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Edward J Berbari

Publications and source records attributed to Edward J Berbari.

5 recordsLinked to original sources
PubMed2006

A single moving dipole model of ventricular depolarization.

Modeling abnormal depolarization of the ventricles may provide a means to localize sites of arrhythmia foci from the body surface recordings. In this paper, we present a single moving dipole (SMD) model of the ventricular depolarization. The model can reproduce characteristic QRS patterns comparable to the clinical recordings when it is located in an inhomogeneous torso model. Our approach involves estimating a series of dipole moments based on vectocardiograms and estimating trajectories based on the three-dimensional isochrone of the ventricular activation. The patterns of body surface potential isochrones are consistent with those from previous studies. The SMD model was also used to simulate posterior wall infarction, which matched the criteria for this diagnosis. In conclusion, our SMD model provided a base for further ventricular depolarization studies and this equivalent dipole approach might be useful in investigating ventricular arrhythmias and their site of origin.

Body Surface Potential Mapping↗
PubMed2005

High-resolution analysis of ambulatory electrocardiograms to detect possible mechanisms of premature ventricular beats.

For generations of electrocardiogram (ECG) analysis, the presence of premature ventricular beats (PVBs) has been characterized as a common event in the ECG without regard to the mechanism which has caused the PVB in the first place. At best, the coupling interval with the preceding sinus beat may be noted. This viewpoint persisted throughout the era of automated ECG analysis, as well as influencing the treatment of more life threatening events by PVB suppression strategies alone. This study proposed three hypotheses which would link the PVB to a specific mechanism or milieu. Each of these hypotheses requires significant signal processing of the continuously recorded high resolution ECG. Data are presented which demonstrate that abnormal intra-QRS potentials may be linked to a reentrant mechanism for the PVBs and that many patients have significant changes in these potentials in the sinus beats preceding the PVB. Changes in the characteristics of the repolarization as measured in the T/U wave period were also observed and could be linked to triggered activity mechanism for some PVBs. Finally, the role of subclinical ST segment changes also indicates that low grade ischemia may play a role in modulating either PVB mechanism. The data generated by this study suggest that a new view toward PVB mechanism as measured by ECG characteristics may warrant a more rational approach to renewed interest identifying the malignant PVBs and their eventual clinical management.

Algorithms↗