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J Appl Physiol 102: 1367-1373, 2007. First published December 21, 2006; doi:10.1152/japplphysiol.00593.2006
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Contraction-relaxation coupling mechanism characterization in the thermodynamic phase plane: normal vs. impaired left ventricular ejection fraction

Yue Wu,1 Yingbo Yu,2 and Sándor J. Kovács1,2,3

1Cardiovascular Biophysics Laboratory, Department of Physics, 2Department of Biomedical Engineering, and 3Cardiovascular Division, Department of Internal Medicine, Washington University, St. Louis, Missouri

Submitted 26 May 2006 ; accepted in final form 12 December 2006

Using simultaneous pressure-volume measurements obtained during cardiac catheterization, we employ the thermodynamic phase-plane (TPP) method to characterize global contraction-relaxation coupling (CRC) between normal and impaired left ventricular (LV) ejection fraction (LVEF) groups. The cardiac cycle inscribes a closed loop in the TPP defined by the coordinates "potential" power [V(dP/dt), ergs/s] and "kinetic" power [P(dV/dt), ergs/s]. The TPP-derived indexes {kappa} and {rho} define the chamber's contractile and CRC attributes, respectively. Data from 33 subjects dichotomized as normal control (n = 22, >50% LVEF) and impaired LVEF (n = 11, <50% LVEF) were analyzed. The results were as follows: {kappa} = 3.0 ± 1.1 and {rho} = –0.38 ± 0.21 for controls and {kappa} = 5.4 ± 1.6 and {rho} = –1.14 ± 0.47 for the impaired LVEF group; {kappa} and {rho} are significantly higher for impaired LVEF than for control (P < 0.001 for both). As {kappa} increased, {rho} decreased (r = –0.69) for all subjects. Hence, ventricles with impaired LVEF are thermodynamically less efficient because they require more potential power per unit of delivered kinetic power than controls. We conclude that TPP-derived indexes of CRC facilitate assessment of chamber efficiency in thermodynamic terms and elucidate the dominant differentiating features in terms of CRC indexes.

left ventricular function; cardiac power; mathematical modeling



Address for reprint requests and other correspondence: S. J. Kovács, Cardiovascular Biophysics Laboratory, Washington Univ. Medical Center, 660 South Euclid Ave., Box 8086, St. Louis, MO 63110 (e-mail: sjk{at}wuphys.wustl.edu)







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