the official journal of korean society of cardiac...

The Official Journal of Korean Society of Cardiac Arrhythmia

Vol.11 No.3September 2010

ISSN 2005-9728

http://arrhythmia.circulation.or.kr

The Korean Society of Cardiac Arrhythmia

Main Topic Reviews

Article Review

ECG & EP Cases

Journal of Cardiac Arrhythmia

© Copyright 2010 Journal of Cardiac Arrhythmia Editorial Board & MMK Co., Ltd.All rights reserved. No part of this publication may be reproduced, stored in a retrieval system or transmitted in any form or by anymeans, electronic, mechanical, photocopying, recording or otherwise without permission in written form from the copyright holder. Thispublication is published by MMK Co., Ltd.

Tel 02-2007-5400 Fax 02-3452-5984 http://www.medimedia.co.kr E-mail: [email protected]

Journal of Cardiac

Arrhythmia

Main Topic Reviews

Article Review

ECG & EP Cases

Journal of Cardiac Arrhythmia

Vol.11 No.3 September 2010

Contents

Cover: Cardiac MRI showed bulging of RV apex withdyskinetic wall motion and focal aneurysm onsystolic phase. (page 41)

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Tai-Ho Rho, MDDivision of Cardiology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea

Diagnosis of bradyarrhythmias

ABSTRACTBradyarrhythmias, as manifested by sick sinus syndrome or AV (atiroventricular) block, cause diverse clinicalsigns and symptoms such as dizziness or syncope, shortness of breaths, fatigue, decreased exercise capacity,and decrease of cognitive functions. Those symptoms or signs are caused by a decreased blood flow to vitalorgans secondary to limited cardiac output. A permanent pacemaker is at present the only treatment forsymptomatic bradycardia, which is known to improve survival and quality of life. The diagnosis of bradycardiaconfirmed simply by proving drop in heart beats. The palpation of radial pulses or apical pulses, or theauscultation of heart beats sometime suffices. However, the diagnosis is usually confirmed by ECG. Episodesof bradyarrhythmias are not frequent in some patients, and in others, bradycardias occur in only specificclinical settings, which make the diagnosis difficult. To overcome these obstacles, ECG is repeated or othercomplicated studies are needed.

Key words: bradycardia sick sinus syndrome AV block

Received: June 25, 2010Accepted: September 30, 2010Correspondence: Tai-Ho Rho, MD, Division of Cardiology, Department ofInternal Medicine, College of Medicine, The Catholic University of Korea,505 Banpo-dong, Seocho-gu, Seoul 137-701, Korea Tel: 82-2-2258-1027, Fax: 82-2-2258-1030E-mail: [email protected]

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References

1. Menozzi C, Brignole M, Alboni P, Boni L, Paparell N, Gaggioli G,Lolli G. The natural course of untreated sick sinus syndrome andidentification of the variables predictive of unfavorable outcome.Am J Cardiol. 1998;82:1205-1209.

2. Sweeney MO, Hellkamp AS, Ellenbogen KA,Glotzer TV, SilvermanR, Yee R, Lee KL, Lamas GA; MOST Investigators. Prospectiverandomized study of mode switching in a clinical trial ofpacemaker therapy for sinus node dysfunction. J CardiovascElectrophysiol. 2004;15:153-160.

3. Harrison 1713-1723,2010. MIP

4. Assar MD, Krahn AD, Klein GJ, Yee R, Skanes AC. Optimalduration of monitoring in patients with unexplained syncope. AmJ Cardiol. 2003;92:1231-1233.

5. Lamas GA, Lee KL, Sweeney MO, Silverman R, Leon A, Yee R,Marinchak RA, Flaker G, Schron E, Orav EJ, Hellkamp AS, GreerS, McAnulty J, Ellenbogen K, Ehlert F, Freedman RA, Estes NA3rd, Greenspon A, Goldman L; Mode Selection Trial in Sinus-Node Dysfunction.. Ventricular pacing or dual-chamber pacing forsinus-node dysfunction. N Engl J Med. 2002;346:1854-1862.

6. Lamas GA, Lee K, Sweeney M, Leon A, Yee R, Ellenbogen K,Greer S, Wilber D, Silverman R, Marinchak R, Bernstein R,Mittleman RS, Lieberman EH, Sullivan C, Zorn L, Flaker G, SchronE, Orav EJ, Goldman L.. The mode selection trial (MOST) in sinusnode dysfunction: design, rationale, and baseline characteristicsof the first 1000 patients. Am Heart J. 2000;140:541-551.

7. Meytes I, Kaplinsky E, Yahini JH, Hanne-Paparo N, Neufeld HN.Wenckebach A-V block: a frequent feature following heavyphysical training. Am Heart J. 1975;90:426-430.

8. Talan DA, Bauernfeind RA, Ashley WW, Kanakis C Jr., Rosen KM.Twenty-four hour continuous ECG recordings in long-distancerunners. Chest. 1982;82:19-24.

9. Krahn AD, Klein GJ, Skanes AC, Yee R. Use of the implantableloop recorder in evaluation of patients with unexplained syncope.J Cardiovasc Electrophysiol. 2003;14:S70-S73.

10. Wilkoff B, Corey J, Blackburn G. A mathematical model of thecardiac chronotropic response to exercise. J Electrophysiol.1989;3:176-180.

11. Katritsis D, Camm AJ. Chronotropic incompetence: a proposalfor definition and diagnosis. Br Heart J. 1993;70:400-402.

12. Brignole M, Menozzi C, Lolli G, Bottoni N, Gaggioli G. Long-term outcome of paced and nonpaced patients with severecarotid sinus syndrome. Am J Cardiol. 1992;69:1039-1043.

13. Zipes DP. Second-degree atrioventricular block. Circulation.1979;60:465-472.

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Joong-Wha Chung, MD Division of Cardiology, Department of Internal Medicine, College of Medicine, Chosun University Hospital, Gwangju, Korea

Sinus node dysfunction

ABSTRACTSinus node dysfunction refers to a broad array of abnormalities in sinus node and atrial impulse formation andpropagation. While the dysfunction can have many causes, it usually is idiopathic. Diagnosis can be difficultbecause of its elusive findings on electrocardiogram or Holter monitor. The mainstay of treatment ispermanent pacemaker placement. The primary objective in this review is to identify the full scope of thesyndrome.

Key words: sinus node dysfunction sick sinus syndrome review

Received: June 1, 2010Revision Received: August 18, 2010Accepted: September 30, 2010Correspondence: Joong-Wha Chung, MD, Division of Cardiology,Department of Internal Medicine, College of Medicine, Chosun UniversityHospital, 588 Susuk Dong, Dong-gu, Gwangju 501-717, KoreaTel: 82-62-220-3399, Fax: 82-62-222-3858E-mail: [email protected]

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Intrinsic causes AmyloidosisArteritisCardiomyopathiesChagas' diseaseCollagen vascular diseaseDiphtheriaFamilial sinoatrial node disordersFatty replacementFriedreich's ataxiaHemochromatosisIdiopathic degenerative fibrotic infiltration*Ischemia/infarctionLeukemiaMetastatic diseaseMuscular dystrophyMyocarditisPericarditisRheumatic heart diseaseSarcoidosisSurgical injury

Extrinsic causesCholinestease deficiency (suggested) HyperkalemiaHypoxiaPhamacologic agents

DigitalisCalcium channel blockersBeta blockers Sympatholytic agentsAntiarrhythmics

Toxins

Pediatric causesCongenital abnormalitiesSinoatrial nodal artery deficiency

Table 1. Causes of sick sinus syndrome

* Most common intrinsic cause (Adopted from Am Fam Physician. 2003;67:1725-1732)

Central nervous systemDementia IrritabilityLethargyLightheadednessMemory lossNocturnal wakefulnessSyncope or pre-syncope

Cardiovascular systemAngina pectorisArterial thromboemboliCerebrovascular accidentCongestive heart failurePalpitations

OtherDigestive disturbancesDizzinessErrors in judgementFacial flushingFatigueOliguria

Table 2. Symptoms of sick sinus syndrome

(Adopted from Am Fam Physician. 2003;67:1725-1732)

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Severe sinus bradycardia

Sinus pauses or arrest

Sinus node exit block

Chronic atrial tachyarrhythmias

Alternating periods of atrial bradyarrhythmias and tachyarrhythmias

Inappropriate responses of heart rate during exercise or stress

Table 3. Manifestations of sinus node dysfuction

ClassWith documented symptomatic bradycardiaSymptomatic chronotropic incompetenceSymptomatic sinus bradycardia that results from required drug therapy for medical conditionsClass a

With heart rate <40 beats/min when a clear associaton between significant symptoms consistent with bradicardia and the actual presence of bradycardia has not been documented

With syncope of unexplained origin when clinically significant abnormalities of sinus node function are discoveredor provoked in electrophysiologic studies

Class b

Minimally symptomatic patients with chronic heart rate <40 beats/min while awake ClassAsymptomatic patients In patients whose symptoms suggestive of bradycardia have been clearly documented to occur in the absence of

bradycardiaWith symptomatic bradycardia caused by nonessential drug therapy

Table 4. Guidelines for permanent pacing in sinus node dysfunction

(From ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities)

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References

1. Dobrzynski H, Boyett MR, Anderson RH. New insights intopacemaker activity: promoting understanding of sick sinussyndrome. Circulation. 2007;115:1921-1932.

2. Issa ZF, Miller JM, Zipes DP. Clinical arrhythmology andelectrophysiology. WB Saunders. 2009, pp 118-126.

3. Jerod ML, John MD, Tomothy RA. Effect of perfusion rate ofcholinergic agonist on sinus node automaticity. J Electrocardiol.1985;18:287-294.

4. Aksena S, Camm AJ. Electrophysiological disorders of the heart.Elsevier. 2005

5. Adan V,Crown LA. Diagnosis and Treatment of Sick SinusSyndrome. Am Fam Physician. 2003;67:1725-1732.

6. . 2009, pp 92-94.7. Lamas GA, Lee KL, Sweeney MO, Silverman R, Leon A, Yee R,

Marinchak RA, Flaker G, Schron E, Orav EJ, Hellkamp AS, GreerS, McAnulty J, Ellenbogen K, Ehlert F, Freedman RA, Estes NA3rd, Greenspon A, Goldman L; Ventricular pacing or dual-chamber pacing for sinus-node dysfunction. N Engl J Med.2002;346:1854-1862.

8. Andrew E. Epstein, etc. ACC/AHA/HRS 2008 Guidelines forDevice-Based Therapy of Cardiac Rhythm Abnormalities, A Reportof the American College of Cardiology/American HeartAssociation Task Force on Practice Guidelines (Writing Committeeto Revise the ACC/AHA/NASPE 2002 Guideline Update forImplantation of Cardiac Pacemakers and Antiarrhythmia Devices)J Am Coll Cardiol. 2008;51:1-62.

9. Menozzi C, Brignole M, Alboni P, Boni L, Paparella N, Gaggioli G,Lolli G: The natural course of untreated sick sinus syndrome andidentification of the variables predictive of unfavorable outcome.Am J Cardiol. 1998;82:1205-1209.

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Dae-Hyeok Kim, MDDivision of Cardiology, Department of Internal medicine, Inha University School of Medicine, Inchoen, Korea

Atrioventricular block

ABSTRACTAtrioventricular block is a disturbance of impulse conduction between the atria and the ventricles. This blockcan be transient or permanent, depending on the anatomical or functional impairment. According to theseverity of the conduction disturbance, first degree, second degree and third degree or completeatrioventricular block is classified. The atrioventricular block may cause variable symptoms, such as dyspnea,dizziness, syncope and cardiac arrest. The pacemaker implantation will be able to resolve the symptom whichis related to atrioventricular block.

Key words: atrioventricular block pacemaker

Received: May 28, 2010Revision Received: August 9, 2010Accepted: September 30, 2010Correspondence: Dae-Hyeok Kim, MD , Division of Cardiology,Department of Internal medicine, Inha University school of Medicine.Korea, 7-206, 3rd Street, Shinheung-Dong, Jung-Gu, Inchoen 400-711,KoreaTel: 82-32-890-2440, Fax: 82-32-890-2447E-mail: [email protected]

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Figure 1. Atrioventricular block in superior part of His.

Figure 2. Atrioventricular block in inferior part of His.RA; right atrium, RV; right ventrcle

Figure 3. First degree AV block Figure 4. Mobitz type AV block

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Acquired AV block Symptomatic patients in whom His-Purkinje block, suspectedas a cause of symptoms, hasnot been established

Patients with second - or third- degree AV block treated witha pacemaker who remainsymptomatic and in whomanother arrhythmia issuspected as cause ofsymptoms

Patinents with second- or third-degree AV block in whomknowledge of the site ofblock or its mechanism orresponse to pharmacologicalor other temporary interventionmay help derect therapy orassess prognosis

Patients with premature, concealed junctionaldepolarizations suspected asa cause of second-or third-degree AV block pattern (e.g.pseudo-AV block)

Symptomatic patients patients in whom the symptoms and presence of AV block are correlated by ECG findings

Asymptomatic patients with transient AV block associated with sinus slowing (e.g. nocturnal type second-degree AV block)

Indication Class (Appropriate) Class (Equivocal) Class (Inapproprite)

Table 1. ACC/AHA guideline for clinical EPS for evaluation of acquired

Class (indicated)

Class (goodsupportive evidence)

Third-degree advanced second-degree AV block at any anatomical level, associated with any one of the following conditions:1. Bradycardia with symptoms (including heart failure) presumed to be caused by AV block2. Arryhythmias and other medical conditions requiring drugs that result in symptomatic

bradycardia 3. Documented periods of asystole of 3.0 sec or any escape rate <40 beats/min in

awake, symptom-free patients4. After catheter ablation of the AV junction; there are no trials to assess outcome

without pacing, and pacing is virtually always planned in this situation unless theoperative procedure is AV junction modification

5. Postoperative AV block that is not expected to resolve after cardiac surgery6. Neuromuscular diseases with AV block, such as myotonic muscular dystrophy, Kearns-

Sayre syndrome, Erb dystrophy (limb-girdle), and peroneal muscular atrophy, with orwithout symptoms, because there may be unpredictable progression of AV conductiondisease

Second-degree AV block regardless of type or site of block, with associated symptomatic bradycardia

C

CB,C

B,C

C

BB

B

B,C

B

B

B

Asymptomatic third-degree AV block at any anatomical site with average awake ventricularrates of 40 beats/min, especially if cardiomegaly or LV dysfunction is present

Asymptomatic type second-degree AV block with a narrow QRS; when type second-degree AV block occurs with a wide QRS, pacing becomes a Class recommendation

Asymptomatic type second-degree AV block at intra-His or infra-His levels found at electrophysiological study performed for other indications First- or second-degree AV block with symptoms similar to those of pacemaker syndrome

IndicationClass Level of Evidence

Table 2. ACC/AHA guideline for permanent pacing in AV acquired block in adult.8

AV block; atrioventricular block, ECG; electrocardiogram

AV block; atrioventricular block

Figure 6. High degree AV blockFigure 5. Mobitz type AV block

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References

1. Mathewson FA, Rabkin SW, Hsu P. Atrioventricular heart block:27 year follow-up experience. Trans Assoc Life Insur Med Dir Am.1976;60:110.

2. Peuch P, Grolleau R, Guimond C. Incidence of different types ofA-V block and their localization by His bundle recordings. In:Wallens HJJ, Lie KI, Janse MJ, eds. The conduction system of theheart. Leiden: Stenfert Kroese. 1976:467-484.

3. Pauch P, Wainwrite RJ. Clinical electrophysiology ofatrioventricular block. Cardiol Clin. 1983;1:209.

4. Zoob M, Smith KS. The aetiology of complete heart block. Br MedJ. 1963;2:1149-1153.

5. Lenegre J. Etiology and pathology of bilateral bundle branchblock in relation to complete heart block. Prog Cardiovasc Dis.1964;6:409-444.

6. Lev M. Anatomic basis for atrioventricular block. Am J Med.1964;37:742-748.

7. Zipess DP, DiMarco JP, Gillette PC. Guidelines for clinicalintracardiac electrophysiologic study. A report of the AmericanCollege of Cardiology/American Heart Association Task Force onAssessment of Diagnostic and Therapeutic procedures, J Am CollCardiol. 1995;26:555.

8. Gregoratos G, Abrams J, Ebstein AE. ACC/AHA/NASPE 2002Guideline update for implantation of cardiac pacemakers andantiarrhythmia device summary article: A report of the AmericanCollege of Cardiology/American Heart Association Task Force onPractice Guidelines (ACC/AHA/NASPE Committee to Update the1998 Pacemaker Guidelines). Circulation. 2002;106:2145.

Figure 7. Complete AV block

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Jung-Hoon Sung, MD, PhD. Division of Cardiology, Department of Internal Medicine, CHA Bundang Medical Center, CHA University, Seongnam-si, Gyeonggi-do, Korea

Permanent cardiac pacing

ABSTRACTModern pacemaker technology has improved the duration and quality of life for individuals withbradyarrhythmias. The use of cardiac pacemaker in patients with bradyarrhythmias has become increasinglypopular ever since its introduction in 1952. A cardiac pacemaker system consists of a cardiac pulse generator,lead electrode and a software of these devices. Each of these devices helps decipher the intrinsic electricalsignals within the heart and provide necessary impulses to synchronize cardiac activity. Patient’s systemic wellbeing, as well as predictive clinical progression, existence of various arrthymias such as atrialtachycardia/fibrillation, possibility of returning to sinus rhythm, atrioventricular synchrony, requirement foratrial pace regulation and chronotropic variability, should be taken into account prior to insertion of artificialpacemaker and adequate post-implantation follow up is crucial.

Key words: bradyarrhythmia cardiac pacemaker pulse generator lead electrode

Received: June 23, 2010Accepted: September 30, 2010Correspondence: Jung-Hoon Sung, MD, PhD. Division of Cardiology,Department of Internal Medicine, CHA Bundang Medical Center, CHAUniversity, 351 Yatap-dong, Bundang-gu, Seongnam-si, Gyeonggi-do 463-712,KoreaTel: 82-31-780-5585, Fax: 82-31-780-5584E-mail: [email protected]

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Figure 1. Selection of pacemaker systems for patients with atrioventricular block. Decisions are illustrated by diamonds.Shaded boxes indicate type of pacemaker. AV; atrioventricular

Figure 2. Selection of pacemaker systems for patients with sinus node dysfunction. Decisions are illustrated bydiamonds. Shaded boxes indicate type of pacemaker. AV; atrioventricular

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References

1. Epstein AE, DiMarco JP, Ellenbogen KA, Estes NA 3rd, FreedmanRA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL,Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ,Stevenson LW, Sweeney MO, Smith SC Jr, Jacobs AK, Adams CD,Anderson JL, Buller CE, Creager MA, Ettinger SM, Faxon DP,Halperin JL, Hiratzka LF, Hunt SA, Krumholz HM, Kushner FG,Lytle BW, Nishimura RA, Ornato JP, Page RL, Riegel B, TarkingtonLG, Yancy CW; American College of Cardiology/American HeartAssociation Task Force on Practice Guidelines (Writing Committeeto Revise the ACC/AHA/NASPE 2002 Guideline Update forImplantation of Cardiac Pacemakers and Antiarrhythmia Devices);American Association for Thoracic Surgery; Society of ThoracicSurgeons. ACC/AHA/HRS 2008 Guidelines for Device-Based

Therapy of Cardiac Rhythm Abnormalities: a report of theAmerican College of Cardiology/American Heart Association TaskForce on Practice Guidelines (Writing Committee to Revise theACC/AHA/NASPE 2002 Guideline Update for Implantation ofCardiac Pacemakers and Antiarrhythmia Devices): developed incollaboration with the American Association for Thoracic Surgeryand Society of Thoracic Surgeons. Circulation. 2008;117;e350-e408.

2. PHILIP J. PODRID, PETTER R. KOWEY. CARDIAC ARRHYTHMIA:mechanisms, diagnosis, and management. 2nd ed; pp 321-328.

3. Kenneth A. Ellenbogen, Mark A. Wood. Cardiac pacing and ICDs.4th ed; pp 47-86.

4. pp 151-185.5. 2004; pp 636-638.6. Bernstein AD, Camm AJ, Fisher JD, Fletcher RD, Mead RH,

Nathan AW, Parsonnet V, Rickards AF, Smyth NP, Sutton R.North American Society of Pacing and Electrophysiology policystatement. The NASPE/BPEG defibrillator code. Pacing ClinElectrophysiol. 1993;16:1776-1780.

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Young-Keun On, MD, PhDDivision of Cardiology, Department of Medicine Cardiac & Vascular Center, Samsung Medical Center, Sungkyunkwan UniversitySchool of Medicine, Seoul, Korea

Catheter ablation for tachycardia-bradycardia syndrome

ABSTRACT

Sinus node (SAN) dysfunction is frequently associated with atrial fibrillation (AF), and can lead to syncopal

attacks after AF termination, a condition forming the basis of the “tachycardia-bradycardia

syndrome.”Although abnormalities of SAN structure have been noted in patients with AF, there is increasing

evidence of a reversible component related to SAN remodeling caused by rapid atrial tachyarrhythmias. It has

been demonstrated that when AF patients show prolonged sinus pauses on AF termination, successful AF

ablation is followed by a marked recovery in SAN function indices. In animal models, atrial tachyarrhythmia

downregulates SAN HCN2/4 and minK subunit expression, along with the corresponding currents funny

current (If) and slow delayed-rectifier current (IKs). Tachycardia-induced remodeling of SAN ion channel

expression, particularly for the “pacemaker” subunit If, may contribute to the clinically significant association

between SAN dysfunction and supraventricular tachyarrhythmias. SAN dysfunction in AF is also associated

with calcium clock malfunctioning, characterized by unresponsiveness to isoproterenol caffeine and the down-

regulation of type 2 ryanodine recepter (RYR2) in SAN. Therefore sinus node dysfunction caused by atrial

tachyarrhythmias could be reversed by curative ablation of AF, thus avoiding the need for pacemaker

implantation. Radiofrequency cathether ablation should be an option of the treatment for the tachycardia-

bradycardia syndrome.

Key words: tachycardia-bradycardia syndrome atrial fibrillation ablation

Received: May 28, 2010Revision Received: August 16, 2010Accepted: September 30, 2010Correspondence: Young-Keun On, MD, PhD. Division of Cardiology,Department of Medicine Cardiac & Vascular Center, Samsung MedicalCenter, Sungkyunkwan University School of Medicine, 50 Irwon-dong,Gangnam-gu, Seoul 135-710, Korea Tel: 82-2-3410-3420, Fax: 82-2-3410-3849E-mail: [email protected]

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Figure 1. Twenty six old lady complained of palpitation, dizziness and pre-syncope. The electrocardiogram showsirregular heart rhythm and rapid heart beats.

Figure 2. Tachycardia-bradycardia syndrome. The electrocardiogram shows rapid heart beats and abrupt termination oftachycardia followed by sinus pause.

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Figure 3. The atrial fibrillation converted to atrial flutter during the ablation of left pulmonary vein antrum.

Figure 4. The atrial flutter was terminated during the ablation of cavotricuspid isthmus and followed by pause and sinusrhythm.

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Figure 5. Intracardiac electrogram shows normal sinus rhythm after the ablation.

Figure 6. After the catheter ablation of atrial fibrillation the patient didn’t complain of palpitation and dizziness and theelectrocardiogram shows normal sinus rhythm.

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References

1. Allessie M, Ausma J, Schotten U. Electrical, contractile andstructural remodeling during atrial fibrillation. Cardiovasc Res.2002;54:230-246.

2. Thery C, Gosselin B, Lekieffre J, Warembourg H. Pathology ofsinoatrial node: correlations with electrocardiographic findings in111 patients. Am Heart J. 1977;93:735-740.

3. Elvan A, Wylie K, Zipes DP. Pacing-induced chronic atrialfibrillation impairs sinus node function in dogs: electrophysiologicalremodeling. Circulation. 1996;94:2953-2960.

4. Hocini M, Sanders P, Deisenhofer I, Jais P, Hsu LF, Scavee C,Weerasoriya R, Raybaud F, Macle L, Shah DC, Garrigue S,Metayer PL, Clementy J, Haissaguerre M. Reverse remodeling ofsinus node function after catheter ablation of atrial fibrillation inpatients with prolonged sinus pauses. Circulation. 2003;108:1172-1175.

5. Yeh YJ, Burstein B, Qi XY, Sakabe M, Chartier D, Comtois P,Wang Z, Kuo CT, Nattel S. Funny current downregulation andsinus node dysfunction associated with atrial tachyarrhythmia-Amolecular basis for tachycardia-bradycardia syndrome.Circulation. 2009;119:1576-1585.

6. Joung B, Lin SF, Chen Z, Antoun PS, Maruyama M, Han S,Piccirillo G, Stucky M, Zipes DP, Chen PS, Das MK. Mechanismsof sinoatrial node dysfunction in a canine model of pacing-induced atrial fibrillation. Heart Rhythm. 2010 ;7:88-95.

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Nam-Ho Kim, MDDivision of Cardiology, Department of Internal Medicine, Wonkwang University Medical School, Iksan, Jeonbuk, Korea

Continuing warfarin therapy is superior to interrupting warfarin with orwithout bridging anticoagulation therapy in patients undergoingpacemaker and defibrillator implantation

Imdad Ahmed, MD, Elie Gertner, MD, William B. Nelson, MD, PhD,* Chad M. House, BS, RDCS, Ranjan Dahiya, MD,*

Christopher P. Anderson, MPH, David G. Benditt, MD, FHRS, Dennis W.X. Zhu, MD* From the *Section of Cardiology and Department of Medicine, Regions Hospital and the University of Minnesota Medical School, Saint Paul, Minnesota, Regions

Hospital, Saint Paul, Minnesota, and Cardiac Arrhythmia and Syncope Center, University of Minnesota Medical School,Minneapolis, Minnesota.

Heart Rhythm. 2010 ;7:745-749.

<

Received: June 27, 2010Revision Received: August 20, 2010Accepted: September 30, 2010Correspondence: Nam-Ho Kim, MD, Division of Cardiology, Department ofInternal Medicine, Wonkwang University Medical School, 344-2 Shinyong-dong, Iksan, Jeonbuk 570-711, KoreaTel: 82-63-859-2523, Fax: 82-63-852-8480E-mail: [email protected]

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Table 1. INR level and perioperative hemorrhagic and thromboembolic complications in all patients

Contined warfarin Bridging Anticoagulation withheld

Outcome (n=222) (n=123) (n=114)

Hematoma 1 (0.45%) 7 (5.7%) 2 (1.75%)p=0.004 p=0.26

Transient ischemic attack 0 1 (0.8%) 4 (3.5%)p=0.35 p=0.01

Mean INR ( SD) 2.57 0.49 1.33 0.20 1.35 0.32INR range 1.5 - 4.7 1.1-1.7 1.0 -1.6

INR; international normalized ratio

Table 2. Length of postoperative hospital stayp

Group No. of days (mean SD)

Continued warfarin (n=222) 1.23 0.12Bridging (n=123) 2.27 0.21

p < 0.0001Anticoagulation withheld (n=114) 1.23 0.13

p = 0.93

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A case of bradycardia dependent Torsa de Pointes

ABSTRACTWe report a case of bradycardia-dependent torsade de pointes. Our patient was presented with recurrent

syncope. Serial electrocardiograms showed high grade atrioventricular (AV) block with frequent torsade de

pointes. The patient's dysrhythmia was abated with cardiac pacing at a moderate rate. His bundLe

electrogram revealed infra-His block and the permanent pacemaker was implanted for the irreversible AV

block.

Key words: bradycardia torsa de pointes

Eui-Seok Hwang, MDDivision of Cardiology, Department of Internal Medicine, Kwandong University Medical School Sung-Soon Kim, MD, PhD.Division of Cardiology, Yonsei Cariovascular Center and Cardiovascular Research Institute, Yonsei University College of Medicine, Korea

Received: June 14, 2010Accepted: Sepember 30, 2010Correspondence: Sung-Soon Kim, MD, PhD. Division of Cardiology,Yonsei Cariovascular Center and Cardiovascular Research Institute, YonseiUniversity College of Medicine, Korea 250 Seungsanno, Seodaemun-gu,Seoul, 120-752, Korea Tel: 82-2-2228-8441, Fax: 82-2-393-2041E-mail: [email protected]

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Figure 1. 12 lead ECG (electrocardiogram) shows sinus rhythm with high grade atrioventricular block and frequent extrasystoles. A series of short-long sequences ensues and culminates in TdP.

Figure 2. Two series of TdP. TdP terminated spontaneously in panel A and defibrillation with bi-phasic 200 J wasneeded to terminate TdP in panel B. HR; heart rate

A

B

A

B

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Figure 3. The 12 lead ECG while the temporary pacemaker has been turned off several days after initial insertion,shows there is a persistent high grade AV block with escape idioventricular rhythm of RBBB. The conducted beats (thesecond and the last beat) shows LBBB morphology. ECG; electricardiogram, AV; artrioventricular

Figure 4. His bundle electrogram (His 12) shows that HV block. In surface ECG tracing (I and V1), there are threedifferent morphologies of QRS complex; the first QRS complex is an AV conduction with LBBB (left bundle branch block),the second one is a fusion beat of normal QRS in which the conducted beat with LBBB and ventricular escape of RBBB(right bundle branch block) morphology fused together and the third is an AV dissociation with idioventricular rhythm ofthe RBBB pattern.ECG; electricardiogram, AV; artrioventricular, HV; his ventricular

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References

1. Viskin S. Long QT syndromes and torsade de pointes. Lancet.1999;354:1625-1633.

2. Volders PG, Sipido KR, Vos MA, Spatjens RL, Leunissen JD,Carmeliet E, Wellens HJ. Downregulation of delayed rectifier K(+)currents in dogs with chronic complete atrioventricular block andacquired torsades de pointes. Circulation. 1999;100:2455-2461.

3. Tsuji Y, Opthof T, Yasui K, Inden Y, Takemura H, Niwa N, Lu Z,Lee JK, Honjo H, Kamiya K, Kodama I. Ionic mechanisms ofacquired QT prolongation and torsades de pointes in rabbits withchronic complete atrioventricular block. Circulation. 2002;106:2012-2018.

4. Topilski I, Rogowski O, Rosso R, Justo D, Copperman Y, GliksonM, Belhassen B, Hochenberg M, Viskin S. The morphology of theQT interval predicts torsade de pointes during acquiredbradyarrhythmias. J Am Coll Cardiol. 2007;49:320-3208.

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Nam-Sik Yoon, MD / Jeong-Gwan Cho, MDDivision of Cardiology, Department of Internal Medicine, Medical School, Chonnam National University, Gwangju, Korea

A case of DDD pacemaker-reprogramming to DDI in a patient withatrial fibrillation

ABSTRACTDDI, defined as AV (atrioventricular) sequential, non-P-synchronous pacing with dual-chamber sensing, allows

sensing in both chambers and inhibition in both chambers, but an atrial event will not trigger a ventricular

response. Occasionally a DDD device to DDI is useful in preventing the patient from experiencing brief rapid

atrial rates. In DDI mode, the rapid atrial fibrillation or flutter waves cannot trigger beats in the ventricle.

Modern pacemakers have programs called automatic mode switching and these algorithms have generally

eliminated the need for fixed DDI pacing. On the other hand, if the atrial fibrillation is intermittent, the DDI

mode will prevent the patient from being paced briefly at maximum tracking rate before being switched to a

slower mode. Another potential use for DDI is in a patient with persistent sinus bradycardia. A DDI pacemaker

with rate responsiveness will pace consistently in the atrium and the rate-responsive device will allow a

somewhat physiologic response to activity.

Key words: pacemaker atrial fibrillation

Received: June 24, 2010Revision Received: August 10, 2010Accepted: September 30, 2010Correspondence: Nam-Sik Yoon, MD, Division of Cardiology, Departmentof Internal Medicine, Medical School, Chonnam National University, 671Jeabongro, Dong-gu, Gwangju, KoreaTel: 82-62-220-6272, Fax: 82-62-225-6260E-mail: [email protected]

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Figure 2. Electrocardiogram after DDDR pacemaker implantation. Pacing spikes are visible in front of P and QRS waves.

Figure 1. Sinus node recovery time was 6,557 ms at 850 ms of baseline sinus cycle length.

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Figure 4. Electrocardiogram after mode change from DDD to DDI.

Figure 3. Electrocardiogram when the patient complained about excertional dyspnea. Atrial fibrillation and ventricularpacing rhythm are visible.

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References

1. Kenneth AE, Mark AW: Cardiac pacing and ICDs, 4th ed.Blackwell Publishing, 2005;276. 2. Tom K: The nuts and bolts of cardiac pacing, Blackwell Futura,2005;83.

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Jin-Seok Kim, MDDepartment of Cardiology, Sejong Heart Institute, Sejong General Hospital. Bucheon, Gyeonggi-do, Korea

Arrhythmogenic right ventricular dysplasia/cardiomyopathy

ABSTRACTArrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is a clinical entity characterized by

ventricular arrhythmias and a specific ventricular pathology showing fibrofatty infiltration of the right

ventricular (RV) free wall. ARVD/C is known as an important cause of sudden cardiac death in young adults.

We reported a case of a 38-year-old female who visited us for palpitation and a history of syncope, and was

diagnosed with ARVD/C. Ventricular arrhythmias such as frequent ventricular premature beats and ventricular

tachycardia were documented. Also, RV enlargement and dysfunction were noted on imaging. Finally, she

received an ICD implantation.

Key words: ventricular tachycardia arrhythmogenic right ventricular dysplasia cardiomyopathy

Received: June 28, 2010Revision Received: August 11, 2010Accepted: September 30, 2010Correspondence: Jin-Seok Kim, MD, Division of Cardiology, Department ofCardiology, Sejong Heart Institute, Sejong General Hospital. 91-121 Sosa-bon-2-dong, Sosa-gu, Bucheon 422-711, KoreaTel: 82-32-340-1155, Fax: 82-32-349-3005E-mail: [email protected]

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Figure 1. Baseline ECG on admission (A) and follow-up (B). A. Frequent ventricular ectopies with LBBB configurationare shown. T wave inversion is noted at precordial leads. B. On follow-up, ECG evolution was noted. It shows deep Twave inversions in V1 to V3.ECG; electrocardiogram

A

B

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Figure 3. Cardiac MRI showed bulging of RV apex with dyskinetic wall motion and focal aneurysm (bold white arrow)on systolic phase (A), and suspected linear enhancement (thin white arrow) along the RV myocardium, especially atapical portion (B).RV; right ventricles

Figure 2. Documented monomorphic ventricular tachycardia with left bundle branch block configuration on 24 hoursHolter recordings.

A B

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References

1. Gamayel C, Pelliccia A, Thompson PD. Arrhythmogenic rightventricular cardiomyopathy. J Am Coll Cardiol. 2001;38:1773-1781.

2. Sen-Chowdhry S,Lowe MD, Sporton SC, McKenna WJ.Arrhythmogenic right ventricular cardiomyopathy: clinicalpresentation, diagnosis, and management. Am J Med.2004;117:685-695.

3. Corrado D, Fontaine G, Marcus FI, McKenna WJ, Nava A, ThieneG, Wichter T. Arrhythmogenic right ventricular dysplasia/cardiomyopathy:need for an international registry. Study Group on ArrhythmogenicRight Ventricular Dysplasia/Cardiomyopathy of the WorkingGroups on Myocardial and Pericardial Disease and Arrhythmias ofthe European Society of Cardiology and of the Scientific Councilon Cardiomyopathies of the World Heart Federation. Circulation.2000;101:e101-106.

4. Corrado D, Basso C, Schiavon M, Thiene G. Screening forhypertrophic cardiomyopathy in young athletes. N Engl J Med.1998;339:364-369.

5. Dalal D, Nasir K, Bomma C, Prakasa K, Tandri H, Piccini J, RoguinA, Tichnell C, James C, Russell SD, Judge DP, Abraham T, SpevakPJ, Bluemke DA, Calkins H. Arrhythmogenic right ventriculardysplasia: a United States experience. Circulation. 2005;112:3823-3832.

6. Nava A, Bauce B, Basso C, Muriago M, Rampazzo A, Villanova C,Daliento L, Buja G, Corrado D, Danieli GA, Thiene G. Clinicalprofi le and long-term follow-up of 37 families witharrhythmogenic right ventricular cardiomyopathy. J Am CollCardiol. 2000;36:2226-2233.

7. Tabib A, Loire R, Chalabreysse L, Meyronnet D, Miras A, MalicierD, Thivolet F, Chevalier P, Bouvagnet P. Circumstances of deathand gross and microscopic observations in a series of 200 casesof sudden death associated with arrhythmogenic right ventricularcardiomyopathy and/or dysplasia. Circulation. 2003;108:3000-3005.

8. Angelini A, Basso C, Nava A, Thiene G, Endomyocardial biopsy inarrhythmogenic right ventricular cardiomyopathy. Am Heart J.1996;132:203-206.

9. McKenna WJ, Thiene G, Nava A, Fontaliran F, Blomstrom-Lundqvist C, Fontaine G, Camerini F. Diagnosis ofarrhythmogenic right ventricular dysplasia/cardiomyopathy TaskForce of the Working Group Myocardial and Pericardial Diseaseof the European Society of Cardiology and of the ScientificCouncil on Cardiomyopathies of the International Society andFederation of Cardiology. Br Heart J. 1994;71:215-218.

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10. European Heart Rhythm Association; Heart Rhythm Society,Zipes DP, Camm AJ, Borggrefe M, Buxton AE, Chaitman B,Fromer M, Gregoratos G, Klein G, Moss AJ, Myerburg RJ, PrioriSG, Quinones MA, Roden DM, Silka MJ, Tracy C, Smith SC Jr,Jacobs AK, Adams CD, Antman EM, Anderson JL, Hunt SA,Halperin JL, Nishimura R, Ornato JP, Page RL, Riegel B, PrioriSG, Blanc JJ, Budaj A, Camm AJ, Dean V, Deckers JW, DespresC, Dickstein K, Lekakis J, McGregor K, Metra M, Morais J,Osterspey A, Tamargo JL, Zamorano JL; American College ofCardiology; American Heart Association Task Force; EuropeanSociety of Cardiology Committee for Practice Guidelines.ACC/AHA/ESC 2006 guidelines for management of patientswith ventricular arrhythmias and the prevention of suddencardiac death; a report of the American College ofCardiology/American Heart Association Task Force and theEuropean Society of Cardiology Committee for PracticalGuidelines (Writing Committee to Develop Guidelines forManagement of Patients With Ventricular Arrhythmias and thePrevention of Sudden Cardiac Death). J Am Coll Cardiol.2006;48:e247-346.

11. Epstein AE, DiMarco JP, Ellenbogen KA, Estes NA 3rd,

Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, HammillSC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH,Silka MJ, Stevenson LW, Sweeney MO, Smith SC Jr, Jacobs AK,Adams CD, Anderson JL, Buller CE, Creager MA, Ettinger SM,Faxon DP, Halperin JL, Hiratzka LF, Hunt SA, Krumholz HM,Kushner FG, Lytle BW, Nishimura RA, Ornato JP, Page RL, RiegelB, Tarkington LG, Yancy CW; American College ofCardiology/American Heart Association Task Force on PracticeGuidelines (Writing Committee to Revise the ACC/AHA/NASPE2002 Guideline Update for Implantation of Cardiac Pacemakersand Antiarrhythmia Devices); American Association for ThoracicSurgery; Society of Thoracic Surgeons. ACC/AHA/HRS 2008Guidelines for Device-Based Therapy of Cardiac RhythmAbnormalities; a report of the American College ofCardiology/American Heart Association Task Force on PracticeGuidelines (Writing Committee to Revise the ACC/AHA/NASPE2002 Guideline Update for Implantation of Cardiac Pacemakersand Antiarrhythmia Devices): developed in collaboration withthe American Association for Thoracic Surgery and Society ofThoracic Surgeons. Circulation. 2008;117:e350-408.

Smith HJ, Allen S, Yu W, Fard S. This is the title. Circulation.

2004;104:276-308

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