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Sanjiv M Narayan

Publications and source records attributed to Sanjiv M Narayan.

16 recordsLinked to original sources
PubMed2006

Acute volume overload elevates T-wave alternans magnitude.

The objective of this study was to determine whether acute volume loading elevates T-wave alternans (TWA) in dogs with structurally normal hearts. TWA predicts sudden cardiac arrest in patients with left ventricular dysfunction and congestive heart failure. However, volume load and ventricular stretch may themselves precipitate arrhythmias. It is unclear to what extent volume load causes TWA. In six male mongrel dogs [25.8 kg (SD 4.2)] under general anesthesia, we measured TWA during progressive atrial pacing to 160 beats/min. Pacing was performed at baseline, at the midpoint and peak of a saline infusion designed to induce acute CHF, and then during diuresis. Dog 1 was hypothermic throughout the protocol and excluded from analysis. For dogs 2-6, 102 ml/kg (SD 30) were infused over 315 min (SD 50), causing pulmonary capillary wedge pressure to rise from 9.6 (SD 3.5) to 21.2 mmHg (SD 1.6) (P < 0.01), and heart rate variability to fall (P < 0.01). TWA magnitude (Valt) rose in all dogs with volume load (P < 0.001). Compared with baseline, TWA at peak infusion had higher magnitude [Valt 3.4 (SD 1.95) vs. 0.5 muV (SD 0.35); P = 0.011] and occurred at lower heart rates [128 (SD 6) vs. 151 beats/min (SD 12); P = 0.008]. Net volume load was linearly related to Valt (P < 0.01), with each 10 ml/kg net volume load increasing Valt by 0.23 muV. Acute volume overload elevates TWA in normal canine hearts. Although dramatic, however, this effect may contribute clinically to abnormal TWA only in patients with marked volume overload. Future studies should examine the interaction of fluid overload, myocardial disease, and arrhythmia susceptibility.

Acute Disease↗
PubMed2006

Cardiac-directed expression of adenylyl cyclase VI facilitates atrioventricular nodal conduction.

OBJECTIVES: The purpose of this study was to test the hypothesis that cardiac-directed expression of adenylyl cyclase VI (AC(VI)) facilitates atrioventricular (AV) nodal conduction. BACKGROUND: Cardiac-directed expression of AC(VI), unlike other strategies to increase cyclic adenosine monophosphate generation, reduces mortality in murine cardiomyopathy. Recent reports suggest that AC(VI) expression may also protect against lethal bradycardia. METHODS: We performed immunofluorescence staining for AC(VI) in the AV node of transgenic mice. We then performed electrophysiologic studies (EPSs) using a 1.7-F octapolar catheter at the AV junction in 11 transgenic AC(VI) mice and 14 control mice. RESULTS: Immunofluorescence staining revealed increased AC(VI) expression in the AV node of transgenic mice versus controls. During EPS, AV intervals approximated PR intervals (R2 = 0.99) and related linearly to atrial-to-His intervals (R2 = 0.98; both p < 0.0001). Thus, we studied AV intervals to avoid electrocardiogram pacing artifacts and inconsistent inscription of His bundle electrograms. At baseline, AC(VI) mice had shorter AV intervals (47 +/- 9 ms) than controls (57 +/- 11 ms; p = 0.02), despite similar sinus rates. In pacing, AV intervals were shorter in AC(VI) mice than controls for a wide cycle-length range (p < 0.01). The AC(VI) mice also had shorter AV Wenckebach cycle lengths (AC(VI): 114 +/- 12 ms; control: 131 +/- 28 ms; p = 0.05) and ventriculo-atrial effective refractory periods (AC(VI): 97 +/- 21 ms; control: 127 +/- 15 ms; p = 0.05). We observed no differences between groups in sinus node function, and ventricular arrhythmias were not inducible. CONCLUSIONS: Cardiac-directed expression of AC(VI) facilitates AV nodal conduction without altering sinus node function. These results suggest the need to define a role for AC(VI) gene transfer in treating diseases of AV conduction.

Adenylyl Cyclases↗
PubMed2006

Diagnostic accuracy of irregularly irregular RR intervals in separating atrial fibrillation from atrial flutter.

Periodic electrocardiographic RR intervals are often used to separate atrial flutter (AFl) from atrial fibrillation (AF), but have not yet been validated. We hypothesized that irregularly irregular electrocardiographic RR intervals poorly identify AF from AFl, and that atrial wavefront regularity affects variability in atrioventricular conduction. We studied the electrocardiographic RR intervals in 66 patients referred for ablation of AFl (21 atypical and 21 typical) and AF (n=24) in relation to intracardiac activation. Receiver-operating characteristics showed that periodicity in 60% of RR intervals provided only 66% sensitivity and 86% specificity for typical AFl and failed to separate atypical AFl from AF. Fewer RR intervals were integer atrial/ventricular ratios in atypical than in typical AFl (50% vs 83%, p=0.005), reflecting greater SDs in atrial cycles (6.98+/-7.02 vs 3.10+/-1.62 ms, p=0.023), more variable AH intervals (56+/-28 vs 18+/-21 ms, p=0.002), longer AH intervals (185+/-65 vs 118+/-31 ms, p=0.01), and greater AH variability for any atrial cycle length (p=0.026). In conclusion, irregularly irregular RR intervals are not specific for AF, are common in AFl, and should not be used to conclusively separate AF from AFl in the absence of sawtooth flutter waves. Future studies should explore the relation among AFl circuit location, cycle variability, and atrioventricular nodal conduction.

Atrial Fibrillation↗
PubMed2006

Relation of T-wave alternans to regional left ventricular dysfunction and eccentric hypertrophy secondary to coronary heart disease.

Left ventricular (LV) hypertrophy and structural disease are associated with exaggerated repolarization dispersion and risk for cardiac arrest. We hypothesized that T-wave alternans (TWA) from the electrocardiogram, reflecting proarrhythmic repolarization dispersion, would increase with extent of eccentric LV hypertrophy and vary spatially with the distribution of myocardial scar. We studied 28 patients with coronary disease, systolic dysfunction, and nonsustained ventricular tachycardia. On echocardiography, 21 patients had wall motion abnormalities and 20 had LV hypertrophy (mass index > or =100 g/m(2)). TWA magnitude (voltage of alternation), which was computed spectrally during ventricular stimulation, varied linearly with LV mass index (p = 0.003). Spatially, positive TWA (magnitude > or =1.9 microV) in orthogonal electrocardiographic axes overlaid scar or wall motion abnormalities in corresponding echocardiographic segments (p <0.05 in x and y axes). After a follow-up of 35 +/- 13 months, positive TWA predicted the combined end point of death or sustained ventricular arrhythmias in all patients (p = 0.025), with a trend for those with echocardiographic LV hypertrophy (p = 0.058). In conclusion, in patients with systolic dysfunction due to coronary artery disease, TWA may indicate arrhythmic contributions from regional myocardial scar and eccentric LV hypertrophy.

Aged↗
PubMed2006

T-wave alternans and the susceptibility to ventricular arrhythmias.

T-wave alternans (TWA) reflects beat-to-beat fluctuations in the electrocardiographic T-wave, and is associated with dispersion of repolarization and the mechanisms for sudden cardiac arrest (SCA). This review examines the bench-to-bedside literature that, over decades, has linked alternans of repolarization in cellular, whole-heart, and human studies with spatial dispersion of repolarization, alternans of cellular action potential, and fluctuations in ionic currents that may lead to ventricular arrhythmias. Collectively, these studies provide a foundation for the clinical use of TWA to reflect susceptibility to ventricular arrhythmias in several disease states. This review then provides a contemporary evidence-based framework for the use of TWA to enhance risk stratification for SCA, identifying populations for whom TWA is best established, those for whom further studies are required, and areas for additional investigation.

Action Potentials↗
PubMed2006

Evaluating fluctuations in human atrial fibrillatory cycle length using monophasic action potentials.

OBJECTIVE: To study fluctuations in intracardiac atrial fibrillation (AF) cycle length (CL). BACKGROUND: Sites of short AF CL may be good ablation targets, and cycle lengthening predicts ablation success. However, the optimum method for measuring AF CL, and its stability, are unclear. We hypothesized that autocorrelation better estimates AF CL than spectral dominant frequency (DF), which is susceptible to double counting, using monophasic action potentials (MAPs) to separate atrial activation from artifact. METHODS: In 28 patients with paroxysmal or persistent AF, we analyzed 49 AF epochs using MAPs at the high (HRA) and low (LRA) right atrium. We estimated AF CL over 2 seconds, 10 seconds, and 2 minutes using spectral DF and autocorrelation in MAPs and filtered bipoles. RESULTS: In the HRA, manually measured CL was 167 +/- 25 ms. Spectral DF poorly estimated AF CL in bipolar signals (R = 0.31; P = NS), due to double counting, but accurately estimated MAP CL (R = 0.73, P < 0.001). Autocorrelation estimated MAP (R = 0.92; P < 0.001) and bipolar (R = 0.83; P < 0.001) CL, with lower errors than spectral DF (P < 0.0001). Over time, changes in DF consistently preceded reciprocal changes in organization (P < 0.001). Finally, excluding inaccurate spectra, DF and AF organization differed between HRA and LRA over 2 seconds, but correlated over 10 seconds and 2 minutes (P < 0.05). CONCLUSIONS: AF CL is better estimated by autocorrelation than spectral DF, particularly for bipoles, and stable when measured for >10 seconds. Notably, changes in AF CL preceded reciprocal changes in organization, yet changes in organization did not precede changes in AF CL. These results may help to interpret AF CL fluctuations.

Action Potentials↗
PubMed2005

Separating atrial flutter from atrial fibrillation with apparent electrocardiographic organization using dominant and narrow F-wave spectra.

OBJECTIVES: The purpose of this study was to separate atrial flutter (AFL) with atypical F waves from fibrillation (AF) with "apparent organization." BACKGROUND: We hypothesized that F-wave spectra should reveal a dominant and narrow peak in AFL, reflecting its single macro-re-entrant wave front, but broad spectra in AF, reflecting multiple wave fronts. METHODS: We identified 39 patients with electrocardiograms (ECGs) of "AFL/AF" or "coarse AF" from 134 consecutive patients referred for ablation: 21 had AFL (18 atypical, 3 typical), 18 had AF, and all were successfully ablated. Filtered atrial ECGs were created by cross-correlating F waves to successive ECG time points. Dominant peaks between 3 and 10 Hz were identified from power spectra of X (lead V5), Y (aVF), and Z (V1) axes, and for each, we calculated height (relative to two adjacent spectral points) and area ratio to envelopes of bandwidth 0.625, 1.25, 2.5, 3.75, and 5 Hz (range 0 to 1, where higher ratios reflect narrower peaks). RESULTS: Dominant peaks had greater relative height for AFL than AF (three-axis mean: 14.2 +/- 6.4 dB vs. 6.6 +/- 2.1 dB; p < 0.001). Peak area ratios were also higher for AFL than AF for all envelopes (p < 0.001). For the 2.5-Hz envelope, the separation (0.61 +/- 0.14 vs. 0.35 +/- 0.05, respectively; p < 0.001) enabled a ratio > or =0.44 to identify all cases of AFL from AF (p < 0.001). A panel of seven cardiologists blinded to clinical data provided lower diagnostic accuracy (82.1%; p < 0.01). CONCLUSIONS: In ambiguous ECGs with atypical F waves, spectral evidence for a solitary activation cycle separates AFL from AF with "apparent organization." This approach might improve bedside ECG diagnosis and shed light on intra-atrial organization of both rhythms.

Algorithms↗
PubMed2005

Separating non-isthmus- from isthmus-dependent atrial flutter using wavefront variability.

OBJECTIVES: The aim of this study was to separate isthmus-dependent atrial flutter (IDAFL) from non-isthmus-dependent atrial flutter (NIDAFL) from the electrocardiogram (ECG) based on functional differences. BACKGROUND: The ECG analyses of F-wave shape suboptimally separate NIDAFL from IDAFL. The authors hypothesized that anatomic and functional differences may result in greater wavefront variability in NIDAFL than IDAFL, allowing their separation. The authors tested this hypothesis in patients undergoing ablation for atrial flutter using a novel ECG algorithm to detect subtle F-wave variability, validated by intracardiac measurements. METHODS: In 62 patients (23 NIDAFL, 39 IDAFL) ECG atrial wavefronts were represented as correlations of an F-wave template to the ECG over time. Correlations in orthogonal ECG lead-pairs were plotted at each time point to yield loops reflecting temporal and spatial regularity in each plane. The ECG analyses were compared with intracardiac standard deviations of: 1) atrial electrograms (temporal variability), and 2) bi-atrial activation time differences (spatial variability). RESULTS: Atrial ECG temporospatial loops were reproducible in IDAFL, but varied in NIDAFL (p < 0.01) suggesting greater variability that correctly classified IDAFL (39 of 39 cases) from NIDAFL (22 of 23 cases; p < 0.001). Intra-atrial mapping confirmed greater temporal variability for NIDAFL versus IDAFL, in lateral (p < 0.01) and septal (p = 0.03) right atrium, and proximal (p = 0.02) and distal (p < 0.01) coronary sinus. Spatial variability was greater in NIDAFL than IDAFL (p = 0.02). CONCLUSIONS: Greater cycle-to-cycle atrial wavefront variability separates NIDAFL from IDAFL and is detectable from the ECG using temporospatial analyses. These results have implications for guiding ablation and support the concept that IDAFL and NIDAFL lie along a spectrum of intracardiac organization.

Algorithms↗
PubMed2005

T-wave alternans phase following ventricular extrasystoles predicts arrhythmia-free survival.

OBJECTIVE: The purpose of this study was to assess the value of T-wave alternans (TWA) following ventricular extrasystoles in predicting arrhythmia-free survival. BACKGROUND: Stratifying risk for sudden death in patients with coronary disease and moderate left ventricular (LV) dysfunction remains a challenge. We hypothesized that, in such patients, a discontinuity in beat-to-beat T-wave alternation (TWA phase reversal) following single ventricular extrasystoles reflects transiently exaggerated repolarization dispersion, and predicts spontaneous ventricular arrhythmias. METHODS: We studied 59 patients with ischemic LV dysfunction (mean LV ejection fraction 38.7 +/- 5.3%) and nonsustained ventricular tachycardia undergoing programmed stimulation. TWA was computed spectrally from the ECG during ventricular pacing, and TWA phase reversal was reflected by a discontinuity in T-wave oscillation after single ventricular extrasystoles. RESULTS: Patients induced into ventricular arrhythmias (n = 36) had greater TWA magnitude (V(alt): 6.60 +/- 6.46 microV vs 2.61 +/- 1.97 microV; P = .001) and more frequent TWA phase reversal (62.1% vs 44.4%; P = .02) than those who were not (n = 23). During a mean follow-up of 36 +/- 12 months, positive TWA (V(alt) > or =1.9 microV) and TWA phase reversal both (P < .05) predicted events (all-cause mortality, ventricular tachycardia, ventricular fibrillation). Univariate predictors of arrhythmia-free survival were TWA phase reversal (P < .005), positive TWA (P < .05), age (P = .008), and LV mass index (P = .043). On multivariate analysis, only TWA phase reversal and age predicted events; if TWA phase was excluded, only positive TWA and age predicted events. CONCLUSION: Phase reversal in TWA following ventricular extrasystoles predicts spontaneous ventricular arrhythmias and all-cause mortality in patients with moderate ischemic LV dysfunction and was a better predictor than positive TWA or programmed ventricular stimulation.

Aged↗
PubMed2005

Abnormal heart rate turbulence predicts the initiation of ventricular arrhythmias.

BACKGROUND: Abnormal heart rate turbulence (HRT) reflects autonomic derangements predicting all-cause mortality, yet has not been shown to predict ventricular arrhythmias in at-risk patients. We hypothesized that HRT at programmed ventricular stimulation (PVS) would predict arrhythmia initiation in patients with left ventricular dysfunction. METHODS: We studied 27 patients with coronary disease, left ventricular ejection fraction (LVEF) 26.7 +/- 9.1%, and plasma B-type natriuretic peptide (BNP) 461 +/- 561 pg/mL. Prior to arrhythmia induction at PVS, we measured sinus cycles after spontaneous or paced premature ventricular contractions (PVCs) for turbulence onset (TO; % cycle length change following PVC) and slope (TS; greatest slope of return to baseline cycle). T-wave alternans (TWA) was also measured during atrial pacing. RESULTS: At PVS, abnormal TO (> or =0%) predicted inducible ventricular tachycardia (VT; n = 10 patients; P < 0.05). TO was greater in inducible than in noninducible patients (2.3 +/- 3.1% vs -0.02 +/- 2.8%, P < 0.05) and correlated with LVEF (P < 0.05) but not with BNP. TS did not differ between groups. Conversely, ambulatory HRT differed significantly from HRT at PVS (TO -0.55 +/- 1.08% vs 0.85 +/- 3.02%, P < 0.05; TS 2.63 +/- 2.09 ms/RR vs 8.70 +/- 6.56 ms/RR, P < 0.01), and did not predict inducible VT but trended (P = 0.05) to predict sustained VT on 739 +/- 179 days follow-up. TWA predicted inducible (P < 0.05) and spontaneous (P = 0.0001) VT but did not co-migrate with HRT. CONCLUSIONS: Abnormal HRT measured at PVS predicted the induction of sustained ventricular arrhythmias in patients with ischemic cardiomyopathy. However, HRT at PVS did not correlate with ambulatory HRT, nor with TWA, both of which predicted spontaneous ventricular arrhythmias. Thus, HRT may reflect the influence of autonomic milieu on arrhythmic susceptibility and is likely complementary to traditional arrhythmic indices.

Aged↗
PubMed2005

Implantable defibrillators with and without resynchronization for patients with left ventricular dysfunction.

In conclusion, sudden cardiac arrest is a major cause of mortality in patients with LV dysfunction, even in asymptomatic patients. Low EF and heart failure may contribute synergistically to this risk, and may confer a risk of sudden death that accumulates over time. Several studies confirm that ICDs are more effective than optimal medical therapy at reducing SCA, although efforts must focus on optimizing medical therapy. Finally, ventricular dyssynchrony is a major risk factor for cardiac mortality that is best ameliorated by CRT. Future studies using markers of mechanical dyssynchrony will likely enhance the ability of CRT to reduce symptoms, hospitalization, and mortality.

Death, Sudden, Cardiac↗
PubMed2004

Temporal and spatial phase analyses of the electrocardiogram stratify intra-atrial and intra-ventricular organization.

We hypothesized that electrocardiogram (ECG) spatial phase analysis would define a spectrum of intracardiac organization from atrial fibrillation (AF), nonisthmus-dependent and isthmus-dependent atrial flutter (AFL) to supraventricular tachycardias (SVT), and similarly for ventricular arrhythmias. We analyzed arrhythmia ECGs of 33 patients with isthmus (n = 9) and nonisthmus (n = 5) dependent AFL and SVT: atrial (n = 3), atrioventricular nodal (n = 3), and orthodromic reciprocating (n = 3) tachycardias, as well as AF (n = 5), ventricular tachycardia (monomorphic, VT-MM; n = 7), and fibrillation (VF; n = 3). ECG spatial phase was considered coherent when the correlation coefficient of an atrial (or ventricular) template to its ECG over time maintained a constant relationship in XY, XZ, and YZ planes. Regularity was quantified spectrally from ECG and correlation series. Spatial coherence occurred in 9/9 cases of isthmus--but only 1/5 of cases of nonisthmus-dependent AFL (p < 0.01; chi2). All showed one dominant spectral peak (temporal coherence). In AF, spatial phase was inconsistent in all planes and spectra were broad band. Temporal and spatial coherence occurred in other SVT. VT-MM maintained spatial phase and a single spectral peak, while VF displayed neither. Our conclusions are that temporal and spatial phase analysis from the ECG stratifies intra-atrial and intra-ventricular organization and reveals subtle variability lost on visual inspection.

Adult↗
PubMed2003

Ventricular filling slows epicardial conduction and increases action potential duration in an optical mapping study of the isolated rabbit heart.

INTRODUCTION: Mechanical stimulation can induce electrophysiologic changes in cardiac myocytes, but how mechanoelectric feedback in the intact heart affects action potential propagation remains unclear. METHODS AND RESULTS: Changes in action potential propagation and repolarization with increased left ventricular end-diastolic pressure from 0 to 30 mmHg were investigated using optical mapping in isolated perfused rabbit hearts. With respect to 0 mmHg, epicardial strain at 30 mmHg in the anterior left ventricle averaged 0.040 +/- 0.004 in the muscle fiber direction and 0.032 +/- 0.006 in the cross-fiber direction. An increase in ventricular loading increased average epicardial activation time by 25%+/- 3% (P < 0.0001) and correspondingly decreased average apparent surface conduction velocity by 16%+/- 7% (P = 0.007). Ventricular loading did not significantly alter action potential duration at 20% repolarization (APD20) but did at 80% repolarization (APD80), from 179 +/- 7 msec to 207 +/- 5 msec (P < 0.0001). The dispersion of APD20 was decreased with loading from 19 +/- 2 msec to 13 +/- 2 msec (P = 0.024), whereas the dispersion of APD80 was not significantly changed. These electrophysiologic changes with ventricular loading were not affected by the nonspecific stretch-activated channel blocker streptomycin (200 microM) and were not attributable to changes in myocardial perfusion or the presence of an electromechanical decoupling agent (butanedione monoxime) during optical mapping. CONCLUSION: Acute loading of the left ventricle of the isolated rabbit heart decreased apparent epicardial conduction velocity and increased action potential duration by a load-dependent mechanism that may not involve stretch-activated channels.

Action Potentials↗
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↗
PubMed2002

Alternans of atrial action potentials during atrial flutter as a precursor to atrial fibrillation.

BACKGROUND: The mechanisms underlying the transition of typical atrial flutter (Afl) to fibrillation (AF) remain unclear. We set out to test the hypothesis that Afl disorganizes to AF via alternans of atrial action potentials. METHODS AND RESULTS: In 38 patients with Afl, monophasic action potentials (MAPs) were recorded at the isthmus and either high or low right atrium (HRA, LRA) during overdrive pacing to 160 ms or to the initiation of AF, whichever came first. MAP duration measured at 90% repolarization was longer at the isthmus in all patients, and failed to shorten with rate, compared with the HRA (n=38) or LRA (n=5). In 20 patients who developed AF, progressive pacing first caused alternans of isthmus MAP duration and amplitude at mean cycle length of 219+/-45 ms, followed by AF at a mean onset cycle length of 184+/-38 ms. Subsets of this group showed spontaneous action potential duration alternans at the isthmus (11 of 20 patients) and 2:1 isthmus conduction block immediately preceding AF (4 of 20 patients). In the 18 patients who did not develop AF, MAP alternans was less common (9 of 18 patients; P<0.0003), and occurred only at faster pacing (cycle length=169+/-25 ms; P<0.05). CONCLUSIONS: In patients with typical Afl, action potential duration rate maladaptation at the isthmus may lead to action potential duration alternans and conduction block preceding the transition to AF. These isthmus characteristics may enable the spontaneous initiation of AF through wavefront fractionation and may explain the benefits of isthmus ablation in preventing AF recurrence.

Action Potentials↗