Charlie Young

Spectrum off electrophysiologic and electropharmacologic characteristics of verapamil-sensitive ventricular tachycardia in patients without structural heart disease

Abstract Verapamil-sensitive ventricular tachycardia (VT) is a well-recognized clinical entity that some authorities believe may result from triggered activity. Despite its uniform response to verapamil, however, there is evidence that this uncommon form of VT may not be as homogeneous as first believed. Standard intracardiac electrophysiologic techniques were used to study verapamilsensitive VT in 32 patients (aged 38 years ± 20 years) without evidence of structural heart disease. More than half of these patients (69%) exhibited VT with a right bundle branch block-type QRS pattern, with the remainder (31%) displaying VT with a left bundle branch block pattern. In 31% of the patients the VT could be induced by fixed-cycle length atrial pacing, whereas in 59% of patients fixed-cycle length ventricular pacing was necessary. A critical range of cycle lengths for VT induction was required in 66% of the patients. Ventricular tachycardia was initiated with single atrial premature extrastimuli in 16% of patients, single ventricular extrastimuli in 50% of patients, and double ventricular premature extrastimuli in 9% of patients. Ventricular tachycardia displaying cycle-length alternans was observed in 28% of patients. In only 19% of patients was it possible to entrain VT during pacing from the right ventricular apex. Isoproterenol infusion was required for tachycardia induction in 50% of patients, 44% of whom had VT with a left bundle branch block QRS pattern, with the remaining 56% exhibiting VT with a right bundle branch block pattern. Beta-adrenergic blockers suppressed 53% of verapamil-sensitive VT in patients tested, whereas adenosine terminated VT in 50% of patients, with 81 % of these patients exhibiting either a left bundle branch block QRS pattern or isoproterenol dependence. Ventricular tachycardia exhibiting a left bundle branch block pattern was more likely to be isoproterenol dependent (p 0.5). Verapamil-sensitive VT exhibits properties expected of both a reentrant and triggered arrhythmia, and it is inconsistently dependent on both exogenous catecholamines for induction and intravenous adenosine for termination. Verapamil-sensitive VT encompasses a heterogeneous group of tachycardias that may result from multiple cellular electrophysiologic mechanisms.

Localization of the origin of the atrioventricular junctional rhythm induced during selective ablation of slow-pathway conduction in patients with atrioventricular node reentrant tachycardia

During radiofrequency catheter ablation of slow atrioventricular node pathway conduction in patients with atrioventricular node reentrant tachycardia, an atrioventricular junction rhythm is frequently observed. The origin and relation to ablation success of this junctional rhythm was examined in this study. By using standard intracardiac electrophysiology techniques, we studied the radiofrequency energy-induced atrioventricular junctional rhythm in 43 consecutive patients with atrioventricular node reentrant tachycardia undergoing selective ablation of slow-pathway conduction. The frequency of atrioventricular junctional activity was correlated with successful and unsuccessful attempts at ablation of slow-pathway conduction. Also, we compared the sequence of retrograde atrial activation of radiofrequency energy-induced atrioventricular junctional beats in a subgroup of 22 patients with the retrograde activation sequence observed during pacing from the right ventricular apex and the site of successful ablation of slow-pathway conduction. A total of 201 radiofrequency-energy applications was delivered in 43 patients with > or = 5 atrioventricular junctional beat(s) induced during 110 (55%) of 201 ablation attempts. Atrioventricular junctional activity was noted during 98% of successful ablations but only 43% of the unsuccessful attempts (sensitivity, 98%; specificity, 57%; negative predictive value, 99%). The mean time to appearance of atrioventricular junctional beats was 8.8 +/- 4.1 sec (mean +/- SD) after the onset of radiofrequency-energy application. In 22 (100%) of 22 patients in whom detailed atrial mapping was performed, the retrograde atrial activation sequence of the radiofrequency-induced atrioventricular junctional beats was earliest in the anterior atrial septum, identical to that seen during pacing from the right ventricular apex. Earliest retrograde atrial activation was at the posterior septum in all patients during pacing from the successful ablation site, a markedly different activation pattern compared with that seen during either radiofrequency ablation or ventricular pacing. Whereas the occurrence of atrioventricular junctional activity during radiofrequency ablation does not necessarily herald a successful ablation of slow atrioventricular node pathway conduction, its absence strongly suggests that the energy is being applied in an unsuccessful fashion. Furthermore, it appears that radiofrequency energy-induced atrioventricular junctional beats originate not from the endocardium in contact with the ablating catheter tip but instead appear to exit remotely from the anterior atrial septal region. This finding supports the existence of specialized tissues in the atrioventricular junction that preferentially transmit the effects of radiofrequency energy to an anterior exit site, possibly identical to the atrial exit site of the retrograde fast atrioventricular node conduction pathway.

Ventricular fibrillation induced by low-energy shocks from programmable implantable cardioverter-defibrillators in patients with coronary artery disease

Many of the newest implantable cardioverter-defibrillators (ICDs) provide the option of programmable low-energy cardioversion for monomorphic ventricular tachycardia (VT). Whereas these devices may provide less myocardial damage and increased comfort in patients receiving frequent shocks for VT, the proarrhythmic effects of low-energy cardioversion from ICDs in patients with structural heart disease are not clear. The purpose of this study was to determine prospectively the per-patient incidence of ventricular fibrillation (VF) induction after low-energy cardioversion of VT by ICDs in patients with coronary artery disease. The estimated cardioversion energy requirement was determined during the course of routine predischarge ICD testing in 40 patients with newly implanted ICDs. Two groups of patients were identified during determination of the cardioversion energy requirement: (1) a non-VF group consisting of 26 of 40 patients (65%) without VF induced by low-energy shock and, (2) a VF group consisting of 14 of 40 patients (35%) who developed VF during low-energy cardioversion. There was no difference between the 2 groups in terms of patient age, sex, concurrent antiarrhythmic drug therapy, VT cycle length, or type of ICD system implanted. Compared with the non-VF group, the VF group was more likely to have both a lower ejection fraction (25 +/- 5% vs 33 +/- 8%; p = 0.005) and a cardioversion energy requirement > 2 J (79 vs 27%; p = 0.005). Our results suggest that low-energy cardioversion is associated with a high per-patient risk of VF induction, and the risk is higher in patients with poorer left ventricular function and, possibly, higher cardioversion energy requirement.(ABSTRACT TRUNCATED AT 250 WORDS)

MULTIPLE ATRIOVENTRICULAR NODAL PATHWAYS IN HUMANS : ELECTROPHYSIOLOGIC DEMONSTRATION AND CHARACTERIZATION

Multiple AV Nodal Pathways. Introduction: Multiple AV nodal pathway physiology can be demonstrated in certain patients with clinical AV reentrant tachycardia.

Efficacy of adenosine in terminating catecholamine-dependent supraventricular tachycardia☆

The purpose of this study was to determine if adenosine is equally effective in terminating catecholamine-dependent and independent supraventricular tachycardia (SVT). The effect of adenosine on termination of SVT was studied in 21 patients: 12 with atrioventricular (AV) reciprocating tachycardia, and 9 with AV node reentrant tachycardia. Group 1 comprised 13 patients who had SVT induced in the absence of exogenous catecholamines, whereas group 2 comprised 8 who needed isoproterenol (1.6 +/- 0.4 micrograms/min) for induction. There was no statistical difference between the 2 groups regarding age, weight, mean arterial pressure during sinus rhythm and SVT, cycle length of SVT, or norepinephrine and epinephrine levels during sinus rhythm and SVT. Cycle length during sinus rhythm was significantly decreased in group 2. The mean dose of adenosine needed to terminate SVT was 52 +/- 6 micrograms/kg of body weight in group 1, and 61 +/- 12 micrograms/kg in group 2 (p > 0.05). In addition to isoproterenol not altering the minimal dose of adenosine necessary to terminate SVT, there was also no correlation between the dose of adenosine (mean 55 +/- 6 micrograms/kg) of each patient, and the corresponding endogenous epinephrine (273 +/- 59 pg/ml) (r = -0.19) and norepinephrine (400 +/- 58 pg/ml) (r = 0.01) levels during SVT, or cycle length of SVT (323 +/- 9 ms) (r = -0.35). The results show that adenosine is equally effective in terminating catecholamine-dependent and independent SVT; higher adenosine doses should not be needed to manage catecholamine-dependent SVT.(ABSTRACT TRUNCATED AT 250 WORDS)

Cellular and Clinical Electrophysiology of Verapamil‐Sensitive Ventricular Tachycardias

Verapamil‐Sensitive Ventricular Tachycardias. Ventricular tachycardia (VT) due to reentry is often associated with organic structural heart disease, such as coronary artery disease with previous myocardiai infarction, and primary or secondary cardiomyopathy. Treatment of this form of VT generally requires the use of potent antiarrhythmic drugs such as procainamide, quinidine, and amiodarone, or nonpharmacologic interventions such as endocardial resection and implantation of cardioverter defibrillators. Some forms of VT, typically occurring in younger patients and not associated with structural heart disease, may be due to a mechanism other than reentry and may be terminated or prevented by Ca2+ channel or beta blockers. Because these tachycardias are often so effectively treated with these rather benign agents, all patients with sustained VT undergoing an electrophysiologic study should be carefully evaluated to rule out the possibility of having these forms of VT. These tachycardias may be induced by treadmill exercise testing, programmed electrical stimulation, and/or catecbolamine infusion. While it appears that the mechanisms of these tachycardias may be caused by triggered activity related to afterdepolarizations or enhanced automaticity, there is evidence that some may in fact be due to reentry involving Ca2+‐dependent slow conduction. The cellular mechanisms of triggered activity and enbanced automaticity, and their relation to clinical ventricular arrhythmias, are discussed. (J Cardiovasc Electrophysiol, Vol. 3. pp. 500–514 October 1992)

Demonstration of a Posterior Atrial Input to the Atrioventricular Node During Sustained Anterograde Slow Pathway Conduction

OBJECTIVES This study sought to demonstrate electrophysiologic evidence for the existence of different anatomic atrial input sites of fast and slow conduction pathways in patients with dual atrioventricular (AV) node physiology. BACKGROUND Although a separate posterior exit site exists for a retrograde slow AV node pathway, it remains unresolved whether a separate atrial input site into the AV node actually exists in patients with dual anterograde AV node pathway physiology. METHODS In 10 patients with dual AV node pathway physiology, atrial pacing at three chosen drive cycle lengths (DCL1, DCL2 and DCL3) was performed at an anterior site (A) just above the His bundle recording site and at a posterior atrial site (P) just below the coronary sinus ostium. DCL3 was chosen as the one cycle length that resulted in a long AH interval consistent with slow pathway conduction. The stimulus to His bundle conduction times (SH) at both sites (SH(P) and SH(A), respectively) and their differences (deltaSH = SH(P) - SH(A)) at each of the three drive cycle lengths were analyzed. RESULTS The mean +/- SD deltaSH values for DCL1 and DCL2 measured 9 +/- 16 and 8 +/- 18 ms, respectively, and the mean deltaSH value at DCL3 measured -34 +/- 24 ms, which was significantly different from the mean deltaSH values at DCL1 and DCL2 (both p < 0.05). CONCLUSIONS The significant change in the deltaSH (SH(P) - SH(A)) value during slow pathway conduction could be accounted for by a corresponding shift of anterograde input from an anterior to a posterior entry site to the AV node. These findings support the notion that a separate anterograde entry site of the slow pathway does exist in patients with dual AV node pathway physiology.

Ventricular pacing threshold and refractoriness after defibrillation shocks in patients with implantable cardioverter-defibrillators.

The aim of this study was to examine the effect of ventricular fibrillation and a subsequent defibrillation shock on ventricular excitability and refractoriness in human beings. We studied 16 consecutive patients with implantable cardioverter-defibrillators undergoing follow-up studies. The pre- and post-shock pacing threshold, ventricular effective refractory period, monophasic action potential duration, and serum catecholamine levels were measured. Compared with the baseline state, immediately after ventricular fibrillation, and a successful defibrillation shock: (1) the ventricular effective refractory period decreased from 251 +/- 24 ms to 222 +/- 30 ms (p < 0.01), (2) the monophasic action potential duration decreased from 210 +/- 16 ms to 179 +/- 23 ms (P < 0.01) at 50% repolarization and from 274 +/- 24 ms to 240 +/- 26 ms (P< 0.01) at 90% repolarization, (3) the pacing threshold was not significantly altered and, (4) serum levels of epinephrine and norepinephrine were elevated. These results show that although ventricular fibrillation and subsequent defibrillation had no effect on the ventricular pacing threshold in human beings, it was associated with a decrease in post-shock monophasic action potential duration and ventricular effective refractory period, contrary to some previously reported findings.

Characteristic electrocardiographic features of manifest left anterior paraseptal accessory atrioventricular connection

Manifest left anterior paraseptal accessory atrioventricular (AV) connections are extremely rare, and their associated electrocardiographic preexcitation pattern has not been well defined. In this report we give an account of the unique surface electrocardiographic (ECG) features exhibited by a patient with a documented left anterior paraseptal accessory AV pathway. Additionally, we show that this unique ECG pattern can be reproduced in patients lacking this pathway by ventricular pacing at this left anterior paraseptal location. A 28-year-old woman with a 10-year history of paroxysmal supraventricular tachycardia was referred for intracardiac electrophysiology study. A 12-lead ECG obtained during atrial-paced rhythm (Fig. 1, A) showed a frontal plane axis of +110 degrees and ventricular preexcitation with a P wave to A wave interval of 60 msec. The h waves were positive in leads II, III, and aVF and negative in lead V1. QRS complexes were isoelectric in lead V1, negative in leads V2 to V4, and positive in leads V5 to V6. With standard percutaneous techniques, intracardiac multipolar electrode catheters were placed in the high right atrium, right ventricular apex, His bundle region, and coronary sinus. To precisely localize the ventricular insertion of the accessory AV connection, a deflectable quadripolar catheter (2 mm interelectrode distance) was positioned along the ventricular side of the mitral annulus with the retrograde transaortic approach. During sinus rhythm with ventricular preexcitation evident, mapping of the mitra] annulus revealed earliest ventricular activation with the tip of the mapping catheter located at a left anterior paraseptal location (Fig. 2, A). During orthodromic AV reciprocating tachycardia, the earliest retrograde atria] activation was recorded at the same site (Fig. 2, B). Simultaneous activation