Successful Catheter Ablation of Bidirectional Ventricular Premature Contractions Triggering Ventricular Fibrillation in Catecholaminergic Polymorphic Ventricular Tachycardia With RyR2 Mutation
2012; Lippincott Williams & Wilkins; Volume: 5; Issue: 1 Linguagem: Inglês
10.1161/circep.111.966549
ISSN1941-3149
AutoresTakashi Kaneshiro, Yoshihisa Naruse, Akihiko Nogami, Hiroshi Tada, Kentaro Yoshida, Yukio Sekiguchi, Nobuyuki Murakoshi, Yoshiaki Kato, Hitoshi Horigome, Mihoko Kawamura, Minoru Horie, Kazutaka Aonuma,
Tópico(s)Cardiovascular Effects of Exercise
ResumoHomeCirculation: Arrhythmia and ElectrophysiologyVol. 5, No. 1Successful Catheter Ablation of Bidirectional Ventricular Premature Contractions Triggering Ventricular Fibrillation in Catecholaminergic Polymorphic Ventricular Tachycardia With RyR2 Mutation Free AccessCase ReportPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessCase ReportPDF/EPUBSuccessful Catheter Ablation of Bidirectional Ventricular Premature Contractions Triggering Ventricular Fibrillation in Catecholaminergic Polymorphic Ventricular Tachycardia With RyR2 Mutation Takashi Kaneshiro, MD, Yoshihisa Naruse, MD, Akihiko Nogami, MD, Hiroshi Tada, MD, Kentaro Yoshida, MD, Yukio Sekiguchi, MD, Nobuyuki Murakoshi, MD, Yoshiaki Kato, MD, Hitoshi Horigome, MD, Mihoko Kawamura, MD, Minoru Horie, MD and Kazutaka Aonuma, MD Takashi KaneshiroTakashi Kaneshiro From the Cardiovascular Division, Institute of Clinical Medicine (T.K., Y.N., H.T., K.Y., Y.S., N.M., K.A.) and Department of Child Health (Y.K., H.H.), Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan; Division of Heart Rhythm Management, Yokohama Rosai Hospital, Yokohama, Japan (A.N.); and Department of Cardiovascular and Respiratory Medicine, Shiga University of Medical Science, Shiga, Japan (M.K., M.H.). , Yoshihisa NaruseYoshihisa Naruse From the Cardiovascular Division, Institute of Clinical Medicine (T.K., Y.N., H.T., K.Y., Y.S., N.M., K.A.) and Department of Child Health (Y.K., H.H.), Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan; Division of Heart Rhythm Management, Yokohama Rosai Hospital, Yokohama, Japan (A.N.); and Department of Cardiovascular and Respiratory Medicine, Shiga University of Medical Science, Shiga, Japan (M.K., M.H.). , Akihiko NogamiAkihiko Nogami From the Cardiovascular Division, Institute of Clinical Medicine (T.K., Y.N., H.T., K.Y., Y.S., N.M., K.A.) and Department of Child Health (Y.K., H.H.), Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan; Division of Heart Rhythm Management, Yokohama Rosai Hospital, Yokohama, Japan (A.N.); and Department of Cardiovascular and Respiratory Medicine, Shiga University of Medical Science, Shiga, Japan (M.K., M.H.). , Hiroshi TadaHiroshi Tada From the Cardiovascular Division, Institute of Clinical Medicine (T.K., Y.N., H.T., K.Y., Y.S., N.M., K.A.) and Department of Child Health (Y.K., H.H.), Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan; Division of Heart Rhythm Management, Yokohama Rosai Hospital, Yokohama, Japan (A.N.); and Department of Cardiovascular and Respiratory Medicine, Shiga University of Medical Science, Shiga, Japan (M.K., M.H.). , Kentaro YoshidaKentaro Yoshida From the Cardiovascular Division, Institute of Clinical Medicine (T.K., Y.N., H.T., K.Y., Y.S., N.M., K.A.) and Department of Child Health (Y.K., H.H.), Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan; Division of Heart Rhythm Management, Yokohama Rosai Hospital, Yokohama, Japan (A.N.); and Department of Cardiovascular and Respiratory Medicine, Shiga University of Medical Science, Shiga, Japan (M.K., M.H.). , Yukio SekiguchiYukio Sekiguchi From the Cardiovascular Division, Institute of Clinical Medicine (T.K., Y.N., H.T., K.Y., Y.S., N.M., K.A.) and Department of Child Health (Y.K., H.H.), Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan; Division of Heart Rhythm Management, Yokohama Rosai Hospital, Yokohama, Japan (A.N.); and Department of Cardiovascular and Respiratory Medicine, Shiga University of Medical Science, Shiga, Japan (M.K., M.H.). , Nobuyuki MurakoshiNobuyuki Murakoshi From the Cardiovascular Division, Institute of Clinical Medicine (T.K., Y.N., H.T., K.Y., Y.S., N.M., K.A.) and Department of Child Health (Y.K., H.H.), Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan; Division of Heart Rhythm Management, Yokohama Rosai Hospital, Yokohama, Japan (A.N.); and Department of Cardiovascular and Respiratory Medicine, Shiga University of Medical Science, Shiga, Japan (M.K., M.H.). , Yoshiaki KatoYoshiaki Kato From the Cardiovascular Division, Institute of Clinical Medicine (T.K., Y.N., H.T., K.Y., Y.S., N.M., K.A.) and Department of Child Health (Y.K., H.H.), Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan; Division of Heart Rhythm Management, Yokohama Rosai Hospital, Yokohama, Japan (A.N.); and Department of Cardiovascular and Respiratory Medicine, Shiga University of Medical Science, Shiga, Japan (M.K., M.H.). , Hitoshi HorigomeHitoshi Horigome From the Cardiovascular Division, Institute of Clinical Medicine (T.K., Y.N., H.T., K.Y., Y.S., N.M., K.A.) and Department of Child Health (Y.K., H.H.), Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan; Division of Heart Rhythm Management, Yokohama Rosai Hospital, Yokohama, Japan (A.N.); and Department of Cardiovascular and Respiratory Medicine, Shiga University of Medical Science, Shiga, Japan (M.K., M.H.). , Mihoko KawamuraMihoko Kawamura From the Cardiovascular Division, Institute of Clinical Medicine (T.K., Y.N., H.T., K.Y., Y.S., N.M., K.A.) and Department of Child Health (Y.K., H.H.), Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan; Division of Heart Rhythm Management, Yokohama Rosai Hospital, Yokohama, Japan (A.N.); and Department of Cardiovascular and Respiratory Medicine, Shiga University of Medical Science, Shiga, Japan (M.K., M.H.). , Minoru HorieMinoru Horie From the Cardiovascular Division, Institute of Clinical Medicine (T.K., Y.N., H.T., K.Y., Y.S., N.M., K.A.) and Department of Child Health (Y.K., H.H.), Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan; Division of Heart Rhythm Management, Yokohama Rosai Hospital, Yokohama, Japan (A.N.); and Department of Cardiovascular and Respiratory Medicine, Shiga University of Medical Science, Shiga, Japan (M.K., M.H.). and Kazutaka AonumaKazutaka Aonuma From the Cardiovascular Division, Institute of Clinical Medicine (T.K., Y.N., H.T., K.Y., Y.S., N.M., K.A.) and Department of Child Health (Y.K., H.H.), Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan; Division of Heart Rhythm Management, Yokohama Rosai Hospital, Yokohama, Japan (A.N.); and Department of Cardiovascular and Respiratory Medicine, Shiga University of Medical Science, Shiga, Japan (M.K., M.H.). Originally published1 Feb 2012https://doi.org/10.1161/CIRCEP.111.966549Circulation: Arrhythmia and Electrophysiology. 2012;5:e14–e17The subject of this report is a 38-year-old woman who often experienced syncope since childhood. Syncope occurred >10 times a year and was associated with convulsion during exercise and emotionally exciting situations. The patient's 13-year-old daughter had also experienced frequent episodes of syncope and developed ventricular fibrillation (VF) during treadmill exercise testing that was successfully defibrillated with electric shock. Witnessing this situation, the patient also lost consciousness, with documented VF that was converted to sinus rhythm by cardiopulmonary resuscitation without electric defibrillation.Both the patient and her daughter were admitted to our hospital. We performed echocardiography, coronary angiography, and cardiac CT, the results of which revealed no structural heart disease. Resting 12-lead ECG did not indicate any abnormalities, including long-QT syndrome or Brugada syndrome. A signal-averaged ECG revealed no late potentials. Treadmill exercise testing easily induced bigeminal ventricular premature contractions (VPCs) with a right bundle branch block configuration and inferior axis (Figure 1A), and the exercise was terminated because of intolerable symptoms. Catecholamine stress test was started with administration of continuous intravenous infusion of epinephrine in a stepwise manner from 0.025 μg/kg per minute.1 During epinephrine infusion at a rate of 0.1 μg/kg per minute, multifocal VPCs (VPC #1, right bundle branch block configuration and superior axis; VPC #2, right bundle branch block configuration and inferior axis [the same VPC configuration as that induced during the treadmill exercise testing]; and VPC #3, left bundle branch block configuration and inferior axis) appeared, and VPC #1 following VPC #2 subsequently induced VF (Figure 1B).Download figureDownload PowerPointFigure 1. A, Twelve-lead ECG recording during treadmill exercise testing. Bigeminal ventricular premature contractions (VPCs) appeared during the second stage of the Bruce protocol. VPC morphology represented a right bundle branch block configuration and inferior axis. Because the patient experienced intolerable symptoms, the test was discontinued. B, Epinephrine stress test. Continuous intravenous infusion of epinephrine was started from a rate of 0.025 μg/kg per minute, and the QT interval did not changed. At a rate of 0.1 μg/kg per minute, VPC #1 (right bundle branch block configuration and superior axis), VPC #2 (right bundle branch block configuration and inferior axis, same as that induced in the treadmill exercise testing), and VPC #3 (left bundle branch block configuration and inferior axis) were induced. Subsequently, VPC #1 following VPC #2 suddenly induced ventricular fibrillation, which was successfully terminated with electric shock.Administration of bisoprolol 5 mg QD was given but failed to suppress the exercise-induced bigeminal VPCs with the same morphology as induced previously. Because frequent deliveries of shock were believed to be likely, even with β-blocker treatment, catheter ablation was offered to the patient before implantable cardioverter-defibrillator (ICD) implantation. Catheter mapping and ablation for the bidirectional VPCs were performed with a 3D electroanatomic mapping system (CARTO; Biosense Webster) and a 3.5-mm-tip irrigation catheter (NaviStar; Thermo Cool) with only local anesthesia. No VPCs, ventricular tachycardia (VT), or VF were inducible with burst pacing and programmed stimulation from both right ventricular apex and right outflow tract during baseline and continuous intravenous infusion of isoproterenol.With epinephrine infusion at a rate of 0.1 μg/kg per minute, VPC #1 and VPC #2 appeared. VPC #1 was nonsustained, and a presystolic Purkinje potential was recorded at the left ventricular inferoseptal area near the posteromedial papillary muscle, which preceded the onset of VPC #1 by 18 ms. The unipolar electrogram from the ablation catheter during VPC #1 showed a QS pattern, and a perfect match of the QRS configuration was obtained by pace mapping (Figure 2). Radiofrequency energy application to this site provoked some ventricular acceleration beats, and several radiofrequency energy applications around the target site finally eliminated all the VPCs, resulting in complete suppression of all VPC #1.Download figureDownload PowerPointFigure 2. Activation mapping and pace mapping for VPC #1. A Purkinje potential was recorded from the left ventricular inferoseptum and preceded the QRS onset by 18 ms. The unipolar electrogram recorded from the distal electrode showed a QS pattern. Perfect pace mapping was obtained at this site. ABL indicates ablation catheter; CS, coronary sinus; His, His bundle; LAO, left anterior oblique; RAO, right anterior oblique; RVa, right ventricular apex; SR, sinus rhythm; VPC, ventricular premature contraction.After the ablation of VPC #1, isolated occurrences of VPC #2 continued, and a local bipolar electrogram recorded on the left coronary cusp showed discrete prepotential that preceded the onset of VPC #2 by 65 ms, and a perfect match of the QRS configuration was obtained by pace mapping (Figure 3). Radiofrequency energy application to the left coronary cusp abolished VPC #2 4 s after the onset of radiofrequency energy application. After successful catheter ablation of bidirectional VPCs, neither VPCs nor VF were inducible, even with an infusion of epinephrine of up to 1.2 μg/kg per minute (a >10 times higher dose than provocation). Precise ablation sites in a 3D electroanatomic mapping merged with contrast-enhanced CT are shown in Figure 4.Download figureDownload PowerPointFigure 3. Activation mapping and pace mapping for VPC #2. A local bipolar electrogram recorded from the LCC showed a discrete prepotential that preceded the QRS onset by 65 ms associated with a QS pattern of unipolar electrogram. Perfect pace mapping was obtained at this site. ABL indicates ablation catheter; CS, coronary sinus; His, His bundle; LAO, left anterior oblique; LCC, left coronary cusp; RAO, right anterior oblique; RVa, right ventricular apex; SR, sinus rhythm; VPC, ventricular premature contraction.Download figureDownload PowerPointFigure 4. Electroanatomic mapping merged with contrast-enhanced CT. Red tags indicate the ABL sites. Blue tags indicate the sites with perfect pace mapping, and yellow tags indicate the sites with Purkinje potentials during sinus rhythm. The sites with perfect pace mapping and the earliest activation for VPC #1 were localized in the inferoseptal site adjacent to the base of the posteromedial papillary muscle (red arrow). Successful ablation site of VPC #2 was on the left coronary cusp (blue arrow). ABL indicates ablation; LAO, left anterior oblique; LCC, left coronary cusp; NCC, noncoronary cusp; RAO, right anterior oblique; RCC, right coronary cusp; VPC, ventricular premature contraction.ICD implantation was performed, and the patient was discharged from the hospital on bisoprolol 2.5 mg QD. Serial Holter ECGs after the ablation showed only 3 to 5 isolated VPCs with a different morphology from the previously observed VPCs, and treadmill exercise testing induced no VPCs at the maximal workload. During 16-month follow-up, neither episodes of syncope nor ICD therapy occurred. Genetic analysis revealed a mutation in the ryanodine receptor gene (RyR2), and a diagnosis of catecholaminergic polymorphic VT (CPVT) was confirmed (Figure 5).2 The patient's daughter was also given a diagnosis of CPVT with same mutation in RyR2 and had catheter ablation for the origins of bidirectional VT. Although she refused ICD implantation, she had not experienced any episode of VT or syncope with β-blocker treatment.Download figureDownload PowerPointFigure 5. Results of genetic analysis. A mutation in the ryanodine receptor gene (RyR2) was detected in both the patient and her daughter. The mutation was not detected in the patient's sister.The generally accepted therapy for CPVT has been β-blockers,3 and the additional administration of flecainide or verapamil to β-blockers has been reported to be effective; however, the effects of those drugs are not fully standardized. For medically refractory cases, sympathetic denervation is one of the alternative treatment options. The ICD is considered the definitive therapy for the prevention of sudden cardiac death; however, failure to prevent sudden cardiac death has been reported in several cases because ICD shock delivery might lead to catecholamine release, resulting in an electric storm.4 This concern prompted the decision to attempt catheter ablation of VPCs triggering VF. Although several reports have described successful catheter ablation of VPCs triggering VF in some patients with structurally normal hearts, such as those with Brugada syndrome, long-QT syndrome, and idiopathic VF, successful catheter ablation of VPCs triggering VF in CPVT has not been reported. Cerrone and colleagues5 reported that the mechanism of CPVT was due to the delayed afterdepolarization-induced triggered activity in a focal Purkinje network in a knock-in (RyR2) mouse. However, whether the Purkinje system is related to the mechanism of VF in CPVT or just trigger origin is still unknown.To our knowledge, this is the first report of successful catheter ablation of the bidirectional VPCs that trigger VF, and this procedure could become one of the adjunctive therapies in patients with CPVT. To clarify the effectiveness and safety of this procedure, more cases and longer-term observation are mandatory.DisclosuresNone.FootnotesCorrespondence to Kazutaka Aonuma, MD, Cardiovascular Division, Institute of Clinical Medicine, Graduate School of Comprehensive Human Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan. E-mail [email protected]tsukuba.ac.jpReferences1. Krahn AD, Gollob M, Yee R, Gula LJ, Skanes AC, Walker BD, Klein GJ. Diagnosis of unexplained cardiac arrest: role of adrenaline and procainamide infusion. Circulation. 2005; 112:2228–2234.LinkGoogle Scholar2. 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Leenhardt A, Denjoy I and Guicheney P (2012) Catecholaminergic Polymorphic Ventricular Tachycardia, Circulation: Arrhythmia and Electrophysiology, 5:5, (1044-1052), Online publication date: 1-Oct-2012. February 2012Vol 5, Issue 1 Advertisement Article InformationMetrics © 2012 American Heart Association, Inc.https://doi.org/10.1161/CIRCEP.111.966549PMID: 22334434 Manuscript receivedJuly 26, 2011Manuscript acceptedJanuary 5, 2012Originally publishedFebruary 1, 2012 Keywordscatecholaminergic polymorphic ventricular tachycardiaarrhythmiacatheter ablationPDF download Advertisement SubjectsArrhythmiasCatheter Ablation and Implantable Cardioverter-Defibrillator
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