© 2003 by European Society of Cardiology
Noninvasive, direct visualization of macro-reentrant circuits by using magnetocardiograms: initiation and persistence of atrial flutter
1Institute of Clinical Medicine, University of Tsukuba Tsukuba, Japan; 2Hitachi Central Research Laboratory, Hitachi Ltd. Kokubunji, Japan
Manuscript submitted 19 November 2002. Accepted after revision 15 June 2003.
Correspondence: Satsuki Yamada, MD, PhD, Institute of Clinical Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan. Tel.: +81-29-853-3210; Fax: +81-29-853-3143. E-mail: satsuyamada-circ{at}umin.ac.jp
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionConclusionAcknowledgementsReferences |
|---|
AIMS: We analysed the cardiac magnetic fields on the body surface to visualize electrical currents noninvasively during reentrant arrhythmias.
METHODS AND RESULTS: Seven patients with counterclockwise atrial flutter (AFL) were studied during 17 episodes of AFL using 64-channel magnetocardiograms (MCGs) and electrophysiological study. Eight of the episodes were paroxysmal AFL, in which MCGs were recorded from the time of spontaneous onset to the time of termination. We constructed iso-magnetic field maps of the tangential components and produced MCG animations. With respect to AFL initiation, an atrial premature complex induced AFL. Prior to the initiation of AFL, atrial fibrillation (AF) transiently occurred. The cardiac magnetic fields revealed a single peak during sinus rhythm or with premature complexes but a disorganized pattern during AF. When AF transformed to AFL, the magnetic fields changed from a disorganized pattern to a single peak at first and then evolved to a circular pattern. During persistent AFL, the magnetic source moved in a counterclockwise circuit.
CONCLUSION: MCG animation can be used to visualize the sequence in which a premature complex transforms sinus rhythm to AFL via AF. Our findings indicate that MCGs can be used to identify noninvasively the mechanisms responsible for atrial tachyarrhythmias.
Key Words: Atrial flutter, atrial fibrillation, cardiac mapping, magnetocardiograms, magnetic source, tangential components
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionAcknowledgementsReferences |
|---|
Magnetocardiograms (MCGs) are noninvasively acquired maps that measure the cardiac magnetic fields on the body surface obtained using a superconducting quantum interference device (SQUID) system[1–
3]. Although MCGs have unique fundamental principles, can be quantified using absolute scales[4], and are less affected by the body tissues compared with 12-lead electrocardiograms (ECGs)[5], their clinical utility has not been established. Several reports have described MCGs studies of His potentials[6,7], ventricular repolarization abnormalities during sinus rhythm[8–10], and arrhythmic foci in patients with premature contractions or Wolff–Parkinson–White syndrome[11–14]. However, there are very few MCG studies of reentrant arrhythmias. Body surface potential mapping applied to atrial arrhythmias can differentiate counterclockwise atrial flutter (AFL) from clockwise AFL[15], although reentrant circuits have not previously been directly visualized on body surface maps.
The aim of our study was to visualize directly reentrant circuits during reentrant arrhythmias using MCGs. We originally developed tangential-component MCGs[16] and created MCG animation loops. We hypothesized that the movement of the magnetic sources in the MCG animation loops would indicate the electrical currents reflected on the body surface. Specifically, we studied counterclockwise AFL, a macro-reentrant circuit in the right atrium[17–19]. In AFL, the reentrant circuit is almost circular in the anterior–posterior view[19], and the cardiac magnetic fields in the anterior chest should be detectable.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionAcknowledgementsReferences |
|---|
Patients
We analysed 17 episodes of counterclockwise AFL in seven patients (six men and one woman) using 64-channel MCGs (Hitachi, Japan). Five patients had cardiovascular disease (two with hypertension, one with mitral stenosis, one with ischaemic heart disease, and one with hypertrophic cardiomyopathy) and two had normal cardiac structures (Table 1). Patients with permanent pacemakers or prosthetic valve placement were excluded from this study because of the presence of excessive magnetic noise in MCGs. Antiarrhythmic drugs had been discontinued for more than five half-lives before the procedures.
|
All seven patients were diagnosed as having counterclockwise AFL based on the findings on ECGs and electrophysiological study (EPS, bandpass filter: 30–400 Hz). Atrial activation was indicated by a negative ‘saw tooth’ pattern in the inferior ECG leads and counterclockwise activation along the tricuspid annulus during EPS[20]
. Nine of the 17 episodes were persistent AFL of at least 3 weeks duration. Eight of the 17 episodes were paroxysmal AFL in the same individual, patient 1. Patient 1 had short and frequent episodes of paroxysmal AFL induced by atrial premature complexes. For the eight episodes, the average duration time, from the onset of the atrial premature complex that induced AFL to the termination of AFL, was 11.2±7.9 s (range: 4.2–21.9 s). This study was approved by the ethics committee of the Tsukuba University Hospital, Tsukuba, Japan. All patients gave written informed consent before entering the study.
MCGs
A 64-channel MCG system was placed in a magnetically shielded room at the University of Tsukuba, Tsukuba, Japan. In this system, a detection coil was used as a first order gradiometer. The measurement area was 17.5 by 17.5 cm (sensor interval: 2.5 cm, sensor arrangement: 8 by 8 matrix, Fig. 1). The distance between the chest wall and the SQUID sensor was about 4.5 cm. Signal to noise ratio and magnetic detection limit were approximately 4 and 7 femto tesla/
Hz. In this study, we analysed beat-to-beat components without signal averaging and baseline correction. Without baseline correction or signal averaging, some SQUID sensors detected magnetic noise <5 pico tesla (pT)/m even if there was no electrophysiological phenomenon, for example, between the end of a T-wave end and the beginning of a P-wave during normal sinus rhythm. Therefore, differentiating electrophysiological phenomena from noise for signals <5 pT m–1 was difficult.
|
The cardiac magnetic fields were recorded from the anterior chest for 2 min. An ECG lead II (bandpass filter: 0.1–100 Hz) was simultaneously recorded. We measured the normal components of the cardiac magnetic fields (sampling interval: 1 ms (1 kHz); bandpass filter: 0.1–50 Hz) and calculated the tangential components of the cardiac magnetic fields using the equation[21,
22]:
 |
where Bz: the measured-normal components (pT) and Bxy': the calculated-tangential components (pT m–1). In the analysis of the normal components, the cardiac magnetic strength, just above a magnetic source (i.e. an electrical source), is zero. However, the magnetic strength is maximal in the tangential components[23,24].
To visualize reentrant circuits, we then created iso-magnetic field maps of the tangential components and produced an MCG animation loop (a minimal interval of 1 ms (1 kHz), a maximal recording time of 2 min). An atrial animation was made from the data in which atrial components were clearly identified during long R–R intervals in order to differentiate atrial components from ventricular components. Arrows were added to the maps to emphasize the relationship between the cardiac magnetic fields and the electrical currents[24]. The arrows indicate electric currents calculated from the cardiac magnetic fields.
Comparison between MCGs, ECGs, and EPS
MCGs and EPS were performed on the same day in different rooms, MCGs in a magnetically shielded room and EPS in an electrophysiological laboratory. We compared MCGs animation loops, ECGs, and EPS at the three time points: initiation of AFL, ongoing AFL, and termination of AFL and characterized the relationship between atrial activation and the cardiac magnetic fields.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionAcknowledgementsReferences |
|---|
Beat-to-beat atrial activation was analysed in all 17 episodes using 64-channel iso-magnetic field maps.
AFL initiation
Spontaneous AFL onsets were studied in patient 1 (Figs. 2 and 3). An atrial premature complex (Fig. 2A) induced atrial fibrillation (AF; Fig. 2B), which then transformed to AFL (Fig. 2C). Two 20-polar catheters were placed in the right atrium. One catheter (RA, 2–5 mm, Daig, Nihon Kohden, Japan) was placed in the posterior right atrium. The other catheter (Halo catheter, 2–5–2 mm, Daig, Nihon Kohden, Japan) was placed along the tricuspid annulus. The earliest recording was recorded at RA 3–4 during sinus rhythm (Fig. 2A, the first beat) and RA 5–6 during an atrial premature complex (Fig. 2A, the second beat). Left atrial mapping was not performed in this patient. During AFL, atrial activation revealed counterclockwise rotation along the tricuspid annulus (Fig. 2C).
|
Eight spontaneous onsets were recorded using MCGs in patient 1 (Fig. 3). For this episode, the time from the onset of the atrial premature contraction (Fig. 3A-2) to the termination of AFL was 21.9 s. The ECG from lead II shows ‘saw tooth’ flutter waves (Fig. 3A-7) for 12.9 s of the total duration time.
|
During sinus rhythm, atrial activation started from the upper left area of the map (red area in Fig. 3B-1). The atrial premature complex (Fig. 3B-2) also started near the region of earliest activation for sinus rhythm in this patient. There were differences in activation time and the shape of the cardiac magnetic fields between sinus rhythm (Fig. 3B-1) and the premature complex (Fig. 3B-2). However, both sinus rhythm and the atrial premature complex had cardiac magnetic fields with a single peak of 60 pT m–1. The cardiac magnetic fields during AF (0.7 s after the premature complex, Fig. 3B-3) showed a disorganized pattern. Specifically, multifocal magnetic sources in the animation activated randomly (Fig. 3B-3, B-4). The cardiac magnetic strength decreased with each peak (40–45 pT m–1). Two seconds later, the cardiac magnetic fields fused into a single peak (Fig. 3B-5), but were still irregularly activated. They then evolved into a circular pattern of activation (Fig. 3B-6). Fifteen seconds later (Fig. 3A-7), the cardiac magnetic fields were represented by a red circle (Fig. 3B-7). Arrows indicating electric currents reveal counterclockwise rotation. The cardiac magnetic strength was 45 pT m–1.
AFL persistence
During AFL, the cardiac magnetic fields showed a circular pattern with counterclockwise rotation (Fig. 4) in all seven patients. The cardiac magnetic strength during AFL was 46±14 pT m–1 (range: 25–71 pT m–1).
|
AFL termination
In patient 1, the AFL sequence terminated when atrial activation passed from the right lateral wall of the right atrium to the coronary sinus ostium, as demonstrated by EPS. In MCGs, the atrial components were obscured by the ventricular components during all eight episodes of termination. Therefore, we could not analyse the termination phase using iso-magnetic field mapping.
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionAcknowledgementsReferences |
|---|
In this study, we analysed reentrant arrhythmias using MCGs. Our system utilizes a new technique, employing a multi-channel system, beat-to-beat analysis, and tangential-component MCGs. The cardiac magnetic fields revealed a single peak during sinus rhythm, a circular pattern during AFL, and a random pattern during AF. Our results demonstrate that unique MCG patterns are associated with AFL and AF.
We were able to visualize transient AF, which antedated AFL. Waldo et al. reported that a transitional rhythm, usually AF, is required for the initiation of type I AFL[25]. When AF transformed to AFL, the cardiac magnetic fields fused a single peak at first, and then changed to a circular pattern. EPS identified a wave front for reentrant arrhythmia using a bandpass filter of 30–400 Hz[26]. Regardless of whether invasive[27,28] or noninvasive procedures are used, it is difficult to measure the refractory period[29] and the excitable gap[30,31]. However, the iso-magnetic field map showed a circular pattern during the persistent phase of AFL. This suggests that MCGs can be used to detect myocardial activities at the wave front and to determine the refractory periods.
The circular patterns obtained by MCGs were larger than reentrant circuits obtained by EPS. The wavelength of the circular pattern was 7.8–12.3 cm during AFL[32]. However, the area of the circle identified by MCGs was as large as the measuring area of 17.5 cm2. The circular patterns are theoretically affected by the number, size, location, and shape of reentry. The circuit enlarges as the distance between the magnetic source and the SQUID sensors increases. A simulation showed the upper link of AFL, anterior or posterior to the superior vena cava, affects the circular patterns, circular or semicircular[33]. As left atrial mapping was not performed in this study, the diagnosis of patient 1 may be controversial. It is not clear if a macro-reentry in the right atrium was built due to focal AF originating from the left atrium[34]. However, in this study we showed the relationship between the cardiac magnetic fields and atrial activation in the right atrium (AFL: a circular pattern, AF: disorganized pattern). Further studies are required to differentiate atrial activation in the right atrium and those in the left atrium and to classify AFL patterns, such as lower loop reentry[35] and a circuit in the posteromedial right atrium (sinus venosum)[36], based on MCGs.
The tangential-component MCG can also be applied to the evaluation of ventricular arrhythmias. The cardiac magnetic fields generated during ventricular tachycardia may be more complex than those generated during AFL because the reentry circuit is small and complex in old myocardial infarctions[37].
Study limitations
This study had some associated limitations. First, EPS and MCGs were performed in different rooms, and were not done at the same time. Although ECG lead II was simultaneously recorded as a standard, more information was required to analyse AF in patient 1. Second, standard MCG maps have not been established. There might be differences between electric currents measured by EPS and the arrows generated by the iso-magnetic field maps. In the MCG animation representing a 1- or 2-ms interval, we can identify electric currents through complex movements of the magnetic source, which were summarized as arrows on the maps. The magnetic source moved along a circuit in AFL, but rapidly appeared and disappeared during AF. These changes were not completely reproduced in the sequential maps. We must identify a better way to reproduce this information. In addition, imaging three-dimensional information is also important.
|
Conclusion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionAcknowledgementsReferences |
|---|
We analysed the tangential components of cardiac magnetic fields in patients with counterclockwise AFL. MCG animation revealed the sequence of activation in which a premature complex transformed sinus rhythm into AFL via AF. This suggests that MCGs can be used to diagnose atrial tachyarrhythmias noninvasively and to investigate mechanisms of how AF converts to AFL.
|
Acknowledgements |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionAcknowledgementsReferences |
|---|
This study was supported by the 6th Japanese Heart Foundation/Pfizer Pharmaceuticals Int. Grant on Cardiovascular Disease Research. We would like to thank Dr Yuichi Noguchi, Mr Toshio Ebashi, and Mr Kazuhiko Akamatsu (Tsukuba Medical Center Hospital, Japan) for their cooperation of magnetic resonance imaging, and Mr Kazunori Muramaki and Mr Kenji Teshigawara (Hitachi Ltd., Japan) for their technical support in data analysis. We would like to thank Dr Denice M. Hodgson (Cardiovascular Diseases Division, Mayo Clinic, U.S.A.) for helpful discussions.
|
Footnotes |
|---|
*Present address: Guggenheim 714, Cardiovascular Diseases Division, Internal Medicine, Mayo Clinic, Rochester, MN 55905, U.S.A. The fellowship is supported by the 19th Medtronic Japan Fellowship for Young Japanese Investigators.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionAcknowledgementsReferences |
|---|
[1] Karp PJ, Katila TE, Saarinen M, Siltanen P, Varpula TT. The normal human magnetocardiogram II. A multipole analysis. Circ Res 1980; 47: 117–130.
[2] Barry WH, Fairbank WM, Harrison DC, Lehrman KL, Malmivuo JA, Wiksmo JP Jr. Measurement of the human magnetic heart vector. Science 1977; 198: 1159–1162.
[3] Baule GM and McFee R. The magnetic heart vector. Am J Cardiol 1970; 79: 223–236.
[4] Cohen D and Kaufman LA. Magnetic determination of the relationship between the S–T segment shift and the injury current produced by coronary artery occlusion. Circ Res 1975; 36: 414–424.
[5] Williamson SJ and Kaufmann L. Biomagnetism. Sources and their detection. J Magn Magn Mater 1981; 22: 147–160.
[6] Farrell DE, Tripp JH, Norgen R. Magnetic study of the His-Purkinje conduction system in man. IEEE Trans Biomed Eng 1980; 27: 345–350.[Web of Science][Medline]
[7] Yamada S, Kuga K, On K, Yamaguchi I. Noninvasive His potential recording by using magnetocardiograms. Circ J 2003; 67: 622–624.[CrossRef][Web of Science][Medline]
[8] Hailer B, Van Leewen P, Lange S, Wehr M. Spatial distribution of QT dispersion measured by magnetocardiography under stress in coronary artery disease. J Electrocardiol 1999; 32: 207–216.[CrossRef][Web of Science][Medline]
[9] Brockmeier K, Schmitz L, Bobadilla Chavez JD, et al. Magnetocardiography and 32-lead potential mapping: reporalization in normal subjects during pharmacologically induced stress. J Cardiovasc Electrophysiol 1997; 8: 615–626.[Web of Science][Medline]
[10] Nomura M, Nakaya Y, Fujino K, et al. Magnetocardiographic studies of ventricular repolarization in old myocardial infarction. Eur Heart J 1989; 10: 8–15.
[11] Weismuller P, Abraham-Fuchs K, Schneider S, et al. Biomagnetic noninvasive localization of accessory pathways in Wolff–Parkinson–White syndrome. Pacing Clin Electrophysiol 1991; 14: 1961–1965.[CrossRef][Medline]
[12] Weismuller P, Abraham-Fuchs K, Schneider S, Richter P, Kochs M, Hombach V. Magnetocardiographic noninvasive localization of accessory pathways in the Wolff–Parkinson–White syndrome by a multichannel system. Eur Heart J 1992; 13: 616–622.
[13] Agren PL, Goranson H, Hindmarsh T, et al. Magnetocardiographic localization of arrhythmia substrate: a methodology study with accessory pathway ablation as reference. IEEE Trans Med Imaging 1998; 17: 479–485.[CrossRef][Web of Science][Medline]
[14] Yamada S, Tsukada K, Miyashita T, et al. Noninvasive diagnosis of arrhythmic foci by using magnetocardiograms — method and accuracy of magneto-anatomical mapping system. J Arrhythmia 2000; 16: 580–586.
[15] SippensGroenewegen A, Lesh MD, Roithinger FX, et al. Body surface mapping of counterclockwise and clockwise typical atrial flutter: a comparative analysis with endocardial activation sequence mapping. J Am Coll Cardiol 2000; 35: 1276–1287.
[16] Tsukada K, Haruta Y, Adachi A, et al. Multichannel SQUID system detecting tangential components of the cardiac magnetic field. Rev Sci Instrum 1995; 66: 5085–5091.[CrossRef]
[17] Kalman JM, Olgin JE, Saxon LA, Fisher WG, Lee RJ, Lesh MD. Activation and entrainment mapping defines the tricuspid annulus as the anterior barrier in typical atrial flutter. Circulation 1996; 94: 398–406.
[18] Nakagawa H, Lazzara R, Khastgir T, et al. Role of the tricuspid annulus as the anterior barrier and the Eustachian valve/ridge on atrial flutter. Relevance to catheter ablation of the septal isthmus and a new technique for rapid identification of ablation success. Circulation 1996; 94: 407–424.
[19] Olgin JE, Kalman JM, Fitzpatrick AP, Lesh MD. Role of right atrial endocardial structures as barriers to conduction during human type I atrial flutter. Activation and entrainment mapping guided by intracardiac echocardiography. Circulation 1995; 92: 1839–1848.
[20] Lesh MD. Catheter ablation of atrial flutter and tachycardia. In Zipes DP and Jalife J (Eds.). Cardiac Electrophysiology. From Cell to Bedside 2000; 3rd edn. Philadelphia WB Saunders pp. 1009–1027.
[21] Construction of tangential vectors from normal cardiac magnetic field components Miyashita T, Kandori A, Tsukada K, et al. 1998; 520–3 IEEE/EMBS 20th Annual International Conference.
[22] A simplified superconducting quantum interference device system to analyze vector components of a cardiac magnetic field Tsukada K, Kandori A, Miyashita T, et al. 1998; 524–527 IEEE/EMBS 20th Annual International Conference.
[23] Tsukada K, Miyashita T, Kandori A, et al. An iso-integral mapping technique using magneto-cardiogram, and its possible use for diagnosis of ischemic heart disease. Int J Card Imaging 2000; 16: 55–66.[CrossRef][Web of Science][Medline]
[24] Tsukada K, Miyashita T, Kandori A, et al. Noninvasive visualization of active regions and current flow in the heart by analyzing vector components of a cardiac magnetic field. Comput Cardiol 1999; 26: 403–406.
[25] Waldo AL and Cooper TB. Spontaneous onset of type I atrial flutter in patients. J Am Coll Cardiol 1996; 28: 707–712.[Abstract]
[26] Josephson ME. Electrophysiologic investigation: technical aspects Clinical Cardiac Electrophysiology: Techniques and Interpretations 2002; 3rd edn. Philadelphia Lippincott Williams & Wilkins pp. 1–18.
[27] Allessie MA, Wijffels M, Dorland R, Van Der Zee L, Vos M. The effects of atrial fibrillation on the monophasic action potential of the caprine atrium. In Franz MR, Schmitt C, Zrenner B (Eds.). Monophasic Action Potentials. Basics and Clinical Application 1997; Berlin Springer pp. 117–125.
[28] Franz MR. Excitable gap, antiarrhythmic actions, electrical remodeling: the role of MAP recording in atrial fibrillation and other atrial tachyarrhythmias. In Franz MR, Schmitt C, Zrenner B (Eds.). Monophasic Action Potentials. Basics and Clinical Application 1997; Berlin Springer pp. 126–138.
[29] Tai CT, Chen SA, Feng AN, Yu WC, Chen YJ, Chang MS. Electropharmacologic effects of class I and class III antiarrhythmia drugs on typical atrial flutter: insights into the mechanism of termination. Circulation 1998; 97: 1935–1945.
[30] Waldo AL, MacLean WAH, Karp RB, Kouchoukos NT, James TN. Entrainment and interruption of atrial flutter with atrial pacing. Studies in man following open heart surgery. Circulation 1977; 56: 737–745.
[31] Tsuchiya T, Okumura K, Tabuchi T, Iwasa A, Yasue H, Yamabe H. The upper turnover site in the reentry circuit of common atrial flutter. Am J Cardiol 1996; 78: 1439–1442.[CrossRef][Web of Science][Medline]
[32] Rensma PL, Allessie MA, Lammers WEJP, Bonke FI, Schalij MJ. Length of excitation wave and susceptibility to reentrant atrial arrhythmias in normal conscious dogs. Circ Res 1988; 62: 395–410.
[33] Yamada S, Tsukada K, Yamaguchi I. Three-dimensional circuit of common atrial flutter. Europace 2000; 1:Suppl B7.
[34] Ndrepepa G, Weber S, Karch MR, et al. Electrophysiologic characteristics of the spontaneous onset and termination of atrial fibrillation. Am J Cardiol 2002; 90: 1215–1220.[CrossRef][Web of Science][Medline]
[35] Cheng J, Cabeen WR, Scheinman MM. Right atrial flutter due to lower loop reentry: mechanism and anatomical substrate. Circulation 1999; 99: 1700–1705.
[36] Friedman PA, Luria D, Fenton AM, et al. Global right atrial mapping of human atrial flutter: the presence of posteromedial (sinus venosa region) functional block and double potentials. A study in biplane fluoroscopy and intracardiac echocardiography. Circulation 2000; 101: 1568–1577.
[37] DeBakker JMT, Coronel R, Tasseron S, et al. Ventricular tachycardia in the infarcted Langendorff-perfused heart: role of the arrangement of surviving cardiac fibers. J Am Coll Cardiol 1990; 15: 1594–1607.[Abstract]
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  F. Kilicaslan, A. Verma, H. Yamaji, N. F. Marrouche, O. Wazni, J. E. Cummings, S. Hao, M. W. Andrews, S. Beheiry, A. Abdul-Karim, et al. The need for atrial flutter ablation following pulmonary vein antrum isolation in patients with and without previous cardiac surgery J. Am. Coll. Cardiol., March 1, 2005; 45(5): 690 - 696. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||