Treatment of a Patient with an Adenosine-Sensitive Ventricular Tachycardia Using Digoxin

Digitalis and Ventricular Tachycardia. Digoxin was used to treat a patient with an adenosine-sensitive ventricular arrhythmia. The patient had an exercise-induced ventricular tachycardia that was evaluated electrophysiologically and displayed characteristics of a triggered arrhythmia. The tachycardia was terminated reproducibly with 12 mg of intravenous adenosine. After treatment with digoxin (serum level = 1.7 ng/mL), the arrhythmia could no longer be initiated with programmed electrical stimulation or exercise treadmill testing. The patient has since remained symptom free for 10 months. The autonomic effects of digitalis are proposed to mediate drug efficacy in this form of ventricular tachycardia.     

Mechanisms of Idiopathic Left Ventricular Tachycardia

Idiopathic Left Ventricular Tachycardia. Idiopathic left ventricular tachycardia (ILVT) differs from idiopathic right ventricular outflow tract (RVOT) tachycardia with respect to mechanism and pharmacologic sensitivity. ILVT can he categorized into three subgroups. The most prevalent form, verapamil-sensitive intrafascicular tachycardia, originates in the region of left posterior fascicle of the left bundle. This tachycardia is adenosine insensitive , demonstrates entrainment, and is thought to he due to reentry. The tachycardia is most often ablated in the region of the posteroinferior interventricular septum. A second type of ILVT is a form analogous to adenosine- sensitive RVOT tachycardia. This tachycardia appears to originate from deep within the interventricular septum and exits from the left side of the septum. This form of VT also responds to verapamil and is thought to he due to cAMP-mediated triggered activity. A third form of ILVT is propranolol sensitive. It is neither initiated or terminated by programmed stimulation, does not terminate with verapamil, and is transiently suppressed by adenosine, responses consistent with an automatic mechanism. Recognition of the heterogeneity of ILVT and its unique characteristics should facilitate appropriate diagnosis and therapy in this group of patients.     

Radiofrequency Catheter Ablation of Left Ventricular Outflow Tract Tachycardia:

Left Ventricular Outflow Tract Tachycardia. Idiopathic ventricular tachycardia (VT) originating from the left ventricular outflow tract (LVOT) is rare. We report two patients whose QRS configuration during VT commonly showed an inferior axis and monophasic R waves in all the precordial leads. The mechanism of these VTs appeared to be triggered activity. From mapping and ablation, the origin of these VTs was determined to be in the most posterior LVOT, corresponding to the aortomitral continuity (left fibrous trigone).     

Case Report: Adenosine Induced Ventricular Fibrillation in a Patient with Stable Ventricular Tachycardia

Adenosine is frequently used in emergency departments and intensive care units for the termination of narrow complex tachycardias. Recently its utility in terminating wide complex tachycardias has been reported in the literature. Adenosine is generally felt to be a safe medication even though its proarrhythmic effects in the setting of narrow complex or supraventricular tachycardias have been well documented. Herein, we describe the first case to our knowledge of adenosine inducing ventricular fibrillation in a patient with a stable wide complex tachycardia that was subsequently proven to be ventricular tachycardia at electrophysiologic study.     

Ventricular Tachycardia

Congenitally Corrected Transposition and VT. Ventricular tachycardia (VT) is an uncommon finding in patients with congenitally corrected transposition of the great arteries (CCTGA). Cardiac death in patients with CCTGA has been attributed to complete heart block, systemic ventricular dysfunction, or severe AV valve regurgitation with heart failure. We descrihe the case of a patient who presented with palpitations and near-syncope that was associated with clinical episodes of VT. Programmed ventricular stimulation revealed easily inducible sustained VT that immediately degenerated to ventricular fibrillation and subsequently required therapy with an implantable cardioverter defibrillator.     

Surgery for Ventricular Tachycardia

The treatment of drug-refractory chronic ventricular tachycardia (VT) has undergone a revolution over the last 50 years. We now have automatic implantable cardioverter defibrillator therapy with pace-terminating capabilities, and catheter ablation of VT has refined mapping and improved methods of lesion generation. Between 1980 and 1993, Houston Methodist Hospital became a leader in the diagnosis and surgical ablation of VT and other arrhythmias. This is a brief account of that period and some of the experiences and lessons that have led to significant advances used today.     

The Duration of Induced Ventricular Tachycardia as Related to Clinically Sustained Ventricular Tachycardia

Programmed electrical stimulation has been extremely useful in the management of patients with sustained ventricular tachycardia or cardiac arrest. However, the definition of sustained ventricular tachycardia is controversial, and the relationship between the duration of induced ventricular tachycardia and the risk for spontaneous ventricular tachycardia has not been adequately defined. Thus, we examined the records of 64 patients with at least three beats of induced ventricular tachycardia during EP studies using single and double premature stimuli in sinus rhythm and during ventricular paced rhythm (two sites, up to three drive cycle lengths) and using ventricular burst pacing to correlate maximum length of induced ventricular tachycardia with the nature of their spontaneous arrhythmias. Forty-nine patients (77%) had ventricular tachycardia requiring intervention to terminate it, which we called sustained. Nine patients (14%) had ten or fewer beats of ventricular tachycardia; four patients (6%) had 11 to 20 beats of ventricular tachycardia; and two patients (3%) had more than 20 beats of ventricular tachycardia which did not require intervention for termination. Inducible sustained ventricular tachycardia had a sensitivity of 88% and a specificity of 92% for identifying patients with clinical sustained ventricular tachycardia or fibrillation. More than 20 beats of inducible ventricular tachycardia had a sensitivity of 92% and a specificity of 92%. More than 10 beats of inducible ventricular tachycardia achieved a sensitivity of 98% and a specificity of 91% for identifying patients with sustained ventricular tachycardia or fibrillation. The criteria used for the duration of inducible ventricular tachycardia are arbitrary and the interpretation of inducible nonsustained ventricular tachycardia must depend on the purpose of the test and the prior probability of each result.     

Bidirectional Ventricular Tachycardia?

A 65‐year‐old woman was admitted to the hospital because of a syncopal episode with documented transient complete atrioventricular block. A DDD pacemaker was implanted. Post implantation, the patient was diagnosed with bidirectional ventricular tachycardia. Analysis of the arrhythmia and differential diagnosis is performed.     

Idiopathic Left Ventricular Aneurysm: An Unusual Substrate of Ventricular Fibrillation and Ventricular Tachycardia

Idiopathic left ventricular aneurysm (LVA) is a very rare clinical condition. This article describes a patient with idiopathic LVA associated with episodes of ventricular tachycardia and ventricular fibrillation. Clinical and instrumental examinations did not reveal the pathogenesis of the aneurysm. The malignant clinical course suggests that an aggressive antiarrhythmic treatment, including ICD implantation, may be warranted.     

Differential Effects of Adenosine on Focal and Macroreentrant Atrial Tachycardia

INTRODUCTION: The effects of adenosine on atrial tachycardia (AT) remain controversial, and the mechanistic implications of adenosine termination have not been fully established. The purpose of this study was to elucidate the differential effects of adenosine on focal and macroreentrant AT and describe the characteristics of adenosine-sensitive AT. METHODS AND RESULTS: Thirty patients received adenosine during AT. Tachycardia origins were identified as focal or macroreentrant during invasive electrophysiologic studies. Responses to adenosine were analyzed and characterized as tachycardia termination, transient suppression, or no effect. Electrophysiologic studies demonstrated a focal origin of tachycardia in 17 patients. Adenosine terminated focal tachycardias in 14 patients (dose 7.3 +/- 4.0 mg) and transiently suppressed the arrhythmias in three others (dose 10.0 +/- 6.9 mg). A macroreentrant mechanism was demonstrated in 13 patients; adenosine terminated only one of these tachycardias and had no effect on the remaining 12 patients (dose 10.2 +/- 2.9 mg). Four classes of adenosine-sensitive AT were identified. Class I consisted of nine patients with tachycardia arising from the crista terminalis; these tachycardias also terminated with verapamil (4/4). Class II consisted of four patients with repetitive monomorphic AT arising from diverse sites in the right atrium; these either slowed or terminated in response to verapamil (2/2). Class III consisted of the three patients with transient suppression and demonstrated electropharmacologic characteristics consistent with an automatic mechanism, including insensitivity to verapamil (2/2). In the one patient with macroreentrant AT that was comprised of decremental atrial tissue, adenosine terminated tachycardia in a zone of decremental slow conduction (Class IV); this tachycardia slowed with verapamil. CONCLUSIONS: Adenosine-sensitive AT is usually focal in origin and arises either from the region of the crista terminalis (inclusive of the sinus node) or from diverse atrial sites with an incessant nonsustained repetitive pattern. Although most forms of macroreentrant AT are insensitive to adenosine, rarely macroreentrant AT with zones of decremental slow conduction can demonstrate adenosine sensitivity.     

Ablation of Ventricular Tachycardia Due to a Postinfarct Ventricular Septal Defect:

Outer Loop Tachycardia. Introduction : Ventricular tachycardia (VT) alter postinfarct ventricular septal defect (VSD) repair has not been well characterized.
Methods and Results: A 55-year-old man developed refractory VT after inferior wall infarction and VSD repair. Entrainment demonstrated a broad reentry circuit path (outer loop) between the tricuspid annulus and VSD patch. A series of radiofrequency (RF) lesions transected this path, abolishing VI' and producing conduction block between the inferior and superior aspects of the basal right ventricular septum.
Conclusion: Some VTs have broad reentry loops requiring ablation by a series of RF lesions across the path to create a line of block. This approach is analogous to that for atrial flutter.     

Adenosine-Sensitive Bundle Branch Reentry

Adenosine-Sensitive Bundle Branch Reentry. Introduction: Bundle branch reentry is an uncommon mechanism for ventricular tachycardia. More infrequently, both fascicles of the left bundle may provide the substrate for such macroreentrant bundle branch circuits, so-called interfascicular reentry. The effect of adenosine on bundle branch reentrant mechanisms of tachycardia is unknown.
Methods and Results : A 59-year-old man with no apparent structural heart disease and history of frequent symptomatic wide complex tachycardias was referred to our center for further electrophysiologic evaluation. During electrophysiologic study, a similar tachycardia was reproducibly initiated only during isoproterenol infusion, which had the characteristics of bundle branch reentry, possibly using a left interfascicular mechanism. Intravenous adenosine reproducibly terminated the tachycardia. Application of radiofrequency energy to the breakout site from the left posterior fascicle prevented subsequent tachycardia induction and rendered the patient free of spontaneous tachycardia during long-term follow-up.
Conclusions : Patients with ventricular tachycardia involving a bundle branch reentrant circuit may be sensitive to adenosine. These results suggest that adenosine may not only inhibit catecholamine-mediated triggered activity but also some catecholamine-mediated reentrant ventricular arrhythmias.     

Alcohol Ablation of Ventricular Tachycardia

Alcohol Ablation of Ventricular Tachycardia. Ventricular tachycardia that is refractory to medical management has been treated with surgical resection, catheter ablation, and antitachycardia pacemaker. In this case report we describe the use of transcoronary alcohol ablation to treat a patient's ventricular tachycardia. This is accomplished by using ethanol to destroy the site of origin or pathways used in ventricular tachycardia.     

Bundle Branch Reentry Ventricular Tachycardia:

Bundle Branch Reentry VT. We describe a patient with bundle branch reentry ventricular tachycardia with 1:1 VA conduction in whom resetting was performed while obtaining simultaneous recordings from the right ventricular apex (V) and His-bundle electrogram. Both the tachycardia return cycle and the V-His interval demonstrated an increasing reset response, while the His-V interval demonstrated a flat reset response. These reset responses are consistent with a partially excitable gap localizing to the V-His portion of the bundle branch reentry circuit.     

A Case with Occurrence of Antidromic Tachycardia After Ablation of Idiopathic Left Fascicular Tachycardia: Mechanism of Left Upper Septal Ventricular Tachycardia

A 36‐year‐old male presented with verapamil‐sensitive narrow QRS tachycardia. The patient underwent the catheter ablation of common idiopathic left fascicular ventricular tachycardia (ILVT) 2 years ago. During narrow QRS tachycardia, the diastolic and presystolic potentials (P1 and P2) were recorded at the left septum. Activation sequences of P1 and P2 were opposite from those in common ILVT. Entrainment of P1 at the upper septum exhibited concealed fusion and S‐QRS equal to P1‐QRS. Radiofrequency current to P1 suppressed VT. Idiopathic left upper septal VT might be the antidromic macroreentry of the common form of ILVT.     

Epicardial Ablation of Ventricular Tachycardia

Epicardial mapping and ablation via a percutaneous subxiphoid technique has been instrumental in improving the working understanding of complex myocardial scars in various arrhythmogenic substrates. Endocardial ablation alone may not be sufficient in patients with ischemic cardiomyopathy, dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, hypertrophic cardiomyopathy, and Chagas disease to prevent recurrent ventricular tachycardia. Multiple observational studies have demonstrated greater freedom from recurrence with adjunctive epicardial ablation compared with endocardial ablation alone. While epicardial ablation is performed predominantly at tertiary referral centers, knowledge of the technical approach, clinical indications, and potential complications is imperative to maximizing clinical success and patient safety.In 1996, Sosa and colleagues modified the pericardiocentesis technique to enable percutaneous access to the pericardial space for mapping and catheter ablation of ventricular tachycardia.1 Originally developed for patients with epicardial scarring due to chagasic cardiomyopathy and patients with ischemic cardiomyopathy refractory to endocardial ablationm,2,3 this approach has since become an essential part of the armamentarium for the treatment of ventricular tachycardia. Myocardial scars are three-dimensionally complex with varying degrees of transmurality, and the ability to map and ablate the epicardial surface has contributed to a greater understanding of scar-related VT in postinfarction cardiomyopathy and nonischemic substrates including idiopathic dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, hypertrophic cardiomyopathy, and chagasic cardiomyopathy. In this review, we highlight the percutaneous approach and discuss clinical indications and potential complications.     

Adenosine-Sensitive Atrial Reentrant Tachycardia Originating from the Atrioventricular Nodal Transitional Area

Adenosine-Sensitive AT from AVN Area. Introduction : Atrial tachycardia shows wide variations in its electrophysiologic properties and sites of origin. We report an atrial tachycardia with ECG manifestations and electrophysiologic characteristics similar to an atypical form of AV nodal reentrant tachycardia (AVNRT).
Methods and Results : This supraventricular tachycardia was observed in 11 patients. It was initiated by atrial extrastimulation with an inverse relationship between the coupling interval of an extrastimulus and the postextrastimulus interval. Its induction was not related to a jump in the AH interval, and its perpetuation was independent of conduction block in the AV node. Ventricular pacing during tachycardia demonstrated AV dissociation without affecting the atrial cycle length. A very small dose of adenosine triphosphate (mean 3.9 ± 1.2 mg) could terminate the tachycardia. The earliest atrial activation during tachycardia was recorded at the low anteroseptal right atrium with a different intra-atrial activation sequence from that recorded during ventricular pacing, where the tachycardia was successfully ablated in 9 of 10 attempted patients. Bidirectional AV nodal conduction remained unatttched after successful ablation.
Conclusion : There may he an entity of adenosine-sensitive atrial tachycardia probably due to focal reentry within the AV node or its transitional tissues without involvement of the AV nodal pathways. This tachycardia can he ablated without disturbing AV nodal conduction from the right atrial septum.     

Idiopathic Ventricular Tachycardia and Fibrillation

Idiopathic Ventricular Tachycardia and Fibrillation. Important data have recently been added to our understanding of sustained ventricular tachyarrhythmias occurring in the absence of demonstrable heart disease. Idiopathic ventricular tachycardia (VT) is usually of monomorphic configuration and can be classified according to its site of origin as either right monomorphic (70% of all idiopathic VTs) or left monomorphic VT. Several physiopathological types of monomorphic VT can be presently individualized, according to their mode of presentation, their relationship to adrenergic stress, or their response to various drugs. The long-term prognosis is usually good. Idiopathic polymorphic VT is a much rarer type of arrhythmia with a less favorable prognosis. Idiopathic ventricular fibrillation may represent an underestimated cause of sudden cardiac death in ostensibly healthy patients. A high incidence of inducibility of sustained polymorphic VT with programmed ventricular stimulation has been found by our group, but not by others. Long-term prognosis on Class IA antiarrhythmic medications that are highly effective at electrophysiologic study appears excellentJfy Cardiovasc Electrophysiol, Vol. 4, pp. 356–368, June 1993 ).