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PubMed2006

Pathogenesis of cardiac conduction disorders in children genetic and histopathologic aspects.

Fetal dysrhythmias are usually transient. Abnormal fetal rates and rhythms during labor are "functional." Fetal dysrhythmias may be associated with congenital heart disease and fetal hydrops. Bradycardia is usually related to fetal distress; supraventricular tachycardia, atrial flutter, and atrial fibrillation may be associated with severe congestive heart failure. Ventricular fibrillation is rare in the fetus and infant and is usually associated with myocardial necrosis with perimembranous septal defect; the nonbranching atrioventricular (AV) bundle may have an aberrant position and result in cardiac arrhythmia. Wolff-Parkinson-White syndrome with conduction abnormalities and left ventricular hypertrophy (LVH) is due to an accessory pathway that bypasses the AV sulcus and results in faster conduction. Carnitine deficiency may be primary or secondary and may result in cardiac arrhythmia. Histiocytoid cardiomyopathy is characterized by cardiomegaly, incessant ventricular tachycardia, and frequently sudden death. Arrhythmogenic right ventricular dysplasia (ARVD) results in ventricular tachycardia and left bundle branch block. Noncompaction of the left ventricle predisposes to potentially fatal arrhythmias. Long Q-T syndromes (LQTS) are a heterogeneous group of disorders with many genetic mutations. Brugada syndrome is an autosomal dominant trait with right bundle branch block and ST elevation. Barth syndrome is an X-linked disorder with dilated cardiomyopathy, cyclic neutropenia and skeletal myopathy. Hypertrophic cardiomyopathy in infancy may be related to metabolic diseases, particularly glycogen storage diseases; the familial form predisposes to sudden death. Arrhythmias following cardiac surgery may occur after closure of a ventricular septal defect (VSD) or damage to the conduction system.

Arrhythmias, Cardiac↗
PubMedDate not supplied

Reentrant tachyarrhythmias in right atria of cardiomyopathic versus healthy Syrian hamster.

We studied the role of acetylcholine (ACh) and calcium overload in the induction of atrial flutter or atrial fibrillation (AF) in right atria from 34 normal male Syrian hamsters (F1B) and 33 cardiomyopathic Syrian hamsters (BIO 14.6) associated with focal myocardial necrosis. Action potential (AP) was recorded with conventional microelectrode techniques and twitch force by a transducer. ACh (0.1, 1 and 10 microM) induced high-frequency AF (around 33 Hz) along with tension oscillations and contracture in 7 of 12 normal hamster atria. These effects of ACh were abolished by tetrodotoxin or quinidine as well as by atropine. In contrast, ACh induced AF only in 1 of 12 myopathic atria. In both normal and myopathic atria, ACh induced similar changes in AP duration, spontaneous rate and force. The effects of calcium overload were tested by means of a high [Ca(2+)](o) (8.1 mM) low [K(+)](o) (1 mM) solution in another series of experiments. This solution also induced incidence of AF higher in normal (10/12) than in myopathic atria (4/12). The calcium load was also increased by high-frequency pacing (32 Hz for 3 or 30 s): AF occurred in normal atria (5/8), but not in myopathic atria (0/8). Measurement of the refractory period revealed a longer refractory period in myopathic than in control atria. We concluded that the lower incidence of AF in myopathic atria was probably due to their longer refractory period and the associated focal myocardial necrosis which then hindered the establishment of such a reentrant rhythm.

Acetylcholine↗
PubMed2005

Implantable dual-chamber defibrillator for the selective treatment of spontaneous atrial and ventricular arrhythmias: arrhythmia incidence and device performance.

INTRODUCTION: Atrial tachyarrhythmias are a common co-morbidity in patients with an ICD indication. Recently introduced ICD's are equipped to independently detect and treat atrial and ventricular tachyarrhythmias. The purpose of this prospective study was to evaluate the incidence and termination of spontaneous atrial and ventricular tachyarrythmias in patients with a history of atrial tachyarrhythmias. METHODS AND RESULTS: Ninety patients, 70% male with an ICD indication and history of atrial tachyarrhythmia (LVEF 45 +/- 6%, [AT/AF indication 55 +/- 10, AT/VT 45 +/- 16], 46% CAD) were enrolled and 89 were implanted with a VENTAK PRIZM AVT (Guidant). Spontaneous atrial and ventricular tachyarrhythmias were printed and evaluated during an average follow-up period of 272 +/- 72 days utilizing the stored intracardial electrogram function of the device. Nineteen patients (21%) presented had only atrial tachyarrhythmias, 32 patients (36%) had both atrial and ventricular tachyarrhythmias and 18 patients (20%) had only ventricular tachyarrhythmias. Patients with only atrial tachyarrhythmias had a total of 3274 atrial episodes; 2002 terminated spontaneously, 1264 were treated with ATP and 8 with shock therapy. ATP was successful in 735 (58%) of 1264 episodes. Patients with both atrial and ventricular tachyarrhythmias had 7277 documented atrial tachyarrhythmias, 5231 terminated spontaneously, 1153 of 2009 were terminated by ATP (57.4%) and 37 by shock therapy (20 patient controlled). Atrial tachyarrhythmias identified as atrial flutter (AT) by the atrial rhythm classification (ARC) algorithm had a higher ATP conversion success rate than episodes identified as atrial fibrillation (AF); 66.7% for AT and 26.4% for AF. Patients with only ventricular tachyarrhythmias had 690 documented episodes, 401 terminated spontaneously, 248 (85.8%) were terminated by ATP and 41 by shock. CONCLUSION: Seventy-seven percent of patients with an ICD indication had spontaneous atrial and/or ventricular tachyharrhythmias within the first 6 months after ICD implantation. ATP therapy terminated 58% of all atrial tachyarrhytmias and 66.7% of the atrial flutters. The dual chamber ICD detected, classified and terminated all ventricular tacharrhythmias appropriately.

Aged↗
PubMed1976

Patient-initiated rapid atrial pacing to manage supraventricular tachycardia.

Patient-controlled rapid atrial pacing was used to manage 12 cases of recurrent supraventricular tachycardia refractory to drug therapy. The pacing system consists of an implanted receiver-lead system and an external patient-activated transmitter. In each case, brief periods (5 to 20 seconds) of rapid atrial pacing were effective in terminating the supraventricular tachycardia and resulted in a return to normal sinus rhythm. In three patients, occasional transient episodes of atrial flutter or atrial fibrillation preceded a spontaneous return to normal sinus rhythm. The pacing system was removed in one patient 13 months postoperatively because of persistent pericarditis; one patient died of an unrelated cerebral hemorrhage 13 months postoperatively. Successful management of supraventricular tachycardia has been maintained in the 10 remaining patients for 15 to 36 months (average 26.4). In more than 6,000 patient applications of rapid atrial pacing, there has been only one failure to convert the tachycardia. Successful application of permanent rapid atrial pacing requires (1) prescreening of patients with temporary external rapid atrial pacing to verify susceptibility to conversion of supraventricular tachycardia and absence of anomalous conduction pathways that may permit conduction of rapid pacing rates to the ventricles, and (2) assessment of the patient's ability to use the transmitter properly.

Adult↗
PubMed1992

Effectiveness of oral sotalol for treatment of pediatric arrhythmias.

Sotalol is a beta blocker with class III activity. Few investigators have reported its use in pediatric patients. From August 1985 to May 1990, 66 patients (mean age 8.7 years; range 9 days to 24 years), including 14 infants aged less than 3 months, were treated with oral sotalol alone (n = 46) or in association with digoxin (n = 20). Supraventricular reentrant tachycardia was present in 38 patients (20 with documented preexcitation), atrial flutter in 10 and atrial ectopic tachycardia in 7. Three patients had other types of supraventricular tachycardia. Tachycardia was of ventricular origin in 6 patients and both of supraventricular and ventricular origin in the remaining 2. Mean dose of oral sotalol was 135 mg/m2/day given in 2 doses. Congenital heart disease was present in 28 patients, 14 with previous cardiac surgery, mostly at the atrial level. Prior treatment with 1 or more antiarrhythmic agent had been unsuccessful in 83% of patients. Mean duration of treatment was 13.3 months (range 2 months to 5 years). Overall, treatment was successful in 79% of cases. Highest rate of success was observed in patients with supraventricular reentrant tachycardia with or without preexcitation (89%) and in those with atrial ectopic tachycardia (85.5%). Atrial flutter could be controlled in 60% of cases. Sotalol seemed less effective in ventricular tachycardia with a complete control of the arrhythmia being achieved in only 17%; however, it decreased the number of runs of ventricular tachycardia and the number of ventricular premature complexes in 50% of patients. There were no adverse effects in 89% of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1991

Surgical treatment of supraventricular tachycardia: experience with 61 patients.

Sixty-one patients underwent operation for supraventricular tachycardia: 52 had tachycardia associated with the atrioventricular accessory pathways; 9 patients had other forms of tachycardia. Accessory pathways were successfully divided in 92.3% of the patients. Classic endocardial approach was used in 30 patients; closed heart ablation of the accessory pathways was performed in 22 patients. There were two reoperations for return of conduction through the accessory pathways. Six patients underwent cryoablation of the His bundle through the right atrial approach. Four patients underwent attempts at curative operations for atrioventricular node reentry tachycardia, atrial flutter, and atrial ectopic tachycardia. Concomitant cardiac surgical procedures were performed in 14 patients. Operative mortality was 1.6%. A satisfactory result, without tachycardia and without medication, was achieved in 93.4% of all patients.

Cryosurgery↗
PubMed2006

Reduction of atrial tachyarrhythmia episodes during the overdrive pacing period using the post-mode switch overdrive pacing (PMOP) algorithm.

BACKGROUND: Early recurrences within 10 minutes after termination of an atrial tachyarrhythmia, such as atrial tachycardia (AT), atrial flutter, or atrial fibrillation (AF) episodes, account for a large part of paroxysmal AT/AF episodes. It is unclear whether these arrhythmias can be suppressed by overdrive pacing. OBJECTIVE: We set out to prove that overdrive pacing is effective in preventing early recurrences of AT/AF. METHODS: This AT500 (DDDRP device, Bakken Research Center Medtronic, Maastricht, The Netherlands) post-mode switch overdrive pacing (PMOP) study is a randomized controlled trial designed to test the efficacy of overdrive pacing on the suppression of early recurring AT/AF episodes. With the PMOP feature, overdrive pacing is activated 12 ventricular beats after device-confirmed termination of an AT/AF episode with a programmed duration and rate. If at least four episodes of 1 minute in duration occurred within the run-in period of 1 month, patients were randomized to one of the three settings (PMOP off and PMOP 10 minutes at 90 bpm or 120 bpm) for 2 months. At 2 and 4 months, patients were crossed over to another arm. At 6 months, all patients were programmed with PMOP on at 90 bpm for 30 minutes. RESULTS: We enrolled 122 and randomized 50 patients. Sixty percent of all stored AT/AF episodes occurred within 10 minutes after a previous episode; 31% occurred after device-determined termination and before the device reached the overdrive rate (17-27 ventricular beats after termination), and 29% of the episodes occurred while the device was pacing at the programmed overdrive rate. Thirty-seven percent of the average percentage of episodes during the overdrive period was prevented by the randomized settings of PMOP 90 bpm/10 min (P = .01, paired t-test, n = 39) and 120 bpm/10 min (P = .03, n = 35). In addition, for the nonrandomized setting of PMOP 90 bpm/30 min, the average number of episodes during the overdrive period was significantly smaller than the percentage of episodes occurring during the corresponding off period of 30 minutes (P = .05, n = 33). No significant differences in burden and episodes were found between the PMOP settings and the corresponding off periods. CONCLUSIONS: This is the first randomized controlled clinical trial to prove that overdrive pacing is effective in preventing early recurrences of AT/AF. However, shortcomings of the PMOP algorithm, such as late activation, need further improvement.

Aged↗
PubMed2006

Paroxysmal atrial fibrillation precipitated by amiodarone-induced thyrotoxicosis five months after cessation of therapy.

Amiodarone is currently indicated for the treatment of life-threatening ventricular dysrhythmias. It is also used for the treatment of supraventricular dysrhythmias and as maintenance therapy after successful cardioversion of atrial flutter or atrial fibrillation. Adverse effects related to its expanded use are increasingly common. We describe a case of amiodarone-induced thyrotoxicosis occurring 5 months after cessation of therapy and discuss the pathophysiology and treatment of this disorder.

Amiodarone↗
PubMed1996

Interatrial septal aneurysms and atrial arrhythmias in infants.

Studies have suggested that interatrial septal aneurysms (IASAs) may be the initiating mechanism of supraventricular tachycardia (SVT) in newborns and infants. A retrospective study was performed to determine the incidence of IASAs in 30 infants with atrial arrhythmias (SVT, atrial flutter, or frequent premature atrial contractions) and their possible relation to the mechanism of atrial arrhythmias. An IASA was defined as dilation of the septum > 5 mm beyond the plane of the atrial septum and associated with redundant tissue and abnormal mobility. The study patients were compared with age and sex-matched control subjects. Four (13%) of the 30 study patients and 2 (7%) of 30 control subjects had an IASA (difference not significant). In contrast to previous reports, this study demonstrates that there is not a significant relation between the presence of IASAs and the onset and recurrence of atrial arrhythmias.

Atrial Flutter↗
PubMed1983

Prosthetic mitral valve motion during cardiac dysrhythmias as determined by echocardiography.

To assess the changes and physiologic mechanisms of prosthetic valve motion during cardiac dysrhythmias as well as the role of atrial systole in the closure of the mitral valve, M-mode echocardiography was performed in 36 patients with normally functioning prosthetic mitral valves (Björk-Shiley, Starr-Edwards, and Beall valve). Premature closure of the prosthetic mitral valve in diastole with a "sharp" closing motion was seen during first-degree atrioventricular block, atrial fibrillation with ventricular rates less than 60 beats/min, and atrial flutter. A "rounded" premature valve closure due to atrial systole was seen during atrial tachycardia and complete heart block. Atrial systole initiates a closing motion of the prosthetic mitral valve at end-diastole, and ventricular systole completes this closure during normal sinus rhythm. When first-degree atrioventricular block is present, atrial systole alone completes this closure before ventricular contraction. Atrial contraction alone also can effectively close the prosthetic mitral valve during atrial flutter and atrial tachycardia. Other factors (such as left ventricular diastolic volume) may play a role in the effective closure of the prosthetic mitral valve during atrial fibrillation with slow ventricular rates and complete heart block. These findings must be considered in the echocardiographic evaluation of suspected malfunctioning prosthetic mitral valves. A baseline postoperative echocardiogram after prosthesis insertion is important for future evaluation when clinically indicated.

Aged↗
PubMed1992

Atrial electrograms and the characterization of atrial fibrillation.

An improved method of calculating magnitude-squared coherence spectra on pairs of short-duration electrogram recordings is discussed. This method is based on adaptive signal processing techniques and yields spectra with higher resolution than those obtained using a straightforward direct method. The high-resolution spectra will make it possible to examine the time-varying relationship between activity at two sites during atrial fibrillation and may be useful for quick rhythm characterization by implanted devices or for constructing coherence maps in research studies. Example high-resolution spectra for sinus rhythm, atrial flutter, and atrial fibrillation are presented.

Atrial Fibrillation↗
PubMedDate not supplied

The electrocardiogram in acute pulmonary embolism.

Electrocardiograms of 90 patients with arteriographically documented acute submassive or massive pulmonary embolism and no associated cardiac or pulmonary disease were studied. Patients were derived from the Urokinase-Pulmonary Embolism Trial National Cooperative Study. In massive embolism, the electrocardiogram was normal in 6 per cent (3 of 50) of patients. With submassive embolism, 23 per cent of patients (9 of 40) had a normal electrocardiogram. Since one or more of the traditional manifestations of acute cor pulmonale (S1Q3T3, right bundle branch block, P pulmonale, or right axis deviation) occurred in only 26 per cent of patients, one could not rely exclusively upon these electrocardiographic abnormalities for the diagnosis of pulmonary embolism. The most common electrocardiographic abnormalities were nonspecific T wave changes which occurred in 42 per cent of patients and nonspecific abnormalities (elevation or depression) of the RST segment which occurred in 41 per cent of patients. Left axis deviation occurring in 7 per cent of the patients was as frequent as right axis deviation. Low voltage QRS complexes, previously undescribed in pulmonary embolism, occurred in 6 per cent of patients. None of the patients had atrial flutter or atrial fibrillation, which appears to occur more typically in patients with pulmonary embolism who have preexistent cardiac disease. All of the varieties of electrocardiographic abnormalities disappeared in some of the patients by 2 wk. Inversion of the T wave was the most persistent abnormality. Larger defects on the lung scan or pulmonary arteriogram occurred in patients with various abnormalities on the electrocardiogram than in patients with normal electrocardiograms. The pulmonary arterial mean pressure and/or right ventricular end-diastolic pressure was significantly higher in patients with several varieties of abnormal electrocardiograms, although the partial pressure of oxygen in arterial blood, in general, did not differ from that in patients with normal electrocardiograms. These hemodynamic correlations, made for the first time in patients, suggest that acute ventricular dilatation, possibly in combination with hypoxemia, is a causative factor of the electrocardiographic changes in acute massive or submassive pulmonary embolism.

Acute Disease↗
PubMed2000

Mechanisms of atrial fibrillation: is a cure at hand?

The mechanisms of atrial fibrillation relate to the presence of random reentry involving multiple interatrial circuits. Triggers for development of atrial fibrillation include rapidly discharging atrial foci (mainly from pulmonary veins) or degeneration of atrial flutter or atrial tachycardia into fibrillation. Therapy for control of atrial fibrillation includes drugs, atrial pacing for those with sinus node dysfunction, or ablation of the atrioventricular junction. Therapeutic maneuvers for cure of atrial fibrillation include surgical or radiofrequency catheter induced linear lesions to reduce the atrial tissue and prevent the requisite number of reentrant wavelets. We need a much better understanding of basic mechanisms before a true cure is at hand.

Animals↗
PubMed1987

Complete sinoatrial block in two patients with bradycardia-tachycardia syndrome.

Electrophysiologic studies with recordings of sinus node electrograms were performed in two patients with bradycardia-tachycardia syndrome. In both patients, the rest electrocardiogram showed apparent sinus bradycardia. Patient 1 had frequent paroxysms of atrial tachycardia with long pauses of up to 10 seconds; Patient 2 had paroxysmal atrial flutter and atrial pauses of up to 8 seconds. Multiple, repetitive, low frequency deflections, with a cycle length ranging from 730 to 960 ms in Case 1 and 570 to 750 ms in Case 2, suggestive of sinus node electrograms, were recorded at a critical area at the junction between the superior vena cava and the right atrium. These low frequency deflections had no relation to spontaneous junctional beats or the spontaneous atrial beats that showed high frequency deflections on the atrial electrogram. However, they could be suppressed by spontaneous or paced atrial beats. Pharmacologic interventions in Case 2 showed that the cycle length of the low frequency deflections shortened after administration of isoproterenol and did not change after propranolol or atropine. Thus, complete sinoatrial exit block with intact entrance conduction can occur in patients with bradycardia-tachycardia syndrome. Under such circumstances, the surface electrocardiographic manifestation of sinus bradycardia may not be of sinus origin.

Adult↗
PubMed2000

Case report: pulmonary vein stenosis following RF ablation of paroxysmal atrial fibrillation: successful treatment with balloon dilation.

Paroxysmal atrial fibrillation and atrial tachycardia may originate from a focal source in one or multiple pulmonary veins. A focal origin facilitates a potential cure amendable to radiofrequency ablation. Herein we report the case of a 16 year old adolescent male with a tachycardia induced cardiomyopathy who presented with very frequent paroxysmal episodes of atrial fibrillation, atrial flutter and atrial tachycardia. The origin of the arrhythmia was mapped to the secondary branches of the left lower pulmonary vein using an octapolar micro-mapping catheter. Immediately following application of three radiofrequency lesions, angiography of the left lower pulmonary vein revealed a region of focal stenosis at the site of energy application, with delayed pulmonary venous emptying. Attempts to relieve any element of spasm using direct administration of nitroglycerin were unsuccessful. Three months later repeat catheterization revealed an unchanged region of tight anatomical stenosis. Balloon dilation of two stenotic areas resulted in dramatic relief of the obstruction and improved venous drainage. Recatheterization 6 months later revealed mild restenosis that was successfully redilated. Intracardiac ultrasound demonstrated focal constriction. Care should be exercised in attempting RF ablation in distal arborization sites of the pulmonary veins in children, because of the small caliber compared to adult subjects. Radiofrequency induced focal areas of stenosis may be amenable to balloon catheter dilation.

Adolescent↗
PubMed2003

Atrial pacing therapies for prevention of atrial fibrillation in patients with implantable defibrillators.

Atrial fibrillation (AF), atrial flutter and atrial tachycardia (AT) occur frequently in patients following implantation of an implantable cardioverter defibrillator (ICD) for the treatment of ventricular tachyarrhythmias. Some new generation ICDs have incorporated atrial antitachycardia pacing therapy (ATP) and atrial pacing algorithms designed specifically for the prevention of AF. In the GEM III AT clinical evaluation, atrial ATP efficacy for termination of AF and AT was assessed. Overall ATP efficacy for AF/AT, based on device classification, was 40% when adjusted using the Generalized Estimating Equations to account for correlated data that arises from utilizing multiple episodes in some patients. However, many episodes of AF/AT were noted to terminate within 10 minutes of onset. Applying a more conservative definition of efficacy, termination within 20 sec of delivery of the last atrial ATP, efficacy for termination of AF/AT was 26%. 50 Hz burst pacing was shown to have minimal efficacy for termination of AF and modest incremental benefit following ramp or burst pacing therapies for AT. These observations provide a more realistic expectation of the value of atrial ATP in the ICD population with AF. Atrial ATP terminates some episodes of AT but previously reported efficacy rates of 40-50% are exaggerated and in part reflect spontaneous terminations of some AF/AT episodes.

Algorithms↗
PubMed2002

How to test mode switching in pacemakers implanted in patients: the MOST study.

Optimal management of atrial arrhythmias with dual chamber pacemakers requires proper performance of automatic mode switching (AMS). The aim of this study was to develop a reliable technique to test the AMS function by using an external electronic device capable of mimicking the occurrence of supraventricular arrhythmias (Supraventricular Arrhythmia Simulator [SAS]). The SAS delivers low voltage pulse trains (200 mV, 20 ms) through two skin electrodes. Each pulse train lasts 15 seconds and starts synchronously with a pacing pulse of the implanted pacemaker to avoid interference from the operator. The pulse train rate is set at 350, 250, and 160 beats/min to simulate AF, atrial flutter, and atrial tachycardia (AT), respectively. Thirty-five patients implanted with Vitatron pacemakers, whose AMS system has been previously validated, were enrolled. Atrial and ventricular sensing were programmed in unipolar mode at 0.5 mV and in bipolar mode at > 2 mV, respectively. All pulses from the SAS were detected by the atrial channel at an amplitude ranging from 1 to 3 mV. The test proved to be safe and reliable at rest and during exercise. AMS occurred immediately at onset or at offset of atrial arrhythmias, and no adverse interference on pacemaker function was seen from the SAS. In conclusion, the described technique and the SAS are safe and reliable for patient and pacemaker function and can be proposed as a useful method to verify proper performance of AMS function irrespective of the type of implanted devices.

Aged↗
PubMed2003

Quantifying intracardiac organization of atrial arrhythmias using temporospatial phase of the electrocardiogram.

INTRODUCTION: Separating nonisthmus-dependent atrial flutter (AFL) from "organized" atrial fibrillation (AF), or isthmus-dependent AFL, may be difficult using ECG characteristics alone. We hypothesized that temporal and spatial phase analysis of ECG atrial waveforms could effectively separate these rhythms by quantifying subtle variations in ECG atrial activation during supraventricular tachycardias (SVT). METHODS AND RESULTS: We studied 52 patients at electrophysiologic study (EPS) who demonstrated isthmus-dependent (n = 15) and nonisthmus-dependent (n = 9) AFL, atrial tachycardia (n = 6), AV nodal reentry (n = 9), orthodromic reciprocating tachycardia (n = 6), and AF (n = 7). Atrial activity was represented as a series of correlations of an atrial template to successive time samples of the arrhythmia ECG. Spatial phase was analyzed as a reproducible relationship of this atrial activity between leads over time; temporal regularity was measured from power spectra. Spatial phase was maintained (coherent) in lead planes V5/aVF (XY), V5/V1 (XZ), and aVF/V1 (YZ) in 15 of 15 cases of isthmus-dependent AFL, but in only 1 of 9 cases of nonisthmus-dependent AFL (P < 0.01; chi2). Temporally, all cases of AFL showed one dominant peak on correlation spectra (magnitude >6 dB), suggesting one activation wavefront, although this was smeared in nonisthmus-dependent cases. In contrast, AF showed inconsistent spatial phase in all planes and broad band spectra, consistent with multiple and/or variable activation paths. All other SVTs showed spatial coherence and one dominant spectral peak. CONCLUSION: Coherence of temporal and spatial phase is a powerful approach to measure the spatial organization of intracardiac activation from the ECG that reveals a spectrum from SVT to isthmus-dependent and nonisthmus-dependent AFL, to AF.

Adult↗