J L Smeets

Surgical therapy has been applied in the treatment of atrial fibrillation for almost two decades. At present, the most commonly used approach is the maze operation developed by Cox. In this operation, atrial fibrillation is prevented by critically located incisional lines. Currently, these lines also are drawn during operation using cryoablation or radiofrequency current. To document the value of the maze operation, randomized studies, not only on arrhythmia prevention but also on atrial transport function and thromboembolic complications, should be performed.

Background —Accurate mapping of the site of origin and activation sequence of a cardiac arrhythmia is essential for a successful catheter ablation procedure. To achieve this, precise and reproducible catheter manipulation is mandatory. The aim of this study was (1) to assess the accuracy of a new nonfluoroscopic mapping system in humans and (2) to report the first result of endocardial activation mapping with this system during sinus rhythm and several types of supraventricular and ventricular tachycardias. Methods and Results —Fifteen patients were studied. Accuracy measurements were performed in 5 of them (patients 5, 6, 7, 8, and 14). The distances between two subsequent catheter positions in the inferior caval vein as determined by the nonfluoroscopic mapping system were compared with measurements made with calipers by four independent investigators using identification marks on the catheter shaft. The difference between these two methods was 0.95±0.8 mm. In 15 patients, activation of the right atrium and/or the right or left ventricle was recorded during sinus rhythm. Three-dimensional activation maps were constructed in patients with atrial and ventricular tachycardias and Wolff-Parkinson-White syndrome. Conclusions —With this new nonfluoroscopic mapping technique, accurate positioning of the catheter tip is possible. A three-dimensional activation map can be reconstructed during sinus rhythm and during supraventricular and ventricular tachycardias of different compartments of the heart.

We performed radiofrequency catheter ablation of idiopathic ventricular tachycardia in six children. In four, the ventricular tachycardia originated in the left ventricle, in two it originated in the right ventricular outflow tract. In 5/6 (83%) the RF procedure was successful; there were no complications.

Precise localization of accessory pathways (APs) is crucial to minimize radiofrequency (RF) energy applications in the Wolff-Parkinson-White (WPW) syndrome. Although several markers have been described for identifying APs, no gold standard has thus far been established. The present study attempted to validate the hypothesis that an early intrinsic deflection (ID) would be identifiable in the unipolar ventriculogram, if this was recorded at or near the site of endocardial breakthrough of the AP. The electrograms of 23 patients with the WPW syndrome who underwent RF ablation were analysed using a computer-based system. A total of 50 electrograms (19 successful and 31 unsuccessful RF energy applications) were studied. The downstroke of the unipolar ventriculogram was measured at 1 msec intervals for the dV/dt; the maximal dV/dt (the most rapid segement of the downstroke) was considered as the ID. The following parameters were found to differentiate between successful and unsuccessful RF ablation attempts: (i) Timing of the ID relative to the delta wave onset (ID-delta = plus 11 +/- 21 msec versus minus 18 +/- 22 msec, p < 0.001). (ii) Timing of the ID relative to the onset of the unipolar ventriculogram (Vu-ID = 14 +/- 7 msec versus 29 +/- 15 msec, p < 0.001). (iii) Maximal dV/dt in the initial 20 msec of the unipolar ventriculogram (367 +/- 146 microV/msec versus 207 +/- 97 microV/msec, p < 0.001). The other parameters (probable AP potential, bipolar ventriculogram timing, continuous electrical activity, unipolar signal morphology) were not helpful in this regard. Hence, the identification of the ID and measurement of its timing is helpful in localising overt APs for successful delivery of RF energy.

A case history is presented of a patient in whom a left-free-wall accessory pathway was surgically ablated to treat symptomatic Wolff--Parkinson--White syndrome. Subsequently, AV-nodal reentrant tachycardia became manifest. The patients's AV-nodal reentrant tachycardia was interrupted by Cox's discrete cryosurgical procedure. As a result of analysis of these cases of dual substrates for reentrant supraventricular tachycardia, ECG and electrophysiological means for differential diagnosis has been developed. These are discussed herein.

Evaluation of the use of radiofrequency energy to interrupt accessory atrioventricular pathways. Prospective study. University Hospital Maastricht. The outcome is presented of radiofrequency catheter ablation of accessory atrioventricular pathways in our first 50 consecutive patients, with a total of 54 accessory pathways. All but one patient suffered from symptomatic tachycardias. A catheter electrode was positioned next to the accessory pathway and 30 second pulses of 40 W radiofrequency energy were used to interrupt the connection. Complete block in conduction was accomplished in 44/54 (81%) of accessory pathways. No complications occurred. Success rate, procedure time and radiation dose were found to be related to the location of the accessory connection. The highest success rate was found in left free wall pathways (24/26; 92%), the lowest in right lateral pathways which seldom occur (1/4; 25%). The total procedure took 1-6 hours. The maximal duration of radiographic imaging was 2.5 hours. Although insufficient information on long-term efficacy is available, current results support the use of radiofrequency ablation of accessory pathways in institutions with expertise in the invasive management of cardiac arrhythmias. Technical improvements leading to reduction in procedure time and radiation dose will facilitate acceptance of this technique by patient and operator.

Nine patients (eight males) are reported with one or more episodes of circulatory collapse in the absence of overt heart disease or other known causes of arrhythmias; sudden arrhythmic death occurred in one of these patients. Age at first episode ranged from 16 to 41 (mean, 28) years. In seven patients, ventricular fibrillation was documented at the time of resuscitation. One patient had ventricular flutter. In the remaining patient, documentation of the arrhythmia during the collapse was not available. Four patients had frequent early ventricular premature beats, and in three of these patients, they were accompanied by episodes of rapid nonsustained polymorphic ventricular tachycardia. Failure to suppress this ectopic activity by drug therapy seems to be of prognostic significance. Of the three patients showing persistence of frequent early ventricular premature beats, one died suddenly, and two had recurrences of symptomatic arrhythmic episodes. The value of noninvasive and invasive tests in the management of these patients is not clear, with the exception of exercise testing in patients with exercise-related arrhythmias and long-term electrocardiographic monitoring in patients with frequent spontaneous ventricular ectopic activity. Follow-up varied from 21 to 192 (mean, 84) months. One patient died suddenly 21 months after his first collapse. Selection of antiarrhythmic drug therapy was largely empirical. In view of the relative rarity of sudden arrhythmic death in the absence of heart disease and the many uncertainties about its mechanism(s) and management, a worldwide registry of these patients is suggested.

Recent knowledge relating to the proarrhythmic actions of antiarrhythmics is reviewed. After establishing the diagnostic criteria the authors discuss the incidence of proarrhythmias illustrating the wide spectrum of "drug-induced arrhythmogenesis" with clinical examples. The possibilities of recognition, prediction and prevention of proarrhythmic events and sudden death are outlined.