scholarly journals End-systolic pressure/volume relationship during dobutamine stress echo: a prognostically useful non-invasive index of left ventricular contractility

2005 ◽  
Vol 26 (22) ◽  
pp. 2404-2412 ◽  
Author(s):  
Aurelia Grosu ◽  
Tonino Bombardini ◽  
Michele Senni ◽  
Vincenzo Duino ◽  
Mauro Gori ◽  
...  
2002 ◽  
Vol 282 (5) ◽  
pp. H1739-H1750 ◽  
Author(s):  
Knut E. Kjørstad ◽  
Christian Korvald ◽  
Truls Myrmel

The end-systolic pressure-volume relationship is regarded as a useful index for assessing the contractile state of the heart. However, the need for preload alterations has been a serious limitation to its clinical applications, and there have been numerous attempts to develop a method for calculating contractility based on one single pressure-volume loop. We have evaluated four of these methods. Pressure-volume data were obtained by combined pressure and conductance catheters in 37 pigs. All four methods were applied to 88 steady-state pressure-volume files, including eight files sampled during dopamine infusions. Estimates of single-beat contractility (elastance) were compared with preload-varied multiple-beat elastance [ E es(MB)]. All methods had a low average bias (−0.3 to 0.5 mmHg/ml) but limits of agreement (±2 SD) were unacceptably high (±2.6 to ±3.8 mmHg/ml). In the dopamine group, E es(MB) showed an increase of 1.7 ± 0.8 mmHg/ml (mean ± SD) compared with baseline ( P < 0.001). None of the single-beat methods predicted this increase in contractility. It is therefore doubtful whether any of the methods allow for single-beat assessment of contractility.


Author(s):  
Tom E. Claessens ◽  
Ernst R. Rietzschel ◽  
Marc L. De Buyzere ◽  
Dirk De Bacquer ◽  
Guy De Backer ◽  
...  

The contractile state of the human left ventricle (LV) is often assessed by its end-systolic elastance (Ees) [1]. This index is calculated as the slope of the linear end-systolic pressure-volume relationship (ESPVR), which connects the upper left corners of pressure-volume loops obtained under various loading conditions (figure 1).


1988 ◽  
Vol 255 (3) ◽  
pp. H679-H684
Author(s):  
J. D. Schipke ◽  
J. Alexander ◽  
Y. Harasawa ◽  
R. Schulz ◽  
D. Burkhoff

We predicted the shape of the end-systolic pressure-thickness relationship (ESPTR) by modeling the left ventricle as thick-walled sphere. To test the validity of the predicted relationships, we then measured the ESPTR over wide volume ranges in seven isolated blood-perfused canine hearts. Both simulation and experiments demonstrated that the ESPTR is curvilinear. However, within a physiological left ventricular systolic pressure range (80–150 mmHg), the ESPTR was described reasonably well by a straight line. Within that pressure range, changes in left ventricular contractile state, assessed by slope changes of the end-systolic pressure-volume relationship, were associated with almost parallel shifts in the ESPTR. In contrast, in a low pressure range (less than 80 mmHg), contractility changes were associated with slope changes of the ESPTR. We conclude that, in general, there are limitations in the application of ESPTR for assessing left ventricular contractility, but if the limitations are recognized and accounted for, then the ESPTR may be useful for assessing contractility changes in vivo.


1997 ◽  
Vol 273 (4) ◽  
pp. H1688-H1695
Author(s):  
Katsuya Onishi ◽  
Kiyotsugu Sekioka ◽  
Ryoichi Ishisu ◽  
Yuji Abe ◽  
Hideyuki Tanaka ◽  
...  

An increase in the responsiveness of the contractile machinery to Ca2+could theoretically enhance the mechanoenergetics of the heart. To clarify this unresolved issue, we studied the effects of MCI-154, a Ca2+ sensitizer, on the mechanoenergetics in terms of the left ventricular contractility index [slope of end-systolic pressure-volume relationship ( E max)] and the relationship between myocardial oxygen consumption (Vo 2) and left ventricular pressure-volume area in excised cross-circulated canine hearts. MCI-154 increased E max by 42 ± 31% (SD), although the slope of the Vo 2-PVA relationship (an indicator of contractile efficiency) was unchanged by MCI-154. Despite equal increases in E max, the relative increase in unloaded Vo 2(ΔVo 2/Δ E max) during infusion of MCI-154 was, however, significantly less than that during CaCl2 infusion (0.0016 ± 0.0018 vs. 0.0059 ± 0.0054; P < 0.05). By contrast, ΔVo 2/Δ E maxfor milrinone was the same as that for CaCl2 (0.0043 ± 0.0041 vs. 0.0039 ± 0.0045; P > 0.05). Basal metabolism in KCl-arrested hearts was unchanged by MCI-154, indicating that MCI-154 consumes less energy than CaCl2 for excitation-contraction coupling. These findings suggest that MCI-154 acts energetically as a Ca2+ sensitizer in beating canine whole hearts.


1994 ◽  
Vol 76 (3) ◽  
pp. 1060-1067 ◽  
Author(s):  
K. R. Walley ◽  
P. C. Hebert ◽  
Y. Wakai ◽  
P. G. Wilcox ◽  
J. D. Road ◽  
...  

Whether systolic contractility or diastolic compliance changes soon after tumor necrosis factor-alpha (TNF-alpha) exposure is not known. Accordingly, we measured hemodynamics, left ventricular contractility using the slope of the end-systolic pressure-volume relationship, and diastolic pressure-volume relationships in six control dogs and in six dogs receiving 60 micrograms.kg-1.h-1 i.v. of TNF-alpha. Mean aortic pressure decreased by 22% 1 h after TNF-alpha infusion and remained decreased (P < 0.05). Cardiac output increased by 19% 1 h after TNF-alpha infusion and remained significantly greater than control values (P < 0.05). Left ventricular contractility decreased by 23% (P < 0.05) 1 h after TNF-alpha infusion and decreased by 52% (P < 0.01) 5 h after TNF-alpha infusion. The diastolic pressure-volume relationship did not change in the TNF-alpha group or the control group. Ejection fraction did not change after TNF-alpha infusion despite the decrease in contractility because afterload decreased. We conclude that TNF-alpha is important in causing the hypotensive, hyperdynamic circulation of sepsis. The new finding that left ventricular contractility is decreased shortly after TNF-alpha infusion suggests that TNF-alpha, or another mediator released very soon after TNF-alpha, is an important myocardial depressant factor.


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