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.

The present study describes the clinical and electrophysiological characteristics of sustained bundle branch reentrant ventricular tachycardia treated with electrical ablation of the right bundle branch. Seven patients presented with syncopal episodes, and six of the seven had documented episodes of ventricular tachycardia. All

What is known and objectives Coronary artery disease (CAD) is the leading cause of death in the United States. For patients on whom guideline‐driven measures have been tried, enhanced external counterpulsation (EECP) is the only truly noninvasive and safe intervention for which a reduction of angina symptoms and nitrate use, increased exercise tolerance, and improvement in myocardial ischaemia have been shown. The objective of this study was to demonstrate, by way of literature review, the efficacy of EECP as a treatment modality for the relief of refractory angina and improvement in quality of life in CAD patients. Methods This article reviewed the safety and efficacy of EECP in patients with refractory angina, by conducting a sweeping search and analysis of existing published literature. Results and Discussion Critical review of a multitude of studies revealed that EECP consistently reduces angina pectoris, extends time to exercise‐induced ischaemia, decreases dependency on nitroglycerine for frequent chest pain, increases maximum workload, and improves the quality of life in patients with symptomatic stable angina. The literature reviewed also indicated that EECP is well‐tolerated by the vast majority of patients, with relatively few adverse events reported. Conclusion The present study suggests that EECP is a safe and likely best available method of treatment for patients presenting with symptomatic CAD not amenable to further revascularization.

We analyzed the effect of functional fascicular block (FFB) on ventriculoatrial conduction time (VACI) during orthodromic tachycardia (OT) in 32 patients with single accessory pathway (AP) of the Kent bundle type. The location of AP was left free wall (LFW-AP) in 21 patients, left posteroseptal in 6, right free wall in 2, and right anteroseptal in 3. FFB either alone or in combination with functional left or right bundle branch block (LBBB or RBBB) occurred predominantly at the onset of OT and was initiated with ventricular extrastimulus technique more often than with atrial extrastimulation. In patients with LFW-AP, isolated functional left anterior fascicular block (LAFB) produced significant prolongation in VACI (15-35 ms). A similar magnitude of VACI increase (20-35 ms) was also observed when LAFB was associated with RBBB. Although 2545-ms prolongation in VACT occurred with functional LBBB and normal axis, an additional 20-55-ms VACIT increase was seen when LAFB accompanied LBBB. Functional LAFB, alone or in combination with bundle branch block, however, did not prolong VACIT in patients with other AP locations. Furthermore, left posterior fascicular block did not produce prolongation of VACI in any of the cases.It is concluded that in patients with the Wolff-ParkinsonWhite syndrome, evaluation of VACT during functional LAFB provides important information regarding AP localization and a clear separation of LFW-AP from all other locations.

The efficacy of cryosurgery alone was evaluated in 15 patients with refractory monomorphic sustained ventricular tachycardias related to inferior wall infarction. Patients were 64 +/- 9 (SD) years old and had a mean left ventricular ejection fraction of 39.2 +/- 11.2%. Thirty different tachycardias were mapped with the origin localized to the septum or inferior wall in 20 (67%), near the mitral valve anulus in 6 (20%) and at the base of the posterior papillary muscle in 4 (13%) tachycardias. Endocardial cryoablation of these sites was performed with 6 to 13 (mean 9.2 +/- 1.8) cryolesions per heart. No mitral valve replacement was performed. There was one postoperative death as a result of sepsis. Cryoablation abolished inducible ventricular tachycardia in 11 patients. Of the other three patients, the tachycardia in two was controlled with a single antiarrhythmic agent that had previously failed to suppress inducible ventricular tachycardia. Thus, clinical success was obtained in 13 (93%) of 14 patients. The remaining patient received an automatic implantable cardioverter defibrillator. Ejection fraction remained unchanged or improved after surgery in 14 patients (93%). There have been no late deaths, recurrence of sustained ventricular tachycardia or significant mitral regurgitation during a mean follow-up period of 19 +/- 7 months. These results compare quite favorably with those previously reported for subendocardial resection alone, and indicate that cryosurgery is highly effective, does not result in deterioration of left ventricular function and preserves mitral valve competence when cryoablation of the posterior papillary muscle is necessary.

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.

Ventricular tachycardia is the commonest underlying mechanism for wide QRS tachycardia. A correct diagnosis can usually be made from clinical and surface electrocardiographic criteria.

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