ABSTRACT
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.
