Significance of fragmented ventricular electrograms observed using intracardiac recording techniques in man.

Abstract

Recent studies using intracardiac recordings (ICR) demonstrate 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. Fragmented VE evidently reflects desynchronized local electrical activity related to conduction delay in the ventricular myocardium and may be necessary for the genesis of reentrant VT in man, a finding similar to that observed during experimental myocardial infarction in the canine heart. Patients (17) were studied using ICR, 5 with and 12 without a documented history of VT. Of these 17 patients, 2 had cardiomyopathy, 5 arteriosclerotic heart disease (3 of 5 had ventricular aneurysm), 5 rheumatic heart disease and 2 congenital heart disease; the remaining 3 had no apparent heart disease. The left and right VE were recorded at multiple sites with variable interelectrode distances and filter frequency settings. Fragmented VE could be recorded in the right VE in 4 patients (23.5%) (1 with and 3 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. Incremental atrial pacing induced progressive prolongation of VE fragmentation without the induction of VT. When VT was induced, it bore no relationship to VE fragmentation. During VT, interruption of VE fragmentation with ventricular extrastimulation did not terminate VT. Recordings of fragmented VE apparently depends on the ICR location, interelectrode distance and filter frequency setting. Fragmentation of the VE can be observed in patients with and without VT. Fragmentation of the VE may reflect fractionated myocardial potentials. It may also represent artifacts associated with intracardiac catheter electrode movement during cardiac systole and diastole. VE recorded as such should be interpreted with caution in defining the mechanism of VT in man.