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.     

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 ).     

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.     

Adenosine-Sensitive Ventricular Tachycardia:

Adenosine-Sensitive VT. Idiopathic ventricular tachycardia (VT) is a term that refers to tachycardia that arises from ventricles devoid of apparent structural abnormalities. This form of VT is now recognized to be related to several distinct entities and includes a reentrant form typically located in the region of the left posterior fascicle, an automatic form that may originate from either ventricle, and a form that originates from the right ventricular outflow tract. This last type can account for up to 80% of cases of idiopathic VT and with few exceptions can be further subdivided into repetitive monomorphic VT and paroxysmal stress-induced VT, Evidence has accumulated suggesting that both forms of VT are related to cAMP-mediated triggered activity. The experimental underpinnings of this conclusion as well as the clinical characteristics of this form of idiopathic VT are elucidated in this review.     

Regular Wide QRS Complex Tachycardia During Atrial Fibrillation in a Patient with Preexcitation Syndrome: A Case Report

AV Conduction in WPW. We report an unusual case of a relatively regular wide QRS complex tachycardia alternating with periods of an irregular narrow QRS complex tachycardia during atrial fibrillation in a patient with Wolff-Parkinson-White syndrome. Both tachycardias resulted from atrial fibrillation, the wide QRS complex tachycardia being due to 2:1 AV conduction of a type I atrial fibrillation across a posteroseptal accessory AV connection.     

Case Report: Spontaneous Atriofascicular Pathway Automaticity Simulating Ventricular Tachycardia

Atriofascicular pathways most commonly present electrocardiographically as an antidromic reciprocating AV reentrant tachycardia. We report the case of a child who presented in infancy with a wide QRS complex tachycardia thought to be supraventricular tachycardia with aberrant conduction, associated with tachycardia-induced cardiomyopathy. Later in life the same patient represented with episodes of palpitations secondary to a wide QRS complex tachycardia, thought to be ventricular tachycardia. Electrophysiologic mapping demonstrated the origin of the wide QRS complex tachycardia was from automatic activity originating from a right anterolateral atriofascicular pathway, which also participated in a reentrant antidromic AV reciprocating tachycardia. Radiofrequency ablation of the atriofascicular pathway successfully eliminated both arrhythmias. The mechanism of the wide QRS complex tachycardia appeared to result from spontaneous automaticity of the atriofascicular pathway.     

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.     

Suppression of Ventricular Tachycardia With Dronedarone: A Case Report

Suppression of Ventricular Tachycardia With Dronedarone . Introduction: Dronedarone is a multichannel blocker with similar electrophysiological properties to amiodarone. Dronedarone has not been studied in humans as an agent to suppress ventricular arrhythmias. Methods: This case report describes the dramatic antiarrhythmic effects of dronedarone in a patient with nonischemic cardiomyopathy and recurrent ventricular tachycardia, which was resistant to multiple antiarrhythmic agents and endocardial catheter ablation. Results: Dronedarone was effective in completely suppressing ventricular tachycardia. Conclusion: Further research is needed to establish a potential larger role for dronedarone in controlling ventricular arrhythmias in humans. (J Cardiovasc Electrophysiol, Vol. 22, pp. 201‐202, February 2011)     

Clinical Results with Catheter Ablation: AV Junction, Atrial Fibrillation and Ventricular Tachycardia

With the limitations of pharmacologic and device therapies for atrial fibrillation and ventricular tachycardia, catheter ablation is assuming a larger role in the management of patients with these common arrhythmias. Multiple case series and clinical trials have helped to define the evolving role of these techniques for ablation of the atrioventricular node, atrial fibrillation, and ischemic ventricular tachycardia. Based on very low complication rates, excellent efficacy and proven outcomes with radiofrequency ablation of the atrioventricular node, this approach with permanent pacing should play a larger role in the treatment of symptomatic patients with permanent atrial fibrillation. While linear ablation of atrial fibrillation has limited clinical utility for the treatment of this common arrhythmia, the results of multiple case series of focal atrial fibrillation ablation indicate the potential for an expanding role of this curative technique. Catheter ablation techniques for ventricular tachycardia in the setting of coronary artery disease have a role as supplemental therapy to the implantable cardioverter defibrillator in patients with recurrent pharmacologically refractory ventricular arrhythmias requiring frequent device interventions.     

Stability: An ICD Detection Criterion for Discriminating Atrial Fibrillation From Ventricular Tachycardia

Stability, An ICD Detection Criterion. introduction: The purpose of this study was to review a new implantable cardioverter defibrillator (ICD) detection criterion, stability, to determine if it can effectively discriminate rapid rhythms of atrial fibrillation from ventricular tachycardia. Inappropriate shocks for rapid atrial fibrillation limit the acceptance of ICDs. The advent of an additional detection criterion, stability, has been postulated to be of value in discriminating rapid atrial fibrillation, which may not warrant treatment, from ventricular tachycardia, which obviously does warrant therapy delivery. Methods and Results: Twenty-six patients were studied during 32 episodes of rapid atrial fibrillation and 24 episodes of monomorphic ventricular tachycardia below 220 beats/min. Each rhythm was repeatedly evaluated by the device at each of the seven stability values available (8, 16, 23, 31, 39, 47, and 55 msec) and then classified as stable or unstable. Upon completion of this acute study, 32 ICD patients bad the stability feature activated and were followed for proper arrhythmia treatment by the device. Using stability windows from 8 to 47 msec, all atrial fibrillation rhythms were appropriately classified as unstable. Three of 6 were classified correctly for the 55-msec window. All ventricular tachycardia rhythms were appropriately classified as stable for all stability windows from 8 to 55 msec. Clinical follow-up confirmed appropriate therapy delivery when coupled with sustained rate duration (SRD). Thirty-two patients followed for 292 patient-months had no episodes of untreated ventricular tachycardia with 428 successfully classified as stable and treated. Only three episodes of suspected atrial fibrillation resulted in therapy delivery as the rhythm duration exceeded the SRD of 30 seconds. Conclusions: The CPI Ventak PRx ICD is highly reliable in appropriately classifying atrial fibrillation as unstable and monomorphic ventricular tachycardia as stable for most stability windows evaluating tachycardias below 220 beats/min. As a result, when testing of atrial fibrillation is not possible, we recommend the routine programming of this stability feature at the 31-msec window with an SRD of 30 seconds. The reliability of this device in discriminating atrial fibrillation from monomorphic ventricular tachycardia may have important clinical implications for other tiered therapy ICDs with this feature as well as for future ICDs in development.     

Parenteral Antiarrhythmic Drug Therapy in Ventricular Tachycardia/Ventricular Fibrillation: Evolving Role of Class III Agents—Focus on Amiodarone

Intravenous Amiodarone. More effective intravenous antiarrhythmic agents are required for treatment of patients with refractory malignant ventricular arrhythmias. More recently, a great deal of interest has been focused on use of intravenous amiodarone for these patients. Uncontrolled early studies showed that intravenous amiodarone was effective in 42% to 81% of treated patients. Recent large cooperative trials have documented the efficacy of intravenous amiodarone in these patients and have shown an efficacy comparable to bretylium in patients with refractory sustained ventricular tachycardia or fibrillation.     

Ventricular Fibrillation Resulting from Synchronized Internal Atrial Defibrillation in a Patient with Ventricular Preexcitation

VF After Synchronized Internal Atrial Defibrillation. This case describes ventricular proarrhythmia as a result of a synchronized internal atrial defibrillation shock in a 29-year-old man with Ebstein's anomaly referred for radiofrequency ablation of a right posterior accessory pathway. During the electrophysiologic study, atrial fibrillation was induced and 3/3 msec shocks of various strengths were delivered between two decapolar defibrillation catheters in the coronary sinus and right atrial appendage. A 2.0-J biphasic shock synchronized to an R wave after a short-long-short ventricular cycle length pattern with a preshock coupling interval of 245 msec induced ventricular fibrillation, which was externally defibrillated with 200 J. This observation has implications for the development of implantable atrial defibrillators.     

Radiofrequency Ablation of Ventricular Fibrillation and Multiple Right and Left Atrial Tachycardia in a Patient with Brugada Syndrome

Brugada syndrome is a well-known form of idiopathic ventricular fibrillation (VF). Few data suggest that this arrhythmia may be triggered by ventricular premature beats (VPBs), and an association with other arrhythmia such as monomorphic ventricular tachycardia (VT) or supraventricular tachycardia (SVT) has been reported. In a highly symptomatic 18-year-old-male patient with this syndrome, frequent episodes of VF, fast polymorphic VT, and fast monomorphic sustained regular tachycardia were observed. The tachycardia episodes were classified as VT or VF and as a consequence received appropriate therapies with the implanted cardioverter defibrillator (ICD). Precipitating VPBs that were stored in the ICD memory and on the electrocardiogram (ECG) exhibited the same morphology as frequent isolated VPBs. During the electrophysiological study, right and left atrial tachycardia (AT) with one-to-one atrioventricular conduction were also induced and successfully ablated. VF was ablated using the same noncontact mapping (NCM) system triggering VPBs from right ventricular outflow tract (RVOT).     

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.     

Ventricular Tachycardia in Patients with Impaired Left Ventricular Function: The Role of Propafenone

The combined occurrence of left ventricular dysfunction and -ventricular tachyarrhythmias portends a high annual mortality. Anti arrhythmic drugs can ameliorate ventricular arrhythmia and may reduce the risk of sudden cardiac death. We administered propafenone to 15 patients with ventricular tachyarrhythmias and left ventricular ejection fractions 40%. Propafenone significantly reduced isolated ventricular premature depolarizations, couplets, and ventricular tachycardia on ambulatory monitoring. Propafenone eliminated all exercise provocable ventricular tachycardia. Propafenone additionally abolished ventricular tachycardia inducible by programmed stimulation in 4 of 7 patients. In 8 patients studied before and during therapy, there was no significant change in left ventricular ejection fraction as determined by nuclear ventriculography. Propafenone was discontinued in 4 patients due to side effects. Seven patients receiving continuing propafenone therapy remain alive with only one patient suffering arrhythmia recurrence. Propafenone is an effective drug for the management of ventricular tachyarrhythmias and may be used for patients with impaired left ventricular function.