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

Johnson, L and Simon, MA and Pinsky, MR and Shroff, SG (2009) Insights into the effects of contraction dyssynchrony on global left ventricular mechano-energetic function. PACE - Pacing and Clinical Electrophysiology, 32 (2). 224 - 233. ISSN 0147-8389

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Background: The effects of dyssynchrony on global left ventricular (LV) mechanics have been well documented; however, its impact on LV energetics has received less attention. Objective: To assess the effects of LV contraction dyssynchrony on global LV mechano-energetic function in a pacing-induced acute model of dyssynchrony. Methods: 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 (MVO2-PVA) relationship quantified LV energetic function. Internal PVA for MVO2 RVOT was calculated based on the MVO2-PVA relationship for RA pacing. Thus, lost PVA (internal PVA-PVARVOT) represents the mechanical energy not observable at the global level. Results: Compared to RA pacing, RVOT pacing depressed LV mechanics as indicated by a rightward shift of ESPVR (i.e., increase in Vd from 0.58 ± 0.10 to 0.67 ± 0.10 mL, P < 0.05). Despite depressed mechanics, RVOT pacing was associated with greater MVO2 such that the MVO2-PVA relationship intercept was markedly increased from 0.025 ± 0.003 to 0.029 ± 0.003 mL•O2/beat/100gLV (P < 0.05). Excess MVO2 (i.e., MVO2 RVOT - MVO2 RA) significantly correlated with lost PVA (R2 = 0.54, P < 0.001). Conclusion: A potential mechanism explaining the observed increase in MVO2 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 MVO2. © 2009, The Authors.


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Item Type: Article
Status: Published
CreatorsEmailPitt UsernameORCID
Johnson, L
Simon, MA
Pinsky, MRpinsky@pitt.eduPINSKY0000-0001-6166-700X
Shroff, SGsshroff@pitt.eduSSHROFF
Date: 1 February 2009
Date Type: Publication
Journal or Publication Title: PACE - Pacing and Clinical Electrophysiology
Volume: 32
Number: 2
Page Range: 224 - 233
DOI or Unique Handle: 10.1111/j.1540-8159.2008.02206.x
Schools and Programs: School of Medicine > Critical Care Medicine
Refereed: Yes
ISSN: 0147-8389
PubMed Central ID: PMC2948864
PubMed ID: 19170912
Date Deposited: 07 Mar 2012 20:09
Last Modified: 22 Jun 2021 14:55


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