This work was funded by the British Heart Foundation.
University of Heidelberg (2006) Proc Physiol Soc 4, SA3
Research Symposium: Godfrey Smith1, Nichola Walker2, Francis L. Burton1, Stuart M. Cobbe2
1. Faculty of Biomedical and Life Sciences, Glasgow University, Glasgow, United Kingdom. 2. Division of Cardiovascular & Medical Sciences, Faculty of Medicine, Glasgow University, Glasgow, United Kingdom.
The pattern of electrical activation of the ventricle of the heart determines the efficiency of ventricular function and the electrical stability of the heart. The pattern of epicardial activation was examined in rabbit hearts with large transmural apical infarcts. The hearts, isolated from adult male New Zealand rabbits under terminal pentobarbitone anaesthesia, were Langendorff-perfused with Tyrode solution. Hearts were isolated 8 weeks after coronary artery ligation performed under halothane anaesthesia. Membrane voltage from the epicardial surface of the left ventricle (LV) including the infarct was monitored using the voltage-sensitive dye RH237. Optical action potentials were detected from the epicardial surface of the infarct; the signal amplitude was ~20% of those in the non-infarcted zone (NZ). Epicardial activation mapping of the mid-region of the LV free wall, including the infarct, showed that during right atrial (RA) or LV endocardial pacing, the activation sequence was not significantly different between infarcted and sham-operated groups. Direct stimulation of the epicardium in the NZ revealed an area of slow conduction velocity (CV ~5 cm s-1, ~10% of normal values) at the margin of the infarct zone (IZ). Within the IZ, CV was ~50% of normal. Epicardial action potential rise time was longer in the IZ (23.4±2.1 vs. 42.4±1.2 ms, p<0.05) and repolarization interval was shorter (88.9±3.7 vs. 73.0±4.4 ms, p < 0.05). Premature stimuli applied to NZ during RA pacing produced regions of very slow conduction (2-3 cm s-1) at the margins of the IZ. Chemical ablation of the endocardium of the LV free wall (including the infarct) dramatically altered the epicardial activation pattern on RA pacing, but the pattern during epicardial stimulation was not significantly altered. In conclusion, the presence of a scar did not disrupt the ventricular epicardial activation pattern during RA or endocardial pacing. Regions of slow conduction were seen in the margin of the IZ during epicardial pacing or with epicardial extra stimuli. Optical action potentials were recordable from the epicardial surface of the transmural infarct scar. These signals were not altered by endocardial ablation. Therefore remnant groups of myocytes in the ventricular wall may support electrical activity even in a transmural scar.
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Where applicable, experiments conform with Society ethical requirements.