Termination of Epicardial Left Ventricular Tachycardia by Pacing without Global Capture

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.

Electroanatomical mapping–guided stereotactic radiotherapy for right ventricular tachycardia storm

Clinical Case: A 53-year-old male patient was referred to our center for the management of severe electrical storm (ES). The patient experienced 76 appropriate shocks within 30 minutes delivered from his implantable cardioverter-defibrillator as a result of recurrent ventricular tachycardia (VT) occurring just after retiring to his hotel room at the end of an uneventful business meeting. The implantable cardioverter-defibrillator was implanted 16 years ago when the patient presented with syncope and had inducible VT at an electrophysiological study. Coronary artery disease was ruled out at that time with coronary angiography. However, the systolic function of the left ventricle was moderately impaired, with an ejection fraction of 38% measured by echocardiography, which also revealed regional wall motion abnormalities. This nonischemic cardiomyopathy was attributed to remote myocarditis. When presenting with ES, the patient was admitted at first to the intensive care unit of the local university hospital. A 12-lead ECG showed monomorphic VT of 188 bpm (Figure 1A). Ventricular tachyarrhythmia was stabilized acutely by sequential drug application of β-blockers, amiodarone, and lidocaine as well as sedation followed by endotracheal intubation under general anesthesia. After the initial cooling-down phase, the patient was transferred to our center for further management. To prevent more episodes of ES and to avoid long-term use of amiodarone with the risk of potentially severe adverse effects, catheter ablation was performed. Figure 1. A , Twelve-lead ECG showing a monomorphic ventricular tachycardia (VT) with inferior axis, Q wave present in lead I and absent in lead aVF, right bundle-branch block pattern with positive QRS complex in V1 through V3 and negative in V4 through V6, and with a pseudo δ-wave and late intrinsicoid deflection, suggesting a left lateral midventricular epicardial origin. B , Stepwise management of electrical storm. Application of different steps should be individualized for …

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) …

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.

Background: Aberrant diastolic Ca2+leak through the cardiac ryanodine receptor (RyR2) is an important cause of heart failure (HF) and lethal arrhythmia. Dantrolene (DAN) specifically binds to the Leu601-Cys620 of N terminal domain in RyR2 and stabilizes the tetrameric structure of RyR2, preventing the Ca2+ leak through RyR2. Our previous study as a proof-of-concept showed that intravenous injection (i.v.) of DAN was effective in termination and prevention of refractory ventricular tachycardia (VT) storm in HF. Research Question: How much is loading dose of DAN i.v. to terminate VT storm in HF? We hypothesized that the optimal dose was within 3mg/kg from our previous study. Aim: This study aimed to verify that 3mg/kg DAN i.v. was optimal for the termination of amiodarone-resistant VT storm in HF. Methods: This was an open-label, uncontrolled, single-center study. The detail in the study design and methods is shown in Fig.1. We studied patients with episodes of VT storm regardless of medications, such as amiodarone and beta-blockers, recommended by HF guidelines. DAN(3mg/kg) was intravenously added on the above guideline treatment. The acute anti-arrhythmic efficacy of DAN was assessed as follows: 1) proportion of patients whose VT storm was terminated by 3mg/kg DAN i.v., 2) incidence rate of VT storm within 24 hours before and after DAN i.v.. Results: The consecutive 7 patients with refractory VT storm were enrolled in this study (median age:72 years old, male/female: 4/3, median LVEF29%). Underlying heart disease included 3 ischemic cardiomyopathy, 3 acute myocardial infarction after successful percutaneous coronary intervention and 1 tachycardia-induced cardiomyopathy. 2 of 7 patients underwent mechanical circulatory support before DAN i.v. because of pulseless VT. All patients were classified as NYHA class III/IV. 3 mg/kg of DAN i.v. ceased VT storm within 60 min in 7/7 (100%) (Fig.2, left). The number of sustained VT within 24 h after DAN i.v. were significantly lower than those within 24 h prior to DAN administration (Fig 2, right). A representative case is shown in Fig.3 The VT storms refractory to amiodarone and landiolol (beta-blocker) as well as sedation showed complete response to 3mg/kg DAN i.v.. Conclusions: DAN, a RyR2 stabilizer, was effective in the termination of VT storm in HF resistant to guideline directed medical treatment. This is the first study to evaluate the optimal dose of DAN i.v. against the refractory VT storm in HF.

Catheter ablation of ventricular tachycardia with radiofrequency currents, with special reference to the termination and minor morphologic change of reinduced ventricular tachycardia

To study electrophysiological characteristics that enable the identification and ablation of sites of chagasic tachycardia. Thirty-one patients with chronic Chagas' heart disease and sustained ventricular tachycardia (SVT) underwent electrophysiological study to map and ablate that arrhythmia. Fifteen patients had hemodynamically stable SVT reproducible by programmed ventricular stimulation, 9 men and 6 women with ages ranging from 37 to 67 years and ejection fraction varying from 0.17 to 0.64. Endocardial mapping was performed during SVT in all patients. Radiofrequency (RF) current was applied to sites of presystolic activity of at least 30 ms. Entrainment was used to identify reentrant circuits. In both successful and unsuccessful sites of RF current application, electrogram and entrainment were analyzed. Entrainment was obtained during all mapped SVT. In 70.5% of the sites we observed concealed entrainment and ventricular tachycardia termination in the first 15 seconds of RF current application. In the unsuccessful sites, significantly earlier electrical activity was seen than in the successful ones. Concealed entrainment was significantly associated with ventricular tachycardia termination. Bystander areas were not observed. The reentrant mechanism was responsible for the genesis of all tachycardias. In 70.5% of the studied sites, the endocardial participation of the slow conducting zone of reentrant circuits was shown. Concealed entrainment was the main electrophysiological parameter associated with successful RF current application. There was no electrophysiological evidence of bystander regions in the mapped circuits of SVT.

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

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.