Activation Delay After Premature Stimulation in Chronically Diseased Human Myocardium Relates to the Architecture of Interstitial Fibrosis
Top Cited Papers
- 17 December 2001
- journal article
- other
- Published by Ovid Technologies (Wolters Kluwer Health) in Circulation
- Vol. 104 (25), 3069-3075
- https://doi.org/10.1161/hc5001.100833
Abstract
Background — Progressive activation delay starting at long coupling intervals of premature stimuli has been shown to correlate with sudden cardiac death in patients with hypertrophic cardiomyopathy. The purpose of this study was to elucidate the mechanism of increased activation delay in chronically diseased myocardium. Methods and Results — High-resolution unipolar mapping (105, 208, or 247 recording sites with interelectrode distances of 0.8, 0.5, or 0.3 mm, respectively) of epicardial electrical activity was carried out during premature stimulation in 11 explanted human hearts. The hearts came from patients who underwent heart transplantation and were in the end stage of heart failure (coronary artery disease, 4; hypertrophic cardiomyopathy, 1; and dilated cardiomyopathy, 6). Eight hearts were Langendorff-perfused. Epicardial sheets were taken from the remaining hearts and studied in a tissue bath. Activation maps and conduction curves were constructed and correlated with histology. Conduction curves revealing prominent increase of activation delay were associated with zones of dense, patchy fibrosis with long fibrotic strands. Dense, diffuse fibrosis with short fibrotic strands only marginally affected conduction curves. The course of conduction curves in patchy fibrotic areas greatly depended on the direction of propagation relative to fiber direction. Conclusions — The study demonstrates that in chronically diseased human myocardium, nonuniform anisotropic characteristics imposed by long fibrotic strands cause a progressive increase of activation delay, starting at long coupling intervals of premature stimuli. The increase strongly depends on the direction of the wave front with respect to fiber direction and the architecture of fibrosis.This publication has 18 references indexed in Scilit:
- Predicting Sudden Cardiac Death From T Wave Alternans of the Surface Electrocardiogram:Journal of Cardiovascular Electrophysiology, 1996
- Fractionated electrograms in dilated cardiomyopathy: Origin and relation to abnormal conductionJournal of the American College of Cardiology, 1996
- Cardiac tissue geometry as a determinant of unidirectional conduction block: assessment of microscopic excitation spread by optical mapping in patterned cell cultures and in a computer modelCardiovascular Research, 1995
- QT dispersion and sudden unexpected death in chronic heart failureThe Lancet, 1994
- Reduced content of connexin43 gap junctions in ventricular myocardium from hypertrophied and ischemic human hearts.Circulation, 1993
- Myocardial electrical propagation in patients with idiopathic dilated cardiomyopathy.JCI Insight, 1993
- Reentry as a cause of ventricular tachycardia in patients with chronic ischemic heart disease: electrophysiologic and anatomic correlation.Circulation, 1988
- Electrophysiologic and anatomic basis for fractionated electrograms recorded from healed myocardial infarcts.Circulation, 1985
- Structural and electrophysiological changes in the epicardial border zone of canine myocardial infarcts during infarct healing.Circulation Research, 1985
- The functional role of structural complexities in the propagation of depolarization in the atrium of the dog. Cardiac conduction disturbances due to discontinuities of effective axial resistivity.Circulation Research, 1982