Ventricular tachycardia termination in a 70-year-old female with arrhythmogenic right ventricular cardiomyopathy.

It is generally accepted that the diagnosis of an epicardial origin of ventricular tachycardia (VT) can be made indirectly by observing VT termination during ablation on the epicardial surface of the heart. There is a caveat, however, which is that termination of VT during radiofrequency current application on the epicardial surface could be due to extension of the lesion beyond the epicardium. Therefore, successful ablation of VT using an epicardial approach does not necessarily prove the reentrant circuit is located superficially. We present a case of a 44-year-old man with VT storm who demonstrated successful termination of VT with radiofrequency current application on the epicardial surface of the heart. This site corresponded to a site where pacing during VT resulted in termination of VT without global capture. Isolated mid-diastolic potentials were only seen at this site as well. We hypothesize that the finding of termination of VT by pacing without global capture supports the argument that the site of pacing is a critical part of the VT circuit.

Effects of intravenous adenosine on verapamil-sensitive “idiopathic” ventricular tachycardia

Amiodarone Is Poorly Effective for the Acute Termination of Ventricular Tachycardia

Based on epicardial mapping, different mechanisms of termination of reentrant ventricular tachycardia by various pharmacological interventions are described. In 40 Langendorff-perfused rabbit hearts, rings of anisotropic left ventricular epicardium were made by a cryoprocedure. Sustained monomorphic ventricular tachycardia based on continuous circus movement of the impulse around the ring was induced by programmed stimulation. Increasing doses of heptanol (n = 10), potassium (n = 10), tetrodotoxin (n = 6), RP62719 (a new class III drug) (n = 4), flecainide (n = 5), and propafenone (n = 5) were administered to terminate ventricular tachycardia. Epicardial mapping (248 points) was used to study the mechanism of termination of ventricular tachycardia. In 28 of 40 hearts, ventricular tachycardia terminated because the drugs produced complete conduction block of the impulse in a segment of the reentrant pathway. In the remaining 12 hearts (heptanol, n = 2; potassium, n = 3; tetrodotoxin, n = 2; RP62719, n = 2; flecainide, n = 1; and propafenone, n = 2), termination of ventricular tachycardia occurred by collision of the circulating impulse with a spontaneous antidromic wave front reflected within the circuit. This phenomenon occurred when the circulating impulse encountered an arc of functional conduction block that did not extend along the whole width of the ring. As a result, the impulse dissociated into a continuing orthodromic circulating wave and a returning antidromic echo-wave caused by microreentry within the ring. Independent of their mechanisms of action, sodium channel blockers, electrical uncouplers, and class III drugs terminate reentrant ventricular tachycardia either by complete conduction block or by collision of the impulse with an echo-wave.

Evaluation of intravenous lidocaine for the termination of sustained monomorphic ventricular tachycardia in patients with coronary artery disease with or without healed myocardial infarction

Although multi-detector computed tomography (MDCT) and cardiac magnetic resonance (CMR) can assess the structural substrate of ventricular tachycardia (VT) in ischemic cardiomyopathy (ICM), non-ICM (NICM), and arrhythmogenic right ventricular cardiomyopathy (ARVC), the usefulness of systematic image integration during VT ablation remains undetermined. A total of 116 consecutive patients (67 ICM; 30 NICM; 19 ARVC) underwent VT ablation with image integration (MDCT 91%; CMR 30%; both 22%). Substrate was defined as wall thinning on MDCT and late gadolinium-enhancement on CMR in ICM/NICM, and as myocardial hypo-attenuation on MDCT in ARVC. This substrate was compared to mapping and ablation results with the endpoint of complete elimination of local abnormal ventricular activity (LAVA), and the impact of image integration on procedural management was analyzed. Imaging-derived substrate identified 89% of critical VT isthmuses and 85% of LAVA, and was more efficient in identifying LAVA in ICM and ARVC than in NICM (90% and 90% vs. 72%, P < 0.0001), and when defined from CMR than MDCT (ICM: 92% vs. 88%, P = 0.026, NICM: 88% vs. 72%, P < 0.001). Image integration motivated additional mapping and epicardial access in 57% and 33% of patients. Coronary and phrenic nerve integration modified epicardial ablation strategy in 43% of patients. The impact of image integration on procedural management was higher in ARVC/NICM than in ICM (P < 0.01), and higher in case of epicardial approach (P < 0.0001). Image integration is feasible in large series of patients, provides information on VT substrate, and impacts procedural management, particularly in ARVC/NICM, and in case of epicardial approach.

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) …

Catheter ablation guided by termination of postinfarction ventricular tachycardia by pacing with nonglobal capture

Endocardial or epicardial ventricular tachycardia in nonischemic cardiomyopathy? The role of 12-lead ECG criteria in clinical practice

Cryoablation of ventricular tachycardia guided by return cycle mapping after entrainment

Ventricular tachycardias can be terminated by a variety of pacemaker techniques, including rapid and slow stimulation. Fast tachycardias are typically poorly tolerated, and require prompt intervention, usually with rapid pacing. Termination of ventricular tachycardia by slow or single capture pacemaker stimulation techniques is attractive, because of its presumed safety and the possibility of using simple implantable pacers. To identify factors favoring termination, single capture stimulation was used in 390 episodes of ventricular tachycardia in 21 patients, 16 with coronary artery disease, able to tolerate ventricular tachycardia for several minutes. Single capture stimulation terminated 223 episodes (57%) in 18 patients, and two were accelerated. Of 157 episodes exposed to 2-3 programmed extrastimuli or rapid pacing 149 (94%) were terminated and 7 were accelerated. Direct current cardioversion was needed in 12 episodes. Without medications, only two patients tolerated VT. Only one patient had reliable termination with single capture stimulation over several days. Systolic blood pressure was similar in episodes terminated and not terminated by single capture stimulation, but the ventricular rate was significantly lower in episodes terminated, 116 +/- 19 vs. 1.33 +/- 24 (p less than 0.001). Termination of ventricular tachycardia was not affected by QRS morphology. Single capture termination of ventricular tachycardia is largely unpredictable, with limited reproducibility over a period of time. Although comparatively safe, single capture techniques are not likely to prove useful in the long-term treatment of many patients with recurrent ventricular tachycardia.

To define the electrophysiological basis for the termination of ventricular tachycardia (VT), three-dimensional cardiac mapping and analysis of the terminal beats of nonsustained VT and beats of sustained VT were performed in six patients with healed myocardial infarcts. Termination of VT was due to activation from multiple initiation sites that were discordant from those responsible for the maintenance of sustained VT in 45% of cases, to repetitive activation from single sites that were discordant from those responsible for the maintenance of sustained VT in 24% of cases, or to activation from sites concordant with the sites of repetitive activation during sustained VT in 31% of cases. Sustained VT was characterized by occasional shifting of initiation sites, even after the tachycardia entered the stable monomorphic phase. Mapping was of sufficient density to define the mechanisms for 21 terminating beats of VT. In 5 cases, termination was due to intramural reentry, which initiated with the total activation time of the preceding beat of 204 +/- 11 milliseconds (ms) but terminated primarily because of a decrease in total activation time (144 +/- 23 ms, P = .03) that was associated with the development of intramural conduction block or with significant changes in the activation sequence along the reentrant circuit. In 16 cases, terminal beats were initiated by a focal mechanism on the basis of the absence of intervening electrical activity from the termination of the preceding beat to the initiation of the terminating beat (172 +/- 9 ms). Focal activation was associated with less conduction delay of the preceding beat (115 +/- 6 ms) than terminating reentrant beats (P < .001) and usually terminated suddenly without oscillations in cycle length or total activation time. Termination of VT is associated with alterations in initiation sites that are most often discordant from those maintaining sustained VT and is due to either reentrant or focal mechanisms.

In order to evaluate the potential use of external cardiac pacing (EXP) in the clinical termination of sustained ventricular tachycardia (VT), we attempted VT terminations in seven patients. All had recurrent sustained monomorphic ventricular tachycardia (mean rate 145 beats/min), which had previously required cardioversion. During subsequent VT episodes, all seven underwent overdrive pacing with EXP at a pulse amplitude of 120 mA, and rates of 200 pulses/min. A total of 18 of 18 episodes of VT were successfully terminated by EXP alone. In one patient, the first attempt at EXP termination of one episode of VT resulted in an acceleration of the tachycardia, which was then terminated by EXP. All patients tolerated EXP well with minimal sedation. We conclude that EXP may be an effective clinical modality for the termination of sustained monomorphic ventricular tachycardia.

Termination of ventricular tachycardia by low-energy shocks delivered during the ventricular refractory period has been reported. We describe a case of reproducible termination of multiple episodes of sustained ventricular tachycardia by a low-current extrastimulus delivered during the effective refractory period of the right ventricle, from the distal bipole of a quadripolar electrode catheter.

High-energy defibrillation shock is the only therapy for ventricular tachyarrhythmias. However, because of adverse side effects, lowering defibrillation energy is desirable. We investigated mechanisms of unpinning, destabilization, and termination of ventricular tachycardia (VT) by low-energy shocks in isolated rabbit right ventricular preparations (n = 22). Stable VT was initiated with burst pacing and was optically mapped. Monophasic "unpinning" shocks (10 ms) of different strengths were applied at various phases throughout the reentry cycle. In 8 of 22 preparations, antitachycardia pacing (ATP: 8-20 pulses, 50-105% of period, 0.8-10 mA) was also applied. Termination of reentry by ATP was achieved in only 5 of 8 preparations. Termination by unpinning occurred in all 22 preparations. Rayleigh's test showed a statistically significant unpinning phase window, during which reentry could be unpinned and subsequently terminated with E80 (magnitude at which 80% of reentries were unpinned) = 1.2 V/cm. All reentries were unpinned with field strengths < or = 2.4 V/cm. Unpinning was achieved by inducing virtual electrode polarization and secondary sources of excitation at the core of reentry. Optical mapping revealed the mechanisms of phase-dependent unpinning of reentry. These results suggest that a 20-fold reduction in energy could be achieved compared with conventional high-energy defibrillation and that the unpinning method may be more effective than ATP for terminating stable, pinned reentry in this experimental model.