Nonexcitatory stimulus delivery improves left ventricular function in hearts with left bundle branch block.
BACKGROUND
Preliminary data in a heart failure animal model and isolated muscle preparation have suggested that nonexcitatory stimulation (NES) improves left ventricular (LV) function.


RESULTS
We compared biventricular (BV) pacing with NES in an animal model with left bundle branch block (LBBB). The left bundle branch (LBB) was ablated in eight normal heart pigs and led to >50% increase in QRS duration (mean 100 +/- 15 msec). End-diastolic LV pressure, end-systolic LV pressure, LV pressure (LV dP/dtmax), aortic pulse pressure, and LV ejection fraction were measured before pre-LBB ablation and compared with post-LBB ablation (AAI pacing), BV pacing, NES delivery, and BV+NES. Moreover, to evaluate LV diastolic function, we measured the early (E wave) and late flows (A wave) through the mitral valve using spectral Doppler. Compared with post-LBB ablation, NES led to a significant increase in LV dP/dtmax (1,047 +/- 224 mmHg/sec vs 897 +/- 116 mmHg/sec; P < 0.05), LV ejection fraction (64% +/- 18% vs 49% +/- 17%; P < 0.05), and aortic pulse pressure (18 +/- 3.6 mmHg vs 16 +/- 2.8 mmHg; P < 0.05). Moreover, improvement in LV hemodynamic parameters was significantly higher during NES delivery when compared with BV pacing. No significant changes in E wave, A wave, and E/A were recorded during NES, NES+BV, and BV pacing.


CONCLUSIONS
Our preliminary data demonstrate that NES is superior to BV pacing in improving LV function in an animal model with LBBB. Moreover, we demonstrated that NES does not affect transmitral valve flow and subsequently LV diastolic function.
Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Ohio 44195, USA.
Nassir F
NF
Marrouche
Stephen V
SV
Pavia
Shaowei
S
Zhuang
Yung-Jin
YJ
Kim
Tomotsugu
T
Tabata
Don
D
Wallick
Eduardo
E
Saad
Ahmad
A
Abdul-Karim
Robert
R
Schweikert
Walid
W
Saliba
Patrick
P
Tchou
Andrea
A
Natale
D000818:Animals; D002037:Bundle-Branch Block / Q000503:physiopathology* / Q000628:therapy*; D002304:Cardiac Pacing, Artificial / Q000379:methods*; D006439:Hemodynamics; D023421:Models, Animal; D009200:Myocardial Contraction / Q000502:physiology; D013552:Swine; D016277:Ventricular Function, Left / Q000502:physiology*