Search

Although pacemaker therapy is characterized by a high degree of reliability, follow-up of pacemaker patients is necessary to provide early detection of pacemaker failure and optimal setting of programable pacemakers as well as to render adequate treatment of underlying disease. The most common cause of pacemaker failure is battery depletion. In spite of the available data on the mean life-expectancy of the various batteries, the individual time of depletion cannot be predicted with accuracy. Furthermore, a defect in the electronic circuitry and/or electrode may still be rarely encountered even though technical standards are high and, occasionally, threshold elevation or lead dislocation may occur in spite of conscientious implantation technique. For patients with programable pacemakers, follow-up monitoring also enables adjustment for optimal pacemaker function. Thus, through lowering of the current or narrowing of the pulse width, the life of the battery can be prolonged or, on incrementation of these 2 parameters, an increasing threshold can be compensated for within certain limits. More important, however, is the possibility of inductive pacemaker rate changes through external programing to yield the most favorable pulse interval with respect to the underlying disease. Since, in addition to impairment of the cardiac conduction system, other disease processes are frequently presented--approximately one in three patients has coronary artery disease and almost half of the patients have congestive heart failure--follow-up visits not only serve the purpose of monitoring pacemaker function but also provide an opportunity to insure an optimal clinical condition of the patient. Accurate interpretation of pacemaker function prerequisites knowledge of the type of stimulation (fixed rate, synchronized, hysteresis, magnet rate, interference frequencies), of the battery (mercury-zinc, lihium, nickel-cadmium, isotope), of the programability (rate, current, pulse width) as well as the location of impulse capture and detection and through ascertainment of secured position of the lead and generator. While the pacemaker rate enables interpretation of the state of charge of the battery, evaluation of capture and tracing threshold permit assessment of the presence of a threshold elevation, lead dislocation, an electrode fracture or a defect in the electronic circuity. Stimulation of extracardiac muscle areas may be indicative of improper positioning and inadequate isolation of the generator, lead dislocation or lead perforation.

In 16 patients with angiographically-documented coronary artery disease and repetitive ventricular responses the effects of oral propafenon 300 mg t.i.d. on the continuous 24-hour ECG were analyzed in a study carried out according to a double-blind, randomized, crossover, placebo-controlled protocol. Comparisons were made for the number of couplets (Lown IVa) and ventricular tachycardias (Lown IVb) as well as the overall incidence of ventricular premature beats during the two last days of a five-day placebo phase and on the second and third day of treatment with propafenon. In 15 further patients with electrocardiographically-documented sustained ventricular tachycardias, the effect of intravenous propafenon (1.5 mg/kg in three minutes) was also investigated. Repeat electrophysiologic studies were performed in eight of the 15 patients after two to 13 days of continuous treatment with oral propafenon 300 mg t.i.d. The stimulation protocol incorporated delivery of a maximum of four extra stimuli during sinus rhythm and during apical right ventricular stimulation at each of four basic intervals (600, 500, 400 and 330 ms) as well as burst stimulation with intervals between 300 and 250 ms. Stimulation was terminated after induction of sustained ventricular tachycardia. In patients in whom ventricular tachycardia could be induced prior to medication with one or two stimuli, after propafenon no more than two extra stimuli were applied. As compared with placebo, propafenon led to a more than 90% reduction in couplets in 56% of the patients and in 64% of the patients there was a complete suppression of ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Guidelines for a step-wise plan of treatment of tachycardias have been compiled based on clinical empirical experience and with the aid of surface electrocardiograms, intracardial electrograms and stimulation techniques. The plan is primarily with the aid of surface electrocardiograms, intracardial electrograms and stimulation techniques. The plan is primarily oriented with respect to the antiarrhythmic efficacy, the adverse reactions and the practicability of the respective agents. Any type of tachycardia, including premature atrial or ventricular contractions, may be regarded as indication for treatment. Treatment is not indicated only in those asymptomatic patients with rare and evanescent tachycardias and in those with less than 300 premature contractions per hour. Beta-adrenergic blockers are the drugs of choice for the persistent sinus tachycardia. Should the latter agents be contraindicated, propafenon, amiodarone or aprindine may be administered. Verapamil and/or digitalis are indicated only for suppression of paroxysmal sinus tachycardias. Atrial premature contractions are best managed with guinidine or disopyramid. An acute reduction of rapid ventricular rates associated with atrial tachycardias, atrial flutter or fibrillation can best be attained through the administration of verapamil prior to digitalis or beta-adrenergic blockers. Re-establishment of sinus rhythm and prophylactic suppression of the latter should be undertaken with quinidine or disopyramid in combination with digitalis and/or either a beta-adrenergic blocker or intravenously-administered verapamil. Verapamil is the drug of choice for initial management of AV-junctional tachycardia for which a combination with digitalis may be considered. An alternative combination is that of a beta-adrenergic blocker and digitalis. For the acute treatment of ventricular tachycardias, lidocain has proved most effective. Although ajmaline and/or propafenon may be given should no response be obtained, electrical cardioversion would be more appropriate. To prevent ventricular tachycardia or when treatment is indicated for ventricular premature beats, ajmaline, propafenon, quinidine, disopyramid or mexiletine, occasionally in combination with a beta-adrenergic blocker should be employed. Verapamil and/or ajmaline, are usually very effective for termination of reciprocal tachycardias. Ajmaline or propafenon in combination with a beta-adrenergic blocker is recommended for the prophylactic treatment of reciprocal tachycardia. In patients who additionally have bradycardia, prolonged QT-intervals or pre-excitation syndromes, the guidelines should be modified accordingly.

During exercise, ventricular arrhythmias may be observed in 50% of healthy subjects and up to 85% of patients with heart disease. For the quantitative as well as qualitative assessment of ventricular arrhythmias, continuous ECG (Holter) monitoring is superior to the Exercise ECG. Both methods together render a 10% increase in sensitivity over that achieved through the use of one method only. In patients with repeated ventricular tachycardias, assessment through electrical stimulation is more preferable than the use of the exercise ECG or continuous ECG monitoring. In patients with coronary artery disease, ventricular arrhythmias during exercise, depending on their incidence and complexity, may indicate a two to eight-fold increase in the likelihood of cardiac death. The reproducibility of ventricular arrhythmias during repeated exercise testing is reported between 30 and 77%. Thus, in the individual patient, the complete absence of an exercise-induced arrhythmia during treatment does not permit differentiation between therapeutic effect and spontaneous variability. Accordingly, the exercise ECG is generally not an adequate method for assessment of antiarrhythmic treatment.