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Load, chamber stiffness, and relaxation are the three established determinants of global diastolic function (DF). Coupling of systolic stiffness and isovolumic relaxation has been hypothesized; however, diastolic stiffness-relaxation coupling (DSRC) remains unknown. The parametrized diastolic filling (PDF) formalism, a validated DF model incorporates DSRC. PDF model-predicted DSRC was validated by analysis of 159 Doppler E-waves from a published data set (22 healthy volunteers undergoing bicycle exercise). E-waves at varying (46-120 bpm) heart rates (HR) demonstrated variation in acceleration time (AT), deceleration time (DT), and E-wave peak velocity. AT, DT, and Epeak were converted into PDF parameters: stiffness (k), relaxation (c), and load (xo) using published numerical methods. Univariate linear regression showed that over a twofold increase in HR, AT, and DT decrease (r = -0.44; P < 0.001 and r = -0.42; P < 0.001, respectively), while, DT/AT remains constant (r = -0.04; P = 0.67). Similarly, k increases with HR (r = 0.55; P < 0.001), while c has no significant correlation with HR (r = 0.08; P = 0.32). However, the dimensionless DSRC parameter ϣ = c²/4k shows no significant correlation with HR (r = -0.03; P = 0.7). Furthermore, ϣ is uniquely determined by DT/AT rather than AT or DT independently. Constancy of w in spite of a twofold increase in HR establishes that stiffness (k) and relaxation (c) are coupled and manifest via a HR-invariant parameter of E-wave asymmetry and should not be considered independent of each other. The manifestation of DSRC through E-wave asymmetry via ϣ underscores the value of DT/AT as a physiological, mechanism-derived index of DF. NEW & NOTEWORTHY: Although diastolic stiffness and relaxation are considered independent chamber properties, the cardiohemic inertial oscillation that generates E-waves obeys Newton's law. E-waves vary with heart rate requiring simultaneous change in stiffness and relaxation. By retrospective analysis of human heart-rate varying transmitral Doppler-data, we show that diastolic stiffness and relaxation are coupled and that the coupling manifests through E-wave asymmetry, quantified through a parametrized diastolic filling model-derived dimensionless parameter, which only depends on deceleration time and acceleration time, readily obtainable via standard echocardiography. [ABSTRACT FROM AUTHOR]

Load, chamber stiffness, and relaxation are the three established determinants of global diastolic function (DF). Coupling of systolic stiffness and isovolumic relaxation has been hypothesized; however, diastolic stiffness-relaxation coupling (DSRC) remains unknown. The parametrized diastolic filling (PDF) formalism, a validated DF model incorporates DSRC. PDF model-predicted DSRC was validated by analysis of 159 Doppler E-waves from a published data set (22 healthy volunteers undergoing bicycle exercise). E-waves at varying (46-120 bpm) heart rates (HR) demonstrated variation in acceleration time (AT), deceleration time (DT), and E-wave peak velocity. AT, DT, and Epeak were converted into PDF parameters: stiffness (k), relaxation (c), and load (xo) using published numerical methods. Univariate linear regression showed that over a twofold increase in HR, AT, and DT decrease (r = -0.44; P < 0.001 and r = -0.42; P < 0.001, respectively), while, DT/AT remains constant (r = -0.04; P = 0.67). Similarly, k increases with HR (r = 0.55; P < 0.001), while c has no significant correlation with HR (r = 0.08; P = 0.32). However, the dimensionless DSRC parameter w = c²/4k shows no significant correlation with HR (r = -0.03; P = 0.7). Furthermore, w is uniquely determined by DT/AT rather than AT or DT independently. Constancy of w in spite of a twofold increase in HR establishes that stiffness (k) and relaxation (c) are coupled and manifest via a HR-invariant parameter of E-wave asymmetry and should not be considered independent of each other. The manifestation of DSRC through E-wave asymmetry via w underscores the value of DT/AT as a physiological, mechanism-derived index of DF. [ABSTRACT FROM AUTHOR]