Cryoablation of ventricular tachycardia guided by return cycle mapping after entrainment

The central common pathway, which is the target for ablation in reentrant ventricular tachycardia, can be localized by entrainment mapping techniques. However, localization of the pathway is not always possible because of the elevated pacing threshold and the low voltage and fractionated potentials at the pathway. We examined whether return cycle mapping after entrainment localizes the pathway without pacing at the pathway or recording the potentials from the pathway and determined the required electrode resolution to localize the pathway. Epicardial mapping was performed with 253 unipolar electrodes during and after entrainment of 13 morphologies of ventricular tachycardia that were induced in dogs 4 days after infarction. The return cycle was calculated by subtracting the first activation time from the second activation time after the last stimulus and the return cycle distribution map was constructed for each stimulation site. The return cycle isochrones equal to the ventricular tachycardia cycle length converged on the lines of conduction block irrespective of the stimulation site, and the central common pathway was localized at the region between the intersections of the return cycle isochrones after entrainment from different stimulation sites. The potentials from the central common pathway were not required to localize the pathway, and the mapping accuracy did not change with or without analysis of the potentials from the pathway. According to the correlation between the electrode resolution and the mapping accuracy, an interelectrode distance of 8.5 mm was estimated as sufficient resolution for successful tachycardia termination during radiofrequency ablation guided by return cycle mapping. Return cycle mapping after entrainment localizes the central common pathway without pacing at the pathway or recording the potentials from the pathway. This new mapping technique could improve the success rate of the ablative procedures.

Structure and function of the ventricular tachycardia isthmus.

Sustained ventricular tachycardia (VT) is an important cause of morbidity and sudden death in patients with heart disease.1 Implantable cardioverter-defibrillators (ICDs) terminate VT episodes, reducing the risk of sudden death. Recurrent VT develops in 40% to 60% of patients who receive an ICD after an episode of spontaneous sustained VT. A first episode of VT occurs in ≈20% of patients within 3 to 5 years after ICD implantation for primary prevention of sudden death in high-risk groups.2–4 ICD shocks reduce quality of life and are associated with an increased risk of death.2–4 Antiarrhythmic drug therapy with amiodarone or sotalol reduces VT episodes but with disappointing incidence of side effects and efficacy.2 Catheter ablation is useful for reducing VT episodes and can be life-saving when VT is incessant.1,5,6 Idiopathic VTs occur in patients without structural heart disease and rarely cause sudden death. Electrophysiological study with catheter ablation is often warranted to confirm the diagnosis, to provide further evidence for the absence of ventricular scar or other disease, and often to cure the arrhythmia. Ablation is also an option for symptomatic nonsustained VT and frequent ventricular ectopy in these patients.1 The appearance of the VT on ECG often suggests its likely cause and associated heart disease (Figure 1). Monomorphic VT has the same QRS complex from beat to beat, indicating repetitive ventricular activation from a structural substrate or focus that can be targeted for ablation. Most are due to reentry through regions of ventricular scar.7 Figure 1. ECG types of VT and most common causes are shown with characteristic ECG features of selected VTs. LBBB indicates left bundle-branch block; LVOT, LV outflow tract; RBBB, right bundle-branch block; L, left; and R, right. Polymorphic VTs have a changing ventricular activation sequence that can be due to …

Options for ventricular tachycardia ablation after double valve replacement

Influence of tachycardia cycle length and antiarrhythmic drugs on pacing termination and acceleration of ventricular tachycardia

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

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

In a randomized, cross-over study we evaluated the efficacy of rate adaptive constant cycle length (BURST) and autodecremental (RAMP) pacing for termination of sustained monomorphic ventricular tachycardia. An external device capable of delivering the same types of antitachycardia pacing as the newer generation implantable cardioverter defibrillators was used. Thirty-one patients with ischemic and nonischemic cardiomyopathy and documented clinical ventricular tachycardia or ventricular fibrillation were examined during routine invasive electrophysiological studies. RAMP and BURST pacing were each attempted in 54 matched pairs of induced ventricular tachycardia. After a therapy was applied, the tachycardia was reinitiated and the other therapy applied during the second episode so that a total of 108 ventricular tachycardia episodes were studied. Overall efficacy of ventricular tachycardia pace termination was 69% and the time required to stop ventricular tachycardia was 14.1 +/- 11.3 seconds. The ability to terminate ventricular tachycardia by RAMP (72%) or BURST (65%) pacing was not significantly different. However, time to terminate ventricular tachycardia by RAMP (11.8 +/- 8.5 sec) was significantly shorter than by BURST (16.4 +/- 13.5), P < .001. Acceleration of ventricular tachycardia was uncommon with both pacing modes, 7/108 (7%). The ability to pace terminate ventricular tachycardia was cycle length dependent. The highest success was with ventricular tachycardia cycle length between 300 and 350 msec. The success rate decreased with faster and also slower ventricular tachycardia. 1. Rate adaptive pacing methods for ventricular tachycardia termination are effective and safe. 2. Autodecremental RAMP pacing afford quicker ventricular tachycardia termination than constant cycle length BURST pacing. 3. The ability to terminate ventricular tachycardia is cycle length dependent with cycle length range of 300-350 msec being most responsive to pace termination.

Ventricular tachycardia reentry circuits in chronic infarct scars can contain slow conduction zones, which are difficult to distinguish from bystander areas adjacent to the circuit during catheter mapping. This study developed criteria for identifying reentry circuit sites using computer simulations. These criteria then were tested during catheter mapping in humans to predict sites at which radiofrequency current application terminated ventricular tachycardia. In computer simulations, effects of single stimuli and stimulus trains at sites in and adjacent to reentry circuits were analyzed. Entrainment with concealed fusion, defined as ventricular tachycardia entrainment with no change in QRS morphology, could occur during stimulation in reentry circuit common pathways and adjacent bystander sites. Pacing at reentry circuit common pathway sites, the stimulus to QRS (S-QRS) interval equals the electrogram to QRS interval (EG-QRS) during tachycardia. The postpacing interval from the last stimulus to the following electrogram equals the tachycardia cycle length. Pacing at bystander sites the S-QRS exceeds the EG-QRS interval when the conduction time from the bystander site to the circuit is short but may be less than or equal to the EG-QRS interval when the conduction time to the circuit is long. The postpacing interval, however, always exceeds the tachycardia cycle length. When conduction in the circuit slows during pacing, the S-QRS and postpacing intervals increase and the slowest stimulus train most closely reflects conduction times during tachycardia. Endocardial catheter mapping and radiofrequency ablation were performed during 31 monomorphic ventricular tachycardias in 15 patients with drug refractory ventricular tachycardia late after myocardial infarction. During ventricular tachycardia, trains of electrical stimuli or scanning single stimuli were evaluated before application of radiofrequency current at the same site. Radiofrequency current terminated ventricular tachycardia at 24 of 241 sites (10%) in 12 of 15 patients (80%). Ventricular tachycardia termination occurred more frequently at sites with entrainment with concealed fusion (odds ratio, 3.4; 95% confidence interval [CI], 1.4 to 8.3), a postpacing interval approximating the ventricular tachycardia cycle length (odds ratio, 4.6; 95% CI, 1.6 to 12.9) and an S-QRS interval during entrainment of more than 60 milliseconds and less than 70% of the ventricular tachycardia cycle length (odds ratio, 4.9; 95% CI, 1.4 to 17.1). Ventricular tachycardia termination was also predicted by the presence of isolated diastolic potentials or continuous electrical activity (odds ratio, 5.2; 95% CI, 1.8 to 15.5), but these electrograms were infrequent (8% of all sites). Combinations of entrainment with concealed fusion, postpacing interval, S-QRS intervals, and isolated diastolic potentials or continuous electrical activity predicted a more than 35% incidence of ventricular tachycardia termination during radiofrequency current application versus a 4% incidence when none suggested that the site was in the reentry circuit. Analysis of the postpacing interval and S-QRS interval suggested that 25% of the sites with entrainment with concealed fusion were in bystander areas not within the reentry circuit. At restudy 5 to 7 days later, 6 patients had no monomorphic ventricular tachycardia inducible, and inducible ventricular tachycardias were modified in 4 patients. None of these 10 patients have suffered arrhythmia recurrences during a follow-up of 316 +/- 199 days, although 4 continue to receive previously ineffective medications. Regions giving rise to reentry after myocardial infarction are complex and can include bystander areas, slow conduction zones, and isthmuses for impulse propagation at which radiofrequency current lesions can interrupt reentry.

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.

Amiodarone Is Poorly Effective for the Acute Termination of Ventricular Tachycardia

Characterization of return cycle responses predictive of successful pacing-mediated termination of ventricular tachycardia

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.

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.

With the development of left ventricular pacing for cardiac resynchronization, there is an interest in the possibility of improving ventricular antitachycardia pacing (ATP) efficacy by pacing from the LV electrode(s). This study assessed the efficacy of pacing delivered from the left coronary vein (LCV) compared to that delivered from the right ventricular apex (RVA) upon ventricular tachycardia (VT) induction and termination. Sixty patients undergoing provocative ventricular electrophysiology (EP) studies in three centers were enrolled. Multipolar EP catheters were placed in the atrium, the RVA, and LCV. VT induction was attempted from the RVA and LCV in random order. Upon detection of monomorphic VT, burst ATP for up to 10 pulses at 88% VT cycle length was delivered from the RVA or LCV, in a random order, and crossed over when possible. Identical VT morphologies were reinduced to allow paired comparison of RVA versus LCV ATP. Data from 55 patients were analyzed. Thirty-four morphologically distinct monomorphic VT types were induced in 22 patients. ATP succeeded in 18 (55%) and VTs in 13 patients. RVA ATP terminated 15 of 23 (65%) VTs, and LCV ATP terminated 10 of 23 (43%) VTs (P = 0.14). ATP delivered ipsilateral to the earliest activation site required 5.0 + or - 2.6 pulses to terminate compared to 4.8 + or - 1.7 pulses when delivered from the contralateral site (P = 0.90). Paired comparison was possible for 13 VT morphologies in 11 patients. Paired RVA and LCV ATP efficacy was identical (54%vs 54%, P = 1.0). ATP delivered from a LCV lead offers no efficacy advantage over pacing from the RVA.