R.N.W. Hauer

Control of radiofrequency lesion size by power regulation.

The influence of power and exposure duration on lesion size in radiofrequency catheter ablation was investigated in 15 closed-chest dogs. Radiofrequency energy was delivered to the right ventricular endocardium between the tip of a standard 6F electrode catheter and a large W and durations of 5, 10, 20, 30, and 60 seconds. At necropsy 1 week later, well-demarcated homogeneous lesions were found when power had exceeded a threshold level that decreased from 1.8 W at 5 seconds to 0.7 W at 60 seconds. Lesion size ranged from 0 to 7.5 mm in depth and 0 to 9 mm in diameter. For the 5, 10, and 20 second ablations, lesion size was determined by exposure duration and power level. However, after a 20 second exposure, lesion size had reached maturity and was related to delivered power only. Therefore, a gradual, controlled growth of the lesion can be obtained by a stepwise increase of the radiofrequency power level with ample exposure duration at each level to allow for stabilization. At levels exceeding 7 W, the formation of a thin insulating layer of blood coagulum on the electrode surface caused an abrupt increase of impedance within approximately 30 seconds. Therefore, lesion size is limited to 8.5 mm in radiofrequency ablation with a standard 6F endocardial electrode catheter.

LocaLisa New Technique for Real-Time 3-Dimensional Localization of Regular Intracardiac Electrodes

BACKGROUND Estimation of the 3-dimensional (3D) position of ablation electrodes from fluoroscopic images is inadequate if a systematic lesion pattern is required in the treatment of complex arrhythmogenic substrates. METHODS AND RESULTS We developed a new technique for online 3D localization of intracardiac electrodes. Regular catheter electrodes are used as sensors for a high-frequency transthoracic electrical field, which is applied via standard skin electrodes. We investigated localization accuracy within the right atrium, right ventricle, and left ventricle by comparing measured and true interelectrode distances of a decapolar catheter. Long-term stability was analyzed by localization of the most proximal His bundle before and after slow pathway ablation. Electrogram recordings were unaffected by the applied electrical field. Localization data from 3 catheter positions, widely distributed within the right atrium, right ventricle, or left ventricle, were analyzed in 10 patients per group. The relationship between measured and true electrode positions was highly linear, with an average correlation coefficient of 0.996, 0.997, and 0.999 for the right atrium, right ventricle, and left ventricle, respectively. Localization accuracy was better than 2 mm, with an additional scaling error of 8% to 14%. After 2 hours, localization of the proximal His bundle was reproducible within 1.4+/-1.1 mm. CONCLUSIONS This new technique enables accurate and reproducible real-time localization of electrode positions in cardiac mapping and ablation procedures. Its application does not distort the quality of electrograms and can be applied to any electrode catheter.

Unfavorable outcome in patients with primary electrical disease who survived an episode of ventricular fibrillation.

BACKGROUND Prognosis in patients with ventricular tachyarrhythmia without structural heart disease (primary electrical disease) has been described as excellent. However, prognosis may be less favourable in the subgroup surviving an episode of ventricular fibrillation. METHODS AND RESULTS We prospectively followed 19 consecutive patients (age, 13 to 66 years; mean age, 33 years) who had survived an episode of documented ventricular fibrillation. Structural heart disease, preexcitation, and long QT syndromes were excluded by thorough cardiologic evaluation. All patients underwent 24-hour Holter monitoring, exercise testing, and programmed electrical stimulation according to a standardized protocol. Holter monitoring revealed episodes of ventricular tachyarrhythmia in 5 patients. Exercise testing reproducibly provoked ventricular tachycardia in 2 patients. Baseline programmed electrical stimulation yielded inducibility of rapid ventricular tachyarrhythmia in 10 patients (53%) and noninducibility in 9 (47%). Nine patients were discharged on antiarrhythmic drug therapy. A defibrillator was implanted in 10 patients. During 43-month follow-up (range, 5 to 85 months; median, 41 months), major arrhythmic events recurred in 7 patients (37%). Four of these patients had noninducibility at baseline programmed electrical stimulation. Two patients on antiarrhythmic drugs had recurrent cardiac arrest: one died suddenly and the other was successfully resuscitated from ventricular fibrillation and subsequently underwent defibrillator implantation. In the other 5 patients, termination of (pre)syncopal episodes was associated with defibrillator shocks. Termination of ventricular fibrillation was documented by Holter recording in one of these patients. Specific markers predictive of a recurrent event could not be identified, although 6 of 7 patients with recurrent events had experienced at least one episode of cardiac arrest or (pre)syncope before the index episode. CONCLUSIONS Patients with primary electrical disease presenting with ventricular fibrillation are at high risk of recurrence of major arrhythmic events during long-term follow-up. Noninducibility at baseline study does not predict an uneventful course. Also, early defibrillator implantation should be considered in these patients.

Endocardial catheter mapping: wire skeleton technique for representation of computed arrhythmogenic sites compared with intraoperative mapping.

Guiding surgical therapy of ventricular tachycardia by preoperative endocardial catheter mapping necessitates improvement of the accuracy of localization of the arrhythmogenic site. We therefore used a new mathematical cineradiographic method during catheter mapping to compute the position of left ventricular arrhythmogenic sites relative to three anatomic reference points: the centers of aortic and mitral valve ostia and the left ventricular apex. To enable the surgeon to identify the position of the computed sites, a wire skeleton (one for each patient) representing a single or multiple arrhythmogenic site(s) relative to the anatomic reference points was constructed. This wire skeleton was inserted into the left ventricular cavity during surgery. Side branches of the device indicated preoperatively localized arrhythmogenic sites. Results in eight consecutive patients were compared with those of intraoperative simultaneous mapping of 64 endocardial sites. Sixteen morphologically distinct monomorphic ventricular tachycardias were mapped by catheter and 15 by intraoperative mapping. In 12 ventricular tachycardias an identical morphology was recorded during both techniques. The distance between arrhythmogenic sites localized with both methods was 1 cm or less in 11 of these 12 ventricular tachycardias and 2 cm in one ventricular tachycardia. These results indicate that endocardial catheter mapping combined with wire skeleton representation of computed positions of arrhythmogenic sites is reliable for guiding surgical therapy of ventricular tachycardia and since some of the ventricular tachycardias were inducible only during either preoperative or intraoperative mapping, both techniques have an additive value. In addition, the wire skeleton proved convenient during surgery by identifying the arrhythmogenic sites.

Endocardial catheter mapping: validation of a cineradiographic method for accurate localization of left ventricular sites.

To guide surgical therapy for ventricular tachycardia by preoperative endocardial catheter mapping, accurate anatomic localization of arrhythmogenic sites is mandatory. For this reason we developed a mathematical cineradiographic method to compute left ventricular sites relative to three anatomic reference points: the centers of aortic and mitral valve ostia and the left ventricular apex. To validate the method 14 epicardial left ventricular markers were implanted in four dogs to simulate arrhythmogenic sites. Distances between markers and the anatomic references were calculated and the results were compared with postmortem measurements. The difference between calculated and measured distances was 0.5 +/- 3.1 mm (mean +/- SD), confirming accurate localization of anatomic marker sites. However, in surgery the results have to be displayed in a practically applicable, unambiguous way. Therefore, wire skeletons were constructed to represent calculated endocardial marker sites relative to the anatomic reference points. To validate this approach, 14 markers were implanted in the left ventricular subendocardium in four dogs. Wire skeletons were constructed, one for each marker site, and inserted postmortem into the left ventricular cavity via a 2 cm incision. In all cases the correct indication of a marker site by the corresponding wire skeleton was confirmed by fluoroscopic inspection in multiple projections. This wire skeleton technique may enhance the practical usefulness of preoperative endocardial catheter mapping.

Body-Surface QRST Integral Mapping Arrhythmogenic Right Ventricular Dysplasia Versus Idiopathic Right Ventricular Tachycardia

BACKGROUND Ventricular tachycardia originating in the right ventricle may arise in the presence or absence of structural heart disease. The two main causes of right ventricular tachycardia are arrhythmogenic right ventricular dysplasia (ARVD) and idiopathic right ventricular tachycardia (IRVT) originating from the outflow tract. This study was carried out to determine whether body-surface QRST integral mapping can differentiate patients with ARVD from patients with IRVT. METHODS AND RESULTS Body-surface QRST integral maps were obtained during sinus rhythm in 8 patients with ARVD, 8 patients with IRVT, and 27 healthy control subjects. QRST integral maps were analyzed both visually and mathematically. All control subjects had a normal dipolar QRST integral map. In all patients with ARVD, a specific dipolar QRST integral map with an abnormally large negative area covering the entire inferior and right anterior thorax was recorded. In 6 of 8 patients with IRVT, a normal map pattern was found, whereas the remaining 2 patients showed an abnormally large negative area on the right anterior thorax. CONCLUSIONS Patients with ARVD display a specific abnormal QRST integral map that may be related to delayed repolarization in the structurally abnormal right ventricle. The majority of patients with IRVT demonstrate a normal QRST integral map. A slightly abnormal QRST integral map was noted in 2 of 8 patients with IRVT, which may be related to minor structural abnormalities, undetectable by the present routine diagnostic techniques. These preliminary results indicate that body-surface QRST integral mapping may become an important diagnostic tool to differentiate patients with ARVD from those with IRVT.

Ventricular tachycardia after in vivo DC shock ablation in dogs. Electrophysiologic and histologic correlation.

BackgroundDC shock catheter ablation for the treatment of ventricular tachycardia (VT) may induce VT episodes that disappear within days. Methods and ResultsA 30-J cathodal shock was delivered to the endocardial left ventricular wall in 15 closed-chest dogs. All dogs had VT during the first day after ablation. Eleven of these dogs were studied on the first day. Extensive epicardial and endocardial activation mapping in vivo, in Langendorff-perfused hearts, and in tissue blocks in a tissue bath localized the site of origin of VT to subendocardial Purkinje fibers in a border zone surrounding the central necrotic ablation lesion. Intracellular recording showed that this zone consisted of a subendocardial superficial layer (SSL) of cells with abnormal characteristics, a resting membrane potential (RMP) of −58 ± 11 mV (mean ± SD), and an action potential amplitude (APA) of 61 ± 20 mV. In addition, the steepness of phase 0 of the action potential was markedly reduced. In three dogs abnormal automaticity was found in a very small area. Immediately below the SSL, cells were normal with an RMP of −78 ± 5 mV and an APA of 107 ± 8 mV. Histology confirmed a thin SSL with edematous and necrotic cells, hemorrhage, and infiltration. The other four dogs were studied at 1 week after ablation when VT was absent. Microelectrode impalement in the SSL was either impossible or showed nearly normal action potential characteristics. Histological examination showed a markedly thickened fibrotic subendocardial layer at places where impalement was impossible. Normal subendocardium was found in other areas of the border zone. ConclusionsOur results indicate that VT after DC shock ablation originates from cells with abnormal automaticity in the superficial subendocardial border zone around the central ablation lesion. Within 1 week edematous and necrotic cells in this border zone are replaced by a fibrotic layer, and this transition is associated with the disappearance of VT. (Circulation 1991;84:267–278)

Change in delay of atrioventricular conduction after radiofrequency catheter ablation for atrioventricular nodal re-entry tachycardia.

OBJECTIVE--To monitor atrioventricular conduction after radiofrequency ablation for atrioventricular nodal re-entry tachycardia. DESIGN--Measurement of PR interval from 12 lead surface electrocardiograms before; at 0, 24, 48, 72, and 96 hours; and at 1 and 6 months after radiofrequency ablation. PATIENTS--40 consecutive patients with atrioventricular nodal re-entry tachycardia. The anterior approach was used in 23 patients, the posterior approach in 17. RESULTS--With the anterior approach the PR interval increased significantly and progressively until 48 hours after ablation (maximum 282 (SD 62.2) ms, before ablation 142 (29.5) ms; P < 0.0001). Up to 96 hours no further change was observed, but one month after ablation the PR interval had decreased to a value not significantly different from that 24 hours after the procedure (231 (51.2) ms). In one patient total atrioventricular block developed 24 hours after an uncomplicated procedure and a permanent pacemaker was implanted. With the posterior approach the PR interval increased slightly in the first 24 hours (156 (22.7) ms, before ablation 144 (21.2) ms P = 0.004), but it had returned to preablation values at 1 month. One patient developed second degree atrioventricular block during the first 24 hours after ablation, despite delivery of all radiofrequency pulses posterior to Kochs triangle at sites without His bundle deflection. PR intervals at 6 months did not differ significantly from the values at 1 month. CONCLUSION--After the anterior approach the progressive delay in atrioventricular conduction up to 48 hours after radiofrequency ablation for atrioventricular nodal re-entry tachycardia warrants continuous in hospital monitoring of patients for at least two days after the procedure.

Unmasking of left free wall ventricular preexcitation by His bundle ablation.

His bundle ablation was performed in a 48 year old man with drug refractory orthodromic atrioventricular reentrant tachycardia and paroxysmal atrial fibrillation. Reentry was caused by a left free wall concealed accessory pathway. Interruption of the His bundle by low energy direct current shock (25 J) was quickly followed by anterograde conduction via the accessory pathway, with various forms of advanced block. The combined effect of unfavourable anterograde conduction (prolonged anterograde effective refractory period and decremental conduction), the left lateral location of the accessory pathway and intra-atrial conduction delay on one side, and normal conduction via the atrioventricular node and His bundle with retrograde concealed conduction into the accessory pathway on the other side resulted in masking of the anterograde conduction capability of the anomalous pathway. This observation does not seem to invalidate the choice of His bundle ablation in similar cases.