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Department Introduction

Department Introduction

Ischemia Heart Disease Group

(3) Arrhythmia Group

The Tohoku University Arrhythmia Group provides leading-edge treatments to patients with arrhythmias. We are able to offer a wide range of electrophysiological procedures: radiofrequency catheter ablation therapy (RFCA), implantation of pacemaker, implantable cardioverter defibrillator (ICD), and biventricular devices, in addition to noninvasive evaluation of arrhythmias. We also conduct diagnosis and treatment of idiopathic ventricular fibrillation including Brugada syndrome.
By using two catheter navigation system (CARTO and EnSite), we offer advanced ablation therapy for complex arrhythmias such as atrial fibrillation and ventricular tachycardia, especially in patients with organic heart diseases including myocardial infarction, dilated cardiomyopathy, or congenital heart disease as well as ordinary supraventricular arrhythmias. We have also been performing device therapies, such as a pacemaker, an implantable cardioverter defibrillator (ICD), and biventricular devices for patients with bradyarrhythmia, tachyarrhythmia, or severe cardiac heart failure, to contribute prevent sudden cardiac death and improve the quality of life.
Furthermore, the effort on clinical research allow us to provide the most effective care to our patients.


  1. Arrhythmia Group Experience
  2. CARTO System
  3. Atrial Fibrillation Ablation
  4. Cardiac Resynchronization Therapy
  5. Brugada Syndrome
  6. Implantable Cardioverter Defibrillator

1. Arrhythmia Group Experience

Arrhythmia Group Experience over the past decade

Arrhythmia Group Experience over the past decade

Details of treatment diseases in 2009

Arrhythmia Group Experience over the past decade

2. CARTO System

CARTO System (electroanatomical mapping system: EAM)
EAM enables to identify complex tachycardia circuits. This navigation system constructs a 3D virtual image of heart on which enables express the anatomical location, tachycardia activation formation (activation mapping), and voltage information (voltage mapping). This system is very useful to find the optimal ablation site, especially in tough cases with left atria focal atrial tachycardia where we reach by using transseptal approach and ventricular tachyarrhythmias based on organic heart diseases.

3. Atrial Fibrillation Ablation

Atrial fibrillation is one of the most common arrhythmia. It is very significant to treat atrial fibrillation and maintain sinus rhythm, leading to improvement of the patient’s symptoms and hemodynamic status, and prevention of a thromboembolism. However, drug therapy is not always effective against atrial fibrillation. Ablation procedure for atrial fibrillation has been recently developing as alternative curative therapy. In 1998, it was reported that atrial fibrillation is triggered by isolated and repetitive atrial premature contraction originated from the pulmonary vein. However, there are also cases in whom initial premature contraction is difficult to be determined  if origins are multifocal. Today the main method for the treatment of atrial fibrillation is the electrical isolation of the pulmonary vein orifice. This method can be done by isolating each of the four pulmonary vein orifices or by isolating the ipsilateral side pulmonary veins in a broad area that includes the atrial muscle. We perform the latter method, which is particularly promising for preventing the occurrence of pulmonary artery stenosis and treating the focal origin at left atrial posterior wall in addition to the pulmonary vein orifice origin.
Figure 1 shows the left atrium and pulmonary vein in an endoscopic view from the posterior surface of the heart using MDCT, the left and right superior and inferior pulmonary vein orifices (two orifices surrounded by a small circle) and the ablation point line (dotted line) respectively. Using the transseptal approach, two ring-shaped electrode catheters are inserted into the orifices of the left superior and inferior pulmonary veins and in the same manner an ablation catheter is inserted into the left atrium (Figure 2). The end point of ablation is disappearance of the right and left pulmonary vein potential and the electrical isolation of pulmonary vein from the left atrium (Figure 3). This ablation therapy makes it possible to control atrial fibrillation that were previously refractory to anti-arrhythmic drugs.

Broad area ipsilateral side pulmonary vein electrical isolation -Left atrium posterior wall image and right and left pulmonary vein orifice image--

Figure. 1
Figure. 2: Catheter position Figure. 3: Intracardiac electrocardiogram (left atrial pulmonary vein potential simultaneous disappearance)
Catheter position Intracardiac electrocardiogram (left atrial pulmonary vein potential simultaneous disappearance)

4. Cardiac Resynchronization Therapy

(1) Indication Criteria of Cardiac Resynchronization Therapy (CRT)
for Severe Cardiac Failure Patients

CRT Indication Criteria
  • NYHA III to IV cardiac failure
  • Refractory to medical therapy
  • Left ventricular ejection fraction (EF) < 35%
  • Left ventricular dyssynchronized movement
    (QRS width is 120 ms or more on the electrocardiogram)
  • From the American Heart Association 2005 guideline




  • In addition to pacing from the right atrium and right ventricle, biventricular pacing is also conducted by pacing from the left ventricular free wall via the coronary sinus.
  • For patients with ventricular arrhythmias, a device also having implantable cardioverter defibrillator function (CRT-D) is used.


(2) Cardiac Resynchronization Therapy (CRT) Using Biventricular Pacing

Cardiac Resynchronization Therapy (CRT) Using Biventricular Pacing


(3)Improvement of Mechanical Dyssynchronyafter CRT

Post-biventricular Pacing Cardiac Asynchronous Contraction Improvement

5. Diagnosis and Treatment of Idiopathic Ventricular Fibrillation including Brugada Syndrome
What is Brugada Syndrome?
  1. Brugada Syndrome is a disorder that causes lethal arrhythmia (idiopathic ventricular fibrillation), which is thought to be one of the main causes of nocturnal sudden death in youth, middle-age, and elderly people.
Characteristics of Brugada Syndrome are:
  1. Distinguishing electrocardiogram finding (so-called, Brugada electrocardiogram)
  2. None of organic cardiac disease accounting for the ECG
  3. Documentation of lethal arrhythmia (ventricular fibrillation)
Diagnosis
  1. Electrocardiogram examination: 12-lead electrocardiogram, special 24-hour electrocardiogram, late potential detection using signal-averaging electrocardiography
  2. Diagnostic imaging: UCG (ultrasound cardiography), MRI (magnetic resonance imaging) or CT (computer tomography) are performed to rule out organic heart diseases
  3. Drug challenge test: Intravenous administration of an anti-arrhythmic drug to clarify the Brugada ECG helps the diagnosis.
  4. Electrophysiological study: Induction test for ventricular arrhythmias by programmed ventricular stimulation is used to evaluate the risk of cardiac event or to determine the indication of implantable cardioverter defibrillator (ICD)
Treatment
  1. An implantable cardioverter defibrillator (ICD) is the only established therapy to prevent sudden cardiac death by lethal arrhythmia.

An implantable cardioverter defibrillator (ICD) is only established therapy to prevent sudden cardiac death by lethal arrhythmia


6. Implantable Cardioverter Defibrillator

An implantable cardioverter defibrillators (ICD) is an implantable electronic device that continuously monitors or senses heart rate, and that delivers an electrical shock to terminate lethal tachyarrhythmias such as ventricular tachycardia or ventricular fibrillation. We have been implanting ICD to the various cases with ventricular tachyarrhythmias since 1996, and perform approximately 20 procedures annually and a cumulative total of approximately 130 procedures to date. In 2006 we started implanting biventricular pacemakers having an implantable cardioverter defibrillator (CRT-D) to add a biventricular pacing function for severe cardiac failure cases.

Publications (since 2000)
  1. Yamaguchi N, Kumagai K, Fukuda K, Wakayama Y, Sugai Y, Hirose M, Shimokawa H. Electrophysiological properties of the right atrial septum in patients with atrial tachyarrhythmias. Tohoku J Exp Med. 2008;215:13-22.
  2. Kumagai K, Fukuda K, Wakayama Y, Sugai Y, Hirose M, Yamaguchi N, Takase K, Yamauchi Y, Takahashi A, Aonuma K, Shimokawa H. Electrocardiographic characteristics of the variants of idiopathic left ventricular outflow tract ventricular tachyarrhythmias. J Cardiovasc Electrophysiol. 2008;19:495-501.
  3. Kumagai K, Suzuki F, Aonuma K, Hiroaki Shimokawa.Atrial Tachycardia Originating from the Upper Left Atrial Septum: Demonstration of Transseptal Interatrial Conduction Using the Infolded Atrial Walls. Journal of Cardiovascular Electrophysiology. 2006;17:907-911.
  4. Hallaq H, Yang Z, Viswanathan PC, Fukuda K et al. Quantitation of protein kinase A-mediated trafficking of cardiac sodium channels in living cells. Cardiovasc Res.72:250-261, 2006.
  5. Kumagai K, Takahashi A, Yamauchi Y, Aonuma K. Ventricular Tachycardia Originating from the Epicardium Identified by Intracoronary Mapping Using a PTCA Guidewire. Journal of Cardiovascular Electrophysiology. 2006;17:670-3.
  6. ter Keurs HE, Wakayama Y et al. Arrhythmogenic Ca(2+) release from cardiac myofilaments. Prog Biophys Mol Biol. 2006;90:151-71.
  7. ter Keurs HE, Wakayama Y et al. Role of sarcomere mechanics and Ca2+ overload in Ca2+ waves and arrhythmias in rat cardiac muscle. Ann N Y Acad Sci. 2006;1080:248-67.
  8. Fukuda K, Davis SS, Nakajima T et al. Oxidative Mediated Lipid Peroxidation Recapitulates Proarrhythmic Effects on Cardiac Sodium Channels. Circ Res. 2005;97:1262-9
  9. ter Keurs HE, Wakayama Y et al. Spatial nonuniformity of contraction causes arrhythmogenic Ca2+ waves in rat cardiac muscle. Ann N Y Acad Sci. 2005;1047: 345-65.
  10. Wakayama Y, Miura M, et al. Spatial nonuniformity of excitation-contraction coupling causes arrhythmogenic Ca2+ waves in rat cardiac muscle. Circ Res .2005;96:1266-73.
  11. Kumagai K, Yamauchi Y, Takahashi A, Yokoyama Y, Sekiguchi Y, Watanabe J, Iesaka Y, Shirato K, Aonuma K. Idiopathic Left Ventricular Tachycardia Originating from the Mitral Annulus. Journal of Cardiovascular Electrophysiology. 2005;16:1029-36
  12. Fukuda K, T Nakajima, PC Viswanathan et al. Compound-specific Na+ channel pore conformational changes induced by local anaesthetics. J Physiol. 2005;564:21-31.
  13. Fukuchi M, Kumagai K, Sakuma M, Kagaya Y, Watanabe J, Tabayashi K, Shirato K. Warfarin-intractable, intraatrial thrombogenesis in a 52-year-old woman with mitral stenosis and chronic atrial fibrillation. Tohoku Journal of Experimental Medicine. 2004;203:59-63.
  14. Kumagai K, Fukuchi M, Ohta J, Baba S, Oda K, Akimoto H, Kagaya Y, Watanabe J, Tabayashi K, Shirato K. Expression of the von Willebrand factor in atrial endocardium is increased in atrial fibrillation depending on the extent of structural remodeling. Circulation Journal. 2004;68:321-7.
  15. Wakayama Y, Miura M et al. Stretch and quick release of rat cardiac trabeculae accelerates Ca2+ waves and triggered propagated contractions. A m J Physiol Heart Circ Physiol. 2001;281:H2133-42.
  16. Miura M, Wakayama Y et al. Effect of transient stretch on intracellular Ca2+ during triggered propagated contractions in intact trabeculae. Can J Physiol Pharmacol. 2001;79:68-72.

( Text by Koji Fukuda )

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