant supraventricular and ventricular tachyarrhythmias in children. The addition of propranolol can significantly enhance the success rate of this class III drug, especially in the treatment of reentry tachycardias due to accessory pathways.

Electrophysiology and indications for pacing in the '80's.

Newer electrophysiological studies have improved our understanding of the pathogenesis of cardiac arrhythmias. Bradycardias originate either from a dysfunction of impulse formation in the sinoatrial node or from a disturbed conduction of the impulse. Different pathogenetic mechanisms are discussed as causes of tachyarrhythmias: circus movement (re-entry) is primarily due to pathological changes in conduction and refractoriness. Focal impulse formation results from local disturbances of depolarization and repolarization of the cell membrane: increased automaticity, abnormal automaticity, triggered activity. Symptomatic bradycardias still represent the standard indication for cardiac pacing particularly with implantable pacemakers. Based on clinical electrophysiology, various types of pacemakers are available at present: atrial triggered and atrial pacing pacemakers, AV-sequential pacemakers, ventricular demand-pacemakers, stand-by pacemakers, and fixed rate pacemakers. The multiprogrammability of newer pacemaker devices is a very useful tool in avoiding secondary interventions. For antitachycardia pacemaker therapy there are essentially three methods in use: 1. overdrive pacing to prevent re-entry phenomena and automaticity and also to suppress tachyarrhythmias based on increased or abnormal automaticity; 2. competitive stimulation for termination of tachycardias by means of single impulses; and 3. rapid atrial stimulation to convert atrial flutter into atrial fibrillation and consequently to normal sinus rhythm. In very rare cases rapid ventricular stimulation is mandatory. The positive results achieved with temporary stimulation methods have led to the development of permanent (implantable) antitachycardia pacemakers for long-term therapy, which have proven to be a low-risk alternative in drug-resistant tachyarrhythmias.