Practical Considerations of Mapping Persistent Atrial Fibrillation With Whole-Chamber Basket Catheters.

OBJECTIVES: This study sought to evaluate basket catheter deployment, catheter-tissue contact, and time-space stability of unipolar atrial electrograms (aEGMs) recorded in persistent atrial fibrillation (AF) patients. BACKGROUND: Panoramic mapping of human AF using multiple-electrode basket catheters may identify AF sources. Although clinical results using this technique are provocative, questions remain about its effectiveness. METHODS: Data were collected from patients (N = 25) undergoing catheter ablation for AF during the multicenter STARLIGHT (Signal Transfer of Atrial Fibrillation Data to Guide Human Treatment) trial (NCT01765075). Left and right aEGM signals were recorded using basket catheters during baseline AF, following ablation and during sinus rhythm. Data were analyzed for basket deployment, peak-to-peak voltage, and electrogram stability and organization. Electrogram stability and organization were evaluated via time-frequency analysis (TFA). RESULTS: Basket catheters displayed equatorial bunching when deployed in atria. Interspline spacing ranged from 1.7 to 64.0 mm in the right atrial and from 1.5 to 85.08 mm in the left atrial basket. Approximately one-third of mapping electrodes failed to demonstrate a median peak-to-peak voltage >2× the low-voltage threshold. Time-space stability and organization was observed in 13 of 22 (59.09%) right atrial and 10 of 22 (45.45%) left atrial baskets. CONCLUSIONS: Despite poor deployment and a large number of low-voltage electrodes, stability and organization was observed in about one-half of the mapped patients. Although this study suggests that basket catheters have limitations for patient-specific AF mapping, concordant activation occurs in some persistent AF patients, which may be amenable to high-density mapping techniques.

Acute clinical evaluation of a left ventricular automatic threshold determination algorithm based on evoked response sensing.

INTRODUCTION: Automatic pacing threshold (AT) testing may simplify device follow-up and improve device longevity. This study's objective was to evaluate the performance of a left ventricular (LV) evoked response sensing-based AT algorithm, for cardiac resynchronization therapy (CRT) devices. METHODS: Patients scheduled for CRT-D/P implant were enrolled. A manual step-down threshold test and a Left Ventricular Automatic Threshold (LVAT) test in each of four pacing vectors-LVTip→Can, LVTip→right ventricle (RV), = LVRing→Can, and LVRing→RV-were conducted. Patients were randomized to either 0.4-ms or 1.0-ms pacing pulse width and in the manual and LVAT test order. A blinded core lab electrophysiologist (EP) determined the threshold using the surface electrocardiogram (gold standard). RESULTS: Data from 70 patients were analyzed. Bipolar LV leads from three major manufacturers were used. A total of 273 AT tests were performed; 12 AT tests did not result in a threshold due to improper testing conditions. Of 261 eligible tests, 234 AT tests (89.6%) returned a threshold measurement. Of the 234 tests, in 233 tests (99.5%) the algorithm-determined threshold matched the EP-determined threshold for that test. A total of 16,689 capture and 526 noncapture beats were collected and the accuracy for detecting capture and noncapture were 98.5% and 99.7% with a two-sided 95% confidence level of (98.4%, 98.7%) and (99.4%, 100%), respectively. No AT threshold measurement was lower than the EP-determined threshold. CONCLUSION: In this study, the results suggest that the LVAT algorithm is accurate at determining pacing thresholds in multiple pacing configurations and a wide range of LV leads in CRT-D/P patients.

Improving contemporary algorithms for implantable cardioverter-defibrillator function.

Implantable cardioverter-defibrillators (ICDs) have been shown in various clinical trials to prevent mortality from sudden cardiac death due to unstable rhythms or ventricular fibrillation. Modern ICDs use sophisticated algorithms to not only deliver therapy on the detection of a malignant rhythm but also reduce the incidence of inappropriate shocks through rhythm discrimination. Current algorithms for detection of malignant rhythms use sophisticated techniques such as real-time processing and analysis of electrograms from a transvenous lead system. The Rhythm ID feature in Boston Scientific ICDs is an example of one such algorithm used for rhythm discrimination. Rhythm ID uses the vector timing and correlation algorithm, which incorporates both timing as well as morphology information for supraventricular tachycardia discrimination. Clinical trials demonstrated high sensitivity and specificity of this feature in discriminating between ventricular tachycardia and supraventricular tachycardia (results published previously). On detection of the unknown rhythm (when the ventricular tachycardia rate detection criteria is met), the vector timing and correlation algorithm compares the unknown rhythm beat-by-beat to a stored template of normal sinus rhythm. The feature correlation coefficient computed over more than 8 points in the time-aligned signals is used for the comparison. The specific discrimination procedure of Rhythm ID depends on the mode (VR or DR) and on whether the test rhythm is an initial detected rhythm or a postshock rhythm. The normal sinus rhythm template against which the suspected rhythm is compared can be periodically updated. This article will cover some of the key aspects of the Rhythm ID feature's decision-making process and the algorithm for template update. The results of previously published clinical studies involving the algorithm's performance also will be reviewed.

Influence of the skeletal muscle activity on time and frequency domain properties of the body surface ECG during evolving ventricular fibrillation in the pig.

AIM OF THE STUDY: To evaluate influence of the skeletal muscle activity (SMA) on time and frequency domain properties of ECG during VF. MATERIALS AND METHODS: We studied the first 9min of electrically induced VF (N=7). We recorded Lead II ECG, 247 unipolar epicardial ventricular electrograms (UEGs) and 3 bipolar skeletal electromyograms (EMGs) near the positions of the ECG electrodes (sampling rate, 500Hz). We reconstructed ECG (RECG) from UEGs using forward-solution transformation matrix. Spectral properties of ECG, RECG, UEGs and MEGs were assessed in the range 2-250Hz by the median frequency (MF) and the upper limit of frequency range containing 99% of spectral energy (Flim(99)). Scaling exponent of ECG, RECG and EMGs was calculated in the ranges of 1-8 and 5-20 sampling intervals (ScE1-8 and ScE5-20, respectively). RESULTS: We observed non-monotonic increases in MF and Flim(99) of the ECG, but not UEGs and RECG, at 1-5min of VF. Maximum values of MF and Flim(99) in ECG, UEGs and RECG were (in Hz): 32+/-29 and 166+/-67; 11+/-2 and 36+/-7; 10+/-2 and 32+/-6, respectively. The transient increases in the high-frequency content of the ECG were correlated with enhanced activity in EMGs, characterized by an almost uniform spectrum in the range 2-250Hz (MF=92+/-29; Flim(99)=245+/-4Hz). Peak values of ScE(1-8) were the highest in EMGs (1.95+/-0.04), intermediate in the ECG (1.59+/-0.26), and the lowest in RECG (1.088+/-0.007). CONCLUSION: SMA significantly contributes to ECG during VF and can bias metrics used for assessment of VF organization.

Ischemic preconditioning protects against arrhythmogenesis through maintenance of both active as well as passive electrical properties in ischemic canine hearts.

BACKGROUND: The mechanisms for the antiarrhythmogenic effects of preconditioning in ischemic hearts, although well demonstrated, are not clear. We measured indices of activation and repolarization using data from a high-resolution epicardial sock electrode array in preconditioned (PC) and non-PC hearts in an attempt to gain further insight into protective mechanisms. METHODS AND RESULTS: Five canine hearts were subjected to a coronary artery occlusion lasting at least 1 hour, and 5 were subjected to a similar occlusion preceded by a preconditioning protocol. Epicardial electrograms were recorded using a 490-electrode sock. Representative beats were selected at intervals of 1 minute for analysis. The mean ST elevation for the PC group both rose slowly after occlusion and also resolved more slowly than the non-PC group. Electrocardiographic markers for propagation such as Total Activation Time, the QRSRMS width, and magnitude of steepest downstroke of the QRS complex all showed that the PC group maintained conduction velocity initially and also varied less dramatically than the control group. The regression line slope computed on a scatter plot of QT width vs cycle length was 0.23 for the PC group and 0.58 for non-PC. During occlusion, the incidence of premature ventricular contractions (PVCs) peaked at approximately 17 minutes followed by a second peak at approximately 27 minutes in the non-PC group, the PC group showed similar peaks at approximately 24 and approximately 53 minutes respectively. CONCLUSION: The slower rate of resolution of ST elevation in PC hearts suggests a delay in gap junction closure, thus maintaining intracellular resistivity and reducing the likelihood of arrhythmia. The speed of conduction is adequately maintained during the early stages of ischemia in PC hearts. The mQTi-mRR regression line, a surrogate measure of rate dependency of repolarization (restitution), has a lower slope in the PC case, thus suggesting a mechanism of reduced arrhythmogenesis. The conclusions are supported by a delay of peak PVCs in PC hearts.

Mechanisms of ischemia-induced ST-segment changes.

Many aspects of ischemia-induced changes in the electrocardiogram lack solid biophysical underpinnings although variations in ST segments form the predominant basis for diagnostic and monitoring of patients. This incomplete knowledge certainly plays a role in the poor performance of some forms of electrocardiogram-based detection and characterization of ischemia, especially when it is limited to the subendocardium. The focus of our recent studies has been to develop a comprehensive mechanistic model of the electrocardiographic effects of ischemia. The computational component of this model is based on highly realistic heart geometry with anisotropic fiber structure and allows us to assign ischemic action potentials to contiguous regions that can span a prescribed thickness of the ventricles. A separate, high-resolution model of myocardial tissue provides us with a means of setting electrical characteristics of the heart, including the status of gap junctional coupling between cells. The experimental counterpart of this model consists of dog hearts, either in situ or isolated and perfused with blood, in which we control coronary blood flow by means of a cannula and blood pump. By reducing blood flow through the cannula for various durations, we can replicate any phase of ischemia from hyper acute to early infarction. Based on the results of these models, there is emerging a mechanism of the electrocardiographic response to ischemia that depends strongly on the anisotropic conductivity of the myocardium. Ischemic injury currents flow across the boundary between healthy and ischemic tissue, but it is their interaction with local fiber orientation and the associated conductivity that generates secondary currents that determine epicardial ST-segment potentials. Results from experiments support qualitatively the findings of the simulations and underscore the role of myocardial anisotropy in electrocardiography.

A study of the dynamics of cardiac ischemia using experimental and modeling approaches.

The dynamics of cardiac ischemia was investigated using experimental studies and computer simulations. An experimental model consisting of an isolated and perfused canine heart with full control over blood flow rate to a targeted coronary artery was used in the experimental study and a realistically shaped computer model of a canine heart, incorporating anisotropic conductivity and realistic fiber orientation, was used in the simulation study. The phenomena investigated were: (1) the influence of fiber rotation on the epicardial potentials during ischemia and (2) the effect of conductivity changes during a period of sustained ischemia. Comparison of preliminary experimental and computer simulation results suggest that as the ischemic region grows from the endocardium towards the epicardium, the epicardial potential patterns follow the rotating fiber orientation in the myocardium. Secondly, in the experimental studies it was observed that prolonged ischemia caused a subsequent reduction in the magnitude of epicardial potentials. Similar results were obtained from the computer model when the conductivity of the tissue in the ischemic region was reduced.