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Am J Physiol Heart Circ Physiol 294: H1589-H1596, 2008. First published January 25, 2008; doi:10.1152/ajpheart.00990.2007
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Physical determinants of left ventricular isovolumic pressure decline: model prediction with in vivo validation

Charles S. Chung and Sándor J. Kovács

Department of Physics, Washington University, St. Louis; and Cardiovascular Biophysics Laboratory, Cardiovascular Division, Washington University School of Medicine, St. Louis, Missouri

Submitted 27 August 2007 ; accepted in final form 22 January 2008

The rapid decline in pressure during isovolumic relaxation (IVR) is traditionally fit algebraically via two empiric indexes: {tau}, the time constant of IVR, or {tau}L, a logistic time constant. Although these indexes are used for in vivo diastolic function characterization of the same physiological process, their characterization of IVR in the pressure phase plane is strikingly different, and no smooth and continuous transformation between them exists. To avoid the parametric discontinuity between {tau} and {tau}L and more fully characterize isovolumic relaxation in mechanistic terms, we modeled ventricular IVR kinematically, employing a traditional, lumped relaxation (resistive) and a novel elastic parameter. The model predicts IVR pressure as a function of time as the solution of d2P/dt2 + (1/µ)dP/dt + EkP = 0, where µ (ms) is a relaxation rate (resistance) similar to {tau} or {tau}L and Ek (1/s2) is an elastic (stiffness) parameter (per unit mass). Validation involved analysis of 310 beats (10 consecutive beats for 31 subjects). This model fit the IVR data as well as or better than {tau} or {tau}L in all cases (average root mean squared error for dP/dt vs. t: 29 mmHg/s for model and 35 and 65 mmHg/s for {tau} and {tau}L, respectively). The solution naturally encompasses {tau} and {tau}L as parametric limits, and good correlation between {tau} and 1/µEk ({tau} = 1.15/µEk – 11.85; r2 = 0.96) indicates that isovolumic pressure decline is determined jointly by elastic (Ek) and resistive (1/µ) parameters. We conclude that pressure decline during IVR is incompletely characterized by resistance (i.e., {tau} and {tau}L) alone but is determined jointly by elastic (Ek) and resistive (1/µ) mechanisms.

relaxation; stiffness; hemodynamics; diastole; mechanics; pressure phase plane; isovolumic relaxation


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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