Noninvasive Identification of Ventricular Tachycardia ... - DIE - UPM

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JACC Vol. 57, No. 2, 2011January 11, 2011:184–94Perez-David et al.VT Substrate and Heterogeneous Tissue Mapping193in 4 patients. No complications were observed during theprocedure. After the RF ablation procedure, all patientswere discharged with an ICD.Follow-up. The mean follow-up was 12 6 months in theSMVT group and 14 5 months in the control group. OneSMVT patient died of cancer and another of heart failure;4 patients had SMVT recurrences. In the control group, 3patients died: 2 of cancer and 1 of stroke. In the controlgroup, 4 patients received an ICD for primary prevention ofsudden cardiac death, 2 patients had an HT channel, and 1of these had VT episodes.DiscussionMain findings. This study provides significant new informationon SMVT substrate: channels of HT are morecommonly identified in SMVT than in control patients, andthe CC detected by endocardial voltage mapping can beidentified by 3D SI mapping.Heterogeneous tissue and SMVT substrate. Haqqani etal. (13) have reported that, in ischemic cardiomyopathypatients, conducting channels within dense scar andadjacent to the mitral annulus were more frequentlyobserved in SMVT patients than in stable control patientsdespite similar left ventricular parameters. We useda noninvasive approach to make a similar observation,namely, that HT and SI channels are more frequentlyobserved in patients with clinical SMVT than in controlpatients and that these channels were mainly located inthe endocardium. Schmidt et al. (10) have indirectlyrelated tissue heterogeneity and VT substrate, showingthat HT mass was associated with inducibility for monomorphicVT. Although we found that HT mass wassimilar in SMVT and control patients, both studiessupport the relation between HT and VT substrate. Thedifference is probably due to the fact that each studyanalyzes a different type of tachycardia (inducible vs.spontaneous) with a different cycle length (231 37 msvs. 364 67 ms).Comparison of voltage mapping and SI mapping. Scarextension by voltage mapping and ceMRI has been comparedelsewhere (14), and some discrepancies have been observed,mainly due to poor wall/catheter contact, or far-field influencesfrom normal myocardium that may lead to underestimation ofendocardial scar dimensions on endocardial voltage maps.Despite these limitations, we observed a significant relationshipbetween the infarct mass (SI 2 SD) and scarextension (1.5 mV), as well as a strong similarity in CCand SI channels with regard to location and orientation.Channel similarity despite scar differences could beexplained by the fact that far-field influences do not seemto affect characterization of CC. The surrounding scarameliorates far-field influences, and CC do not affect thesurrounding scar areas because of the reduced amount ofmyocytes embedded in these zones.Prior studies. Although some authors have analyzedceMRI in VT patients, a clear understanding of VTsubstrate in the scar has not been established. Codreanu etal. (14) compared ceMRI data in post-infarction VT patientsfor whom electroanatomic mapping data were available,but they did not provide data on the VT substrate.Desjardins et al. (15) showed that critical sites of postinfarctionarrhythmias were confined to areas of high SI, butthe VT substrate inside the scar was also not differentiated.Our study adds further information by describing thepresence of HT channels in the scar and a methodology forSI mapping that identifies endocardial VT substrate in thesame way as voltage mapping.Study limitations. The main limitation of our study isthe low number of patients included due to restrictionsaffecting the use of MRI in ICD patients. Although mostpatients had an inferior infarction, as previously reportedin SMVT patients (16), these patients were not specificallyselected, as consecutive patients with infarcts atdifferent locations were included. To maintain blindnessto MRI results, SI maps were not merged in CARTOonline; therefore, evidence of perfect correlation between CCand SI channels is not provided, nevertheless offline synchroniccomparison with CARTO Merge proves similar location andorientation of SI channels and CC. Although no activationmapping during tachycardia was systematically obtained, theconsistency in the relationship between the SMVT circuit andCC is supported by pacing, activation mapping, and successfulablation sites. Only a few SMVTs of 320 ms were included.In the control group, 33% of patients had an HT channel, butbecause no electrophysiological study was performed, we cannotstate explicitly that they were related to an SMVT.Clinical implications. The HT and SI channels could helpto identify patients at risk of SMVT, and this informationcould be useful to identify primary prevention patients inwhom prophylactic substrate ablation could reduce ICD discharges(17). Signal-intensity mapping could identify CC andfacilitate ablation procedures by merging into 3D mappingsystems (18).AcknowledgmentsThe authors thank Juan Felipe Cerezo for software development,Thomas O’Boyle for language revision, and AntonioMoratalla for technical assistance.Reprint requests and correspondence: Dr. Ángel Arenal, Unidadde Arritmias, Servicio de Cardiología, Hospital General UniversitarioGregorio Marañón, C/Dr. Esquerdo, 46 28007 Madrid,Spain. E-mail: arenal@secardiologia.es.REFERENCES1. de Bakker JM, van Capelle FJ, Janse MJ, et al. Reentry as a cause of ventriculartachycardia in patients with chronic ischemic heart disease: electrophysiologicand anatomic correlation. Circulation 1988;77:589–606.2. de Bakker JM, Coronel R, Tasseron S, et al. Ventricular tachycardia in theinfarcted Langendorff-perfused human heart: role of the arrangement ofsurviving cardiac fibers. J Am Coll Cardiol 1990;15:1594–607.
194 Perez-David et al. JACC Vol. 57, No. 2, 2011VT Substrate and Heterogeneous Tissue Mapping January 11, 2011:184–943. Soejima K, Stevenson WG, Maisel WH, Sapp JL, Epstein LM.Electrically unexcitable scar mapping based on pacing threshold foridentification of the reentry circuit isthmus: feasibility for guidingventricular tachycardia ablation. Circulation 2002;106:1678–83.4. Arenal A, del Castillo S, Gonzalez-Torrecilla E, et al. Tachycardiarelatedchannel in the scar tissue in patients with sustained monomorphicventricular tachycardias: influence of the voltage scar definition.Circulation 2004;110:2568–74.5. Hsia HH, Lin D, Sauer WH, Callans DJ, Marchlinski FE. Anatomiccharacterization of endocardial substrate for hemodynamically stablereentrant ventricular tachycardia: identification of endocardial conductingchannels. Heart Rhythm 2006;3:503–12.6. Amado LC, Gerber BL, Gupta SN, et al. Accurate and objectiveinfarct sizing by contrast-enhanced magnetic resonance imaging in acanine myocardial infarction model. J Am Coll Cardiol 2004;44:2383–9.7. Kim RJ, Albert TSE, Wible JH, et al., for the GadoversetamideMyocardial Infarction Imaging Investigators. Performance of delayedenhancementmagnetic resonance imaging with gadoversetamide contrastfor the detection and assessment of myocardial infarction: aninternational, multicenter, double-blinded, randomized trial. Circulation2008;117:629–37.8. Bello D, Fieno DS, Kim RJ, et al. Infarct morphology identifiespatients with substrate for sustained ventricular tachycardia. J Am CollCardiol 2005;45:1104–8.9. Yan AT, Shayne AJ, Brown KA, et al. Characterization of theperi-infarct zone by contrast-enhanced cardiac magnetic resonanceimaging is a powerful predictor of post-myocardial infarction mortality.Circulation 2006;114:32–9.10. Schmidt A, Azevedo CF, Cheng A, et al. Infarct tissue heterogeneityby magnetic resonance imaging identifies enhanced cardiac arrhythmiasusceptibility in patients with left ventricular dysfunction. Circulation2007;115:2006–14.11. Josephson ME. Clinical Cardiac Electrophysiology. 3rd edition. Philadelphia,PA: Lippincott Williams & Wilkins, 2002.12. Arenal A, Glez-Torrecilla E, Ortiz M, et al. Ablation of electrogramswith an isolated, delayed component as treatment of unmappablemonomorphic ventricular tachycardias in patients with structural heartdisease. J Am Coll Cardiol 2003;41:81–92.13. Haqqani HM, Kalman JM, Roberts-Thomson KC, et al. Fundamentaldifferences in electrophysiologic and electroanatomic substratebetween ischemic cardiomyopathy patients with and without clinicalventricular tachycardia. J Am Coll Cardiol 2009;54;166–73.14. Codreanu A, Odille F, Aliot E, et al. Electroanatomic characterizationof post-infarct scars: comparison with 3-dimensional myocardial scarreconstruction based on magnetic resonance imaging. J Am CollCardiol 2008;52:839–42.15. Desjardins B, Crawford T, Good E, et al. Infarct architecture andcharacteristics on delayed enhanced magnetic resonance imaging andelectroanatomic mapping in patients with postinfarction ventriculararrhythmia. Heart Rhythm 2009;6:644–51.16. Stevenson WG, Wilber DJ, Natale A, et al., Multicenter ThermacoolVT Ablation Trial Investigators. Irrigated radiofrequency catheterablation guided by electroanatomic mapping for recurrent ventriculartachycardia after myocardial infarction: the multicenter thermocoolventricular tachycardia ablation trial. Circulation 2008;118:2773–82.17. Reddy VY, Reynolds MR, Neuzil P, et al. Prophylactic catheterablation for the prevention of defibrillator therapy. N Engl J Med2007;357:2657–65.18. Reddy VY, Malchano ZJ, Holmvang G, et al. Integration of cardiacmagnetic resonance imaging with three-dimensional electroanatomicmapping to guide left ventricular catheter manipulation feasibility in aporcine model of healed myocardial infarction. J Am Coll Cardiol2004;44:2202–13.Key Words: ablation y heterogeneous imaging y magnetic resonanceimaging y ventricular tachycardia.
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