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Right Ventricular Electrical Activation in Patients With Repaired Tetralogy of Fallots

2019; Lippincott Williams & Wilkins; Volume: 12; Issue: 6 Linguagem: Inglês

10.1161/circep.119.007141

ISSN

1941-3149

Autores

Zakaria Jalal, Frédéric Sacher, Emmanuelle Fournier, Hubert Cochet, Nicolas Derval, Michel Haı̈ssaguerre, Elvis Teijeira Fernández, Xavier Iriart, Arnaud Denis, Sylvain Ploux, Xavier Pillois, Pierre Bordachar, Jean‐Benoît Thambo,

Tópico(s)

Cardiac pacing and defibrillation studies

Resumo

HomeCirculation: Arrhythmia and ElectrophysiologyVol. 12, No. 6Right Ventricular Electrical Activation in Patients With Repaired Tetralogy of Fallots Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBRight Ventricular Electrical Activation in Patients With Repaired Tetralogy of FallotsInsights From Electroanatomical Mapping and High-Resolution Magnetic Resonance Imaging Zakaria Jalal, MD, PhD, Frédéric Sacher, MD, PhD, Emmanuelle Fournier, MD, Hubert Cochet, MD, PhD, Nicolas Derval, MD, Michel Haissaguerre, MD, PhD, Elvis Teijeira Fernandez, MD, Xavier Iriart, MD, Arnaud Denis, MD, Sylvain Ploux, MD, PhD, Xavier Pillois, PhD, Pierre Bordachar, MD, PhD and Jean-Benoît Thambo, MD, PhD Zakaria JalalZakaria Jalal Zakaria Jalal, MD, PhD, University Hospital of Bordeaux, Ave Magellan, 33600 Pessac, France. Email E-mail Address: [email protected] Department of Pediatric and Adult Congenital Cardiology (Z.J., E.F., X.I., J.B.-T.), Bordeaux University Hospital (CHU), Pessac. IHU Liryc, Electrophysiology and Heart Modeling Institute, Foundation Bordeaux Université, Pessac-Bordeaux (Z.J., F.S., H.C., N.D., M.H., E.T.F., X.I., A.D., S.P., X.P., P.B., J.-B.T.). INSERM, Centre de recherche Cardio-Thoracique de Bordeaux, France (Z.J., F.S., H.C., N.D., M.H., E.T.F., A.D., P.B., J.-B.T.). , Frédéric SacherFrédéric Sacher Electrophysiology and Ablation Unit (F.S., N.D., M.H., A.D., S.P., P.B.), Bordeaux University Hospital (CHU), Pessac. IHU Liryc, Electrophysiology and Heart Modeling Institute, Foundation Bordeaux Université, Pessac-Bordeaux (Z.J., F.S., H.C., N.D., M.H., E.T.F., X.I., A.D., S.P., X.P., P.B., J.-B.T.). INSERM, Centre de recherche Cardio-Thoracique de Bordeaux, France (Z.J., F.S., H.C., N.D., M.H., E.T.F., A.D., P.B., J.-B.T.). , Emmanuelle FournierEmmanuelle Fournier Department of Pediatric and Adult Congenital Cardiology (Z.J., E.F., X.I., J.B.-T.), Bordeaux University Hospital (CHU), Pessac. , Hubert CochetHubert Cochet Department of Radiology (H.C., E.T.F.), Bordeaux University Hospital (CHU), Pessac. IHU Liryc, Electrophysiology and Heart Modeling Institute, Foundation Bordeaux Université, Pessac-Bordeaux (Z.J., F.S., H.C., N.D., M.H., E.T.F., X.I., A.D., S.P., X.P., P.B., J.-B.T.). INSERM, Centre de recherche Cardio-Thoracique de Bordeaux, France (Z.J., F.S., H.C., N.D., M.H., E.T.F., A.D., P.B., J.-B.T.). , Nicolas DervalNicolas Derval Electrophysiology and Ablation Unit (F.S., N.D., M.H., A.D., S.P., P.B.), Bordeaux University Hospital (CHU), Pessac. IHU Liryc, Electrophysiology and Heart Modeling Institute, Foundation Bordeaux Université, Pessac-Bordeaux (Z.J., F.S., H.C., N.D., M.H., E.T.F., X.I., A.D., S.P., X.P., P.B., J.-B.T.). INSERM, Centre de recherche Cardio-Thoracique de Bordeaux, France (Z.J., F.S., H.C., N.D., M.H., E.T.F., A.D., P.B., J.-B.T.). , Michel HaissaguerreMichel Haissaguerre Electrophysiology and Ablation Unit (F.S., N.D., M.H., A.D., S.P., P.B.), Bordeaux University Hospital (CHU), Pessac. IHU Liryc, Electrophysiology and Heart Modeling Institute, Foundation Bordeaux Université, Pessac-Bordeaux (Z.J., F.S., H.C., N.D., M.H., E.T.F., X.I., A.D., S.P., X.P., P.B., J.-B.T.). INSERM, Centre de recherche Cardio-Thoracique de Bordeaux, France (Z.J., F.S., H.C., N.D., M.H., E.T.F., A.D., P.B., J.-B.T.). , Elvis Teijeira FernandezElvis Teijeira Fernandez Department of Radiology (H.C., E.T.F.), Bordeaux University Hospital (CHU), Pessac. IHU Liryc, Electrophysiology and Heart Modeling Institute, Foundation Bordeaux Université, Pessac-Bordeaux (Z.J., F.S., H.C., N.D., M.H., E.T.F., X.I., A.D., S.P., X.P., P.B., J.-B.T.). INSERM, Centre de recherche Cardio-Thoracique de Bordeaux, France (Z.J., F.S., H.C., N.D., M.H., E.T.F., A.D., P.B., J.-B.T.). , Xavier IriartXavier Iriart Department of Pediatric and Adult Congenital Cardiology (Z.J., E.F., X.I., J.B.-T.), Bordeaux University Hospital (CHU), Pessac. IHU Liryc, Electrophysiology and Heart Modeling Institute, Foundation Bordeaux Université, Pessac-Bordeaux (Z.J., F.S., H.C., N.D., M.H., E.T.F., X.I., A.D., S.P., X.P., P.B., J.-B.T.). , Arnaud DenisArnaud Denis Electrophysiology and Ablation Unit (F.S., N.D., M.H., A.D., S.P., P.B.), Bordeaux University Hospital (CHU), Pessac. IHU Liryc, Electrophysiology and Heart Modeling Institute, Foundation Bordeaux Université, Pessac-Bordeaux (Z.J., F.S., H.C., N.D., M.H., E.T.F., X.I., A.D., S.P., X.P., P.B., J.-B.T.). INSERM, Centre de recherche Cardio-Thoracique de Bordeaux, France (Z.J., F.S., H.C., N.D., M.H., E.T.F., A.D., P.B., J.-B.T.). , Sylvain PlouxSylvain Ploux Electrophysiology and Ablation Unit (F.S., N.D., M.H., A.D., S.P., P.B.), Bordeaux University Hospital (CHU), Pessac. IHU Liryc, Electrophysiology and Heart Modeling Institute, Foundation Bordeaux Université, Pessac-Bordeaux (Z.J., F.S., H.C., N.D., M.H., E.T.F., X.I., A.D., S.P., X.P., P.B., J.-B.T.). , Xavier PilloisXavier Pillois IHU Liryc, Electrophysiology and Heart Modeling Institute, Foundation Bordeaux Université, Pessac-Bordeaux (Z.J., F.S., H.C., N.D., M.H., E.T.F., X.I., A.D., S.P., X.P., P.B., J.-B.T.). , Pierre BordacharPierre Bordachar Electrophysiology and Ablation Unit (F.S., N.D., M.H., A.D., S.P., P.B.), Bordeaux University Hospital (CHU), Pessac. IHU Liryc, Electrophysiology and Heart Modeling Institute, Foundation Bordeaux Université, Pessac-Bordeaux (Z.J., F.S., H.C., N.D., M.H., E.T.F., X.I., A.D., S.P., X.P., P.B., J.-B.T.). INSERM, Centre de recherche Cardio-Thoracique de Bordeaux, France (Z.J., F.S., H.C., N.D., M.H., E.T.F., A.D., P.B., J.-B.T.). and Jean-Benoît ThamboJean-Benoît Thambo Department of Pediatric and Adult Congenital Cardiology (Z.J., E.F., X.I., J.B.-T.), Bordeaux University Hospital (CHU), Pessac. IHU Liryc, Electrophysiology and Heart Modeling Institute, Foundation Bordeaux Université, Pessac-Bordeaux (Z.J., F.S., H.C., N.D., M.H., E.T.F., X.I., A.D., S.P., X.P., P.B., J.-B.T.). INSERM, Centre de recherche Cardio-Thoracique de Bordeaux, France (Z.J., F.S., H.C., N.D., M.H., E.T.F., A.D., P.B., J.-B.T.). Originally published22 May 2019https://doi.org/10.1161/CIRCEP.119.007141Circulation: Arrhythmia and Electrophysiology. 2019;12:e007141Surgical repair of tetralogy of Fallot almost universally induces a right bundle branch block (RBBB). The noninvasive assessment of right ventricular (RV) activation, using ECG or transthoracic echocardiography, has become a mainstay in the follow-up of these patients because QRS duration has been identified as a predictor of sudden death, ventricular arrhythmias, or hemodynamic impairment.1 Although the origin of this RBBB is mainly related to surgical lesions of the conduction pathways, its evolutive course is seemingly associated with infundibular or global RV remodeling and fibrosis.2,3 In this setting, this prospective study aimed to (1) characterize RV electrical activation in patients with repair of tetralogy of Fallot with hemodynamic and arrhythmic complications using endocardial electroanatomical mapping and (2) study the anatomical, surgical, and ventricular volumetric features associated with RV activation.Consecutive repair of tetralogy of Fallot patients referred for endocardial electrophysiological study (EPS) were included prospectively between 2011 and 2016. Indications for electrophysiological study were as follows: (1) symptomatic arrhythmia and (2) pulmonary valve dysfunction requiring valve replacement (pulmonary valve replacement). An 8F ablation catheter (Navi-Star, Biosense Webster) was inserted under conscious sedation through the femoral vein up to the RV allowing the generation of electroanatomical voltage maps followed by programmed ventricular pacing.3 RV activation maps were constructed from the same recordings, on which the following data were analyzed: (1) RV activation delay, measured between the onset of surface QRS serving as reference and the first endocardial RV activation; (2) RV apical activation (measured between the first RV activation and the first electrogram activated in the apex); (3) RV activation duration (RVAD) measured between the first and the last RV endocardial activation (excluding low-voltage peri-scar zones [<0.5 mV] with fragmented electrograms on which the measurements were not reproducible); and (4) RV activation pattern defined as the activation sequence of the following 4 RV regions: septum, apex, anterior free wall, and the infundibulum.In addition, the patients underwent a standardized protocol including 12-lead ECG and 1.5T magnetic resonance imaging (Aera, Siemens Medical Systems, Erlangen, Germany) assessing ventricular volumetry, function, and fibrosis using high spatial resolution sequences (Figure [A] through [C]). Data are presented as median (interquartile range) or number (percentage). Comparisons between the quantitative variables of the different subgroups were performed using the Student t test when n≥20 and the Mann-Whitney test if n<20. For nominal variables, a χ2 test was used if n≥5 in all groups and Fisher exact test if at least 1 group had n<5. A linear regression test was used for correlation analyses. A probability P 50% of the maximum being considered as cicatricial. The septal and infundibular scar areas are measured on a surface map of the enhancements over the entire right ventricular (RV; C). D–G, Electroanatomical RV voltage and activation mapping of a 30-year-old patient admitted for before pulmonary valve replacement. Anterior (D and E) and posterior (F and G) views of the RV. D and F, RV activation maps: electrical activation emerges at the mid portion of the interventricular septum (in red) and propagates toward the apex followed by the infundibulum before ending in the anterior free wall. E and G, RV voltage maps: low-voltage areas (red) correspond to surgical scars at the level of the ventricular septum defect (VSD) and infundibular patches. When analyzing the activation pattern as a function of the surgical scars substrate, we can observe that the septal activation breakthrough is followed by 2 spreads of activation: (1) toward the basal septum which undergoes a conduction block (* in F) in an area which corresponds to the VSD patch on the corresponding voltage map (G) and (2) toward the apex followed by the anterior free wall. This propagation wave (F) appears to bypass the infundibular scar visible on the corresponding voltage map (E). IVS indicates interventricular septum; PA, pulmonary artery; RVOT, right ventricular outflow tract; and TA, tricuspid annulus.Fifty-six consecutive patients were included (median age 29 years [23–45], male n=40 [71.4%], right ventriculotomy n=56 [100%]) as part of a preoperative pulmonary valve replacement assessment (n=36) and for ablation (n=20). Complete RBBB was present in 90.6% (n=48) of cases (median QRS duration 159 ms [140–171], 9 patients [17%] had QRS ≥180 ms, and 27 [51%] had QRS ≥160 ms).Median magnetic resonance imaging–indexed RV end-diastolic volume and end-systolic volume were 152 mL/m2 (135–175.5) and 105 mL/m2 (96–127), respectively. Quantitative analysis of myocardial fibrosis was available in 37 patients (72.5%). The median total RV, RV septal scar, and RV infundibular fibrotic surface areas were 18.9 cm2 (14.2–24.6); 6.7 cm2 (4.6–9); and 10.8 cm2 (7.8–14.9), respectively. Total RV and infundibular fibrotic areas were significantly increased in patients with a QRS ≥180 ms (31.1 versus 15.5 cm2; P=0.007 and 18 versus10 cm2; P=0.017, respectively).Endocardial mapping showed a median RV activation delay of 21 ms (8–35) and a prolonged RVAD of 134 ms (118–157). Median apical activation time was 30 ms (0–56); 16 patients (28.5%) had central RBBB (apical activation time >40 ms), whereas the remaining patients (n=40, 71.5%) had peripheral RBBB.4 Patients with a QRS≥180 ms and RV end-diastolic volume ≥150 mL/m2 had a significantly longer RVAD (155 ms versus 131 ms; P=0.0013 and 143 ms versus 126 ms; P=0.034, respectively). The linear correlations with RVAD were weak albeit significant with regard to QRS duration (r=0.44; P<0.001)5 and RV end-diastolic volume (r=0.32; P<0.05).The RV activation sequence found in the majority of patients was as follows: a single breakthrough located in the interventricular septum (80.4%), then frontwave propagation toward the apex (69.6%), followed by the infundibulum (67.9%). The latest region was the free wall (76.8%) or the infundibulum (19.6%; Figure [D] through [G]). Patients whose infundibulum was the latest activated region had a significantly longer RVAD (164 ms versus 130.5 ms; P=0.001). When superimposing voltage and activation maps, surgical scars were found to impact the electrical activation according to 2 pathways (Figure [D] through [G]):The propagation of the activation originating from the basal septum incurred a conduction block at the basal portion of the interventricular septum in an area corresponding to the VSD patch on voltage maps.The impulse propagating on the RV anterior wall appeared to bypass the ventriculotomy scars and infundibular/transannular patches.To our knowledge, this is the largest cohort including repair of tetralogy of Fallot patients with arrhythmic and valvular complications in whom RV activation was assessed invasively. In conclusion, we showed that (1) there was a predominant activation sequence ending in the RV free wall in a majority of patients, (2) the RV activation was significantly prolonged in the whole RV including areas free from scars, due in particular to anatomic factors and to RV dilatation, and (3) surface QRS duration only partially reflects RV activation process. Additional studies focusing on ventricular electromechanical coupling and involving LV activation are needed to improve our understanding of the underlying mechanisms leading to long-term complications in these patients.Sources of FundingThis study received financial support from the French Government as part of the "Investments of the future" program managed by the National Research Agency (ANR), Grant reference ANR-10-IAHU-04.DisclosuresDr Sacher received speaking honoraria from Biosense Webster. The other authors report no conflicts.Footnotes*Drs Bordachar and Thambo contributed equally to this work.Zakaria Jalal, MD, PhD, University Hospital of Bordeaux, Ave Magellan, 33600 Pessac, France. Email [email protected]comReferences1. Gatzoulis MA, Till JA, Somerville J, Redington AN. Mechanoelectrical interaction in tetralogy of Fallot. QRS prolongation relates to right ventricular size and predicts malignant ventricular arrhythmias and sudden death.Circulation. 1995; 92:231–237.LinkGoogle Scholar2. Horowitz LN, Alexander JA, Edmunds LH. Postoperative right bundle branch block: identification of three levels of block.Circulation. 1980; 62:319–328.LinkGoogle Scholar3. Uebing A, Gibson DG, Babu-Narayan SV, Diller GP, Dimopoulos K, Goktekin O, Spence MS, Andersen K, Henein MY, Gatzoulis MA, Li W. Right ventricular mechanics and QRS duration in patients with repaired tetralogy of Fallot: implications of infundibular disease.Circulation. 2007; 116:1532–1539. doi: 10.1161/CIRCULATIONAHA.107.688770LinkGoogle Scholar4. Deanfield J, McKenna W, Rowland E. Local abnormalities of right ventricular depolarization after repair of tetralogy of Fallot: a basis for ventricular arrhythmia.Am J Cardiol. 1985; 55:522–525.CrossrefMedlineGoogle Scholar5. Kapel GFL, Brouwer C, Jalal Z, Sacher F, Venlet J, Schalij MJ, Thambo JB, Jongbloed MRM, Blom NA, de Riva M, Zeppenfeld K. Slow conducting electroanatomic isthmuses: an important link between QRS duration and ventricular tachycardia in tetralogy of Fallot.JACC Clin Electrophysiol. 2018; 4:781–793. doi: 10.1016/j.jacep.2018.02.002CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Rodríguez‐García J, Pijuan‐Domenech A, Francisco‐Pascual J, Dos‐Subirà L, Miranda‐Barrio B, Santos‐Ortega A and Rivas‐Gándara N (2021) Right ventricular resynchronization in a patient with repaired tetralogy of Fallot and severe ventricular dysfunction, Pacing and Clinical Electrophysiology, 10.1111/pace.14340, 44:12, (2119-2123), Online publication date: 1-Dec-2021. Oliver-Ruiz J and Peinado-Peinado R (2021) Prevención de arritmias ventriculares y muerte súbita en adultos con tetralogía de Fallot reparada. ¿Una historia interminable?, Revista Española de Cardiología, 10.1016/j.recesp.2021.05.004, 74:11, (905-908), Online publication date: 1-Nov-2021. Oliver-Ruiz J and Peinado-Peinado R (2021) Preventing ventricular arrhythmias and sudden cardiac death in adults with repaired tetralogy of Fallot: a never-ending story?, Revista Española de Cardiología (English Edition), 10.1016/j.rec.2021.05.018, 74:11, (905-908), Online publication date: 1-Nov-2021. 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June 2019Vol 12, Issue 6 Advertisement Article InformationMetrics © 2019 American Heart Association, Inc.https://doi.org/10.1161/CIRCEP.119.007141PMID: 31113235 Originally publishedMay 22, 2019 Keywordsechocardiographyarrhythmiahemodynamicelectrophysiologytetralogy of FallotPDF download Advertisement SubjectsCongenital Heart DiseaseElectrophysiology

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