Fragmented ventricular electrograms were recorded in the left ventricle of 100% and the right ventricle of 23.5% of patients, regardless of ventricular tachycardia history, and may represent artifacts.
Observational (n=17)
Does the presence of fragmented ventricular electrograms on intracardiac recordings correlate with the mechanism of ventricular tachycardia in humans?
Fragmented ventricular electrograms can be observed in patients with and without ventricular tachycardia, are highly dependent on recording techniques, and may represent artifacts rather than solely reflecting arrhythmogenic substrate.
Recent studies using intracardiac recordings (ICR) have demonstrated that fragmentation of the ventricular electrogram (VE) can be detected in patients with chronic ventricular tachycardia (VT) associated with cardiomyopathy or arteriosclerotic heart disease with ventricular aneurysm. This study suggests that fragmented VE reflects desynchronized local electrical activity related to conduction delay in the ventricular myocardium and may he necessary for the genesis of reentrant VT in man, a finding similar to that observed during experimental myocardial infarction in the canine heart. We studied 17 patients using ICR, five with and 12 without a documented history of VT. Of these 17 patients, two had cardiomyopathy, five arteriosclerotic heart disease (three of five had ventricular aneurysm), five rheumatic heart disease and two congenital heart disease; the remaining three had no apparent heart disease. The left and right VEs were recorded at multiple sites with variable interelectrode distances and filter frequency settings. Fragmented VE could be recorded in the right VE in four patients (23.5%) (one with and three without VT) and in the left VE in all 17 patients (100%) using interelectrode distances of 12 mm or greater and filter frequency settings of 40-500 Hz or less. Furthermore, we observed that (1) incremental atrial pacing could induce progressive prolongation of VE fragmentation without the induction of VT; (2) when VT was induced, it bore no relationship to VE fragmentation; and (3) during VT, interruption of VE fragmentation with ventricular extrastimulation did not terminate VT. These findings suggest that (1) recordings of fragmented VE depend on the ICR location, interelectrode distance and filter frequency setting; (2) fragmentation of the VE can be observed in patients with and without VT; and (3) fragmentation of the VE may reflect fractionated myocardial potentials, but it may also represent artifacts associated with intracardiac catheter electrode movement during cardiac systole and diastole. Therefore, VE recorded as such should be interpreted with caution in defin- ing the mechanism of VT in man.
Waxman et al. (Mon,) conducted a observational in Patients with and without a documented history of ventricular tachycardia (n=17). Intracardiac recordings (ICR) was evaluated on Presence of fragmented ventricular electrograms (VE). Fragmented ventricular electrograms were recorded in the left ventricle of 100% and the right ventricle of 23.5% of patients, regardless of ventricular tachycardia history, and may represent artifacts.