Author + information
- Received June 29, 1995
- Revision received November 14, 1995
- Accepted December 13, 1995
- Published online April 1, 1996.
- Jacques M.T. de Bakker, PhDa,*,
- Frans J.L. van Capelle, PhD*,
- Michiel J. Janse, MD*,
- Sara Tasseron, RT*,
- Jessica T. Vermeulen, MD*,
- Nicolaas de Jonge, MD† and
- Jaap R. Lahpor, MD†
- ↵*Address for correspondence: Dr. Jacques M. T. de Bakker, Department of Experimental Cardiology, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands.
Objectives. We sought to investigate the origin of the fractionated electrogram and its relation to abnormal conduction in cardiomyopathic myocardium.
Background. Patients with dilated cardiomyopathy have a high incidence of ventricular tachycardias. Electrograms recorded in these patients are often fractionated.
Methods. High resolution mapping (200-μm interelectrode distance) of the electrical activity was carried out in 11 superfused papillary muscles and 6 trabeculae from 7 patients who underwent heart transplantation because of dilated cardiomyopathy. Similar measurements were taken in four papillary muscles from dog hearts in which electrical barriers had been artificially made. Ten human preparations were studied histologically.
Results. All preparations revealed sites with fractionated electrograms. In three human preparations, activation patterns showed a discernible line of activation block running parallel to the fiber direction. Fractionated electrograms were recorded at sites contiguous to the line of block. In five preparations, fractionated electrograms were recorded at sites where lines of block were not identified. In these preparations, electrical barriers consisted of short stretches of fibrous tissue. In the remaining nine preparations, fractionated electrograms were recorded, both from sites contiguous to distinct obstacles and sites without evidence of a barrier.
Conclusions. Our observations showed that fractionated electrograms recorded in myocardium damaged by cardiomyopathy were due to both distinct, long strands and short stretches of fibrous tissue. Delayed conduction was caused by curvation of activation around the distinct lines of block and by the wavy course of activation between the short barriers. The latter reflects extreme nonuniform anisotropy.
- Received June 29, 1995.
- Revision received November 14, 1995.
- Accepted December 13, 1995.
- American College of Cardiology