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Fractionated electrograms in dilated cardiomyopathy: origin and relation to abnormal conduction
J M de Bakker1, F J van Capelle, M J Janse
1Department of Experimental Cardiology, Academic Medical Center, Amsterdam, The Netherlands.
Insights
Fractionated electrograms in cardiomyopathy stem from fibrous tissue, causing abnormal heart conduction. This study clarifies the link between myocardial damage and electrical signal disturbances.
Area of Science:
- Cardiovascular Electrophysiology
- Cardiac Pathology
- Myocardial Tissue Engineering
Background:
- Dilated cardiomyopathy (DCM) is associated with a high risk of ventricular tachycardias.
- Fractionated electrograms are frequently observed in patients with DCM.
Purpose of the Study:
- To investigate the origin of fractionated electrograms.
- To understand their relationship to abnormal conduction in cardiomyopathic hearts.
Main Methods:
- High-resolution electrical mapping of human and canine cardiac muscle.
- Histological examination of myocardial tissue samples.
- Artificial creation of electrical barriers in canine models.
Main Results:
- Fractionated electrograms were consistently found in affected myocardial preparations.
- Activation patterns revealed lines of block and delayed conduction around fibrous tissue.
- Both distinct, long strands and short stretches of fibrous tissue were identified as sources.
Conclusions:
- Fractionated electrograms in cardiomyopathy result from fibrous tissue infiltration.
- Abnormal conduction is caused by activation patterns around these fibrous barriers.
- Nonuniform anisotropy contributes to delayed conduction pathways.
Objectives:
We sought to investigate the origin of the fractionated electrogram and its relations 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-microM 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.