Karen J. Friday

Catheter ablation of atrioventricular junction using radiofrequency current in 17 patients. Comparison of standard and large-tip catheter electrodes.

BackgroundTwo catheter electrode systems were compared for delivering radiofrequency current for ablation of the atrioventricular junction. Seventeen patients with drug-resistant supraventricular tachyarrhythmias were studied. Methods and ResultsA 6F or 7F catheter with six or eight standard electrodes (1.25 mm wide, 2.5-mm spacing) was used in the first seven patients (group 1). A 7F quadripolar catheter with a large-tip electrode (4 mm long; surface area, 27 mm2) was used in the final 10 patients (group 2). Both ablation catheters were positioned to record a large atrial potential and a small but sharp His bundle potential from the distal bipolar electrode pair. Radiofrequency current was applied between a large skin electrode on the left posterior chest and either 1) each individual electrode on the standard-tip electrode catheter at 40 V (group 1) or 2) the large-tip electrode at 50–60 V (group 2). Radiofrequency current was limited to 40 V in group patients because of the strong potential for an early impedance rise when higher voltage is applied through tandard electrodes. Complete atrioventricular block was achieved in six of seven group 1 patients and all 10 group 2 patients. A junctional escape rhythm followed ablation in five or six group 1 patients (mean cycle length, 1,066±162 msec) and eight of 10 group 2 patients (mean cycle length, 1,281±231 msec). Atrioventricular block was produced in a mean of 4.7±4.6 radiofrequency current applications delivered over a period of 42±45 minutes using thelarge-tip electrode (group 2) compared with 46±22 applications using standard electrodes (15.9±10.2 applications delivered through the standard-tip electrode) over a period of 147±59 minutes (group 1). For the application producing atrioventricular block, the large-tip electrode used higher voltage (58±17 versus 38 + 5 V, p <0.03) and had lower impedance (103±22 versus 148 + 40Qk, p <0.01), resulting in greater power (33.0±13.0 versus 10.2 ±0.6 W, p <0.003) and shorter time to block (8±3 versus 22±3 seconds, p <0.001). Current delivery through standard electrodes was limited by an impedance rise occurring 7±7 seconds after the onset of one or more radiofrequency current applications at 10±1 W in six of seven patients. Using the large-tip electrode, an impedance rise occurred in five of 10 patients, but at 25±10 W and after 21±9 seconds. Atrioventricular block occurred before the impedance rise in three of these five patients. Complete atrioventricular block persisted in 15 of 16 patients at a mean follow-up of 8.7 months. Atrioventricular conduction returned at 1 month in one group 2 patient and was successfully ablated by a second procedure. Three group 1 patients died 0.5–2 months after ablation, and a fourth patient underwent cardiac transplantation after 10 months. Pathological examination of the heart in two of these patients showed necrosis of the atrioventricular node and origin of the His bundle, without injury to the middle or distal His bundle. All 10 group 2 patients are alive and subjectively improved after ablation. ConclusionsWe conclude that catheter-delivered radiofrequency current effectively produces complete atrioventricular block (94%) without requiring general anesthesia or the risk of ventricular dysfunction or cardiac perforation. The large-tip electrode allows a threefold increase in delivered power and markedly decreases the number of pulses and time required to produce atrioventricular block.

Electrogram patterns predicting successful catheter ablation of ventricular tachycardia.

Ventricular tachycardia in patients with remote myocardial infarction is thought to be due to reentry. To improve the efficacy of catheter ablation, we sought to identify electrograms identifying essential components of the reentrant circuit. In this study we compared the efficacy of shocks delivered at sites of early ventricular activation during tachycardia (presumably exit sites from the reentrant circuit) with that of shocks delivered at sites recording mid-diastolic potentials that were not continuous with the main ventricular potential recorded during the QRS complex, but that always remained associated with the tachycardia during initiation, termination, and resetting with extrastimuli (presumably activation of a segment of the slowly conducting region of the reentrant circuit). A total of 20 attempts was made to ablate 14 monomorphic ventricular tachycardias in 10 patients with remote myocardial infarction with use of one to five shocks of 50 to 370 J (200 J in 70%). All seven tachycardias in which isolated mid-diastolic potentials were targeted were successfully ablated, although one required a second attempt. Twelve attempts were made to ablate seven tachycardias by delivering shocks at sites of early activation during tachycardia when mid-diastolic potentials were not identified. Only three attempts (25%) were successful. Activation preceded the QRS complex by 60, 85, and 120 msec in the three successful attempts and by 20 to 110 msec (median 55 msec) in the nine unsuccessful attempts. For the total 20 attempts, there was no significant difference between successful and nonsuccessful ablation in the number of shocks or total energy delivered.(ABSTRACT TRUNCATED AT 250 WORDS)

New catheter technique for recording left free-wall accessory atrioventricular pathway activation. Identification of pathway fiber orientation

The ability to record accessory atrioventricular (AV) pathway activation consistently may be uniquely beneficial in improving pathway localization, identifying anatomic relations, and providing insight into unusual conduction properties. For the purpose of recording left AV accessory pathway activation, an electrode catheter was specially designed for use in the coronary sinus. The orthogonal catheter has three sets of four electrodes spaced evenly around the circumference. Electrograms were recorded at low gain (less than 1 cm/mV) between adjacent electrodes on the same set (interelectrode distance, 1.5 mm, center to center). This provides a recording dipole perpendicular to the atrioventricular groove to enhance recording of accessory pathway activation while minimizing overlapping atrial or ventricular potentials. The orthogonal electrode catheter was used in the electrophysiological study of 48 consecutive patients with 59 left AV accessory pathways. The catheter could be advanced along the coronary sinus beyond the site of earliest retrograde atrial activation in 49 of the 59 accessory pathways. Activation potentials were recorded from 45 of the 49 (92%) accessory pathways accessible to the catheter (5 of 5 anterior, 8 of 8 anterolateral, 15 of 16 lateral, 5 of 5 posterolateral, 5 of 5 posterior, and 7 of 10 posteroseptal). Accessory pathway potentials were validated by dissociating them from both atrial and ventricular activation by programmed-stimulation techniques. During surgery, accessory pathway potentials were identified from orthogonal catheter electrodes in the coronary sinus in 14 of 16 accessory pathways (12 patients). Epicardial mapping confirmed the location of the accessory pathway, and direct pressure over the orthogonal catheter electrode that recorded the accessory pathway potential resulted in transient conduction block in nine of the 14 accessory pathways. Orthogonal electrode maps of the coronary sinus identified an oblique course in 39 of 45 recorded accessory pathways. Thirty-two of 38 left free-wall accessory pathways were oriented with atrial insertion 4-30 mm (median, 14 mm) proximal (posterior) to the ventricular insertion. In the remaining six free-wall accessory pathways, the lateral excursion could not be determined because either only the atrial end of the accessory pathway was recorded or activation of multiple pathway fibers prevented tracking of individual strands. The seven recorded posteroseptal pathways exhibited accessory pathway potentials throughout an 8-18-mm (median, 10 mm) length of the proximal coronary sinus, but fiber orientation was difficult to determine.(ABSTRACT TRUNCATED AT 400 WORDS)

Ventricular Tachyarrhythmias Related to Early Afterdepolarizations and Triggered Firing: Relationship to QT Interval Prolongation and Potential Therapeutic Role for Calcium Channel Blocking Agents

The ventricular tachyarrhythmias associated with the long QT syndromes have remained enigmatic because of the striking heterogeneity in the events precipitating the arrhythmia (intense sympathetic stimulation vs drug administration or electrolyte abnormalities which prolong repolarization). The absence of comprehensive diagnostic criteria and rational therapy stems from a poor understanding of the mechanistic bases for these arrhythmias. The purpose of this report is to demonstrate the use of current tool s (pacing, monophasic action potential recordings and drugs) to explore new characteristics of these arrhythmias in patients which might be compared to those observed in experimental models. Although limited in scope, recent experimental observations suggest that arrhythmias with many of these characteristics might result from triggered firing associated with early afterdepolarizations (Brachmann , et al., 1983; Da-

Localization of left free-wall and posteroseptal accessory atrioventricular pathways by direct recording of accessory pathway activation.

With the advent of catheter ablation techniques, precise localization of accessory AV pathways (AP) assumes greater importance. In an efort to define the course of AP fibers, we attempted to record activation of 56 left free‐wall and 23 posteroseptal APs in 62 patients undergoing eiectrophysiological study. The coronary sinus (CS) and great cardiac vein (GCV) were mapped using orthogonal catheter electrodes, which provide a recording dipole perpendicular to the AV groove. The tricuspid annulus (TA) was mapped using a 2 mm spaced octapolar electrode catheter. Potentials were considered to represent AP activation only if they could be dissociated from both atrial and ventricular activation by programmed stimulation. Orthogonal catheter electrodes in the CS and GCV were advanced heyond the site of earliest retrograde atrial activation and/or earliest antegrade ventricular activation in 45 of the 56 left free‐wall APs, and AP potentials were recorded from 42 (93%). An oblique course was identified in 36 APs, with the ventricular insertion being recorded 4–30 mm (median 15 mm) distal or anterior to the atrial insertion. In three patients, antegrade and retrograde conduction proceeded over different (but close) parallel fibers. AP potentials were recorded from 19 of 23 posteroseptal pathways. Ten pathways (left posteroseptal) were recorded from the CS, beginning 5–11 mm (median 9 mm) distal to the os, with potentials extending 8–18 mm (median 11 mm) distally. Four pathways (midseptal) were recorded along the TA, anterior to the CS ostium and posterior to the His bundle catheter. Five pathways (right posteroseptal) were recorded along the TA, directly opposite or immediately posterior to the CS ostium. One of the patients had both midseptal and left posteroseptal pathways and three patients had both right posteroseptal and left posteroseptal pathways. We conclude: 1) left free‐wall APs transit the AV groove obliquely and may be comprised of multiple, closely spaced, parallel fihers; 2) the anatomical location of “posteroseptal” pathways is variable and the presence of fibers at multiple sites is common; and 3) direct recordings of AP activation facilitate tracking of the accessory pathway along its course from atrium to ventricle and help identify the presence of multiple fibers.

Thrombosis of Aortic St Jude Valve

Abstract Two patients with thrombus due to a St Jude aortic prosthesis are described. Possible etiological factors are discussed.

Use of intracardiac recordings to determine the site of drug action in paroxysmal supraventricular tachycardia

Paroxysmal supraventricular tachycardia most often results from atrioventricular (AV) reentry using an accessory AV pathway (Wolff-Parkinson-White syndrome) or reentry within the region of the AV node. In AV reentry, using an accessory pathway, suppression of the tachycardia may be achieved by depressing either anterograde AV nodal conduction or retrograde accessory pathway conduction. Intracardiac recordings and programmed electrical stimulation have established that beta-adrenergic antagonists and calcium channel blockers principally affect AV nodal conduction (anterograde limb of the reentrant circuit), whereas class IA and IC agents principally affect the accessory AV pathway (retrograde limb). Pharmacologic therapy has been more effective when directed at the limb in which conduction is most marginal at the tachycardia rate (weak limb). In individual patients, intracardiac recordings and programmed electrical stimulation can be used to identify the weak limb, indicating the class of agents most likely to be effective. Specialized techniques allowing direct recording of accessory pathway activation suggest that limitations in accessory pathway conduction may be explained by anatomic impediments. Conduction is most limited at the atrial interface of the accessory pathway in some patients, whereas in others the ventricular interface may be the limiting factor. Class IA and IC agents appear to have the greatest effect at sites where conduction is most tenuous, i.e., at the anatomic impediments. Similar considerations apply to AV nodal reentry. Anterograde slow AV nodal pathway conduction is most often depressed by digitalis preparations, beta-adrenergic antagonists, and calcium channel blockers, whereas retrograde fast AV nodal pathway conduction is more often depressed by class IA and IC agents. Intracardiac recordings and programmed electrical stimulation can also be used in these patients to identify the weak limb and direct pharmacologic therapy. Direct catheter recordings of AV nodal conduction remain elusive, limiting knowledge of the different conduction properties of the anterograde and retrograde limbs and the site(s) of drug action. Studies in progress, comparing the retrograde AV nodal conduction time during tachycardia with that during ventricular pacing at the same rate, suggest that the His bundle may be incorporated in the reentrant circuit in some patients. It appears that verapamil more readily depresses retrograde fast pathway conduction in these patients than in those in whom the His bundle does not form part of the reentrant circuit, but the reasons for this are unknown.

Methods and results of noninvasive detection of ventricular late potentials

In 1973, Boineau and Cox [1] showed that electrograms from ischemic regions of the canine heart were delayed and fractionated. Waldo and Kaiser [2] described bridging of the diastolic interval with low level electrical activity. Then Scherlag et al. [3], Hope et al. [4], Williams et al. [5] and El-Sherif et al. [6, 7], all working in the same laboratory, evolved an animal model for monitoring and relating this delayed or continuous electrical activity to the generation of ventricular arrhythmias. A wide variety of observations verified the relationship between late potentials and ventricular arrhythmias. These included patterns such as 2:1 block in the ischemic/infarct zone as well as progressive beat-by-beat prolongation of late potentials evolving to continuous electrical activity anteceding ectopic ventricular discharges and ventricular tachycardia. Other studies [8–10] also described prolongation and conduction block of late potentials as a function of heart rate and drugs. Multi-electrode epicardial mapping by El-Sherif et al. [11] and Wit et al. [12] has further verified these late activated areas as the substrate of reentry. An editorial comment by Josephson and Wit [13] clearly emphasizes the role of continuous electrical activity in defining reentry as a mechanism of ventricular tachycardia. Initial studies in man on late potentials were reported by Josephson et al. [14] and Fontaine et al. [15] which were recorded from the endocardial and epicardial surface, respectively, of patients with ventricular tachycardia.

Drug-induced torsades de pointes: clinical and experimental observations bearing on mechanism

Torsades de pointes associated with the administration of quinidine or other class 1A antiarrhythmic agents, phenothiazines, or tricyclic antidepressants is a very distinctive and unusual ventricular tachyarrhythmia. It occurs in the setting of pronounced QTU interval prolongation and has a characteristic pause-related pattern of initiation [1–6]. The incidence of this arrhythmia does not seem to increase with increasing severity of ventricular disease, and may occur in patients with seemingly normal hearts [6–8]. Similarly, the incidence does not seem to increase with increasing drug dose. Torsades de pointes typically occurs at usual or low doses and serum drug levels [3–5, 9–14], and may occur after months of uncomplicated drug therapy without the appearance of other known inciting factors, such as hypokalemia and hypomagnesemia [5, 6, 15]. Susceptible patients have a high risk of recurrence of this arrhythmia upon exposure to any of the other drugs which broaden the T wave and enhance the U wave [5, 14, 16–21], whereas the majority of patients will not develop torsades de pointes regardless of the number of agents tried.