Rate dependence of mechanically induced electrophysiological changes in right ventricle of anaesthetized lambs during pulmonary artery occlusion

• Published in: Acta physiologica Scandinavica 2004-01, Vol.180 (1), p.13-19
• Main Authors: Chen, R., Penny, D. J., Greve, G., Lab, M. J.
• Format: Article
• Language: English
• Subjects: Action Potentials; Anesthesia; Animals; arrhythmia; Arrhythmias, Cardiac - physiopathology; Biological and medical sciences; Blood Pressure - physiology; Constriction; dispersion; early afterdepolarization; Fundamental and applied biological sciences. Psychology; Heart Rate - physiology; mechano-electrical feedback; pacing; Pulmonary Artery - physiology; Sheep; stretch; Ventricular Function, Right - physiology; Vertebrates: anatomy and physiology, studies on body, several organs or systems
• ISSN: 0001-6772; 1365-201X
• DOI: 10.1046/j.0001-6772.2003.01201.x

Aim:  Mechanically induced early afterdepolarization (EAD) is morphologically similar but different in the mechanisms with drug‐induced EAD, which lead to arrhythmia. Pacing suppresses the drug‐induced EAD and arrhythmia, however the effect of pacing on mechanically induced EAD and arrhythmia is not clear. This study addressed this issue in right ventricle (RV) of anaesthetized lambs. Methods:  Six lambs were anaesthetized, and their hearts exposed. Nine monophasic action potential (MAP) electrodes were placed on RV apex, outflow and inflow regions, and recorded before, during, and after a 10 s occlusion of pulmonary artery at a number of pacing rates. Results:  Pacing significantly reduced the baseline MAP duration at 90% repolarization (MAPD90), decreased the reduction of MAPD at early repolarization at the peak of occlusion. Nonetheless, the percentage of reduction was not significantly different among them. Pacing was able to reduce the frequencies, size of mechanically induced EADs. MAPD90 at the peak of occlusion was all shortened during pacing rather than some lengthened at intrinsic rate. Therefore, the dispersion of MAPD90 at the peak of occlusion reduced from 86 ± 6 ms at intrinsic rate to 42 ± 4 ms at 120 beats min−1 , 38 ± 3 ms at 150 beats min−1 and 26 ± 3 ms at 170 beats min−1. Ultimately, pacing reduced/suppressed mechanically induced premature ventricular beats. These alterations were inversely related to heart rates. Conclusion:  Pacing reduces/suppresses both stretch‐induced EADs and arrhythmia. These modulations are remarkably similar to those on other EADs by the pacing.