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Slow conduction in the infarcted human heart. 'Zigzag' course of activation
J M de Bakker1, F J van Capelle, M J Janse
1Interuniversity Cardiology Institute of The Netherlands, Department of Experimental Cardiology, Academic Medical Center, Amsterdam.
Insights
Slow conduction in infarcted heart muscle creates dangerous arrhythmias. This study reveals a "zigzag" activation pathway through surviving muscle bundles, separated by scar tissue, explaining this phenomenon.
Area of Science:
- Cardiovascular Physiology
- Cardiac Electrophysiology
- Myocardial Infarction Research
Background:
- Ventricular tachycardias in chronic myocardial infarction arise from reentry.
- Slow conduction zones within infarcted areas facilitate reentry.
- Understanding slow conduction mechanisms is crucial for managing arrhythmias.
Purpose of the Study:
- To elucidate the mechanism of slow conduction in the chronic infarcted human heart.
- To investigate how myocardial infarction affects cardiac electrical propagation.
Main Methods:
- Studied activation spread in human infarcted papillary muscles post-heart transplantation.
- Utilized high-resolution mapping in areas of slow conduction.
- Analyzed activation delays and conduction velocities in relation to tissue structure.
Main Results:
- Observed significant activation delays (up to 45 ms) perpendicular to fiber direction.
- Identified activation spread within parallel tracts (0.6-1 m/s) separated by collagenous septa.
- Found that tracts formed a complex network, allowing perpendicular conduction where septa were interrupted.
Conclusions:
- Slow conduction perpendicular to fiber direction results from a "zigzag" activation course.
- Activation propagates along elongated pathways formed by branching/merging myocytes.
- Collagenous septa dictate the network structure and influence conduction patterns in infarcted hearts.
Background:
Ventricular tachycardias occurring in the chronic phase of myocardial infarction are caused by reentry. Areas of slow conduction, facilitating reentry, are often found in the infarcted zone. The purpose of this study was to elucidate the mechanism of slow conduction in the chronic infarcted human heart.
Methods And Results:
Spread of activation was studied in infarcted papillary muscles from hearts of patients who underwent heart transplantation because of infarction. Recordings were carried out on 10 papillary muscles that were superfused in a tissue bath. High-resolution mapping was performed in areas revealing slow conduction. Activation delay between sites perpendicular to the fiber direction and 1.4 mm apart could be as long as 45 milliseconds. Analysis of activation times revealed that activation spread in tracts parallel to the fiber direction. Conduction velocity in the tracts was between 0.6 and 1 m/s. Although tracts were separated from each other over distances up to 8 mm, they often connected with each other at one or more sites, forming a complex network of connected tracts. In this network, wave fronts could travel perpendicular to the fiber direction. Separation of tracts was due to collagenous septa. At sites where tracts were interconnected, the collagenous barriers were interrupted.
Conclusions:
Slow conduction perpendicular to the fiber direction in infarcted myocardial tissue is caused by a "zigzag" course of activation at high speed. Activation proceeds along pathways lengthened by branching and merging bundles of surviving myocytes ensheathed by collagenous septa.