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

Amiodarone Is Poorly Effective for the Acute Termination of Ventricular Tachycardia

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

Automatic adjustment of ventricular antitachycardia pacing and individualized device therapy

Time-domain and spectral turbulence analyses of the signal-averaged electrocardiogram have different predictive values for sustained ventricular tachycardia in patients with myocardial infarction

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.

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

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.

HomeCirculationVol. 106, No. 2Ventricular Tachycardia Associated With Myocardial Infarct Scar Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBVentricular Tachycardia Associated With Myocardial Infarct ScarA Spectrum of Therapies for a Single Patient Kyoko Soejima, MD and William G. Stevenson, MD Kyoko SoejimaKyoko Soejima From the Cardiovascular Division, Department of Internal Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, Mass. and William G. StevensonWilliam G. Stevenson From the Cardiovascular Division, Department of Internal Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, Mass. Originally published9 Jul 2002https://doi.org/10.1161/01.CIR.0000019361.34897.75Circulation. 2002;106:176–179Case: A 73-year-old woman is referred for management of recurrent ventricular tachycardia (VT). She had suffered an inferior wall myocardial infarction in 1970. Fifteen years later, she presented with a wide QRS tachycardia, palpitations, and dizziness. Therapy with amiodarone was initiated but discontinued in 1997 because of toxicity, and she received an implantable cardioverter-defibrillator (ICD). She did well until July 2000, when she had several shocks from the ICD, all of which were preceded by syncope. Interrogation of the ICD confirmed 23 episodes of VT, 20 asymptomatic runs terminated by antitachycardia pacing (ATP), and 3 episodes requiring cardioversion from the ICD. Her left ventricular ejection fraction was 25%. Sotalol failed to prevent VT recurrences and mexiletine produced nausea and tremor.She was referred for catheter ablation. An echocardiogram revealed akinesis of the inferior wall and no left ventricular thrombus. In the electrophysiology laboratory, programmed stimulation induced 5 different morphologies of VT (Figure 1) with rates ranging from 180 to 220 bpm. Because the induced VTs were unstable, producing hypotension and often changing from one VT to another, catheter mapping and ablation were performed largely during sinus rhythm, guided by electrogram characteristics and pacing during sinus rhythm (pace-mapping) that marked the location of the infarct scar and likely reentry paths in the subendocardium. After placement of lines of radiofrequency (RF) lesions through these abnormal regions, only ventricular flutter (280 bpm) was inducible; the slower VTs were no longer inducible. There have been no VT recurrences in the 18 months of follow-up after ablation. Download figureDownload PowerPointFigure 1. Twelve-lead ECGs of the inducible VTs were obtained in the electrophysiology laboratory.DiscussionVentricular arrhythmias associated with myocardial infarction (MI) occur in 2 distinct phases. During the acute phase of infarction, polymorphic VT that degenerates to ventricular fibrillation is most common. In the weeks that follow, the healing infarct undergoes structural changes. Fibrosis creates areas of conduction block and also increases separation of myocyte bundles, slowing conduction through myocyte pathways in the border of the infarct.1,2 These pathways or channels can support stable reentry circuits, leading to monomorphic VT, when an appropriate trigger (such as a change in sinus rate or a premature depolarization) occurs. After surviving the acute phase of the infarct, monomorphic VT may emerge at any time. With present management of myocardial infarction, the incidence of sustained VT is relatively low, and fewer than 5% of infarct survivors have inducible VT when studied early after the infarct.3 Patients with large infarcts, often those who are not successfully reperfused, are at greatest risk for VT. Although the first 6 months after infarction is thought to be the period of greatest risk for VT and sudden death, some patients develop VT much later, as in the case presented above. Whether late development of VT is related to electrical and mechanical remodeling or additional ischemic events contributing to the development of the substrate for the VT is not known. Because the arrhythmia substrate for late VT is relatively fixed, this type of VT tends to be recurrent and difficult to suppress with medications.Antiarrhythmic Drugs and ICDsAntiarrhythmic drugs are frequently prescribed because they alter the electrophysiological properties of the reentrant circuit and suppress potential triggers for the development of VT. However, within 2 years, >40% of patients being treated for sustained VT will experience recurrences.4 There is a risk that a VT recurrence will cause sudden death, particularly in patients with depressed ventricular function and those who have presented with a hemodynamically poorly tolerated VT.5Three recent trials support the superiority of ICDs over antiarrhythmic drug therapy for prolonging survival and preventing sudden death in survivors of sustained ventricular arrhythmias.6,7,8 Thus, an ICD is first-line therapy for these patients. For many patients, placement of an ICD prevents the side effects of antiarrhythmic drugs. The most effective drug, amiodarone, produces side effects in almost 75% patients within 5 years. These side effects include hypothyroidism (5% to 25%), blue skin (1% to 6%), corneal pigmentation (1%), pulmonary toxicity (1% per year), tremor, or other neurological toxicity. ICD risks include device failure, lead fractures, and infection, but these are infrequent. ICDs also provide back-up pacing that protects against bradyarrhythmia.Although ICDs extend survival, they only treat the arrhythmia when it occurs, and do not prevent arrhythmia recurrences. Follow-up is required for the infrequent possibility of device malfunction. Within a year of ICD implantation, 68% of patients have recurrent episodes of VT.6 Most monomorphic VTs can be terminated by antitachycardia pacing, which is painless and often asymptomatic, but some patients require electrical cardioversion via the ICD. When VT initially recurs, and particularly when it becomes frequent, an evaluation is required to address potential aggravating factors, such as myocardial ischemia, electrolyte abnormalities, or decompensated heart failure. Most patients with frequent monomorphic VT require additional therapy to reduce VT episodes.Interactions Between ICDs and Antiarrhythmic AgentsAntiarrhythmic drug therapy decreases the frequency of VT episodes in patients with ICDs and may make the VT more amenable to antitachycardia pacing therapy. For some patients, drug therapy is problematic. The antiarrhythmic agent may slow the sinus rate, causing the patient to be paced, potentially with loss of AV synchrony, or producing adverse hemodynamic effects from right ventricular pacing. Antiarrhythmic agents may slow the rate of VT when it occurs such that it falls below the detect rate of the ICD, or falls into the range where sinus tachycardia can also occur, making distinction of sinus tachycardia from VT difficult. Some drugs, notably amiodarone, can increase the energy required for defibrillation, theoretically reducing the likelihood that ventricular fibrillation would be effectively treated by the ICD.AblationRF catheter ablation is a useful adjuvant therapy for frequent episodes of symptomatic VT. Initial ablation studies used careful mapping during VT to identify a critical part of the VT reentry circuit where the relatively small RF ablation lesions could interrupt reentry. The presence of hemodynamically stable VT facilitated mapping and ablation attempts. Patients with unstable VTs that did not allow detailed mapping were largely excluded from initial ablation attempts. Developments in the understanding of the nature of reentrant circuits and in methods to identify the region of the infarct scar and potential reentrant circuit paths through the scar now allow catheter ablation to be effective for many patients who have multiple and unstable VTs.9,10Catheter mapping systems allow electrophysiological data to be integrated in a 3-dimensional anatomic reconstruction of the ventricle (Figure 2A). The map of the left ventricle in Figure 2A, was created during sinus rhythm. The catheter was moved from point to point around the ventricle. At each point, the electrogram amplitude was plotted and color coded, with normal amplitude areas (>1.5 mV) indicated as purple and progressively lower-amplitude regions indicated by blue, green, yellow, and red regions. This patient has a large infero-posterior low-amplitude region consistent with her prior infarction. The area is much larger than that which can be completely ablated by RF energy; however, additional data can be obtained to focus the ablation to an appropriate region.10Download figureDownload PowerPointFigure 2. A, Voltage map of the left ventricle, constructed with an electroanatomic mapping system by moving the mapping catheter point by point over the endocardial surface, is shown. For each point, the electrogram amplitude is indicated by colors: purple indicates >1.5 mV (normal); blue, green, yellow, and red indicate progressively lower-amplitude abnormal regions. The left ventricle is viewed from the PA projection. The infarct area is identified as the extensive low-voltage area (red, yellow, green colors) in the inferior wall. Sites at which pace mapping and limited entrainment mapping were performed are shown with white tags. The gray regions indicate areas of dense scar that create fixed conduction block. B, The locations of RF lesions placed to interrupt pathways between the mitral annulus and areas of dense scars are shown as red tags. EM indicates entrainment mapping; PM, pace mapping matched.Inducing VT once in the electrophysiology laboratory allows confirmation of the diagnosis. In addition, the QRS morphology of the VT is obtained for use as a rough guide to the location of the reentry circuit in the infarct. In lead V1, a right bundle-branch block–like morphology VT suggests a left ventricular origin, and left bundle-branch block–like morphology predicts an origin in the right ventricle or in the interventricular septum. Dominant S waves in V2, V3, and V4 suggest an exit near the apex. Dominant R waves in these leads suggest an exit closer to the mitral annulus. Then, during sinus rhythm, pacing from the mapping catheter (pace-mapping) at sites around the infarct region and comparing the paced QRS with the VT morphology helped identify the VT reentrant circuit.11 The circuits can be large and multiple circuits are common.In the case presented, 5 different VTs were inducible. Figure 2A shows that pace mapping at a site in the low-voltage infarct region, located between two areas of dense unexcitable scar (gray regions), produced a QRS morphology similar to that of one of the VTs. To gain further confirmation that this region was involved in VT, the mapping catheter was placed at the site and VT was induced. After assessing the pattern of electrical activation, burst pacing was initiated to terminate VT. The effects of pacing (entrainment mapping) confirmed that this site was in the circuit12 (Figure 3). During stable sinus rhythm, a line of RF lesions (line 1) was then created through the target region. After the initial RF line was created, programmed stimulation induced other VT morphologies. On the basis of pace-mapping, additional RF lesions (line 2) were created (Figure 2B), which abolished inducible monomorphic VT. Download figureDownload PowerPointFigure 3. An example of entrainment mapping is shown. VT had been induced by right ventricular pacing. Pacing during VT was then performed from the mapping catheter in the left ventricle. The tachycardia was then promptly terminated by rapid burst pacing (not shown) to restore stable sinus rhythm. At this site, pacing accelerates VT to the pacing rate (cycle length of 280 ms) without changing the QRS morphology of the VT. This often indicates that the pacing site, where the mapping catheter is located, is in the reentry circuit. Additional measurements (the postpacing interval and stimulus to QRS interval) confirm that the site is in the reentry circuit. RF ablation was therefore performed at this and adjacent sites, abolishing VT. Abl indicates ablation catheter; RVA, right ventricular apex; VTCL, ventricular tachycardia cycle length.The Role of VT AblationICDs are first-line therapy for many patients with recurrent VT. When antiarrhythmic drug therapy fails to control symptomatic recurrences of VT, catheter ablation should be considered and can be expected to reduce the frequency of recurrent VT in >75% of patients.9,10,13,14 In experienced centers, ablation is now performed regardless of whether the VT rate is rapid and is associated with hemodynamic collapse. The major procedural risks are related to thromboembolism (1.2%), perforation (0.3%), and vascular access complications.15 The procedures can be long and are facilitated by the use of 3-dimensional reconstructions of the ventricular anatomy.When ablation fails, it is usually because of existence of portions of the reentrant circuits deep to the endocardium where they cannot be interrupted with standard endocardial ablation techniques. Ablation with saline-irrigated cooled ablation catheters and percutaneous epicardial mapping and ablation approaches are being evaluated that may allow some of these VTs to be ablated.16,17 Nonpharmacological therapies, such as RF ablation, have an increasingly important role in the management of VT after myocardial infarction, thus expanding the array of options available to clinicians.FootnotesCorrespondence to William G. Stevenson, MD, Cardiovascular Division, Brigham and Women's Hospital 75 Francis St, Boston, MA 02115. E-mail [email protected] References 1 Wit A, Janse MJ. The Ventricular Arrhythmia of Ischemia and Infarction: Electrophysiological Mechanisms. Mount Kisco, NY: Futura; 1993.Google Scholar2 De Bakker JMT, Van Capelle FJL, Janse MJ, et al. Slow conduction in the infarcted human heart: "zigzag" course of activation. Circulation. 1993; 88: 915–926.CrossrefMedlineGoogle Scholar3 Andresen D, Steinbeck G, Bruggemann T, et al. Risk stratification following myocardial infarction in the thrombolytic era. J Am Coll Cardiol. 1999; 33: 131–138.CrossrefMedlineGoogle Scholar4 The ESVEM investigators. Determinants of predicted efficacy of antiarrhythmic drugs in the electrophysiologic study versus electrocardiographic monitoring trial. Circulation. 1993; 87: 323–329.CrossrefMedlineGoogle Scholar5 Wyse DG, Talajic M, Hafley GE, et al. Antiarrhythmic drug therapy in the multicenter unsustained tachycardia trial (MUSTT): drug testing and as-treated analysis. J Am Coll Cardiol. 2001; 38: 344–351.CrossrefMedlineGoogle Scholar6 The Antiarrhythmics versus Implantable Defibrillators (AVID) Investigators. A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. N Engl J Med. 1997; 337: 1576–1583.CrossrefMedlineGoogle Scholar7 Connolly SJ, Gent M, Roberts RS, et al. Canadian implantable defibrillator study (CIDS); a randomized trial of the implantable cardioverter defibrillator against amiodarone. Circulation. 2000; 101: 1297–1302.CrossrefMedlineGoogle Scholar8 Kuck KH, Cappato R, Siebels J, et al. Randomized comparison of antiarrhythmic drug therapy with implantable defibrillators in patients resuscitated from cardiac arrest. The cardiac arrest study Hamburg (CASH). Circulation. 2000; 102: 748–754.CrossrefMedlineGoogle Scholar9 Marchlinski FE, Callans DJ, Gottlieb CD, et al. Linear ablation lesions for control of unmappable ventricular tachycardia in patients with ischemic and nonischemic cardiomyopathy. Circulation. 2000; 101: 1288–1296.CrossrefMedlineGoogle Scholar10 Soejima K, Suzuki M, Maisel WH, et al. Catheter ablation in patients with multiple and unstable ventricular tachycardias after myocardial infarction: short ablation lines guided by reentry circuit isthmuses and sinus rhythm mapping. Circulation. 2001; 104: 664–669.CrossrefMedlineGoogle Scholar11 Stevenson WG, Sager PT, Natterson PD, et al. Relation of pace mapping QRS configuration and conduction delay to ventricular tachycardia reentry circuits in human infarct scars. J Am Coll Cardiol. 1995; 226: 481–488.Google Scholar12 Stevenson WG, Khan H, Sager P, et al. Identification of reentry circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction. Circulation. 1993; 88: 1647–1670.CrossrefMedlineGoogle Scholar13 Stevenson WG, Friedman PL, Sweeney MO. Catheter ablation as an adjunct to ICD therapy. Circulation. 1997; 96: 1378–1380.CrossrefMedlineGoogle Scholar14 Strickberger SA, Man KC, Daoud EG, et al. A prospective evaluation of catheter ablation of ventricular tachycardia as adjuvant therapy in patients with coronary artery disease and implantable cardioverter- defibrillator. Circulation. 1997; 96: 1525–1531.CrossrefMedlineGoogle Scholar15 Hindricks G. The Multicentre European Radiofrequency Survey (MERFS): complications of radiofrequency catheter ablation of arrhythmias. The Multicentre European Radiofrequency Survey (MERFS) investigators of the Working Group on Arrhythmias of the European Society of Cardiology. Eur Heart. 1993; 14: 1644–1653.CrossrefMedlineGoogle Scholar16 Calkins H, Epstein A, Packer D, et al. Catheter ablation of ventricular tachycardia in patients with structural heart disease using cooled radiofrequency energy: results of a prospective multicenter study. Cooled RF Multi Center Investigators Group. J Am Coll Cardiol. 2000; 35: 1905–1914.CrossrefMedlineGoogle Scholar17 Soejima K, Delacretaz E, Suzuki M, et al. Saline-cooled versus standard radiofrequency catheter ablation for infarct related ventricular tachycardias. Circulation. 2001; 103: 1858–1862.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Darden D and Hoffmayer K (2022) The role of coronary artery disease and revascularization in electrical storm: A multidisciplinary team approach, Coronary Artery Disease, 10.1097/MCA.0000000000001144, Publish Ahead of Print Ciuffo L, Bruña V, Martínez‐Sellés M, Vasconcellos H, Tao S, Zghaib T, Nazarian S, Spragg D, Marine J, Berger R, Lima J, Calkins H, Bayés‐de‐Luna A and Ashikaga H (2020) Association between interatrial block, left atrial fibrosis, and mechanical dyssynchrony: Electrocardiography‐magnetic resonance imaging correlation, Journal of Cardiovascular Electrophysiology, 10.1111/jce.14608, 31:7, (1719-1725), Online publication date: 1-Jul-2020. Rosellini E, Lazzeri L, Maltinti S, Vanni F, Barbani N and Cascone M (2019) Development and characterization of a suturable biomimetic patch for cardiac applications, Journal of Materials Science: Materials in Medicine, 10.1007/s10856-019-6327-6, 30:11, Online publication date: 1-Nov-2019. Akhyari P, Barth M and Lichtenberg A (2017) 7.25 Cardiac Patch with Cells: Biological or Synthetic Comprehensive Biomaterials II, 10.1016/B978-0-08-100691-7.00157-9, (482-505), . Castellano D, Blanes M, Marco B, Cerrada I, Ruiz-Saurí A, Pelacho B, Araña M, Montero J, Cambra V, Prosper F and Sepúlveda P (2014) A Comparison of Electrospun Polymers Reveals Poly(3-Hydroxybutyrate) Fiber as a Superior Scaffold for Cardiac Repair, Stem Cells and Development, 10.1089/scd.2013.0578, 23:13, (1479-1490), Online publication date: 1-Jul-2014. Amraoui S, Denis A, Derval N, Zemmoura A, Sacher F, Jais P, Ploux S, Bordachar P, Ritter P, Haissaguerre M and Hocini M (2014) Le futur de la rythmologie interventionnelle, Archives des Maladies du Coeur et des Vaisseaux - Pratique, 10.1016/S1261-694X(14)70608-X, 2014:226, (17-31), Online publication date: 1-Mar-2014. Serpooshan V, Zhao M, Metzler S, Wei K, Shah P, Wang A, Mahmoudi M, Malkovskiy A, Rajadas J, Butte M, Bernstein D and Ruiz-Lozano P (2014) Use of bio-mimetic three-dimensional technology in therapeutics for heart disease, Bioengineered, 10.4161/bioe.27751, 5:3, (193-197), Online publication date: 1-May-2014. Wang B, Williams L, de Jongh Curry A and Liao J (2014) Preparation of Acellular Myocardial Scaffolds with Well-Preserved Cardiomyocyte Lacunae, and Method for Applying Mechanical and Electrical Simulation to Cardiac . N, T, M, B, R, M, B, K and P (2014) site appropriate following right ventricle Online publication date: Le A, A, L, S and D in for cardiac therapies, Online publication date: M, M, S, N, A, E, and M as a for and Journal of and Online publication date: and M for myocardial on Biological Online publication date: Rosellini E, Barbani N and P of Scaffolds for Myocardial and of Biomaterials Myocardial . M, J, D and S for cardiac Materials and Online publication date: Akhyari P, Barth M and Lichtenberg A Cardiac Patch with Cells: Biological or Synthetic Comprehensive . S, M, R, J, M and S of for myocardial Journal of Materials Science: Materials in Medicine, Online publication date: N and M Acellular Cardiac as a Scaffold for In and Online publication date: D and A of with Disease, . J, S and D of by Journal of Online publication date: D, A, A, P, S, I, E, S, P, and and Mechanical Within a Myocardial Patch A, Online publication date: K and J and and in . M, G, S, R and R for Cardiovascular of and Medicine, S, J, M, R, R, M and the of Cardiovascular Online publication date: S, S, J, J, S and with Journal of Materials Online publication date: N and R and of heart using Journal of Materials A, Online publication date: and The Development of for Online publication date: Wang S, I, A, T, Wang S, R, R and Stem and After and Online publication date: N Cardiac Online publication date: T, T, A, T, V, J, J and A In of in Journal of and Online publication date: and R the heart by of the in cardiac Medicine, Online publication date: M, and H of the in Myocardial Online publication date: P and S Therapies for Ventricular Pacing and Electrophysiology, Online publication date: S, P, I, S, A, T, D, R and (2017) The Use of as an Scaffold for the of Online publication date: J, N and S of the with Myocardial Stem and . J Ventricular Online publication date: A, J, J and de a la de de de Online publication date: J, H, M, E, F, M, and Mechanical and of Cardiac from and Online publication date: H, M, J, and A In - . A, J, J and de Radiofrequency Catheter Ablation of Ventricular Tachycardia in Patients With an Implantable de Online publication date: F, F, J, J, J, E, J, D and J Cells: Cardiac for and Online publication date: Ventricular Tachycardia and Associated with Electrical the of the Journal of Cardiovascular Electrophysiology, D, S, M and K Catheter ablation of ventricular tachycardia guided by cardiac Online publication date: N Ventricular in The Journal of Cardiovascular Online publication date: and of the and of on the of Journal of Biomaterials Online publication date: T, D, R, K, T, P, N, and R (2017) in the Ventricular Online publication date: K, P, D, R, and R Ventricular With Online publication date: M, and H of the in Myocardial T, H, S, N, and A conduction slowing and conduction A and D, R and The of electroanatomic mapping during radiofrequency ablation of ventricular tachycardia in patients after myocardial infarction, July 106, 2 Originally

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.

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 …

The purpose of this investigation is to define whether the antiarrhythmic drug moricizine has beneficial or adverse effects on currently used antitachycardia and antifibrillatory devices. These studies were performed in a dog model of sustained monomorphic ventricular tachycardia (VT). In 11 dogs, the left anterior descending artery and all surrounding epicardial collateral feeder vessels were ligated. Defibrillator patches were implanted and the dogs were allowed to recover. After a 7-day recovery period, effective refractory period (ERP), end diastolic threshold (EDT), VT induction, and VT and ventricular fibrillation (VF) termination data were collected before and after moricizine infusion (2 mg/kg). In this experimental model, moricizine caused the following electrophysiological changes: a prolongation of the ERP from 173 +/- 14 to 182 +/- 15 (P < 0.02) with no significant effect on the EDT for pacing; a prolongation of the VT cycle length from 175 +/- 18 to 201 +/- 23 msec (P < 0.003); an increased cycle length required for overdrive pacing from 136 +/- 20 to 157 +/- 22 msec (P < 0.01); no effect on the energy required to cardiovert VT; an increase in the defibrillation threshold from 7.5 +/- 4 to 9.4 +/- 4 joules (P < 0.006) and; in 5 of the 8 dogs with VT, the VT could be initiated with somewhat less aggressive stimulation. Significant beneficial electrophysiological physiological effects were noted on the VT cycle length, including a proportionately prolonged overdrive pacing cycle length for VT termination.(ABSTRACT TRUNCATED AT 250 WORDS)

The automatic implantable cardioverter defibrillator (AICD) has significantly decreased mortality in high risk ventricular tachycardia (VT) patients. The AICD provides treatment based on ventricular rate, sometimes leading to high energy shocks in conscious patients with stable VT, or patients with sinus or supraventricular tachycardia. Other physiological parameters, such as maximal positive and negative systolic right ventricular (RV) dP/dt (RV + dP/dtmax, RV - dP/dtmax, respectively), may be included in detection algorithms for future implantable defibrillators. We studied frequency band limited positive and negative RV dP/dtmax before, during, and after 13 episodes of VT lasting at least 40 beats in duration in nine male patients. The mean (+/- SEM) RV + dP/dtmax, dropped by 120 +/- 28 mmHg/sec (P less than 0.001) during the first five beats of VT. RV + dP/dtmax then slowly rose toward baseline levels until a significant overshoot occurred during the first ten beats following VT termination (delta = 234 +/- 58 mmHg/second, P less than 0.002). RV + dP/dtmax correlated poorly with mean arterial pressure (r = 0.32, P greater than 0.1), systolic blood pressure (r = 0.19, P greater than 0.1), and VT cycle length (r = 0.34, P greater than 0.1). Conversely, RV - dP/dtmax rose during the first ten beats of VT (74 +/- 27 mmHg/sec, P greater than 0.05) and then slowly drifted back toward baseline levels. Like RV + dP/dtmax, RV - dP/dtmax overshot baseline levels during the recovery phase (-108 +/- 48 mmHg/sec, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

To prospectively determine whether mechanical behavior of left ventricular wall segments that contain different degrees of scar tissue and are located at different distances from the interface between infarcted and noninfarcted myocardial tissue can help predict inducibility of monomorphic ventricular tachycardia (VT) in patients with ischemic cardiomyopathy. This HIPAA-compliant study was institutional review board approved; written informed consent was obtained from all patients. Forty-six patients (36 men, 10 women; mean age +/- standard deviation, 61.6 years +/- 11.9) with prior myocardial infarction (MI) and left ventricular dysfunction were referred for defibrillator implantation and underwent an electrophysiologic examination and tagged contrast-enhanced magnetic resonance (MR) imaging. Peak circumferential shortening strain (Ecc) and time to peak Ecc were measured in 12 segments from short-axis sections. Remote, adjacent, and border zones were defined according to increasing proximity to the MI. Patients in whom monomorphic VT could be induced (ie, inducible patients) were considered positive for inducibility. Relationships between inducibility of monomorphic VT, peak Ecc, and time to peak Ecc were analyzed with one-way analysis of variance and Bonferroni test. Inducible patients had more infarcted and border zone sectors and a shorter time to peak Ecc than did noninducible patients in the border zone and adjacent and infarcted regions (P < .001). Peak Ecc in the border zone of inducible patients (-11.42% +/- 0.46 [standard error]) was greater than that in noninducible patients (-10.18% +/- 0.38; P < .05). Ratio of Ecc in border zone and in remote regions was greater (P < .05) in inducible patients than in noninducible patients (1.31 +/- 0.27 vs 0.64 +/- 0.13, respectively). Enhanced border zone function defined as greater Ecc and earlier time to peak Ecc showed positive correlation to VT inducibility in patients with prior MI and left ventricular dysfunction.

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

Muscle sympathetic nerve traffic during spontaneous- versus adenosine-mediated termination of idiopathic right ventricular outflow tract tachycardia