Key result
Pacing at higher rates reduced the dispersion of MAPD90 at the peak of pulmonary artery occlusion from 86 ms to 26-42 ms and suppressed mechanically induced premature ventricular beats.
Why the study?
Does pacing reduce mechanically induced early afterdepolarizations and arrhythmias in the right ventricle of anaesthetized lambs during pulmonary artery occlusion?
Does pacing reduce mechanically induced early afterdepolarizations and arrhythmias in the right ventricle of anaesthetized lambs during pulmonary artery occlusion?
Pacing reduces stretch-induced early afterdepolarizations and arrhythmias in a lamb model of pulmonary artery occlusion, similar to its effects on drug-induced EADs.
Higher-rate pacing may suppress stretch-induced ventricular arrhythmias in acute RV strain models; extends drug-induced EAD observations but leaves clinical translation open.
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.
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Chen et al. (2004) studied Mechanically induced early afterdepolarization and arrhythmia (n=6). Pacing vs. Intrinsic rate was evaluated on Dispersion of MAPD90 at the peak of occlusion. Pacing at higher rates reduced the dispersion of MAPD90 at the peak of pulmonary artery occlusion from 86 ms to 26-42 ms and suppressed mechanically induced premature ventricular beats.
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