Congenital EP Featured Articles of July 2017

Congenital Pediatric Cardiac EP Reviews of July/August 2017 Manuscripts

 

A Multicenter Review of Ablation in the Aortic Cusps in Young People

Nguyen MB, Ceresnak SR, Janson CM, Fishberger SB, Love BA, Blaufox AD, Motonaga KS, Dubin AM, Nappo L, Pass RH.

Pacing and Clinical Electrophysiology. 2017; 40:798-802.

 

Take Home Points:

 

  • Catheter ablation in the aortic cusps for the treatment of arrhythmias in young patients is infrequently pursued, but can be performed safely and with high success.
  • Overall experience with aortic cusp ablation in young patients remains limited, but highly supports the following: comprehensive mapping of arrhythmia targets endocardially before pursuing the aortic cusp sites; appropriate imaging of the aortic cusps and coronary arterial origins before, during, and after ablation; and post-procedural assessments to evaluate aortic valve and ventricular function.

 

Philip-Chang_Headshot (small)Comment from Dr. Philip Chang (Gainesville, FL), section editor of Congenital Electrophysiology Journal Watch:  Though rarely done in young patients, overall experience with catheter ablation within the aortic cusps has been growing, primarily within the adult electrophysiology community, and published results have generally been favorable across a variety of arrhythmia types.  Experience with this ablation approach in young patients is limited and far less published.  In this study, Pass et al. sought to provide a multicenter review of the experience with this ablation approach from 5 medium-large sized pediatric EP centers.

 

Following IRB approval at all centers, retrospective review was performed and all cases in patients <21yo and involving aortic cusp ablation were included.  The authors collected general demographic data along with cardiac-specific data, procedural details, and any reported complications for descriptive analysis.

 

A total of 13 patients/cases were found and included with the cohort’s median age being 16yo (range 10-20.5yo), median weight 57.5 kg (range 31-108 kg), median BSA 1.58 m2 (range 1.12-2.33 m2), and fairly even gender distribution (54% male).  All subjects had structurally normal hearts, preserved ventricular function, and no aortic valve pathology.  Standard and conventional diagnostic EPS and conventional intracardiac mapping and attempted arrhythmia treatment were incorporated before pursuing aortic cusp mapping and ablation in all cases.  Electroanatomic mapping (EAM) was incorporated in the majority of cases (12/13).  When aortic cusp mapping and ablation was pursued, aortic root angiography was performed first in RAO and LAO projections.  Selective coronary angiography was not performed based on the procedural description and details provided by the authors.  A standard 4-mm tip RF ablation catheter was used in 11/13 cases (85%) while irrigated-tip RF ablation was performed in the remaining 2 cases.  For standard RF delivery, powers were limited to 30-50 W and maximum temperature limit was 60o C.  Power was <35 W for irrigated RF deliveries.  Cryoenergy was used in 1 case before changing to RF due to lack of success.  Acute success with aortic cusp ablation using RF energy was achieved in all cases.  Post-ablation aortic root angiography was performed in all cases.  Intracardiac echo (ICE) was utilized in the most recent 3 cases included in the cohort.  Post-procedural echo and ECG assessments were performed within 14 days after the procedure.  Of note, the authors did not report the exact percentage of cases that aortic cusp ablation accounted for at individual centers or collectively.  The approach to anticoagulation and target ACT values were not reported.

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Table 1 outlines the variables collected from the 13 cases included.  Ventricular arrhythmias (VT or PVCs) accounted for 69% of the arrhythmias treated (9/13 cases) and most of these were ablated within the noncoronary cusp (NCC; 8/9 cases).  The authors noted the unusually high proportion of NCC targets for ventricular arrhythmias in this young cohort in comparison to what is more typically noted in adult patients.  A total of 3 cases involved anteroseptal pathways (2 concealed, 1 WPW) and the last case involved ectopic atrial tachycardia.  Pseudoaneurysm involving the femoral arterial access site occurred in 1 patient.  Otherwise, no other complications were reported either acutely during the procedure or on post-procedural assessment.  Recurrence of PVCs occurred in 1 case over a median follow-up time of 20 months (range 7-86 months), which was described by the authors as involving very minimal intra-procedural PVC burden that prevented detailed mapping.  Table 2 outlines the respective cusps where ablation was performed in each arrhythmia subtype.  The authors did not report the total number of ablation lesions or duration of RF deliveries that were performed in each case or collectively.

 

Though limited by very small sample size despite its multicenter design, the study provides some important insights for consideration.  First, acute success with low complication rate can be achieved in the majority of patients where the target for ablation is mapped to the aortic cusps.  The authors acknowledged the sample size limitation, but also highlight this as a demonstration of how infrequent aortic cusp mapping and ablation appears to be of necessity (13 cases across 5 institutions over a 6-7 year period).  The exact percentages that these cases accounted for was not reported but would be expected to be extremely low.  While the low percentage likely reflects the low incidence of arrhythmia targets from the cusp locations, the authors also noted that the rarity may also reflect lack of performance secondary to concerns over potential complications.  The small sample size, along with relative paucity of published experience and data also call for more experience and pooling of data to determine best practices in terms of procedural setup, angiography, integration of ICE, necessity of EAM, and post-procedural monitoring and follow-up.

 

The Utility of Exercise Testing in Risk Stratification of Asymptomatic Patients with Type 1 Brugada Pattern

Subramanian M, Prabhu MA, Harikrishnan MS, Shekhar SS, Pai PG, Natarjan K.

J Cardiovasc Electrophysiol 2017; 28:677-683.

 

Take Home Points:

 

  • Treadmill exercise testing may provide data that can aid in the identification of higher risk groups of asymptomatic patients with type 1 Brugada pattern on ECG
  • Treadmill exercise testing in patients with type 1 Brugada pattern on ECG demonstrates ECG changes at peak exercise and recovery that reflect Na channel dysfunction as well as autonomic imbalances that may contribute, in part, to the basis of developing ventricular arrhythmias.

 

Comment from Dr. Philip Chang (Gainesville, FL), section editor of Congenital Electrophysiology Journal Watch:  Risk stratification of asymptomatic patients who are found to have type 1 Brugada patterns of standard 12-lead ECG remains challenging.  While ICD therapy can provide survival benefit, the low true sudden death event rate and relatively high complication rate with ICDs further complicates the determination of who warrants primary prevention ICD implantation in this patient population.  Subramanian et al. sought to evaluate the utility of standard treadmill exercise testing in uncovering ECG changes that could help identify higher risk patients among a group of subjects with type 1 Brugada patterns on ECG.

 

Following IRB approval, the authors performed a retrospective, case controlled analysis of their experience with exercise testing in otherwise asymptomatic patients >18yo with a spontaneous or pharmacologically induced type 1 Brugada pattern on ECG and no structural cardiac abnormalities over the time period January 2007-December 2015.  A total of 75 patients were included with the majority (72.2%) noted to have spontaneous type 1 patterns while the remaining subjects had an induced type 1 pattern with flecainide.  An ICD was implanted in 22/75 study patients with the majority (20/22) for inducible VT/VF during EPS and 1 patient each for family history of Brugada with sudden death (1/22) and history of spontaneous nonsustained VT (1/22).  The control group was comprised of age- and sex-matched healthy subjects.  Standard symptom-limited exercise testing with Bruce protocol was performed.  All subjects were not on any antiarrhythmic medications.  Testing involved 12-lead ECG collections at rest, at the end of each exercise stage, at peak exercise, and at 1-minute intervals during a 6-minute recovery phase (further divided into early and late recovery segments).  Clinical follow-up was conducted every 6 months or sooner if syncope or ICD therapy occurred (in patients implanted with ICDs).

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Tables 1 and 2 show baseline comparisons between study and control subjects (table 1) and comparisons between study subjects with and without major arrhythmic events (MAEs; table 2).  Subjects with type 1 Brugada patterns had significantly longer PR intervals and slower resting heart rates compared to controls.  Among type 1 Brugada patients with and without MAEs, there were no significant differences in variables.

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Exercise testing resulted in measurable changes in S wave upslope, J point, and maximum ST segment elevation during exercise and recovery in patients with type 1 Brugada pattern, and particularly in those who experienced subsequent MAEs. (Figure 2)  Changes were noted in the precordial leads but interestingly, also in lead aVR as well.  The authors noted longer QRS complex durations at peak exercise in type 1 Brugada patients compared to controls (p <0.001).  They also noted significantly slower and delayed heart rate recovery during the recovery period among type 1 Brugada patients compared to controls (p <0.05).  Nonsustained VT occurred in early recovery in 1 patients with a type 1 Brugada pattern.  Over a mean follow-up duration of 77.9 ± 28.9 months, 8/72 study patients (11.1%) had MAEs (5 VT/VF on ICD and 3 sudden deaths) and 3 patients were lost to follow-up.

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Regression analysis showed precordial S wave upslope duration ratio ≥ 30% at peak exercise, aVR augmented J point elevation ≥ 0.3 mV in late recovery, and delayed heart rate recovery ≤ 40% of maximum heart rate in late recovery as being independent predictors of MAEs in type 1 Brugada patients. (Table 3)  Furthermore, they noted a cumulative risk with increasing number or risk factors in the same patient. (Figure 5)

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This study offers several interesting insights with regards to the management of the asymptomatic type 1 Brugada pattern patient.  First, it offers insights into measurable changes on a noninvasive testing modality that is commonly done and widely available that could help to determine which asymptomatic patients may be at higher risk of arrhythmic events.  Second, the changes that occur during exercise testing also appear to highlight a potential autonomic influence, which may vary from patient to patient and may contribute to higher SCD risk in some compared to others.  This offers new avenues to pursue in terms of therapies to modulate autonomics and perhaps new functional analyses in certain genetic mutations which may be more affected by autonomic factors.  The notable ECG changes in lead aVR are also a novel insight, particularly as most attention is focused on the right precordial leads in Brugada syndrome.  Finally, the presence of measurable ECG changes with standard exercise testing also provides insights into ways to monitor treatment response and titrate medical therapy in Brugada syndrome (though pharmacotherapy to treat Brugada syndrome is very limited to begin with).

There are several limitations noted in this study, including some limitations to the applicability and extrapolation to pediatric patients since this was an adult cohort that excluded patients <18yo.  The overall sample size of the study cohort was small in this single institution study and there may be regional and international variations in disease phenotype and practice composition.  This may be 1 explanation as to the rather high MAE incidence of 11.1%.  Nearly a quarter of study patients also had pharmacologic testing done, though the authors did not disclose the reasons for testing and therefore whether these patients were truly asymptomatic is in question.  The integration of genetic testing was also not discussed.

 

 

CHD EP July 2017

 

  1. Management of postoperative junctional ectopic tachycardia in pediatric patients: a survey of 30 centers in Germany, Austria, and Switzerland.

Entenmann A, Michel M, Herberg U, Haas N, Kumpf M, Gass M, Egender F, Gebauer R.

Eur J Pediatr. 2017 Jul 21. doi: 10.1007/s00431-017-2969-x. [Epub ahead of print]

PMID: 28730319

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  1. Genotype Positive Long QT Syndrome in Patients With Coexisting Congenital Heart Disease.

Ebrahim MA, Williams MR, Shepard S, Perry JC.

Am J Cardiol. 2017 Jul 15;120(2):256-261. doi: 10.1016/j.amjcard.2017.04.018. Epub 2017 Apr 27.

PMID: 28532774

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  1. Increased risk of thromboembolic events in adult congenital heart disease patients with atrial tachyarrhythmias: Bias due to the data sparsity.

Ayubi E, Safiri S, Mansournia MA.

Int J Cardiol. 2017 Jul 15;239:20. doi: 10.1016/j.ijcard.2017.02.133. No abstract available.

PMID: 28560967

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  1. How to Perform Transconduit and Transbaffle Puncture in Patients who have previously undergone the Fontan or Mustard Operation.

Uhm JS, Kim NK, Kim TH, Joung B, Pak HN, Lee MH.

Heart Rhythm. 2017 Jul 14. pii: S1547-5271(17)30877-9. doi: 10.1016/j.hrthm.2017.07.020. [Epub ahead of print] No abstract available.

PMID: 28716702

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  1. A focus on pharmacological management of catecholaminergic polymorphic ventricular tachycardia.

Barbanti C, Maltret A, Sidi D.

Mini Rev Med Chem. 2017 Jul 7. doi: 10.2174/1389557517666170707100923. [Epub ahead of print]

PMID: 28685702

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  1. Does pharmacological therapy still play a role in preventing sudden death in surgically treated Tetralogy of Fallot?

Bronzetti G, Brighenti M, Bonvicini M.

Mini Rev Med Chem. 2017 Jul 7. doi: 10.2174/1389557517666170707101411. [Epub ahead of print]

PMID: 28685697

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  1. Major adverse events and atrial tachycardia in Ebstein’s anomaly predicted by cardiovascular magnetic resonance.

Rydman R, Shiina Y, Diller GP, Niwa K, Li W, Uemura H, Uebing A, Barbero U, Bouzas B, Ernst S, Wong T, Pennell DJ, Gatzoulis MA, Babu-Narayan SV.

Heart. 2017 Jul 6. pii: heartjnl-2017-311274. doi: 10.1136/heartjnl-2017-311274. [Epub ahead of print]

PMID: 28684436 Free Article

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  1. Prevention of Sudden Cardiac Death in Adults With Congenital Heart Disease: Do the Guidelines Fall Short?

Vehmeijer JT, Koyak Z, Budts W, Harris L, Silversides CK, Oechslin EN, Bouma BJ, Zwinderman AH, Mulder BJM, de Groot JR.

Circ Arrhythm Electrophysiol. 2017 Jul;10(7). pii: e005093. doi: 10.1161/CIRCEP.116.005093.

PMID: 28696220

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  1. Where to Throw That Shoe? Catheter Ablation of Atrioventricular Nodal Reentrant Tachycardia in Congenital Heart Disease.

Sherwin ED, Berul CI.

Circ Arrhythm Electrophysiol. 2017 Jul;10(7). pii: e005525. doi: 10.1161/CIRCEP.117.005525. No abstract available.

PMID: 28687672

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  1. Atrioventricular Nodal Reentrant Tachycardia in Patients With Congenital Heart Disease: Outcome After Catheter Ablation.

Papagiannis J, Beissel DJ, Krause U, Cabrera M, Telishevska M, Seslar S, Johnsrude C, Anderson C, Tisma-Dupanovic S, Connelly D, Avramidis D, Carter C, Kornyei L, Law I, Von Bergen N, Janusek J, Silva J, Rosenthal E, Willcox M, Kubus P, Hessling G, Paul T; Pediatric and Congenital Electrophysiology Society.

Circ Arrhythm Electrophysiol. 2017 Jul;10(7). pii: e004869. doi: 10.1161/CIRCEP.116.004869. Epub 2017 Jul 7.

PMID: 28687669

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  1. Appearance of QRS fragmentation late after Mustard/Senning repair is associated with adverse outcome.

Helsen F, Vandenberk B, De Meester P, Van De Bruaene A, Gabriels C, Troost E, Gewillig M, Meyns B, Willems R, Budts W; FH and BV contributed equally to this study.

Heart. 2017 Jul;103(13):1036-1042. doi: 10.1136/heartjnl-2016-310512. Epub 2017 Feb 9.

PMID: 28183791

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  1. Localized atrial reentrant tachycardia in tetralogy of Fallot: Ultra-high-resolution mapping and termination by nonpropagated atrial pacing stimulus.

Lee A, Kite J, Davison O, Haqqani HM.

Heart Rhythm. 2017 Jul;14(7):1102-1103. doi: 10.1016/j.hrthm.2017.03.007. Epub 2017 Mar 18. No abstract available.

PMID: 28323170

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  1. Congenital heart block and immune mediated sensorineural hearing loss: possible cross reactivity of immune response.

Bason C, Pagnini I, Brucato A, Maestroni S, Puccetti A, Lunardi C, Cimaz R.

Lupus. 2017 Jul;26(8):835-840. doi: 10.1177/0961203316682099. Epub 2016 Dec 5.

PMID: 27913750

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  1. Atrial undersensing secondary to quiet timer blanking in pediatric and congenital heart disease patients.

von Alvensleben JC, Schaffer M, Brateng C, Collins KK.

Pacing Clin Electrophysiol. 2017 Jul;40(7):843-849. doi: 10.1111/pace.13101. Epub 2017 Jun 14.

PMID: 28436549

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  1. Discrimination between QRS and T Waves Using a Right Parasternal Lead for S-ICD in a Patient with a Single Ventricle.

Nishiyama T, Kimura T, Nishiyama N, Aizawa Y, Fukuda K, Takatsuki S.

Pacing Clin Electrophysiol. 2017 Jul;40(7):904-907. doi: 10.1111/pace.13046. Epub 2017 Mar 3.

PMID: 28185283

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  1. Pediatric Dosing of Intravenous Sotalol Based on Body Surface Area in Patients with Arrhythmia.

Li X, Zhang Y, Liu H, Jiang H, Ge H, Zhang Y.

Pediatr Cardiol. 2017 Jul 28. doi: 10.1007/s00246-017-1683-9. [Epub ahead of print]

PMID: 28755092

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  1. Radiofrequency ablation of fast ventricular tachycardia causing an ICD storm in an infant with hypertrophic cardiomyopathy.

Ergul Y, Ozyilmaz I, Bilici M, Ozturk E, Haydin S, Guzeltas A.

Pacing Clin Electrophysiol. 2017 Jul 27. doi: 10.1111/pace.13154. [Epub ahead of print]

PMID: 28749010

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  1. NS1643 enhances ionic currents in a G604S-WT hERG co-expression system associated with long QT syndrome 2.

Huo J, Guo X, Lu Q, Qiang H, Liu P, Bai L, Huang CLH, Zhang Y, Ma A.

Clin Exp Pharmacol Physiol. 2017 Jul 25. doi: 10.1111/1440-1681.12820. [Epub ahead of print]

PMID: 28741726

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  1. Contemporary Outcomes in Patients With Long QT Syndrome.

Rohatgi RK, Sugrue A, Bos JM, Cannon BC, Asirvatham SJ, Moir C, Owen HJ, Bos KM, Kruisselbrink T, Ackerman MJ.

J Am Coll Cardiol. 2017 Jul 25;70(4):453-462. doi: 10.1016/j.jacc.2017.05.046.

PMID: 28728690

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  1. What endocardial right ventricular pacing site shows better contractility and synchrony in children and adolescents?

Silvetti MS, Ammirati A, Palmieri R, Pazzano V, Placidi S, Ravà L, Remoli R, Saputo FA, Verticelli L, Drago F.

Pacing Clin Electrophysiol. 2017 Jul 25. doi: 10.1111/pace.13153. [Epub ahead of print]

PMID: 28744930

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  1. Potential utility of pulsed Doppler for prenatal diagnosis of fetal ventricular tachycardia secondary to long QT syndrome.

Miyoshi T, Sakaguchi H, Shiraishi I, Yoshimatsu J, Ikeda T.

Ultrasound Obstet Gynecol. 2017 Jul 25. doi: 10.1002/uog.18819. [Epub ahead of print]

PMID: 28741754

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  1. Plakophilin-2 is required for transcription of genes that control calcium cycling and cardiac rhythm.

Cerrone M, Montnach J, Lin X, Zhao YT, Zhang M, Agullo-Pascual E, Leo-Macias A, Alvarado FJ, Dolgalev I, Karathanos TV, Malkani K, Van Opbergen CJM, van Bavel JJA, Yang HQ, Vasquez C, Tester D, Fowler S, Liang F, Rothenberg E, Heguy A, Morley GE, Coetzee WA, Trayanova NA, Ackerman MJ, van Veen TAB, Valdivia HH, Delmar M.

Nat Commun. 2017 Jul 24;8(1):106. doi: 10.1038/s41467-017-00127-0.

PMID: 28740174 Free PMC Article

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  1. The impact of intrauterine treatment on fetal tachycardia: a nationwide survey in Japan.

Ueda K, Maeno Y, Miyoshi T, Inamura N, Kawataki M, Taketazu M, Nii M, Hagiwara A, Horigome H, Shozu M, Shimizu W, Yasukochi S, Yoda H, Shiraishi I, Sakaguchi H, Katsuragi S, Sago H, Ikeda T; ; on behalf of Japan Fetal Arrhythmia Group.

J Matern Fetal Neonatal Med. 2017 Jul 19:1-6. doi: 10.1080/14767058.2017.1350159. [Epub ahead of print]

PMID: 28720014

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  1. Utility of Echocardiography in Detecting Silent Complications After Pediatric Catheter Ablations.

Amdani SM, Sallaam S, Karpawich PP, Aggarwal S.

Pediatr Cardiol. 2017 Jul 15. doi: 10.1007/s00246-017-1680-z. [Epub ahead of print]

PMID: 28711964

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  1. Bridge to Success: A Better Method of Cryoablation for Atrioventricular Nodal Reentrant Tachycardia in Children.

Reddy CD, Ceresnak SR, Motonaga KS, Avasarala K, Feller C, Trela A, Hanisch D, Dubin AM.

Heart Rhythm. 2017 Jul 14. pii: S1547-5271(17)30875-5. doi: 10.1016/j.hrthm.2017.07.018. [Epub ahead of print]

PMID: 28716699

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  1. Uptake of Predictive Genetic Testing and Cardiac Evaluation for Children at Risk for an Inherited Arrhythmia or Cardiomyopathy.

Christian S, Atallah J, Clegg R, Giuffre M, Huculak C, Dzwiniel T, Parboosingh J, Taylor S, Somerville M.

J Genet Couns. 2017 Jul 11. doi: 10.1007/s10897-017-0129-0. [Epub ahead of print]

PMID: 28699125

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  1. Does pharmacological therapy still play a role in preventing sudden death in surgically treated Tetralogy of Fallot?

Bronzetti G, Brighenti M, Bonvicini M.

Mini Rev Med Chem. 2017 Jul 7. doi: 10.2174/1389557517666170707101411. [Epub ahead of print]

PMID: 28685697

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  1. Therapy Of Cardiac Arrhythmias In Children: An Emerging Role Of Electroanatomical Mapping Systems.

Matteo C, Maurizio M, Viviana T, Scarano M, Paolo B, Giuseppe D.

Curr Vasc Pharmacol. 2017 Jul 5. doi: 10.2174/1570161115666170705155542. [Epub ahead of print]

PMID: 28677509

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  1. [Clinical analysis of pacing therapy and treatment of complications during follow-up in children].

Zhao PJ, Chen YW, Li F, Li Y, Yang JP, Wu JJ.

Zhonghua Er Ke Za Zhi. 2017 Jul 2;55(7):514-518. doi: 10.3760/cma.j.issn.0578-1310.2017.07.009. Chinese.

PMID: 28728260

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  1. Successful use of sirolimus for refractory atrial ectopic tachycardia in a child with cardiac rhabdomyoma.

Ninic S, Kalaba M, Jovicic B, Vukomanovic V, Prijic S, Vucetic B, Kravljanac R, Vujic A, Kosutic J.

Ann Noninvasive Electrocardiol. 2017 Jul;22(4). doi: 10.1111/anec.12435. Epub 2017 Feb 19.

PMID: 28217909

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  1. Effects of Acute Carbon Monoxide Poisoning on ECG and Echocardiographic Parameters in Children.

Ozyurt A, Karpuz D, Yucel A, Tosun MD, Kibar AE, Hallioglu O.

Cardiovasc Toxicol. 2017 Jul;17(3):326-334. doi: 10.1007/s12012-016-9389-4.

PMID: 27778147

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Select item 27509882

 

  1. Risk factors for sudden cardiac death in childhood hypertrophic cardiomyopathy: A systematic review and meta-analysis.

Norrish G, Cantarutti N, Pissaridou E, Ridout DA, Limongelli G, Elliott PM, Kaski JP.

Eur J Prev Cardiol. 2017 Jul;24(11):1220-1230. doi: 10.1177/2047487317702519. Epub 2017 May 9.

PMID: 28482693

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  1. To the Editors-Risk factors for complications in the implantation of epicardial pacemakers in neonates and infants.

Kean AC, Rodefeld MD.

Heart Rhythm. 2017 Jul;14(7):e53. doi: 10.1016/j.hrthm.2017.03.021. Epub 2017 Apr 5. No abstract available.

PMID: 28389305

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  1. Skin sympathetic nerve activity precedes the onset and termination of paroxysmal atrial tachycardia and fibrillation.

Uradu A, Wan J, Doytchinova A, Wright KC, Lin AYT, Chen LS, Shen C, Lin SF, Everett TH 4th, Chen PS.

Heart Rhythm. 2017 Jul;14(7):964-971. doi: 10.1016/j.hrthm.2017.03.030. Epub 2017 Mar 24.

PMID: 28347833

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  1. Efficacy of Flecainide in the Treatment of Catecholaminergic Polymorphic Ventricular Tachycardia: A Randomized Clinical Trial.

Kannankeril PJ, Moore JP, Cerrone M, Priori SG, Kertesz NJ, Ro PS, Batra AS, Kaufman ES, Fairbrother DL, Saarel EV, Etheridge SP, Kanter RJ, Carboni MP, Dzurik MV, Fountain D, Chen H, Ely EW, Roden DM, Knollmann BC.

JAMA Cardiol. 2017 Jul 1;2(7):759-766. doi: 10.1001/jamacardio.2017.1320.

PMID: 28492868

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  1. Transesophageal and invasive electrophysiologic evaluation in children with Wolff-Parkinson-White pattern.

Koca S, Pac FA, Kavurt AV, Cay S, Mihcioglu A, Aras D, Topaloglu S.

Pacing Clin Electrophysiol. 2017 Jul;40(7):808-814. doi: 10.1111/pace.13100. Epub 2017 Jun 1.

PMID: 28436586

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Congenital EP Featured Articles of June 2017

 

Congenital and Pediatric Cardiac EP Reviews of June 2017 Manuscripts

 

Prospective Study of Adenosine on Atrioventricular Nodal Conduction in Pediatric and Young Adult Patients After Heart Transplantation.

Flyer JN, Zuckerman WA, Richmond ME, Anderson BR, Mendelsberg TG, McAllister JM, Liberman L, Addonizio LJ, Silver ES.

Circulation. 2017 Jun 20;135(25):2485-2493. doi: 10.1161/CIRCULATIONAHA.117.028087. Epub 2017 Apr 27.

PMID: 28450351

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Take Home Points:

  • Supraventricular tachycardia can be seen in up to 50% of children and adults after heart transplantation.
  • Adenosine, a endogenous nucleoside that results in sinus slowing and AV block, has been considered relatively contraindicated in heart transplant recipients due to post-transplant denervation
  • Adenosine use at low doses of 25 μg/kg or 1.5 mg were found to be effective in causing AV block in healthy heart transplant patients in sinus rhythm
  • AV block was seen in 96% of patients with escalating adenosine administration up to maximal dose of 200 μg/kg or 12 mg
  • There were no adverse events seen after adenosine administration including no clinically significant asystole (≥ 12 seconds) requiring rescue ventricular pacing
  • The use of adenosine during supraventricular tachycardia in post-heart transplants patients was not evaluated and therefore, the dosing, response and safety of adenosine in that scenario cannot be commented on based on this study.

 

A PatelComment from Dr. Akash Patel (San Francisco), section editor of Congenital Electrophysiology Journal Watch:  Previous limited data has suggested heart transplant patients are at adverse risk to adenosine in the setting of cardiac denervation after transplantation. In particular, adenosine exposure in this setting has been thought to lead to excessive AV block and bradycardia. Due to this concern, adenosine is relatively contraindicated in post-heart transplant patients and thus uncommonly used. However, up to 50% of children and adults with heart transplantation can be affected by supraventricular tachycardia with adenosine potentially providing a therapeutic and/or diagnostic option.  This single center prospective study from New York Presbyterian/Morgan Stanley Children’s Hospital, Columbia University Medical Center aimed to improve our understanding of the safety and efficacy of adenosine in pediatric and young adult patients who have undergone heart transplantation with hopes to reconsider its use in this population.

 

All healthy patients ≥ 2 weeks post-cardiac transplantation were included if they agreed to consent and were excluded if there was evidence of rejection (clinical/humeral/cellular), graft vasculopathy, concurrent use of intravenous inotropic medication, concurrent treatment for rejection, conduction disease (first-, second-, or third-degree AV block, preexisting sinus node dysfunction), or systolic ventricular dysfunction. At the time of routine post-cardiac transplant catheterization, eligible patients underwent adenosine testing.

The study group included 80 patients (55% male) with a median age of 13.6 years (Range: 1.1 – 24 year). The median weight was 50.4 kg (Range: 7.8 – 120 kg). The indications for transplantation included cardiomyopathy (60%), congenital heart disease (30%), retransplantation (7.5%), and other (2.5%). The most common type of transplantation was bicaval (71%) followed by biatrial (28%). Prior history of rejection was seen in 49%. There was use of dipyridamole in 53% which is a medication known to effect adenosine metabolism. This medication was stopped 3 days before catheterization in all patients. There was use of antiarrhythmic drugs – beta-blocker (24%) and digoxin (2.5%)- but no data on indications or prior arrhythmia status. The cardiac catheterization procedures were done under general anesthesia in 64%.

After catheterization and biopsy were complete but before the removal of central access, a 4F quadripolar pacing catheter was introduced into the right ventricle with pacing thresholds tested and outputs set appropriately. Adenosine was given via central access in serial escalating doses based on weight until AV block or clinically significant asystole (either a sinus pause or AV block ≥ 12 seconds which were the predetermined criterion to initiate ventricular pacing) were seen. If patients weighed <60 kg, patients were given 12.5, 25, 50, 100, and 200 μg/kg of adenosine. If patients weighed ≥ 60 kg, patients were given 0.8, 1.5, 3, 6, and 12 mg.  See below.  The median maximal dose of adenosine given was 3.6 mg (IQR: 2.0 – 6.0 mg).

June EP v1

The primary outcome of the study was to assess the safety of adenosine.  There were no patients (0%) who had clinically significant asystole requiring rescue ventricular pacing after adenosine administration during the escalating adenosine protocol. See below.

 June EP V2

 

The secondary objective was to assess the efficacy of adenosine in the post-heart transplant patient. There was AV block seen in 77/80 (96%) of the cohort (see above).  There was sinus pause > 2 seconds seen in 4 (5%). The effect of AV nodal blockade was seen at doses as low as 25 μg/kg (< 60 kg) or 1.5 mg (≥ 60kg) in 12%. As expected, incremental escalations in dosing increased the percent of patients demonstrating AV nodal block. At up to initial standard dosing of 100 μg/kg (< 60 kg) or 6 mg (≥ 60kg), there was AV nodal blockade seen in 72%.  See Below.

June EP V3The AV nodal effects of adenosine varied in duration. The median longest R-R interval during AV block was 1.9 seconds (IQR: 1.4 – 3.2 seconds) (Example See Figure Below (A)) The mean total adenosine effect was 4.3 seconds (SD: ±2.0 seconds)  (Example: See Figure Below (B)). The absolute longest R-R interval and total adenosine effect in any patient was 8.4 seconds. The median consecutive non-conducted P waves during the longest pause were 2 (IQR, 1–3). The authors stated no variable predicted adenosine effect including prior rejection, maximal dose, weight, or time from transplant.

June EP v6

The use of adenosine was well tolerated with typical symptoms reported in the non-anesthetized group including shortness of breath, discomfort, chest pain, headache, and flushing. There were no adverse symptoms that resulted in premature termination of the protocol.

This study demonstrates the safety of adenosine use in a large healthy pediatric and young adult post-cardiac transplant cohort with no adverse effects including no clinically significant asystole requiring rescue ventricular pacing.  The authors conclude that adenosine is effective in causing AV node blockade at much lower doses – 25 μg/kg (< 60kg) or 1.5mg (≥ 60 kg) –  than PALS or ACLS standard dosing. As the effect is dose-dependent, gradual dose escalation can be considered up to maximal doses of 200 μg/kg (< the 60kg) or 12 mg (≥60kg) until AV blockade is achieved.

This study however does not address if and why lower doses are required and if there is an exaggerated response with adenosine use in post-transplant patients. In particular, it is unclear if the same lower doses given centrally in healthy age-based controls would have resulted in the same effect. In addition, in 1990 Ellenbogen et al (Circulation 1990;81: 821-828  PMID: 2306833) demonstrated there was evidence of a supersensitivity effect in adult patients. Since the dose escalation was terminated once AV block was seen, it is unclear if maximal dosing in all 80 patients would have resulted in an exaggerated response. The study design did not allow for answering these important questions but did show safety with their adenosine dose escalation protocol.  The authors discuss the roles of cardiac denervation and reinnervation as it may play a factor in these issues, but interesting the study showed safe adenosine effect as early as 25 days post-transplant and overall no correlation between time of transplant and effective adenosine dose suggesting other factors may play a role.

Clearly there are limitations to this study with the most notable being that patients are known to be healthy, were not in supraventricular tachycardia at the time of adenosine administration, and the route of adenosine administration was via central access. From a practical standpoint, adenosine is often given peripherally and used in an acute setting. Therefore, the effect of adenosine in the “healthy patient” is a less likely scenario as their rejection status and function may not be known and they may be on antiarrhythmics or other medications that may affect the response to adenosine. Nevertheless, this study demonstrates that adenosine may be used safely in this population but a cautious approach using low doses should be undertaken.

 

Additional EP Articles Worth Reading.

 

Intraoperative arrhythmias in children with congenital heart disease: transient, innocent events? Houck CA, Ramdjan TTTK, Yaksh A, Teuwen CP, Lanters EAH, Bogers AJJC, de Groot NMS.Europace. 2017 Jun 28. doi: 10.1093/europace/eux072. [Epub ahead of print]

PMID: 28666343

 

Cardiac Fibroblast Transcriptome Analyses Support a Role for Interferogenic, Profibrotic and Inflammatory Genes in Anti-SSA/Ro-Associated Congenital Heart Block.

Clancy RM, Markham AJ, Jackson T, Rasmussen SE, Blumenberg M, Buyon JP.

Am J Physiol Heart Circ Physiol. 2017 Jun 16:ajpheart.00256.2017. doi: 10.1152/ajpheart.00256.2017. [Epub ahead of print]

PMID: 28626076

 

Cardiac Arrhythmias in Adults with Congenital Heart Disease.

Balaji S, Mandapati R, Shivkumar K.

Card Electrophysiol Clin. 2017 Jun;9(2):xv-xvi. doi: 10.1016/j.ccep.2017.04.001. No abstract available.

PMID: 28457248

 

Genotype-Phenotype Correlation of SCN5A Mutation for the Clinical and Electrocardiographic Characteristics of Probands With Brugada Syndrome: A Japanese Multicenter Registry.

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Circulation. 2017 Jun 6;135(23):2255-2270. doi: 10.1161/CIRCULATIONAHA.117.027983. Epub 2017 Mar 24.

PMID: 28341781

 

 

CHD EP June 2017

 

  1. Intraoperative arrhythmias in children with congenital heart disease: transient, innocent events?

Houck CA, Ramdjan TTTK, Yaksh A, Teuwen CP, Lanters EAH, Bogers AJJC, de Groot NMS.

Europace. 2017 Jun 28. doi: 10.1093/europace/eux072. [Epub ahead of print]

PMID: 28666343

 

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  1. Cardiac Fibroblast Transcriptome Analyses Support a Role for Interferogenic, Profibrotic and Inflammatory Genes in Anti-SSA/Ro-Associated Congenital Heart Block.

Clancy RM, Markham AJ, Jackson T, Rasmussen SE, Blumenberg M, Buyon JP.

Am J Physiol Heart Circ Physiol. 2017 Jun 16:ajpheart.00256.2017. doi: 10.1152/ajpheart.00256.2017. [Epub ahead of print]

PMID: 28626076

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