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Pacing Clin Electrophysiol. 2009 Feb;32(2):224-33. doi: 10.1111/j.1540-8159.2008.02206.x.

Insights into the effects of contraction dyssynchrony on global left ventricular mechano-energetic function.

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Department of Bioengineering, Cardiovascular Systems Laboratory, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.



The effects of dyssynchrony on global left ventricular (LV) mechanics have been well documented; however, its impact on LV energetics has received less attention.


To assess the effects of LV contraction dyssynchrony on global LV mechano-energetic function in a pacing-induced acute model of dyssynchrony.


Using blood-perfused isolated rabbit heart preparations (n = 11), LV pressure, coronary flow, and arteriovenous oxygen content difference were recorded for isovolumic contractions under right atrial (RA) pacing (control) and simultaneous RA and right ventricular outflow tract (RVOT) pacing (dyssynchrony). LV mechanical function was quantified by the end-systolic pressure-volume relationship (ESPVR). Myocardial oxygen consumption-pressure-volume area (MVO(2)-PVA) relationship quantified LV energetic function. Internal PVA for MVO(2 RVOT) was calculated based on the MVO(2)-PVA relationship for RA pacing. Thus, lost PVA (internal PVA-PVA(RVOT)) represents the mechanical energy not observable at the global level.


Compared to RA pacing, RVOT pacing depressed LV mechanics as indicated by a rightward shift of ESPVR (i.e., increase in V(d) from 0.58 +/- 0.10 to 0.67 +/- 0.10 mL, P < 0.05). Despite depressed mechanics, RVOT pacing was associated with greater MVO(2) such that the MVO(2)-PVA relationship intercept was markedly increased from 0.025 +/- 0.003 to 0.029 +/- 0.003 mL*O(2)/beat/100gLV (P < 0.05). Excess MVO(2) (i.e., MVO(2 RVOT)- MVO(2 RA)) significantly correlated with lost PVA (R(2)= 0.54, P < 0.001).


A potential mechanism explaining the observed increase in MVO(2) with dyssynchrony may be that the measured PVA at the global level underestimates the internal PVA at the cellular level, which is likely to be the true determinant of MVO(2).

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