The incidence of sustained bundle branch reentrant (BBR) tachycardia as a clinical or induced arrhythmia or both continues to be underreported. At our institution, BBR has been the underlying mechanism of sustained monomorphic ventricular tachycardia in approximately 6% of patients, whereas mechanisms unrelated to BBR were the cause in the rest. Data gathered from 20 consecutive patients showed electrophysiologic characteristics that suggest this possibility. These include induction of sustained monomorphic tachycardia with typical left or right bundle branch block morphology or both and atrioventricular dissociation or ventriculoatrial block. On intracardiac electrograms, all previously published criteria for BBR were fulfilled, and in addition, whenever there was a change in the cycle length of tachycardia, the His to His cycle length variation produced similar changes in ventricular activation during subsequent complexes with no relation to the preceding ventricular activation cycles. Compared with patients with ventricular tachycardia due to mechanisms unrelated to BBR, patients with BBR had frequent combination of nonspecific intraventricular conduction defects and prolonged HV intervals (100% vs. 11%, p <0.001). When this combination was associated with a tachycardia showing a left bundle branch block pattern, BBR accounted for the majority compared with mechanisms unrelated to BBR (73% vs. 27%, p< 0.01). The above finding in patients with dilated cardiomyopathy should raise the suspicion of sustained BBR because dilated cardiomyopathy was observed in 95% of the patients with BBR. Twelve of the 20 patients were treated with antiarrhythmic agents, and the other eight were managed by selective catheter ablation of the right bundle branch with electrical energy. Our data suggest that sustained BBR is not an uncommon mechanism of tachycardia; it can be induced readily in the laboratory and is amenable to catheter ablation by the very nature of its circuit. The clinical and electrophysiologic features outlined in this study should enable one to correctly diagnose this important arrhythmia. (Circulation 1989;79:256-270) M acroreentry within the His-Purkinje system commonly referred to as bundle branch reentry (BBR) is a frequently observed phenomenon in the laboratory.1-3Although scattered cases of sustained BBR tachycardia have been reported, no large series dealing with this phenomenon exists in the literature.4-11 The incidence of BBR as a mechanism of sustained ventricular tachycardia (VT), therefore, continues to be underreported in the literature, and consequently, there is less awareness of sustained BBR tachycardia as a significant clinical arrhythmia.

Seventeen patients (16 men and 1 woman) were challenged with isoproterenol after their initially inducible sustained ventricular tachyarrhythmia (monomorphic tachycardia in 14 patients and fibrillation in 3) was completely suppressed by class I antiarrhythmic drugs. Coronary artery disease was documented in 11 patients, dilated cardiomyopathy in 2 and no structural heart disease in the remaining 4 patients. The initial presentation was aborted sudden cardiac death (five patients), syncope (eight patients) and symptomatic nonsustained ventricular tachycardia (four patients). The antiarrhythmic drug that rendered the initial ventricular tachyarrhythmias noninducible was class IA in 11 cases, class IC in 5 and combined class IA and IB in 1. The original ventricular tachyarrhythmia became reinducible in 10 patients (group A) and remained noninducible in 7 patients (group B) after isoproterenol infusion at a rate necessary to achieve a 20% increase in heart rate. Despite the results of isoproterenol challenge, all patients were maintained on their electrophysiologically guided antiarrhythmic regimen. During a mean follow-up period of 13 +/- 9 months, 3 of the 10 patients in group A experienced clinical recurrence of tachyarrhythmia; no recurrence was noted in group B. In conclusion, reinducibility of ventricular tachyarrhythmia after beta-adrenergic stimulation seems to identify a subgroup of patients at high risk of subsequent arrhythmic events. Beta-adrenergic blockade or surgical therapy may be indicated in some patients with a positive isoproterenol challenge.

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The results suggest that 1) initiation of ventricular tachycardia during programmed ventricular stimulation occurs with minimal conduction latency; 2) because of the large overlap in coupling intervals where VF or VT were induced, a single coupling interval cannot be recommended to adequately separate these groups; and 3) induction of VF was preceded by increased latency and prolongation of the local activation time. These parameters should not be allowed to prolong if VF is to be avoided during programmed stimulation. In addition, 4) the initiation of VF during electrophysiological studies is often associated with the presence of structural heart disease; such structural disease may promote conduction latency and the development of VF.

We describe our first 20 cases of cryoablation of atrial fibrillation (AF) using transesophageal echocardiography (TEE). Continuous procedural monitoring with TEE by a cardiologist and senior sonographer assists the electrophysiologist in performance of the cryoballoon procedure of AF. Previously using intracardiac echocardiography (ICE) we have found TEE to have better overall procedural imaging, and monitoring for pericardial effusion or thrombus formation. We have found TEE monitoring to be helpful with positioning for interatrial septal (IAS) puncture, catheter tip avoidance of the left atrial appendage (LAA), and guidance of the balloon catheter into each pulmonary vein (PV), with proper positioning within each PV orifice, and documentation of PV occlusion for the cryoballoon procedure. Procedural equipment and the cryoballoon protocol used are presented in detail. The role of TEE imaging during the procedure and in preventing potential dangers is illustrated. It is the goal of this study to demonstrate how the electrophysiology and echocardiography laboratories work together in this cryoablation procedure.

(Echocardiography 2011:28:809‐811)

Multiple defibrillations by the automatic implantable cardioverter/defibrillator (AICD) have been reported to result in localized epicardial damage. No data exist, however, regarding whether this damage can be detected in the clinical setting or whether it interferes with the detection of true myocardial infarction. Forty-nine patients who received defibrillations by patch electrodes were studied prospectively. We attempted to document the presence of myocardial injury with the following three commonly used modalities for the detection of myocardial infarction: serial electrocardiographic changes, serial creatine phosphokinase (CPK) and CPK-MB release, and technetium 99m pyrophosphate scanning. Fifteen patients received defibrillations by AICD patches at the time of AICD generator replacement. Nine patients received defibrillations at the time of new AICD lead placement. The average total energy delivered was 85±29 J. None of these patients had detectable myocardial injury. Ten patients had defibrillations by the AICD patches at the time of bypass operation. One patient in this group developed acute myocardial infarction in the inferior wall after posterior descending coronary bypass operation, as detected by electrocardiogram, 'mTc pyrophosphate scanning, and CPK-MB analysis. Fifteen patients were evaluated for spontaneous AICD discharges. Thirteen had a maximum of five consecutive shocks, and cumulative energy delivered was not greater than 330 J. None of these patients had detectable injury. Two patients had CPK-MB release of 15.3% and 7.5%, respectively. One of these patients had a positive 99mTc pyrophosphate scan. These two patients received 12 and 17 rapid and consecutive AICD discharges, respectively, with cumulative delivered energy of 360 and 510 J, respectively. Twenty-one patients in this series developed nonspecific ST-T segment changes that normalized within 48-72 hours after AICD discharges. We conclude that 1) defibrillation efficacy testing limited to 85±29 J does not cause detectable myocardial injury; 2) spontaneous discharges of the AICD with a maximum cumulative energy of 330 J does not result in detectable myocardial injury when the rate of discharge for five rapid shocks is less than one shock per minute; 3) rapid consecutive (more than 12 at less than 1 minute apart) AICD discharges can result in a positive 9mTc pyrophosphate scan and CPK-MB release (however, electrocardiographic changes consistent with new myocardial infaretion are rare); 4) the appearance of new Q waves or persistent (after 48-72 hours) T wave changes, together with significant release of CPK isoenzymes, is probably because of myocardial infarction caused by vascular occlusion; and 5) transient (48-72 hours) ST-T segment changes are common after AICD discharges. (Circulation

Concealed anterograde penetration of the atrioventricular (AV) node has been used to explain a wide variety of electrocardiographic findings. The effects of atrial rate acceleration on this phenomenon remain undefined. To examine the dynamic interrelations between conducted and nonconducted beats at different atrial rates, a unique atrial pacing protocol of functional 2 :1 AV block was used in 10 patients. The pacing protocol involved abrupt transitions from 2:1 to 1:1 AV conduction and enabled quantification of conduction delay produced by nonpropagated impulses over extremes of atrial rate. Stable 2:1 AV conduction was maintained over a mean range of atrial paced cycle lengths of 289±29.6 to 223+±33.0 msec, respectively. The mean AV conduction time during 2:1 and corresponding 1:1 drives at the longest atrial paced rates were 169+±33.5 and 136.5+±26.9 msec, respectively-revealing a significant effect of nonpropagated impulses on subsequent conduction. Surprisingly, at the shortest atrial paced rates, the mean AV conduction times were 191.5+31.8 and 161.0+23.3 msec, respectively. The lack of significant changes in conduction time between 2:1 and 1:1 drives at the extremes of atrial rate (32.5 vs. 30 msec, p=NS) suggests that the effect of concealed conduction is "fixed" and independent of rate. Clinical implications and postulated electrophysiologic mechanisms are discussed. (Circulation 1989;80:43-50) A n often-observed accompaniment of rapid atrial pacing and supraventricular tachycardias is the production of functional block at the atrioventricular (AV) nodal level, resulting in a 2: 1 atrioventricular response.' Lewis and Master2 first noted that the AV nodal conduction time of propagated impulses during 2: 1 response was longer than that during 1:1 conduction at exactly half the atrial rate. This phenomenon has been attributed to partial anterograde penetration of the AV node during nonconducted impulses; an effect later termed "concealed conduction" by Langendorf.