Majority Of Ventricular Tachycardias Research Articles

Structure and function of the ventricular tachycardia isthmus.

Catheter ablation of postinfarction reentrant ventricular tachycardia (VT) has received renewed interest owing to the increased availability of high-resolution electroanatomic mapping systems that can describe the VT circuits in greater detail, and the emergence and need to target noninvasive external beam radioablation. These recent advancements provide optimism for improving the clinical outcome of VT ablation in patients with postinfarction and potentially other scar-related VTs. The combination of analyses gleaned from studies in swine and canine models of postinfarction reentrant VT, and in human studies, suggests the existence of common electroanatomic properties for reentrant VT circuits. Characterizing these properties may be useful for increasing the specificity of substrate mapping techniques and for noninvasive identification to guide ablation. Herein, we describe properties of reentrant VT circuits that may assist in elucidating the mechanisms of onset and maintenance, as well as a means to localize and delineate optimal catheter ablation targets.

Weathering an Adenosine-Insensitive Right Ventricular Outflow Tract Ventricular Tachycardia Storm in an Adolescent Female: A Case Report

Majority of ventricular tachycardias (VT) are associated with structural disease. However, 10% are idiopathic, such as right ventricular outflow tract (RVOT) VT. A vast majority of RVOT VT demonstrates sensitivity to adenosine, consistent with a triggered mechanism. We present the case of a 15-year-old female patient with palpitations, lightheadedness and dyspnea and a past history of a similar episode of incessant palpitations a month ago, which necessitated electrical cardioversion and amiodarone. On admission, a wide complex tachycardia was documented. Detailed analysis of her wide complex tachycardia showed left bundle branch block (LBBB) morphology, atrioventricular dissociation and positive QRS complexes in inferior leads, suggestive of RVOT VT storm. The patient’s arrhythmia was not responsive to adenosine; hence, adenosine-insensitive RVOT VT was considered. Synchronous cardioversion terminated the tachyarrhythmia. On electrophysiological studies, the VT was induced and localized at the RVOT via 3D-electroanatomical mapping. Radiofrequency ablation of the focus was performed, immediately terminating the tachycardia. The patient was discharged well.

Challenges and Pitfalls of Entrainment Mapping of Ventricular Tachycardia: Ten Illustrative Concepts.

The use and interpretation of entrainment mapping, or continuous resetting, of a reentrant tachycardia has been regarded as the gold standard for delineation of the components of a reentrant circuit.1,2 The response during and after overdrive pacing, whereby 2 wavefronts enter the circuit antidromically (with fusion) and orthodromically, is used to confirm reentry as the arrhythmia mechanism and determine the relationship of the pacing site to the circuit. The fulfillment of classical criteria outlined by Waldo and colleagues3,4 were synthesized into an anatomic concept for scar-related ventricular tachycardia (VT) by Stevenson et al5 to portray the structural and architectural basis of circuit conduction meandering between regions of fibrosis. In this construct, a central corridor, or protected isthmus, is bordered between 2 regions of dense scar with a single entrance that is distinct from a single exit, which yields the QRS morphology.6 This reentrant model has been central to our current mechanistic understanding of scar-mediated VT and is critically important for differentiating critical sites from bystander sites and regions that are unlikely to interrupt or eliminate reentry.7 However, the nature of reentrant VT in man is more complex than our idealized working construct for many reasons. In clinical practice, the majority of VT is hemodynamically unstable, which precludes the ability to perform entrainment mapping and activation mapping of the entire circuit.8 Differences in the circuit between patients with untolerated and tolerated VT are not well understood. VT circuits are 3 dimensionally complex with transmural conduction and circuit conduction is unlikely to be planar, as depicted by electroanatomic mapping of the myocardial surface. Exits may be multiple9,10 and patterns other than loop reentry around scar are likely. Channels of preserved myocardium are frequently not “normal” in voltage (>1.5 mV) …

Reasons for Recurrent Ventricular Tachycardia After Catheter Ablation of Post-Infarction Ventricular Tachycardia

The purpose of this study was to assess the determinants of ventricular tachycardia (VT) recurrence in patients who underwent VT ablation for post-infarction VT. The factors that predict recurrence of VT after catheter ablation in patients with prior infarctions are not well described. Catheter ablation was performed in 98 consecutive patients (88 males [90%]; mean age 67 ± 10 years; ejection fraction 27 ± 13%) with post-infarction VT. Electrograms from the implantable cardioverter-defibrillator were analyzed, and VTs were classified as clinical, nonclinical, or new clinical. A total of 725 VTs were induced during the ablation procedure. All VTs were targeted. In 76 patients, 105 clinical VTs were inducible. Critical sites were identified with entrainment mapping and pace-mapping (≥10 of 12 matching leads) for 75 of 105 clinical VTs (71%) and for 278 of 620 nonclinical VTs (45%). Post-ablation, the clinical VT was not inducible in any patient, and all VTs were rendered noninducible in 63% of the patients. Over a mean follow-up period of 35 ± 23 months, 65 of 98 patients (66%) had no recurrent VTs and 33 (34%) had VT recurrence. A new VT occurred in 26 of 33 patients (79%), and a prior clinical VT recurred in 7 patients (21%). Patients with recurrent VT had a larger scar area as assessed by electroanatomic mapping compared with patients without recurrent VTs (93 ± 40 cm(2) vs. 69 ± 30 cm(2); p = 0.002). In patients with repeat procedures, the majority of inducible VTs for which a critical area could be identified were at a distance of 6 ± 3 mm to the prior ablation lesions. Patients with recurrent VTs have a larger scar as assessed by electroanatomic mapping. Most recurrent VTs were new, and the majority of these VTs were mapped to the vicinity of prior ablation lesions in patients with repeat procedures.

Catheter Ablation of Ventricular Tachycardia

The majority of ventricular tachycardias (VTs) occurs in patients with structural heart disease, predominantly coronary heart disease. Implantable cardioverter defibrillators (ICDs) are first-line therapy in patients with VT and structural heart disease. In patients who receive an ICD after a spontaneous sustained VT, recurrent VT episodes or an electrical storm are major problems. In addition, in patients with an ICD implanted for primary prevention of sudden cardiac death, 20% will experience at least one VT episode within 3-5 years after ICD implantation. Catheter ablation has a high acute success rate in eliminating clinical VT. However, several factors make catheter ablation of VT more difficult than ablation of supraventricular tachyarrhythmias. (1) The infarct region is often large. (2) The induced VT can be unstable or hemodynamically only poorly tolerated and therefore "unmappable". (3) Though most commonly located in the subendocardium, the critical VT zone can occasionally be epicardial or intramural in location. (4) In many cases, several reentrant circuits may coexist making ablation of a single form of VT a palliative procedure which does not obviate the risk of sudden death. Thus, catheter ablation of sustained VT in the setting of structural heart disease can only be considered an adjunctive therapy which, in general, will require ICD therapy. Numerous "modern" mapping technologies have been developed, which have increased success rates of catheter ablation of VT in patients with and without structural heart disease. The aim of the present article is to review current three-dimensional mapping systems in comparison to conventional mapping and to describe a reasonable, tailored approach for the individual patient with VT.

Ventricular Tachycardia in Patients With Normal Hearts

Ventricular tachycardia or ventricular fibrillation can occur in patients with structurally normal hearts. Up to 10% of patients with ventricular tachycardia may have a structurally normal heart. The incidence of idiopathic ventricular fibrillation is less well defined. The prognosis in patients with idiopathic ventricular tachycardia is generally good, but some patients may have a more malignant course with syncope or even rare sudden death. The majority of ventricular tachycardias in patients with structurally normal hearts arise from the right ventricular outflow tract, but up to one-third of these ventricular tachycardias may arise from other right or left ventricular sites. The mechanism of these arrhythmias is not well understood and may be multifactorial, including triggered activity, abnormal automaticity, and reentry. Some left ventricular tachycardias are fascicular tachycardias. Treatment of idiopathic ventricular tachycardia is recommended for symptomatic patients; various therapeutic strategies are reviewed in this article. Catheter ablation appears to be very promising therapy and may be curative in over 90% of patients. In fact, radiofrequency catheter ablation as therapy for symptomatic idiopathic ventricular tachycardia is rapidly becoming early therapy in patients refractory to or intolerant of beta-blockers or calcium channel blockers. (Cardiol Rev 1993;1:6, 336-343)

Localization of breakthrough site of canine monomorphic ventricular tachycardia by pacemapping. A vectorial approach.

The precision and limitations of ventricular pacemapping as a method to localize the site of earliest breakthrough of ventricular tachycardia (VT) were investigated in a canine model of experimental myocardial infarction. Forty-one episodes of VT induced in 10 animals were mapped using a standard grid of 64 endocardial and epicardial bipolar electrodes to determine the site of earliest endocardial or epicardial breakthrough of activation during VT. Each of these 64 recording sites was also used for ventricular pacing during sinus rhythm at cycle lengths comparable to those of the VTs. Orthogonal X, Y, and Z Frank electrocardiographic (ECG) leads were recorded during all episodes of VT and ventricular pacing from all sites after the chest was closed in all animals. Surface ECG waveforms corresponding to each VT and each ventricular pacing were compared pairwise by measuring the Euclidean metric difference between the VT and ventricular pacing vectors with the orthogonal ECG leads as their X, Y, and Z components. The pacing site that generated the vector most similar to VT vector (smallest vectorial difference) was defined as the predicted breakthrough site. This predicted site of breakthrough was identical to the actual site of breakthrough determined by activation sequence mapping during VT for only nine VTs (22%). However, for an additional 27 VTs (66%), the observed and predicted breakthrough locations were at adjacent (1 cm or less apart) recording sites. For five VTs (12%), the two sites were remote, the distance between them exceeding 1 cm. In this model, locating the breakthrough site by pacemapping is exact in only a small minority of VTs. However, when orthogonal surface ECG leads are used for comparison, pacemapping can predict the site of earliest breakthrough during VT with a 1-cm resolution in the majority of VTs.