Introduction: Different analysis techniques have been developed to help understand and characterize the mechanisms responsible for atrial arrhythmias. We tested the hypothesis that Fast Fourier Transform (FFT) analysis of recorded atrial electrograms (AEGs) will rapidly and accurately identify regular and irregular patterns of atrial activation, and, thereby, may provide evidence suggestive of underlying mechanisms of atrial tachyarrhythmias.Methods and Results: During induced atrial tachyarrhythmias in both the canine sterile pericarditis model and canine rapid ventricular pacing-induced congestive heart failure model; 380-404 AEGs were recorded simultaneously from epicardial electrodes on both atria. From AEGs, atrial activation sequences were determined during atrial flutter (AFL), focal atrial tachycardia (AT), and atrial fibrillation (AF). Four-second recording segments of each AEG were subjected to FFT analysis. Frequencies found during FFT analyses in all studies precisely corresponded to the cycle lengths of the AEGs. In AFL and AT, one dominant frequency peak was found throughout both atria. In AF due to multiple unstable reentry circuits, multiple and broad frequency peaks were found in both atria. In AF due to a stable rapid rhythm (driver) in the left atrium with fibrillatory conduction to the rest of the atria, one dominant frequency peak in areas with 1:1 conduction from the driver, and multiple and/or broad frequency peaks in areas with fibrillatory conduction produced by the driver were found. Computation time for all FFT analyses took < 5 minutes.Conclusion: FFT analysis accurately and rapidly identifies global atrial activation patterns during AFL, AT, and AF, thereby assisting in determining arrhythmia mechanisms.

BACKGROUND:Cardiac resynchronization therapy (CRT) for congestive heart failure patients with delayed left ventricular (LV) conduction is clinically beneficial in approximately 70% of patients. Unresolved issues include patient selection, lead placement, and efficacy of LV pacing alone. Being an electrical approach, detailed electrical information during CRT is critical to resolving these issues. However, electrical data from patients have been limited because of the requirement for invasive mapping. OBJECTIVES:The purpose of this study was to provide observations and insights on the variable electrophysiologic responses of the heart to CRT using electrocardiographic imaging (ECGI). METHODS:ECGI is a novel modality for noninvasive epicardial mapping. ECGI was conducted in eight patients undergoing CRT during native rhythm and various pacing modes. RESULTS:In native rhythm (six patients), ventricular activation was heterogeneous, with latest activation in the lateral LV base in three patients and in the anterolateral, midlateral, or inferior LV in the remainder of patients. Anterior LV was susceptible to block and slow conduction. Right ventricular pacing improved electrical synchrony in two of six patients. LV pacing in three of four patients involved fusion with intrinsic excitation resulting in electrical resynchronization similar to biventricular pacing. Although generally electrical synchrony improved significantly with biventricular pacing, it was not always accompanied by clinical benefit. CONCLUSION:Results suggest that (1) when accompanied by fusion, LV pacing alone can be as effective as biventricular pacing for electrical resynchronization; (2) right ventricular pacing is not effective for resynchronization; and (3) efficacy of CRT depends strongly on the patient-specific electrophysiologic substrate.

Introduction: Renin‐angiotensin‐aldosterone system activation may be involved in the pathogenesis of atrial arrhythmias in congestive heart failure (CHF). The effects of aldosterone blockade on atrial tachyarrhythmias have not been evaluated. This study's aim was to determine whether selective aldosterone blockade suppresses atrial tachyarrhythmia inducibility and modifies atrial electrical and/or structural remodeling in a canine model of rapid ventricular pacing (RVP)‐induced CHF.

OBJECTIVES/BACKGROUND Cardiac arrhythmias are a leading cause of death and disability. Electrocardiographic imaging (ECGI) is a noninvasive imaging modality that reconstructs potentials, electrograms, and isochrones on the epicardial surface from body surface measurements. We previously demonstrated in animal experiments through comparison with simultaneously measured epicardial data the high accuracy of ECGI in imaging cardiac electrical events. Here, images obtained by noninvasive ECGI are compared to invasive direct epicardial mapping in open heart surgery patients.METHODS Three patients were studied during sinus rhythm and right ventricular endocardial and epicardial pacing (total of five datasets). Body surface potentials were acquired preoperatively or postoperatively using a 224-electrode vest. Heart-torso geometry was determined preoperatively using computed tomography. Intraoperative mapping was performed with two 100-electrode epicardial patches.RESULTS Noninvasive potential maps captured epicardial breakthrough sites and reflected general activation and repolarization patterns, localized pacing sites to similar to 1 cm and distinguished between epicardial and endocardial origin of activation. Noninvasively reconstructed electrogram morphologies correlated moderately with their invasive counterparts (cross correlation = 0.72 +/- 0.25 [sinus rhythm], 0.67 +/- 0.23 [endocardial pacing], 0.71 +/- 0.21 [epicardial pacing]). Noninvasive isochrones captured the sites of earliest activation, areas of slow conduction, and the general excitation pattern.CONCLUSIONS Despite limitations due to nonsimultaneous acquisition of the surgical and noninvasive data under different conditions, the study demonstrates that ECGI can capture important features of cardiac electrical excitation in humans norrinvasively during a single beat. It also shows that general excitation patterns and electrogram morphologies are largely preserved in open chest conditions.

In anisotropic tissue (e.g., right atrium), nonuniform conduction may cause conduction block/delay, or form a functional line of block, thus, providing a substrate for the initiation/maintenance of atrial arrhythmias. We tested the hypothesis that the activation patterns generated by bipolar, linear, triple site stimulation create more uniform propagation compared to single site stimulation, thereby, minimizing or eliminating potential substrates for initiation/maintenance of reentrant atrial arrhythmias. The canine sterile pericarditis model and normal dogs were studied. A plunge wire electrode pair was placed at the superior aspect of the crista terminalis (CT) for single site pacing. For triple site pacing, three bipolar pairs were placed perpendicular and parallel to the superior aspect of the CT in a linear fashion. Rapid pacing using different electrode configurations was performed at 200 ms and 300 ms cycle lengths up to 6 sec. During pacing, 404 unipolar atrial electrograms were recorded simultaneously from electrode arrays placed on the atria. The data demonstrate that linear triple site pacing creates more uniform linear propagation with less or no conduction delay/block, in contrast to single site pacing which creates elliptical impulse propagation. These findings may help develop alternative pacing techniques for termination and/or prevention of atrial arrhythmias.

Introduction: Dogs with rapid ventricular pacing (RVP)‐induced congestive heart failure (CHF) have inducible atrial tachycardia, flutter, and fibrillation (AF). We tested the hypothesis that rapid atrial activation in multiple regions and at different rates is responsible for sustained AF in this CHF model. Methods and Results: We studied 12 episodes of sustained (>10 minutes) AF induced in 12 dogs with CHF produced by 3–6 weeks of RVP at 230 beats/minute. High‐density mapping of AF was performed using 382 unipolar atrial electrograms recorded simultaneously from epicardial electrodes on the right (RA) and left atria (LA) and Bachmann's bundle. AF mechanisms were based on Fast Fourier Transform (FFT) analysis and activation sequence mapping. A driver was defined as a rapid stable activation region with a single dominant frequency peak in FFT analysis. During AF, three FFT and activation patterns were seen: (1) a single LA driver (7.8 ± 1.1 Hz) near the pulmonary veins (PVs) with irregular activation in the rest of the atria (n = 4); (2) simultaneous, multisite, biatrial drivers at differing frequencies (LA vs RA dominant frequency gradient: 1.3 ± 0.8 Hz) near the PVs (8.4 ± 0.3 Hz) and high RA (8.5 ± 1.5 Hz) (n = 7); and (3) biatrial irregular activation with multiple and/or broadband frequency peaks without a dominant frequency. (LA: 7.1–11.4 Hz; RA: 5.9–7.7 Hz) (n = 1). Atrial drivers had either a focal activation pattern or were due to a macroreentrant circuit around the PVs. Conclusions: In this CHF model, FFT analysis and activation sequence mapping demonstrate that sustained AF is characterized by single and multiple, stable LA and RA drivers with predominant sources in the PVs and high RA causing fibrillatory conduction.

We report the first clinical application of electrocardiographic imaging (ECGI), a new, noninvasive imaging modality for arrhythmias, in an athlete with focal ventricular tachycardia (VT) originating from a left ventricular (LV) diverticulum. A reconstructed map of the epicardial activation sequence during a single premature ventricular complex (PVC) of an identical QRS morphology to the clinical VT, generated from 224-electrode body surface ECGs and a chest CT (ECGI), localized the PVC to the site of the diverticulum. This correlated with subsequent maps obtained using standard techniques. We describe the first case that used ECGI to guide diagnosis and therapy of a clinical tachyarrhythmia.

From the Department of Medicine (Cardiology), Radiology, and Biomedical Engineering, Case Western Reserve University/University Hospitals of Cleveland, Cleveland, Ohio, the Cardiovascular Center Aalst/OLV Hospital, Aalst, Belgium, and the Department of Medicine (Cardiology) Brigham and Women’s Hospital, Boston, Massachusetts. Present affiliation: Cardiac Bioelectricity and Arrhythmia Center, Washington University in St. Louis, St. Louis, issouri.

BACKGROUND:The mechanisms of chronic atrial fibrillation (AF) are not well understood. We performed epicardial mapping of chronic AF in patients undergoing open heart surgery to test the hypothesis that chronic AF is due to a left atrial "driver" with a regular, short cycle length, resulting in fibrillatory conduction to the rest of the atria.METHODS AND RESULTS:Nine patients with chronic AF (1 month to >15 years' duration) were studied at open heart surgery, 8 before and 1 during cardiopulmonary bypass. During AF, atrial electrograms (AEGs) were recorded for 1 to 5 minutes from 404 epicardial electrodes arranged in bipoles along with ECG lead II or ventricular electrogram. Four-second segments of each bipolar AEG were also subjected to fast Fourier transform analysis. Two patterns of atrial activation were present during AF. In pattern 1 (7/9 patients), AEGs from parts of the atria demonstrated a short, regular cycle length with identical beat-to-beat morphology, and the rest of the atria were activated irregularly, and AEGs that demonstrated constant morphology and cycle length were localized to parts of the left atria (5/7), the right atria (1/7), or both atria (1/7). In pattern 2 (2/9 patients), AEGs showed no evidence of regular activation or constant morphology.CONCLUSIONS:In 9 patients with chronic AF, the commonest recorded AEG pattern showed an area of regular, rapid rhythm, consistent with the possibility that a driver causing fibrillatory conduction is one mechanism of AF in these patients.

A stable rhythm of very short cycle length (CL) in the left atrium (LA) can cause fibrillatory conduction, particularly in the right atrium (RA). Fast Fourier transform (FFT) analysis reliably identifies LA to RA conduction path(s) during atrial fibrillation (AF). We tested the hypotheses that FFT analysis of atrial electrograms (AEGs) during AF simulation will reliably identify the critical LA driver CL that causes RA fibrillatory conduction (i.e., the critical conduction breakdown CL) and that a longer critical conduction breakdown CL is found in atria of abnormal (sterile pericarditis) compared to normal dogs. We paced from Bachmann's bundle and the posterior-inferior LA at rapid rates to mimic an LA driver. During pacing, 4 sec of FFT analysis of 203 bipolar AEGs was performed and showed: 1) a single dominant frequency peak at the pacing CL in both atria when the atria followed the pacing in a 1:1 manner; 2) multiple and broad frequency peaks on the RA and parts of the LA at the conduction breakdown CL; and 3) the conduction breakdown CL is longer in pericarditis than normal dogs. FFT analysis allowed reliable detection of the critical CL of an LA driver that induces RA fibrillatory conduction.