scholarly journals P1510 Assessment of left ventricular relaxation time constant by noninvasive left ventricular pressure-strain loop: invasive validation

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
V Meledin ◽  
D Haberman ◽  
G Gandelman ◽  
L Poles ◽  
G Goland ◽  
...  

Abstract Introduction Left ventricular (LV) relaxation time constant, Tau (τ), is one of the best indexes to evaluate left ventricular diastolic function and is usually assessed invasively. Tau is the time constant of the exponential regression Pt =(P0-P∞)e-t/τ+P∞ that expresses left ventricular isovolumic pressure decay, where Pt is LV pressure (LVP) at time t, P0 is LVP at dP/dtmin and P∞ is the asymptotic pressure, to which relaxation would lead if completed without LV filling. Several noninvasive methods were developed to calculate Tau, however, they are time-consuming and complicated. Recently, a simple method regional left ventricular pressure–strain loops and myocardial work was introduced and validated. We hypothesize that left ventricular relaxation time constant can be derived and calculated from the LV pressure–strain loops. Objective To calculate noninvasively Tau using LV pressure–strain loops and compare it to invasive Tau assessment. Methods The study includes patients with preserved LV systolic function without significant valvular disease that were scheduled to elective coronary catheterization. During catheterization, a fluid-filled catheter was placed in the LV to measure pressure. Echocardiography was performed simultaneously with LV pressure recording. Three standard apical views were acquired and subsequently 2D strain analysis was performed using commercially available GE software and LV pressure–strain loops were calculated. Doppler signal was used for timing of valvular events. Tau was calculated by the equation τ =P/(-dP/dt) that is a derivative of the ventricular pressure decline P = P0e-t/τ+PB with respect to time. The pressure between peak negative dP/dt and the lowest LV pressure shortly after mitral valve opening was used for this calculation. The study was approved by the institutional ethics committee. Results Forty patients, (mean age 65.1 ± 10.9 years, 27 male, BSA1.93 ± 0.18 m2) were included in the study. Heart rate and the mean blood pressure at the time of catheterization were 69.9 ± 11.8 min-1 and 85.2 ± 18.8 mmHg, respectively. The mean LV end diastolic diameter was 44 ± 4 mm, the LV mass was 86.7 ± 25.2 g/m2, LVEF 58.4 ± 6.6% and GLS 21.0 ± 3.2%. Tau, calculated noninvasively using derivative method was significantly lower than invasively derived measurement (40.1 ± 13.4 vs 49.8 ± 7.7 msec, p = 0.002). However, a significant positive correlation was observed between the two methods (r =0.67, p <0.001, Figure). Conclusions This preliminary study demonstrates that Tau estimated by a noninvasive method using LV pressure–strain loops has a good correlation with Tau measured invasively. Therefore, Tau can be estimated noninvasively using novel left ventricular pressure–strain loop method. Abstract P1510 Figure.

2008 ◽  
Vol 2 (1) ◽  
pp. 28-30 ◽  
Author(s):  
Bai Xufang

Left ventricular relaxation time constant, Tau, is the best index to evaluate left ventricular diastolic function. The measurement is only available traditionally in catheter lab. In Echo lab, several methods of non-invasive measurement of Tau have been tried since 1992, however almost all the methods are still utilizing the same formula to calculate Tau as in catheter lab, which makes them inconvenient, time-consuming and sometimes not very accurate. A simple method to calculate Tau in patients with mitral regurgitation has been developed just based on Weiss’ formula and simplified Bernoulli’s equation. Similarly, formulas are developed here by pure mathematical derivative to calculate Tau by continuous-wave Doppler in patients with aortic regurgitation.


2008 ◽  
Vol 2 (1) ◽  
pp. 9-11 ◽  
Author(s):  
Xufang Bai

Left ventricular relaxation time constant, Tau, is the best index to evaluate left ventricular diastolic function, but the measurement is only available traditionally in catheter lab. In Echo lab, several methods of non-invasive measurement of Tau have been tried since 1992, however almost all the methods are still utilizing the same formula to calculate Tau as in catheter lab, which makes them inconvenient, time-consuming and sometimes not very accurate. Based on Weiss’ formula and simplified Bernoulli’s equation, a simple method is developed by pure mathematical derivative to calculate Tau by continuous-wave Doppler in patients with mitral regurgitation.


2001 ◽  
Vol 65 (7) ◽  
pp. 610-616
Author(s):  
Kazumasa Harada ◽  
Yasuyuki Sugishita ◽  
Tatsuya Shimizu ◽  
Atsushi Yao ◽  
Hiroshi Matsui ◽  
...  

1989 ◽  
Vol 256 (2) ◽  
pp. H428-H433 ◽  
Author(s):  
R. J. Henning ◽  
J. Cheng ◽  
M. N. Levy

We determined the effects of vagal stimulation on the time constant (tau) of left ventricular isovolumic pressure decay and on the maximum rates of left ventricular pressure change (dP/dt) during contraction and relaxation in anesthetized dogs. In each dog, the atria were paced at a constant rate of 150 beats/min. We recorded left ventricular pressure waveforms in the absence (control) and in the presence of vagal stimulation at frequencies of 1, 2, and 3 Hz. During the control periods and during vagal stimulation at each frequency, we determined tau, the maximal rate of contraction, and the maximal rate of relaxation from left ventricular pressure waveforms recorded at medium (100 mmHg), high (130 mmHg), and low (73 mmHg) afterloads. Vagal stimulation at a frequency of 3 Hz increased tau by 23%. This effect of vagal stimulation on tau was most pronounced at the high afterload. Vagal stimulation at 3 Hz decreased the maximal rate of relaxation by 19%, but it decreased the maximal rate of contraction by only 8%. Thus vagal stimulation significantly decreased the rate of left ventricular relaxation and had a greater depressant effect on ventricular relaxation than on contraction.


1987 ◽  
Vol 253 (2) ◽  
pp. H307-H316 ◽  
Author(s):  
I. Vergroesen ◽  
M. I. Noble ◽  
J. A. Spaan

The effect of cardiac relaxation on the intramyocardial blood volume was studied by measuring the integrated difference between arterial inflow and great cardiac venous outflow. In nine anesthetized goats, the left main coronary artery was perfused under constant pressure. The great cardiac vein was drained under pressure control. The venous flow signal was amplified so that the integrated intramyocardial blood volume was constant in the beating heart. With normal vasomotor tone, the mean change in vascular volume was 3.01 +/- 0.18 (SE) ml/100 g left ventricle (LV); 67% of the volume change was achieved in 1.60 +/- 0.09 s. For the fully dilated bed (adenosine infusion), the values were 4.13 +/- 0.33 ml/100 g and 0.96 +/- 0.06 s, respectively. The volume change could be correlated with the venous pressure during cardiac arrest (Pvd) and the change in mean left ventricular pressure after cardiac arrest (r = 0.95). The correlation improved when data were selected for Pvd less than 6 mmHg to r = 0.98. We assumed that the change in vascular transmural pressure can be approximated as half the mean left ventricular pressure change. The intramyocardial vascular compliance was then estimated as 0.104 +/- 0.012 and 0.146 +/- 0.028 ml X mmHg-1 X 100 g-1 for control and adenosine conditions, respectively. The long time constants excluded the large epicardial veins as the site of volume change; they were much longer than the duration of diastole in the beating heart. We conclude that the intramyocardial vascular compartment is capable of volume expansion on the order of 20% of its normal volume when myocardial compression by ventricular systole is suspended.


Sign in / Sign up

Export Citation Format

Share Document