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Multifocal Atrial Tachycardia4 James McCord, MD; and Steven Rorzak, MD is typically seen in elderly patients with severe illnesses, most tachycardia ofthe arrhythmia may be delayed afterdepolarizations leading The mechanism COPD. commonly Multifocal atrial but this has not been firmly established. The initial treatment of multifocal triggered activity,should include supportive measures and aggressive reversal of precipitating atrial tachycardia causes. Since multifocal atrial tachycardia is commonly a secondary phenomenon, the role for antiarrhythmic therapy is unclear. Metoprolol, magnesium, and verapamil have been evaluated in a few treatment studies, and may have a role in the treatment of multifocal atrial tachycardia. to (CHEST 1998; 113:203-09) Key words: magnesium; metoprolol; multifocal atrial tachycardia; verapamil Abbreviations: AV=atrioventricular; CHF=congestive heart failure; M AT=multifocal atrial PE=pulmonary embolism HP he term multifocal atrial tachycardia (MAT) was ¦*¦ first used in 1968 by Shine et al,1 but this rhythm has been described previously by other names such as chaotic atrial tachycardia,2 chaotic atrial rhythm,3 chaotic atrial mechanism,4 and repetitive multifocal atrial tachycardia.56 In addition, in the paroxysmal 1930s, there were rhythms described as "polymorphe extrasystole"7 and "anarchi auriculaire"8 that represented MAT. probably Shine et al1 defined MAT (Fig 1) as a rhythm with atrial rate >100 beats/min, at least three morpho¬ and irregularP P-P intervals, logically distinct P waves,between waves (to further an isoelectric baseline differentiate MAT from atrial fibrillation and atrial flutter). Some authors have suggested that there should be three distinct P waves different from the sinus P wave,9 while others have stated that two distinct P waves in addition to the sinus P wave are There is no clear consensus adequate forthisdiagnosis.10 criteria for MAT have Other issue. regarding been suggested, such as >50% of all atrial beats an varying R-R intervals, varying P-R being ectopic, and atrial rate >120 beats/min,12 but intervals,11 these are less well accepted. MAT can easily be misinterpreted as atrial fibril¬ lation on an ECG. One retrospective study showed that in patients hospitalized with MAT, only 22% had their ECG interpreted correctly on admission.13 The differentiation of atrial fibrillation from MAT is Henry Ford Hospital, De¬ accepted June 13. Manuscript received April 30, 1997; revision MD, ReprintFord requests: James McCord, MD, or Steven Borzak, Cardiovascular Division, 2799 W Grand Hospital, Henry MI 48202 *From the Cardiovascular Division, troit. Blvd, Detroit, important because their atrial ECG may from MAT.23 tachycardia; differ. Intraatrial fibrillation treatments help distinguish Population The prevalence of MAT in the hospitalized popu¬ lation has been estimated to be 0.05 to 0.32%o.1'2-414 Review of >300 patients with MAT from nine studies demonstrated an average age of 72 years, and an in-hospital mortality rate of 45%o.1-4111316 The mortality rate is most likely a consequence of high the severe underlying illnesses of these patients, rather than a direct result of the arrhythmia itself. MAT occurs even less commonly in the pediatric In 28 patients from six reports, the ages population. to 18 years, but these young from ranged did newborn have serious medical conditions as as not patients their adult counterparts:1722 54% had no other condition besides the arrhythmia, 21% had congen¬ ital heart disease, and 25% had a variety of other conditions. Also, a few young adults have been noted to have MAT without any underlying illness.23 Clinical Setting COPD An exacerbation of COPD is the most common setting in which MAT arises. COPD was present in 55% of patients with MAT described in various studies1-41113-16'24"33 (Table 1). Patients with the and COPD have a high mortality rate: arrhythmia 80% in one study.1 CHEST / 113 / 1 / JANUARY, 1998 Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21757/ on 05/12/2017 203 tions.34 Theophylline may also be arrhythmogenic by causing increased urinary excretion of potassium and magnesium,3538 and thereby hypokalemia and hypomagnesemia. Similarly, the development of MAT has been related to P-agonist therapy. Six of 14 patients with MAT who had aggressive treatment with nebulized isoproterenol had termination of the arrhythmia when the drug therapy was discontinued.4 Hypoxemia Hypoxemia was present in 43% of patients with MAT in several studies.21126 In one study, 85% of MAT patients were in acute respiratory distress.15 Hypoxemia may contribute to the arrhythmia in COPD, but may cause MAT in other settings as well. In two studies, 17% of MAT cases occurred in the postoperative setting,13 where hypoxemia associated with atelectasis or pneumonia might have contrib¬ Figure 1. The rhythm strip demonstrates multiple P-wave atrial rate >100 beats/min, and varying P-P configurations, intervals. Right ventricular hypertrophy is noted in \\. The of COPD may promote the ar¬ rhythmia. study of 16 patients with MAT, all had cessation of the arrhythmia when theophylline therapy was discontinued.11 Twelve patients had theophylline levels >20 ng/mL. Five of these pa¬ tients had theophylline therapy restarted, and MAT recurred in all. An apparent direct relationship was shown between the theophylline level and the num¬ ber of atrial ectopic beats.11 A study of 50 patients with MAT showed that patients treated with theo¬ had significantly faster ventricular rates phylline when compared to similar patients not receiving the drug.33 Ry increasing cyclic adenosine monophos¬ phate in myocardial cells, theophylline may promote catecholamine-mediated delayed afterdepolariza- uted. treatment In one Pulmonary Embolism A weak relationship between MAT and pulmonary embolism (PE) may exist. In a study of 50 patients with MAT, PE was present in 4 of 14 patients who had autopsies.33 In another study of 31 patients with MAT, there were eight autopsies and only one of these had a PE.14 In three other PE was studies, cited in 14%), 10%, and 16% ofthe cases of MAT, but none of these studies described how PE was diag¬ nosed.3'4-11 An association between PE and MAT was not found in a subgroup analysis of the Prospective Table 1.Clinical Characteristics First Author Arsura26 Hazard25 Levine27 Iseri30 Kouvaras32 Shine1 Phillips14 Wang15 Lipson2 COPD, No. CHF, No. (%) (%) 6/11 (55) 20/25 (80) 3/6 (50) 5/8 (63) 5/9 (56) 10/32 (31) 26/31 (84) 10/41 (24) 12/31 (39) Scher13 30/37 (81) 17/56 (30) Levine11 16/16 Kones4 (100) LowK+, No. (%) of Patients With MAT Afib/Aflutter,* No. (%) Hypoxemia, No. PE, No. (%) 10/11 (91) 5/25 (20) 4/32 (13) (17) 10/31 (32) 22/37 (59) 6/56(11) 2/16 (13) 18/31 (58) 3/6 (50) 3/8 (38) 2/9 (22) 13/32 (41) 7/41 9/31 (29) Berlinerblau3 Habibzadeh33 29/50 (58) McCord51 14/14 (100) Others16'24-28-29"31 38/55 (69) Totals 250/453 (55) 74/269 (28) * Afib/Aflutter=atrial fibrillation/atrial flutter. 5/31 (16) 2/37 (5) 5/25 (25) (20) 4/14 (29) 4/16 41/178 (23) 12/31 19/41 17/31 (38) (46) (55) 1/8 10/31 (12) (32) 5/37 (14) 5/16 (31) 1/16 (16) 3/31 (10) 4/14 (28) 25/58 (43) 14/106 (13) 5/31 (16) 53/134 (40) 204 Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21757/ on 05/12/2017 Reviews atrial flutter.2'31415 The arrhythmia typically lasts 1 days, but a few cases of chronic MAT have been documented.2-413 Paroxysms of atrial fibrilla¬ tion or atrial flutter have been shown in 16 to 55% of patients with MAT (Table 2). Intra-atrial masses, such as tuberculomas or metastatic lesions, have been associated with the arrhythmia.4 Finally, al¬ MAT with digoxin though onea author has associated of toxicity,10 preponderance studies do not support an association between MAT and digoxin use or Investigation of Pulmonary Embolism Diagnosis trial. Of 117 patients with angiographically con¬ firmed PE, 4% had atrial fibrillation, 1% had atrial flutter, but none had MAT. However, patients with preexisting cardiac or pulmonary disease were ex¬ cluded from this analysis.39 Thus, a relationship between PE and MAT cannot be excluded. to 10 Congestive Heart Failure and Electrolyte Abnormalities There appears to be an association of congestive heart failure (CHF) with MAT. Heart failure was present in 28% of patients with MAT in several studies, but most patients had coexisting lung disease (Table 1). In nine studies, 23% of patients with MAT had potassium levels <3.5 mEq/L, perhaps medi¬ ated by diuretic treatment of CHF (Table 1). There have been reports of potassium and magnesium associated with conversion of MAT to replacement sinus rhythm.40 In a small study of eight patients, three of whom were hypokalemic and hypomagnesemic, all converted to normal sinus rhythm after potassium and magnesium administration.30 Magne¬ sium modulates many of the potassium transport systems, which may explain why treatment of refrac¬ tory hypokalemia is responsive to reversal of hypo- toxicity.131315 Mechanisms Delayedhasafterdepolarization leading to "triggered been as the mechanism for activity" proposed never but this has been our MAT,274144 provedare(tooscil¬ knowledge). Delayed afterdepolarizations lations in the cardiac myocyte membrane potential that occur following repolarization of an action po¬ tential. When the delayed afterdepolarization is large enough to reach threshold potential, the resultant action potential is termed "triggered." Afterdepolar¬ izations stand in contrast to increased automaticity, as an afterdepolarization is dependent on the occur¬ rence of a previous action potential, while automatic occur de novo. rhythms Indirect evidence suggests that MAT may be due to triggered activity. Intracellular calcium overload promotes triggered activity. Many conditions associ¬ ated with MAT lead to intracellular calcium over¬ load, such as catecholamine excess,45 phosphodies- magnesemia.35 Other Clinical MAT is ously Settings frequently transient and may spontane¬ rhythm, atrial fibrillation, or convert to sinus Table 2.MAT Studies Reference No. Intervention No. of Patients Decrease in Ventricular Rate, p Value Conversion to NSR* Placebo-controlled studies 24 28 Metoprolol IV 9 Verapamil IV 9 Placebo 12 Verapamil IV 5 24 7 3 <0.01 Magnesium IV 9 24 3 <0.05 NS Metoprolol IV 15 Metoprolol po 10 Metoprolol po 11 Verapamil IV 6 Verapamil IV 16 Verapamil IV 13 32 40 32 16 22 22 19 <0.001 <0.001 <0.01 <0.0001 <0.0005 <0.001 <0.01 32 <0.001 NS* NS Placebo 5 51 Placebo 5 3/9 1/9 2/12 1/5 0/5 4/9 0/5 Uncontrolled observational studies 25 26 27 29 16 30 31 32 53 52 Magnesium IV 8 Magnesium IV or IM Amiodarone IV or po Flecainide IV 4 Diltiazem 8 8 9 24 8/15 3/10 11/11 3/6 8/16 3/13 7/8 8/8 9/9 3/4 4/8 *NSR=normal sinus rhythm. fNS=not significant. CHEST / 113 / 1 / JANUARY, 1998 Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21757/ on 05/12/2017 205 inhibition,11 acidemia,46 and hypoxemia.47 Triggered activity can be further potentiated by terase hypokalemia48 or hypomagnesemia49 Verapamil, which inhibits in vitro atrial triggered activity,715 has been used in the treatment of MAT.16-24-27"29 How¬ ever, the efficacy of verapamil for MAT has been inconsistent (Table 2), and delayed afterdepolariza¬ tion leading to triggered activity has never been demonstrated in the setting of MAT (to our knowl¬ edge). agents to treat patients with MAT16-24"32-51"53 (Table 2). However, these studies were limited to small numbers of patients, and only four were controlled.24-28'51-53 The studies involved metoprolol, verapamil, magnesium, diltiazem, flecainide, and amiodarone. Metoprolol Arsura et al24 performed controlled study that a double-blind, placebo- compared metoprolol with verapamil (Table 2). Metoprolol demonstrated THERAPEUTIC INTERVENTIONS Reversal of precipitating causes remains the cor¬ of treatment for MAT, as this may be all that is required to control the arrhythmia,1'2-4-13 and harmful effects of antiarrhythmic agents potentially avoided. be COPD, CHF, electrolyte imbal¬ may ance, hypoxemia, and PE should be treated with consideration of the arrhythmia-promoting effects of some therapies. Theophylline and (3-agonist therapy should be decreased or discontinued if clinically feasible. If a patient remains in MAT, antiarrhythmic therapy can be considered for restoration of sinus or rate control. rhythm Class 1 antiarrhythmic agents have been used without perceived success in uncontrolled settings. These include lidocaine, quinidine, procainamide, and phenytoin.1'2'4'13'1519"21 In addition, electrical cardioversion is not effective in converting MAT to nerstone rhythm.2'415 digoxin has not been evaluated in a controlled study, but observational reports sug¬ gest that digoxin is not effective in controlling the rate or restoring sinus rhythm in patients with MAT.1215 This may be because slowing atrioventricular (AV) conduction does not address the atrial mechanism of the tachycardia. Digoxin promotes which may worsen afterdepolarizations delayed when there is CHF or intermittent MAT. sinus To our knowledge, However, atrial fibrillation, both of which are common in the setting of MAT, digoxin may be beneficial. Digoxin should be used cautiously as these patients may be to digoxin toxicity.1 Ventricular ar¬ especially prone death have been reported rhythmias, AV block, andhas been administered to when excessive digoxin MAT patients who were incorrectly diagnosed as atrial fibrillation.1-15-18-50 In one study, pa¬ havingwith MAT who were receiving digoxin had a tients mortality rate when compared higher significantly not This result, how¬ with patients taking digoxin.33worse the reflect ever, may general prognosis of with heart who failure are more patients likely to be receiving digoxin. Thirteen studies have used other antiarrhythmic a significant reduction in ventricular rate of 24%, while verapamil and placebo had no effect on rate. With metoprolol, more patients converted to sinus rhythm. The only adverse effect was a transient drop in RP with metoprolol from 150/70 mm Hg to 80/60 mm Hg in one patient that responded promptly to fluids. In two other studies, metoprolol demonstrated significant decreases in ventricular rate of 35% and 32% 25,26 jn j-ne study of Hazard and Rurnett,25 one third of discharged patients were maintained on a regimen of oral metoprolol. There was no worsening of pulmonary status; in fact, the average Po2 in¬ creased significantly from 77 to 89 mm Hg in metoprolol-treated patients. However, there was no control group for comparison. In the study of Arsura et al,26 all 11 patients converted to normal sinus rhythm after metoprolol. Verapamil Verapamil resulted in a significant ventricular rate in three decrease in studies,162729 but in two other studies that were double-blind and placebocontrolled, there was no significant change24-28 (Ta¬ ble 2). Verapamil may worsen hypoxemia by negat¬ ing hypoxic pulmonary vasoconstriction in underventilated alveoli,16 but worsening oxygenation was not a consistent finding. Hazard and Rurnett25 showed a decrease in average Po2 of 105 to 78 mm significant while Salerno et al29 showed no significant Hg, decrease in oxygenation. Salerno et al gave the largest dose of IV verapamil (average, 17 mg) and showed that pretreatment with calcium gluconate decreased the hypotensive effect of significantlywithout blocking the heart rate-lowering verapamil effect (RP decreased 11% with calcium as opposed to 27% without calcium). Magnesium study of Iseri et al,30 during "high-dose" magnesium (Table 3) infusion, there was a significant decrease in heart rate, and 88% of patients converted to normal sinus rhythm. Only one patient had a In the 206 Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21757/ on 05/12/2017 Reviews Table 3.Drug Protocols for MAT Reference No. Drug Dose 24 Metoprolol Verapamil 10 mg IV over 5 min 10 mg IV over 5 min 2 g IV over 1 min, then 2 g/h over 5 h 300 mg po tid or 450-1,500 mg IV over 2-24 h 2 mg/kg IV bolus over 10 min, then 1.5 mg/kg for 1 h 0.15 mg/kg IV bolus over 5 min, then 0.005 mg/kg/min for 1 h 20-45 mg IV bolus, then 10-25 mg/h Magnesium 30 32 Amiodarone Flecainide 53 Verapamil Diltiazem 52 of MAT and the average serum magne¬ from 1.6 to 3.5 mEq/L. Utilizing the same protocol, McCord et al51 showed that magne¬ sium caused a significant decrease in heart rate as compared with placebo, but only four of nine mag¬ nesium-treated patients converted to sinus rhythm. Cohen et al31 treated MAT patients with either magnesium sulfate IV or IM. Although no ventricu¬ lar rates were reported, all patients treated IM converted to sinus rhythm within 1 to 2 h, while all patients treated IV converted to sinus rhythm within 4 to 8 h. Cohen et al attributed this difference to the higher sustained magnesium level in the first few hours for the IM-treated group. No side effects were reported in the magnesium studies. Of note, in all of these studies, metoprolol, verapamil, and magne¬ sium decreased ventricular rate by suppressing atrial ectopic beats, not by blocking AV conduction. recurrence sium level rose Other Agents Kouvaras et al32 administered either oral or IV amiodarone to patients with MAT. The four patients who received IV dosing converted to sinus rhythm within 45 min during a 2-h infusion of amiodarone. One of these patients reverted to MAT and required additional IV dosing. Of five patients who received oral amiodarone, two converted to sinus rhythm on the third day, one on the fourth day, and two on the fifth day. All nine patients subsequently received oral maintenance doses. Since MAT is frequently tran¬ sient, it is uncertain if conversion to sinus rhythm represents an effect of amiodarone. Adcock et al,52 in a preliminary report, studied patients with MAT who received IV diltiazem as a bolus and then maintenance infusion. Over a 4-h period, four patients converted to sinus rhythm, and during the infusion, there was a mean decrease in ventricular rate of 35 beats/min. There was no control group. Rarranco et al53 studied six patients with MAT: four received flecainide and two received verapamil. After an IV bolus and then maintenance infusion over 1 h, three of four patients who received flecain¬ ide and zero of two patients who received verapamil in sinus rhythm. Two of the patients who received flecainide converted to sinus rhythm during the 10-min bolus. The effect on ventricular rates was were not reported. Limitations of these trials include few patients (between 4 and 25), limited follow-up (<24 h in most studies), and uncontrolled study design (only 4 studies were controlled). Discussion Should MAT be treated with antiarrhythmic agents? The arrhythmia is typically an epiphenomenon of an underlying disorder, and perhaps should not be directly treated. MAT is commonly transient and will often resolve after precipitating causes are reversed. If the arrhythmia persists, the clinical significance of the tachycardia must be evaluated before the use of antiarrhythmics is considered. MAT would be clinically significant if it were to cause hypotension, CHF, or myocardial ischemia as can atrial fibrillation. Although atrial fibrillation causing can be demonstrated with improvement in hypotension RP after electrical cardioversion, this phenomenon has not been shown in MAT. The arrhythmia is not respon¬ sive to electrical cardioversion, and hypotension in this setting is most likely secondary to underlying conditions such as PE or sepsis. Theoretically, MAT could exacerbate myocardial ischemia or CHF, but this has not been described commonly in the literature. In fact, it is surprising how infrequently unstable angina or myocardial in¬ farction has been described in this elderly popula¬ tion.54 Myocardial ischemia, although uncommon in MAT patients, may be the only compelling reason to the arrhythmia itself. Unfortunately, since only a small number of pa¬ tients have been studied, and the clinical significance of the arrhythmia is unclear, the role of antiarrhyth¬ mic therapy remains uncertain. The clinical rele¬ vance of persistent tachycardia must be evaluated on an individual basis; potential benefits of antiarrhyth¬ mic therapy must be weighed against actual risks. Since metoprolol is the only agent shown to be treat CHEST / 113 / 1 / JANUARY, 1998 Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21757/ on 05/12/2017 207 effective for rate control in a double-blind, placebocontrolled trial,24 it should be the first agent consid¬ ered in the treatment of MAT. Metoprolol's mech¬ anism of action may be the blunting of the stimulus that supports the milieu for adrenergic MAT. The use of metoprolol in the setting of MAT is limited, however, because |3-blockers may worsen CHF or bronchospasm. In two of the three studies was an ex¬ involving metoprolol,24-26 bronchospasm third the while exclusion criterion, study did plicitmention exclusion criteria.25 If (3-blockers are not esmolol with its short relatively contraindicated, adverse effects be considered as half-life may any may resolve soon after discontinuation.55 If metoprolol is not effective or contraindicated, Resides "high-dose" magnesium may be considered. is the only agent metoprolol, high-dose magnesium shown to have efficacy in a placebo-controlled trial.51 The use of high-dose magnesium was shown to be safe in the three MAT trials. The mechanism of action of magnesium may be the inhibition of afterdepolarizations.49 The use of magnesium may be limited by renal failure, but side effects such as headache are minor and transient. flushing andmeasures If these fail, dien verapamil may be con¬ sidered. In the two studies that used a control group, however, verapamil was no better than placebo. The use of verapamil is also limited in the presence of CHF or hypotension. The hypotensive effect may be limited with calcium.29 Although amiodarone, by pretreatmentflecainide and diltiazem, may have potential in the treatment of MAT, they cannot routinely be recom¬ mended because to our knowledge, only one study with a small number of patients evaluated each of these three patients with MAT, who were drugs. Finally, treated with radioto medical therapy, were refractory and ablation AV pace¬ frequency junctionAll three permanent maker placement.56-57 patients had a success¬ ful ablation, and reported improvement in their symptoms of palpitations and dyspnea. This method may prove useful in patients with persistent and symp¬ tomatic MAT. basis for this rhythm is hy¬ electrophysiologic be to afterdepolarizations, which could be pothesized further mediated by the high adrenergic state encoun¬ measures and rever¬ tered in these The ment to sinus rhythm and potential side ef¬ spontaneously fects of antiarrhythmic agents can be avoided. If a patient remains in MAT and the tachycardia is consid¬ ered clinically significant, a certain priority of antiarcould be considered: (3-blockers rbythmic agents or and then vera¬ esmolol), (metoprolol these magnesium, have been evaluated in However, agents pamil. few studies involving small numbers of patients. References 2 3 4 5 Febiger, 1956; 527 DL, Eaddy JA. Repetitive multifocal paroxysmal atrial tachycardia with second degree A-V block, type I, and 6 Abrahms 7 8 9 10 MAT is most typically encountered in elderly pa¬ tients with COPD, and although the arrhythmia is uncommon, its incidence may increase as does the 15 with atrial fibrillation. The distinction quendy confused as incorrect diagnosis may lead to ineffectual and possibly harmful therapy. is crucial, concealed and aberrant A-V conduction. Am J Cardiol 1965; 15:871-73 Langeron L. Troubles electriques de la contraction auriculaire precedeant la fibrillation de l'oreilleitte: existence d'un stade pre-fibrillatoire. Arch Mai Coeur 1932; 25:34-39 Duclos F. L'Anarchie auriculaire comme etat prefibrillatoire. Arch Mai Coeur 1935; 28:393-403 Kastor JA. Multifocal atrial tachycardia. N Engl J Med 1990; 332:1713-17 Chung EK. Appraisal of multifocal atrial tachycardia. Br Heart J 1971; 33:500-04 11 Levine JH, Michael JR, Guarnieri T. 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Philadelphia: Lea & 1 Shine Conclusions concomitant medical problems, and the high mortality rate is most likely due to the severity of their underlying illness. MAT can be difficult to diagnose and is fre- patients. Supportive causes should be the initial treat¬ as many patients will convert strategy sal of precipitating prognostic factors in patients with multifocal atrial tachycar¬ dia [abstract]. Am Rev Respir Dis 1988; 137(suppl):475 Phillips J, Spano J, Burch G. Chaotic atrial mechanism. Am Heart J 1969; 78:171-79 WTang K, Goldfarb BL, Gobel FL, et al. Multifocal atrial tachycardia: a clinical analysis in 41 cases. Arch Intern Med 1977; 137:161-64 16 Hazard PB, Burnett CR. Verapamil in multifocal atrial tachy¬ cardia: hemodynamic and respiratory changes. Chest 1987; 91:68-70 17 Farooki ZQ, Green EW. Multifocal atrial tachycardia in two neonates. Br Heart J 1977; 39:872-74 18 Bisset GS III, Seigel SF, Guam WE, et al. Chaotic atrial tachycardia in childhood. 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