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The effect of left ventricular pacing on transmural activation delay in myopathic human hearts
Andreu Porta-Sánchez1, Paul Angaran1, Stéphane Massé1
1The Hull Family Cardiac Fibrillation Management Laboratory, University Health Network, Toronto General Hospital, 150 Gerrard Street West, Gerrard Wing, 3-526, Toronto, ON, Canada M5G 2C4.
Insights
Left ventricular epicardial pacing (LVEpiP) in myopathic hearts does not reduce global delays. However, LVEpiP shortens transmural activation times, highlighting the LV endocardium's importance in pacing.
Area of Science:
- Cardiology
- Electrophysiology
- Cardiac Pacing
Background:
- Global epicardial activation delay is a concern in myopathic hearts.
- Transmural activation delay has not been previously evaluated in this context.
Purpose of the Study:
- To compare transmural electrical activation delay during left ventricular epicardial pacing (LVEpiP) and right ventricular endocardial pacing (RVEndoP) in human myopathic hearts.
- To evaluate global epicardial activation delay during LVEpiP versus RVEndoP.
Main Methods:
- Langendorff-perfused explanted human hearts from seven patients.
- Epicardial mapping with a 112-electrode sock array.
- Transmural mapping using 100 unipolar electrodes from 25 plunge needles.
Main Results:
- No significant difference in global epicardial activation times between LVEpiP (147±8 ms) and RVEndoP (156±17 ms).
- Significantly shorter LV transmural activation time with LVEpiP (125±44 ms) compared to RVEndoP (172±43 ms).
- LV endocardial layer showed earliest activation during LVEpiP.
Conclusions:
- LVEpiP does not decrease global epicardial activation delays in myopathic hearts compared to RVEndoP.
- LVEpiP facilitates early LV endocardial activation, underscoring its significance even with epicardial lead placement.
Aims:
Left ventricular (LV) epicardial pacing (LVEpiP) in human myopathic hearts does not decrease global epicardial activation delay compared with right ventricular (RV) endocardial pacing (RVEndoP); however, the effect on transmural activation delay has not been evaluated. To characterize the transmural electrical activation delay in human myopathic hearts during RVEndoP and LVEpiP compared with global epicardial activation delay.
Methods And Results:
Explanted hearts from seven patients (5 male, 46 ± 10 years) undergoing cardiac transplantation were Langendorff-perfused and mapped using an epicardial sock electrode array (112 electrodes) and 25 transmural plunge needles (four electrodes, 2 mm spacing), for a total of 100 unipolar transmural electrodes. Electrograms were recorded during LVEpiP and RVEndoP, and epicardial (sock) and transmural (needle) activation times, along with patterns of activation, were compared. There was no difference between the global epicardial activation times (LVEpiP 147 ± 8 ms vs. RVEndoP 156 ± 17 ms, P = 0.46). The mean LV transmural activation time during LVEpiP was significantly shorter than that during RVEndoP (125 ± 44 vs. 172 ± 43 ms, P < 0.001). During LVEpiP, of the transmural layers endo-, mid-myocardium and epicardium, LV endocardial layer was often the earliest compared with other transmural layers.
Conclusion:
In myopathic human hearts, LVEpiP did not decrease global epicardial activation delays compared with RVEndoP. LV epicardial pacing led to early activation of the LV endocardium, revealing the importance of the LV endocardium even when pacing from the LV epicardium.
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