Time constant of isovolumic pressure fall: new numerical approaches and significance

Martin, Gladys; Gimeno, J.; Cosı́n, Juan; Guillem, M. I.

doi:10.1152/ajpheart.1984.247.2.h283

Cited by 33 publications

(30 citation statements)

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“…Prior studies that directly measured P 4 have reported far smaller values (Ϫ7 mm Hg) in normal hearts, 10 although similar data from failing hearts are not available. The increase in P 4 with load reduction was nonphysiologic because if anything, the asymptote should decrease as external constraining forces 22,25 and possibly elastic recoil 26,27 are enhanced. Again, using a purely mathematical manipulation by maintaining a constant P 4 value, we found the apparent load variability of the monoexponential time constants was minimized without compromising quality of fit.…”

Section: Discussionmentioning

confidence: 99%

Analysis of Isovolumic Relaxation in Failing Hearts by Monoexponential Time Constants Overestimates Lusitropic Change and Load Dependence

Senzaki

Kass²

2010

Circ: Heart Failure

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Background-Failing hearts display slow relaxation with apparent increased load sensitivity. However, inaccuracies of monoexponential analysis can contribute to these observations, and different qualitative and quantitative results might be obtained by alternative models. We tested whether pressure relaxation of failing hearts consistently deviates from a monoexponential waveform, leading to overestimations of lusitropic change and load sensitivity by monoexponentialderived time constants. Methods and Results-Fourteen dogs were studied before and after tachycardia pacing-induced heart failure. Relaxation time constants were derived by monoexponential fits ( E ) with zero or nonzero asymptotes and by a logistic fit ( L ). L assumes nonlinear relations between pressure and its first derivative, whereas E assumes a linear dependence. Load sensitivity of was tested by comparing beats during vena caval occlusion. E prolonged by 75% to 80% with heart failure, 3 times more than L (PϽ0.01). E displayed marked load sensitivity in failing hearts, shortening during preload reduction, whereas L was little changed by the same loading maneuver. Neither L nor E varied with preload in control hearts. The discrepancy between E and L results was due to nonmonoexponential decay reflected by nonlinear pressure-time derivative of pressure plots, which was enhanced with heart failure (PϽ0.01). This nonlinearity was reduced by ␤-adrenergic stimulation, lowering preload sensitivity of E to control levels. Conclusions-Isovolumic relaxation in failing hearts deviates from a monoexponential waveform, leading to overestimated relaxation delay and increased load sensitivity of monoexponential time constants. This deviation is under ␤-adrenergic modulation. The logistic model improves the fit-to-real pressure decay in failing hearts, providing more stable measures of relaxation. (Circ Heart Fail. 2010;3:268-276.)

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Section: Discussionmentioning

confidence: 99%

Analysis of Isovolumic Relaxation in Failing Hearts by Monoexponential Time Constants Overestimates Lusitropic Change and Load Dependence

Senzaki

Kass²

2010

Circ: Heart Failure

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“…The slope of the relationship (−1/Tau) can be calculated using the so-called derivative method popularised by RAFF and GLANTZ [74] to help calculate the LV relaxation time constant. Overall, numerous, mathematical tools that take the pressure asymptote into account are available to reliably calculate the time constant (Tau) of exponential decay processes [59,74,75]. Cardiac physiologists are well aware of such tools allowing the accurate calculation the LV relaxation time constant, as has been documented in many previously published studies.…”

Section: Rc-time: a Critical Evaluation And New Proposalmentioning

confidence: 99%

Pulmonary vascular resistance and compliance relationship in pulmonary hypertension

et al. 2015

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Right ventricular adaptation to the increased pulmonary arterial load is a key determinant of outcomes in pulmonary hypertension (PH). Pulmonary vascular resistance (PVR) and total arterial compliance (C) quantify resistive and elastic properties of pulmonary arteries that modulate the steady and pulsatile components of pulmonary arterial load, respectively. PVR is commonly calculated as transpulmonary pressure gradient over pulmonary flow and total arterial compliance as stroke volume over pulmonary arterial pulse pressure (SV/PApp). Assuming that there is an inverse, hyperbolic relationship between PVR and C, recent studies have popularised the concept that their product (RC-time of the pulmonary circulation, in seconds) is "constant" in health and diseases. However, emerging evidence suggests that this concept should be challenged, with shortened RC-times documented in post-capillary PH and normotensive subjects. Furthermore, reported RC-times in the literature have consistently demonstrated significant scatter around the mean. In precapillary PH, the true PVR can be overestimated if one uses the standard PVR equation because the zero-flow pressure may be significantly higher than pulmonary arterial wedge pressure. Furthermore, SV/PApp may also overestimate true C. Further studies are needed to clarify some of the inconsistencies of pulmonary RC-time, as this has major implications for our understanding of the arterial load in diseases of the pulmonary circulation. @ERSpublications Empiric estimates of pulmonary arterial load are prone to errors and may result in overestimation of RC-time

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“…Because of some deviation of LV pressure decay from an exponential decline, a higher starting point or a higher end point will erroneously prolong . 53 This usually has no implications except when values are compared under widely varying LV loading conditions (eg, between control subjects and hypertensive patients). P inf is the final pressure to which LV pressure would decay in the absence of LV filling.…”

Section: Pitfalls Of Diastolic Dysfunction Indexesmentioning

confidence: 99%

Doppler Echocardiography Yields Dubious Estimates of Left Ventricular Diastolic Pressures

2009

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For normal cardiac performance, the left ventricle (LV) must be able to eject an adequate stroke volume at arterial pressure (systolic function) and fill without requiring an elevated left atrial (LA) pressure (diastolic function). These systolic and diastolic functions must be adequate to meet the needs of the body both at rest and during stress. Response by Tschöpe and Paulus on p 809Systolic function is conveniently (although not always accurately) measured as the ejection fraction (EF), calculated as stroke volume divided by end-diastolic volume. 1 The LV EF is easily interpreted. The lower limit of normal is Ϸ50%. The lower the EF is, the greater the reduction in systolic function. Diastolic function has been more difficult to evaluate. 2 Traditionally, invasive measures of LV diastolic pressure-volume relations and the rate of LV pressure fall during isovolumetric relaxation have been used. However, these methods are not practical for routine clinical use and do not adequately evaluate all aspects of diastolic filling. 3 Comprehensive echocardiographic evaluation of the dynamics of LV filling using blood pool and tissue Doppler has now progressed so that it provides clinically important information that can be used to direct patient care. We present data that support the use of echocardiographic evaluation of diastolic function to recognize cardiac dysfunction in patients with heart failure, especially those with preserved EF; to guide the management of patients by identifying those with and without elevated left filling pressures regardless of underlying EF; and to determine prognosis in a wide variety of patient populations. LV FillingAlthough the LV end-diastolic pressure-volume relation describes the passive properties of the LV, LV filling is not a passive or slow process. 3 In fact, the peak flow rate across the mitral valve is equal to or greater than the peak flow rate across the aortic valve. Understanding the physiological basis of LV filling provides the basis for the interpretation of the information available from a comprehensive echocardiographic evaluation of LV filling dynamics.During LV ejection, energy is stored as the myocytes are compressed and the elastic elements in the myocardial wall are compressed and twisted. 4 Relaxation of myocardial contraction allows this energy to be released as the elastic elements recoil. This causes LV pressure to fall rapidly during isovolumetric relaxation. Furthermore, for the first 30 to 40 milliseconds after mitral valve opening, relaxation of LV wall tension is normally rapid enough to cause the LV pressure to continue to decline despite an increase in LV volume. 5 This fall in LV pressure produces an early diastolic pressure gradient from the LA that extends to the LV apex (Figure 1). 6 This accelerates blood out of the LA andThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.

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Time constant of isovolumic pressure fall: new numerical approaches and significance

Cited by 33 publications

References 0 publications

Analysis of Isovolumic Relaxation in Failing Hearts by Monoexponential Time Constants Overestimates Lusitropic Change and Load Dependence

Analysis of Isovolumic Relaxation in Failing Hearts by Monoexponential Time Constants Overestimates Lusitropic Change and Load Dependence

Pulmonary vascular resistance and compliance relationship in pulmonary hypertension

Doppler Echocardiography Yields Dubious Estimates of Left Ventricular Diastolic Pressures

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