Control of rapid ventricular response by radiofrequency catheter modification of the atrioventricular node in patients with medically refractory atrial fibrillation.

BACKGROUND: Pharmacological control of rapid ventricular response to atrial fibrillation may be difficult in some patients. Alternative treatments, including curative surgery or atrioventricular (AV) node ablation with pacemaker implantation, have significant potential morbidity. In view of evidence that dual AV nodal physiology may exist in a significant percentage of the population, even in those without AV nodal reentrant tachycardia, we postulated that control of ventricular response might be achieved by radiofrequency (RF) catheter ablation in the region of the AV nodal slow pathway with its short refractory period. METHODS AND RESULTS: Ten patients underwent attempted AV node modification using a 4-mm-tipped electrode catheter positioned in the middle or posterior septum, between the His bundle and coronary sinus ostium on the tricuspid valve annulus. RF energy was applied at 16 to 30 W for up to 60 seconds, until average ventricular response fell below 100 beats per minute. Reduction of maximal ventricular response below 120 beats per minute was confirmed with atropine 1 mg IV. If required, additional ablations were performed progressively more posteriorly up to the coronary sinus ostium. Patients with successful AV node modification were discharged off AV node-blocking drugs and followed in the clinic at regular intervals. Twenty-four-hour ambulatory ECG recordings and/or treadmill stress tests were obtained before and after ablation for statistical comparison of maximum ventricular rate. Resting average ventricular rate was determined during electrophysiology study before and after ablation. In 7 of 10 patients (70%), maximum ventricular rate was reduced from a mean of 164 +/- 12 to 123 +/- 16 beats per minute (P < .01) and average ventricular rate from a mean of 128 +/- 11 to 83 +/- 10 beats per minute after ablation. Mean minimum ventricular rate was 54 +/- 11 beats per minute after ablation. These 7 patients have remained symptom free from rapid ventricular response for a mean of 14 +/- 8 months (range, 1 to 22). Three remain off all AV node-blocking drugs, 3 remain on digoxin alone, which was previously ineffective, and 1 remains on a beta-blocker for angina. In the 3 patients who did not respond to AV node modification, complete AV node ablation and permanent pacemaker implantation was performed in 2 and DC cardioversion after amiodarone loading was performed in 1. CONCLUSIONS: RF catheter modification of AV node conduction is effective in controlling rapid ventricular response to atrial fibrillation in a significant percentage of medically refractory patients. A possible mechanism of RF modification of AV node conduction is AV nodal slow pathway ablation. Large-scale clinical trials will be needed to determine the overall efficacy and safety of this technique.

Relation between upper limit of vulnerability and defibrillation threshold in humans.

BACKGROUND: In the canine model, an upper limit of shock strength exists that can induce ventricular fibrillation during the vulnerable period of the cardiac cycle. This shock strength (the upper limit of vulnerability) closely correlates with the defibrillation threshold and supports the "upper limit of vulnerability" hypothesis of defibrillation. It is not known whether an upper limit of vulnerability exists in humans or whether this limit correlates with the defibrillation threshold. METHODS AND RESULTS: In 13 patients undergoing implantable cardioverter-defibrillator implantation, the shock strengths associated with a 50% probability of reaching the upper limit of vulnerability (ULV50) and a 50% probability of reaching the defibrillation threshold (DFT50) were determined by the up-down algorithm. The ULV50 was determined only for the mid-upslope of the positive T waves and for the mid-downslope of the negative T waves. No major complications occurred during surgery. An upper limit of vulnerability was demonstrated in each patient. The ULV50 was 300 +/- 138 V or 6.8 +/- 5.8 J, which was significantly lower than the DFT50 of 347 +/- 167 V (p = 0.038) or 9.1 +/- 7.3 J (p = 0.013). The correlation between the ULV50 and the DFT50 was significant (r = 0.90, p < 0.001 for voltage; r = 0.93, p < 0.001 for energy). CONCLUSIONS: An upper limit of vulnerability is present in humans. There is a significant correlation between the ULV50 and the DFT50, and the ULV50 is significantly lower than the DFT50.

Radiofrequency modification of atrioventricular conduction by selective ablation of the low posterior septal right atrium in a patient with atrial fibrillation and a rapid ventricular response.

A case is presented of a 58-year-old woman with atrial fibrillation and uncontrolled ventricular responses up to 180 beats/min despite therapy with digoxin. Radiofrequency energy was applied to the low posteroseptal right atrium in an attempt to modify "slow fiber" conduction. This resulted in a decrease in ventricular rate from 125 to 50 beats/min. Follow-up Holter monitor demonstrated an average heart rate of 64 beats/min (range 43-112). On exercise tolerance test, the maximum heart rate was 126. Modification of the low posterosepta right atrium may prove to be an alternative to AV node or His bundle ablation and pacemaker implantation in patients with poorly controlled atrial fibrillation and rapid ventricular response. The mechanism by which this approach was effective may be ablation of slow conducting AV nodal fibers with a short refractory period.

Interaction between accessory pathways resulting in inability to induce reciprocating tachycardia.

A 44-year old male with Wolff-Parkinson-White syndrome presented with atrial fibrillation. The patient was found at the electrophysiological study to have two accessory pathways, one concealed and the other conducting exclusively in the anterograde direction. After radiofrequency catheter ablation of the anterograde conducting pathway, orthodromic reciprocating tachycardia, which previously could not be induced despite an aggressive protocol, was easily induced. Ablation of the concealed pathway resulted in termination of the tachycardia and suppression of inducibility. We propose that interaction between the two accessory pathways resulted in an inability to induce reciprocating tachycardia.

Risk of ventricular dysrhythmias during 1-hour infusions of amphotericin B in patients with preserved renal function.

In order to assess the safety of 1-h infusions of amphotericin B (AMB), we prospectively monitored 213 1-h infusions of AMB (dose range, 0.27 to 0.89 mg/kg of body weight) in 27 patients with creatinine clearances of > 25 ml/min. Holter monitor tracings during 1-h infusions were compared with those during a 4-h baseline period of monitoring. There were no ventricular dysrhythmias during 1-h infusions of AMB that were not present during baseline monitoring. Nausea and/or rigors were noted for 32 (15%) infusions in six (22%) patients. No patient exhibited a temperature rise of > 1 degree C. We conclude that, in doses of up to 0.9 mg/kg, AMB does not appear to induce asymptomatic ventricular dysrhythmias when administered over 1 h to patients with creatinine clearances of > 25 ml/min.

Radiofrequency catheter ablation for the treatment of human type 1 atrial flutter. Identification of a critical zone in the reentrant circuit by endocardial mapping techniques.

BACKGROUND: Recent studies of human type 1 atrial flutter demonstrated reentry in the right atrium and an area of slow conduction in the low posteroseptal right atrium. Direct-current catheter ablation of this area has been only moderately successful in preventing recurrence. Therefore, we performed endocardial activation mapping and entrainment pace mapping during atrial flutter to determine the critical site for radiofrequency ablation of this arrhythmia. METHODS AND RESULTS: Twelve consecutive patients (seven men and five women; age, 21-73 years) with type 1 atrial flutter (mean cycle length, 253 +/- 39 msec) underwent right atrial endocardial activation and entrainment pace mapping using standard transvenous catheter techniques to localize the atrial flutter reentrant circuit, the area of slow conduction, and the exit site from the area of slow conduction. Upon identifying appropriate sites, radiofrequency energy (16-29 W) was applied via a 4-mm tipped catheter. Activation mapping of atrial flutter revealed a counterclockwise reentrant wave front originating just inferior or posterior to the coronary sinus ostium, proceeding superiorly in the atrial septum to the right atrial free wall, then inferiorly toward the tricuspid annulus and finally medially between the inferior vena cava and the tricuspid annulus, where low-amplitude fragmented electrical activity was noted. Entrainment pace mapping from this area produced an exact P wave match to atrial flutter on 12-lead ECG with a long (greater than 40 msec) stimulus-to-P interval indicating slow conduction, whereas pacing just inferior or posterior to the coronary sinus ostium produced an exact P wave match with a short stimulus-to-P interval (less than 40 msec), presumably identifying the exit site from the area of slow conduction. Radiofrequency energy (one to 14 applications) was effective in terminating and preventing reinduction of atrial flutter in 10 patients. In two patients, atrial flutter was not terminated during radiofrequency energy application but during subsequent pacing attempts. Sites where ablation was successful, located just inferior or posterior to the coronary sinus ostium, were characterized by discrete electrograms with activation times of -20 to -50 msec before P wave onset and exact entrainment pace maps with a stimulus-to-P interval of 20 to 40 msec, consistent with the exit site from the area of slow conduction. Follow-up (mean, 16 +/- 9 weeks; range, 2-31 weeks) revealed recurrence of the original atrial flutter in two patients, one of whom underwent repeat ablation without further recurrence, self-limited infrequent recurrence of a new atrial flutter or atrial fibrillation in three suppressed by beta-blocker or digoxin, and no recurrence in seven. CONCLUSIONS: 1) Radiofrequency energy applied to a critical area in the atrial flutter reentrant circuit, inferior or posterior to the coronary sinus ostium, will terminate and prevent arrhythmia reinduction. 2) Long-term follow-up in a larger series of patients will be required to confirm efficacy of this technique, although short-term results look promising.

Demonstration of accessory pathway interaction by computerized mapping in preexcitation syndrome.

While interaction between the normal conduction system and an accessory pathway (AP) has been reported, interaction between two APs has not been well documented. With the assistance of computerized mapping techniques, we recently operated on a patient with two APs. One of these two APs had slow anterograde conduction velocity and was concealed during sinus rhythm and atrial pacing. Intraoperative computerized mapping studies revealed that the interaction between the APs was responsible for the anterograde conduction block of the slow AP during sinus rhythm and atrial pacing. This is the first direct demonstration of inhibition of conduction of one AP by the other AP in a patient with preexcitation syndrome.