Variation in Tau, the time constant for isovolumic relaxation, along the left ventricular base-to-apex axis

1999 ◽  
Vol 94 (1) ◽  
pp. 41-48 ◽  
Author(s):  
K.L. Davis ◽  
U. Mehlhorn ◽  
E.R. Schertel ◽  
H.J. Geissler ◽  
D. Trevas ◽  
...  
Keyword(s):  
Time Constant ◽  
Left Ventricular ◽  
Left Ventricular Base ◽  
Isovolumic Relaxation

Physical determinants of left ventricular isovolumic pressure decline: model prediction with in vivo validation

2008 ◽  
Vol 294 (4) ◽  
pp. H1589-H1596 ◽  
Author(s):  
Charles S. Chung ◽  
Sándor J. Kovács
Keyword(s):  
Time Constant ◽  
Mean Squared Error ◽  
Elastic Stiffness ◽  
Elastic Parameter ◽  
Left Ventricular ◽  
Rapid Decline ◽  
Function Characterization ◽  
Isovolumic Relaxation

The rapid decline in pressure during isovolumic relaxation (IVR) is traditionally fit algebraically via two empiric indexes: τ, the time constant of IVR, or τL, 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 τ and τL 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/d t2 + (1/μ)dP/d t + EkP = 0, where μ (ms) is a relaxation rate (resistance) similar to τ or τL 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 τ or τL in all cases (average root mean squared error for dP/d t vs. t: 29 mmHg/s for model and 35 and 65 mmHg/s for τ and τL, respectively). The solution naturally encompasses τ and τL as parametric limits, and good correlation between τ and 1/μ Ek (τ = 1.15/μ Ek − 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., τ and τL) alone but is determined jointly by elastic ( Ek) and resistive (1/μ) mechanisms.

scholarly journals The dependence of the time constant of left ventricular isovolumic relaxation (tau) on pericardial pressure.

Circulation ◽  
1990 ◽  
Vol 81 (3) ◽  
pp. 1071-1080 ◽  
Author(s):  
M A Frais ◽  
D W Bergman ◽  
I Kingma ◽  
O A Smiseth ◽  
E R Smith ◽  
...  
Keyword(s):  
Time Constant ◽  
Left Ventricular ◽  
Pericardial Pressure ◽  
Isovolumic Relaxation

Spatio-temporal attributes of left ventricular pressure decay rate during isovolumic relaxation

2012 ◽  
Vol 302 (5) ◽  
pp. H1094-H1101 ◽  
Author(s):  
Erina Ghosh ◽  
Sándor J. Kovács
Keyword(s):  
Relaxation Rate ◽  
Time Constant ◽  
Kinematic Model ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Decay Rates ◽  
Pressure Decay ◽  
Spatio Temporal ◽  
Isovolumic Relaxation

Global left ventricular (LV) isovolumic relaxation rate has been characterized: 1) via the time constant of isovolumic relaxation τ or 2) via the logistic time constant τ L. An alternate kinematic method, characterizes isovolumic relaxation (IVR) in accordance with Newton's Second Law. The model's parameters, stiffness Ek, and damping/relaxation μ result from best fit of model-predicted pressure to in vivo data. All three models (exponential, logistic, and kinematic) characterize global relaxation in terms of pressure decay rates. However, IVR is inhomogeneous and anisotropic. Apical and basal LV wall segments untwist at different times and rates, and transmural strain and strain rates differ due to the helically variable pitch of myocytes and sheets. Accordingly, we hypothesized that the exponential model (τ) or kinematic model (μ and Ek) parameters will elucidate the spatiotemporal variation of IVR rate. Left ventricular pressures in 20 subjects were recorded using a high-fidelity, multipressure transducer (3 cm apart) catheter. Simultaneous, dual-channel pressure data was plotted in the pressure phase-plane (dP/d t vs. P) and τ, μ, and Ek were computed in 1631 beats (average: 82 beats per subject). Tau differed significantly between the two channels ( P < 0.05) in 16 of 20 subjects, whereas μ and Ek differed significantly ( P < 0.05) in all 20 subjects. These results show that quantifying the relaxation rate from data recorded at a single location has limitations. Moreover, kinematic model based analysis allows characterization of restoring (recoil) forces and resistive (crossbridge uncoupling) forces during IVR and their spatio-temporal dependence, thereby elucidating the relative roles of stiffness vs. relaxation as IVR rate determinants.

Myocardial relaxation. II. Hemodynamic determinants of rate of left ventricular isovolumic pressure decline

1980 ◽  
Vol 239 (1) ◽  
pp. H1-H6 ◽  
Author(s):  
W. H. Gaasch ◽  
A. S. Blaustein ◽  
C. W. Andrias ◽  
R. P. Donahue ◽  
B. Avitall
Keyword(s):  
Steady State ◽  
Time Constant ◽  
Volume Expansion ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Relaxation Velocity ◽  
Anesthetized Dogs ◽  
Isoproterenol Infusion ◽  
Isovolumic Relaxation ◽  
Hemodynamic Determinants

The hemodynamic determinants of the time constant of left ventricular (LV) isovolumic pressure (P) decline were studied in 32 anesthetized dogs. The time constant, tau (an index of LV relaxation), was determined from the best exponential fit of the equation P = Poe-t/r, to LVP measured at 5-ms intervals during isovolumic relaxation; Po = LVP at maximum negative dP/dt and t = time. At a constant heart rate of 120 beats/min, tau was determined during steady-state increases in preload (volume expansion), increases in afterload (methoxamine infusion), reductions in afterload (nitroprusside infusion), and in variably afterloaded beats at a constant preload (single-beat interventions). tau was directly related to LV systolic pressure and length during the alterations in LV loading conditions, but tau was not closely related to the extent of fiber shortening. During isoproterenol infusion, relaxation was more rapid (tau), and following the administration of propranolol, relaxation was prolonged (tau). While data from the variably afterloaded contractions indicate the presence of systolic load-dependent LV relaxation velocity, the steady-state studies do not exclude the possibility that altered contractility through reflex or other mechanisms contributes to the observed changes in tau.

Influence of heart rate on left ventricular isovolumic relaxation time: a Doppler study in healthy newborns

2004 ◽  
Vol 17 (4) ◽  
pp. 330-331 ◽  
Author(s):  
Antonio De Merulis ◽  
Giulio Calcagni ◽  
Paolo Versacci ◽  
Renato Lucchini ◽  
Flavia Ventriglia ◽  
...  
Keyword(s):  
Heart Rate ◽  
Relaxation Time ◽  
Left Ventricular ◽  
Isovolumic Relaxation Time ◽  
Doppler Study ◽  
Isovolumic Relaxation

Dynamic Change in the Left Ventricular Base With or Without a Rigid Mitral Valve Prosthesis

ASAIO Journal ◽  
1997 ◽  
Vol 43 (5) ◽  
pp. M396
Author(s):  
TAKESHI KOMODA ◽  
ROLAND HETZER ◽  
JOSEPH HOFMEISTER ◽  
YU-GUO WENG ◽  
JOHANN OELLINCER ◽  
...  
Keyword(s):  
Mitral Valve ◽  
Dynamic Change ◽  
Left Ventricular ◽  
Valve Prosthesis ◽  
Mitral Valve Prosthesis ◽  
Left Ventricular Base

scholarly journals Childhood and adult exposure to secondhand tobacco smoke and cardiac structure and function: results from Echo-SOL

Open Heart ◽  
2018 ◽  
Vol 5 (2) ◽  
pp. e000831 ◽  
Author(s):  
Melissa Suzanne Burroughs Peña ◽  
Katrina Swett ◽  
Robert C Kaplan ◽  
Krista Perreira ◽  
Martha Daviglus ◽  
...  
Keyword(s):  
Left Ventricular ◽  
Structure And Function ◽  
Cardiac Structure ◽  
Isovolumic Relaxation Time ◽  
Shs Exposure ◽  
Cardiac Structure And Function ◽  
And Function ◽  
Relationship Of ◽  
The Relationship ◽  
Isovolumic Relaxation

ObjectiveTo describe the relationship of household secondhand smoke (SHS) exposure and cardiac structure and function.MethodsParticipants (n=1069; 68 % female; age 45–74 years) without history of tobacco use, coronary artery disease or severe valvular disease were included. Past childhood (starting at age <13 years), adolescent/adult and current exposure to household SHS was assessed. Survey linear regression analyses were used to model the relationship of SHS exposure and echocardiographic measures of cardiac structure and function, adjusting for covariates (age, sex, study site, alcohol use, physical activity and education).ResultsSHS exposure in childhood only was associated with reduced E/A velocity ratio (β=−0.06 (SE 0.02), p=0.008). SHS exposure in adolescence/adult only was associated with increased left ventricular ejection fraction (LVEF) (1.2 (0.6), p=0.04), left atrial volume index (1.7 (0.8), p=0.04) and decreased isovolumic relaxation time (−0.003 (0.002), p=0.03). SHS exposure in childhood and adolescence/adult was associated with worse left ventricular global longitudinal strain (LVGLS) (two-chamber) (0.8 (0.4), p= 0.049). Compared with individuals who do not live with a tobacco smoker, individuals who currently live with at least one tobacco smoker had reduced LVEF (−1.4 (0.6), p=0.02), LVGLS (average) (0.9 (0.40), p=0.03), medial E′ velocity (−0.5 (0.2), p=0.01), E/A ratio (−0.09 (0.03), p=0.003) and right ventricular fractional area change (−0.02 (0.01), p=0.01) with increased isovolumic relaxation time (0.006 (0.003), p=0.04).ConclusionsPast and current household exposure to SHS was associated with abnormalities in cardiac systolic and diastolic function. Reducing household SHS exposure may be an opportunity for cardiac dysfunction prevention to reduce the risk of future clinical heart failure.

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