Patrick Tchou

Sustained bundle branch reentry as a mechanism of clinical tachycardia

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 less than 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 less than 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 amendable 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.

Transcatheter electrical ablation of right bundle branch. A method of treating macroreentrant ventricular tachycardia attributed to bundle branch reentry.

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 patients had depressed left ventricular ejection fraction with cardiomegaly. Six of the seven had dilated cardiomyopathy in the absence of significant coronary disease. Twelve-lead electrocardiograms in all seven patients during sinus rhythm were remarkably similar; six demonstrated intraventricular conduction defect resembling left bundle branch block, and one showed left anterior fascicular block. All patients showed prolonged His-to-ventricle intervals during sinus rhythm. Sustained ventricular tachycardia (with atrioventricular dissociation) because of bundle branch reentry was induced in all patients during baseline electrophysiological study. The His-to-ventricle intervals during tachycardia were similar to those seen during sinus rhythm. Electrical ablation of the right bundle branch was accomplished in each patient with delivery of two electrical shocks (170-310 J) through electrode catheters. Right bundle branch block developed on their surface electrocardiogram immediately after the ablation. Follow-up electrophysiological studies showed no inducible ventricular tachycardia. Clinical follow-up showed no recurrence of syncope or ventricular tachycardia. From the data presented, the following can be concluded. First, right bundle branch ablation is a safe and promising means of treating ventricular tachycardia because of bundle branch reentry and can obviate the need for antiarrhythmic drug therapy and its frequent undesirable side effects. Second, there are common clinical and electrophysiological characteristics that are frequently seen in patients with this tachycardia, and the recognition of these common characteristics should alert the physician to a bundle branch reentrant mechanism of ventricular tachycardia.

Echocardiographic demonstration of decreased left ventricular dimensions and vigorous myocardial contraction during syncope induced by head-up tilt

Two-dimensional echocardiography was performed during a head-up tilt test in 11 control subjects (group I) and 18 patients with recurrent unexplained syncope. In four patients (group II), the head-up tilt test was negative at baseline and after isoproterenol infusion. Syncope was induced during baseline head-up tilt in nine patients (group III) and after isoproterenol challenge in five (group IV). The echocardiographic variables assessed were left ventricular end-systolic and end-diastolic areas and percent fractional shortening. At the end of head-up tilt, end-systolic area decreased by 4.5 +/- 1.3 and 3.0 +/- 1.2 cm2 in groups III and IV, respectively, compared with 0.5 +/- 0.7 and 0.2 +/- 0.1 cm2 in groups I and II, respectively (p less than 0.04). Similarly, end-diastolic area decreased by 5.5 +/- 2.6 cm2 in group III compared with 2.7 +/- 1.9 and 1.75 +/- 0.4 cm2 in group I and II, respectively (p less than 0.04). Additionally, at the end of the baseline study, fractional shortening was significantly greater in group III and group IV (43 +/- 5%) than in groups I and II (p less than 0.01). In conclusion, syncope induced by head-up tilt is associated with vigorous myocardial contraction and a significant decrease in left ventricular end-systolic dimensions. This left ventricular hypercontractility may play an important role in the pathogenesis of syncope induced by head-up tilt.

Localization of the fast and slow pathways in atrioventricular nodal reentrant tachycardia by intraoperative ice mapping.

BackgroundAtrioventricular (AV) nodal reentrant tachycardia is classically described as a reentrant rhythm entirely contained within the compact AV node. Although the concepts of longitudinal dissociation of two intranodal pathways and a distal common pathway are accepted, the proximal portion of the circuit remains undefined. Current reports suggest that the two pathways may be separable by atrial tissue and not contained entirely within the compact node. Methods and ResultsWe used an ice mapping method to demonstrate the slow and fast pathways of the reentrant circuit and their relation to the atrial septum around the AV node. Six patients with the usual form (slow-fast) of AV nodal reentrant tachycardia were mapped during surgery. In most patients, antegrade slow pathway localization was posterior and inferior to the compact AV node along the tricuspid annulus; in two patients, it was superior along the tendon of Todaro. Retrograde fast pathway localization was anterior or superior to the compact AV node in all patients. In all patients, anatomic distinction was made between the two pathways and the compact node. ConclusionsWe conclude that no upper common pathway exists within the compact AV node in the usual type of nodal reentrant tachycardia and that the perinodal atrial tissue is a requisite part of the tachycardia circuit.

Useful clinical criteria for the diagnosis of ventricular tachycardia

Misdiagnosis occurs upon initial presentation to medical attention in a considerable number of patients referred for evaluation of wide QRS tachycardia. In order to improve diagnostic accuracy (ventricular versus supraventricular tachycardia), the answers to two key bedside questions were prospectively evaluated: (1) Had the patient experienced a prior myocardial infarction? (2) Did symptoms of tachyarrhythmia start only after the infarction? A patient presenting with a wide QRS tachycardia was considered to have ventricular tachycardia if he or she answered in the affirmative to both of these questions. Of 31 consecutive patients referred with electrocardiographically documented sustained wide QRS tachycardia that was reproduced in the electrophysiology laboratory, the diagnoses made when the patients first presented to medical attention were ventricular tachycardias in 17 patients and supraventricular tachycardias in 14 patients. Following electrophysiologic evaluation, 29 were diagnosed as having ventricular tachycardia and two as supraventricular tachycardia. If the diagnoses were made solely on the basis of responses to the bedside questions mentioned earlier, 28 of the 29 patients having a final diagnosis of ventricular tachycardia would have been correctly identified. It is concluded that the use of these two questions can be very helpful in improving the clinical diagnosis of ventricular tachycardia.

Psychological Support and Psychiatric Management of Patients with Automatic Implantable Cardioverter Defibrillators

There are well over 6, 000 automatic implantable cardioverter defibrillators (AICD) that have been implanted in the United States since 1980. The device clearly reduces arrhythmic mortality in high risk patients. Many AICD patients have other cardiac diseases, most commonly, coronary artery disease with associated prior myocardial infarctions. These patients have special psychosocial stresses that may make them vulnerable to depression and other psychological disturbances. Psychological support together with psychiatric treatment, if needed, should be provided to these patients. Use of psychotropic medications should be closely monitored, especially in this population, as many of these drugs can exacerbate ventricular tachyarrhythmias. Special precautions should also be taken when administering electroconvulsive therapy in these patients.

Efficacy of cryosurgery alone for refractory monomorphic sustained ventricular tachycardia due to inferior wall infarction.

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.

Incidence and clinical significance of ventricular fibrillation induced with single and double ventricular extrastimuli

Of 718 patients evaluated for suspected or documented ventricular tachyarrhythmias, ventricular fibrillation (VF) was induced in 28 (incidence 3.9%) by single and double extrastimuli. Nine of the 28 patients had suspected but no clinically documented ventricular tachycardia (VT) or VF (group 1), 11 had documented VT (group 2) and 8 had out of hospital VF (group 3). In group 1, electropharmacologic control was achieved in 8 patients with the initial agent tested; however, symptoms recurred in 6 patients. In 4 patients the drug was discontinued. After a follow-up of 26 +/- 11 months in group 1, no patient had died. In only 2 of 19 patients in groups 2 and 3 were arrhythmias controlled with the initial agent; 15 patients had VT and 2 VF. Control with class I agents was achieved in 9 of 19 patients and none died until the drug regimen was changed empirically in 3 of these 9. Ten patients, all from groups 2 and 3, were treated empirically with amiodarone; 3 died. All patients died either suddenly or in VT. The mortality rate in groups 2 and 3 after a mean follow-up of 24 +/- 9 months was 32% (p less than 0.05). Continued symptoms and no deaths in group 1 suggests a nonclinical nature of induced VF. Control of induced VF on serial drug testing in group 2 and 3 also indicates a false-negative drug efficacy response, as pharmacologic control of emergent VT on subsequent studies appeared essential to their survival despite control of induced VF. Thus, even with single or double premature stimuli, induction of VF can be a nonclinical response, especially in patients without clinical VF.

Development of a Construct of Psychological Dependency in Patients with the Automatic Implantable Cardioverter Defibrillator: A Quality of Life Issue

Cardiologists involved with implantation and continuous follow-up of patients implanted with the automatic implantable cardioverter defibrillator (AICD) have begun to question how the patient interacts psychologically with the device. Research to date on the psychological complications of AICD implantation has been sparse. A retrospective, descriptive study was designed to structure and assess the numerous variables associated with AICD implantation and psychosocial outcome.