Half-logistic time constant: a more reliable lusitropic index than monoexponential time constant regardless of temperature in canine left ventricle

2008 ◽  
Vol 86 (3) ◽  
pp. 78-87 ◽  
Author(s):  
Ju Mizuno ◽  
Hiromi Matsubara ◽  
Satoshi Mohri ◽  
Juichiro Shimizu ◽  
Shunsuke Suzuki ◽  
...  
Keyword(s):  
Time Constant ◽  
Time Course ◽  
Least Squares Method ◽  
Diastolic Pressure ◽  
Time Derivative ◽  
Left Ventricular ◽  
Monoexponential Model ◽  
Increasing Temperature ◽  
T Tau ◽  
Pressure Fall

Temperature changes influence cardiac diastolic function. The monoexponential time constant (tauE), which is a conventional lusitropic index of the rate of left ventricular (LV) pressure fall, increases with cooling and decreases with warming. We have proposed that a half-logistic time constant (tauL) is a better lusitropic index than tauE at normothermia. In the present study, we investigated whether tauL can remain a superior measure as temperature varies. The isovolumic relaxation LV pressure curves from the minimum of the first time derivative of LV pressure (dP/dtmin) to the LV end-diastolic pressure were analyzed at 30, 33, 36, 38, and 40 °C in excised, cross-circulated canine hearts. tauL and tauE were evaluated by curve-fitting using the least squares method and applying the half-logistic equation, P(t) = PA/[1 + exp(t/tauL)] + PB, and the monoexponential equation, P(t) = P0exp(–t/tauE) + P∞. Both tauL and tauE increased significantly with decreasing temperature and decreased with increasing temperature. The half-logistic correlation coefficient (r) values were significantly higher than the monoexponential r values at the 5 above-mentioned temperatures. This implies that the superiority of the goodness of the half-logistic fit is not temperature dependent. The half-logistic model characterizes the amplitude and time course of LV pressure fall more reliably than the monoexponential model. Hence, we concluded that tauL is a more useful lusitropic index regardless of temperature.

Relaxation time constant of isolated rabbit left ventricle

1987 ◽  
Vol 253 (3) ◽  
pp. H512-H518
Author(s):  
P. Schiereck ◽  
J. H. Nieuwenhuijs ◽  
E. L. de Beer ◽  
M. W. van Hessen ◽  
F. A. van Kaam ◽  
...  
Keyword(s):  
Time Constant ◽  
Diastolic Pressure ◽  
Time Derivative ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Relaxation Time Constant ◽  
Contraction Phase ◽  
End Diastolic Volume ◽  
The Difference ◽  
First Time

Experiments were performed on isolated rabbit left ventricles. Controlled ejections during otherwise isovolumic contractions were studied. The time constant of relaxation was defined as the slope of the linear approximation of the ln(P)-t relation over a 40-ms period starting 20 ms after the minimum of the first time derivative of left ventricular pressure (dP/dt) of the isovolumic contraction. Variations in time of ejection, its amplitude, and velocity are applied independently. No direct effect of the variations in time and velocity of the ejection on the time constant of relaxation was found. This is in conflict with the findings of Hori et al. (Circ. Res. 55: 31-38, 1984). The difference is due to the influence of the recovery of pressure directly after the end of ejection in their study. This effect is present especially when ejection was timed to take place late in the contraction phase. The effect of the variation of the amplitude of the ejection on the time constant was similar to the effect of the end-diastolic pressure on the end-diastolic volume. It is concluded that the time constant of relaxation depends linearly on the same processes that are responsible for the height of the end-diastolic pressure.

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

1984 ◽  
Vol 247 (2) ◽  
pp. H283-H294 ◽  
Author(s):  
G. Martin ◽  
J. V. Gimeno ◽  
J. Cosin ◽  
M. I. Guillem
Keyword(s):  
Relaxation Rate ◽  
Time Constant ◽  
Diastolic Pressure ◽  
Left Ventricular Pressure ◽  
Exponential Model ◽  
Left Ventricular ◽  
Beta Agonist ◽  
Base Line ◽  
Autonomic Blockade ◽  
Pressure Fall

The effects of left ventricular diastolic pressure changes on the values of the time constant (T) of isovolumic pressure fall are controversial. Normally, T is calculated either by linear regression of 1n left ventricular pressure (LVP) vs. time (TL) or by using an exponential model with asymptote (PB, extrapolated base-line pressure to which LVP would fall if decay continued indefinitely). This study, in intact dogs, has been designed to revise the effects that drugs that alter load (angiotensin and nitroprusside, without and with autonomic blockade) and inotropism (isoproterenol and propranolol) might have on the relaxation rate using different numerical methods. We found that 1) the upward or downward translation of the LVP curve had an important effect on the value of TL calculated by the semilogarithmic method; 2) when a model with asymptote was used, the simultaneous changes of T and PB, were not related to the dose of the drug; 3) the values of TL and the -dP/dt values extrapolated to 15 mmHg from a model with PB, were much more sensitive to beta-agonist or antagonist drugs than to others whose action was through load alteration. We feel that some of the earlier studies on relaxation rate determinants should be revised as possibly some of the conclusions have been based on artifacts introduced by the method chosen for the computation of the relaxation parameters.

Dynamic changes in conduction velocity and gap junction properties during development of pacing-induced heart failure

2007 ◽  
Vol 293 (2) ◽  
pp. H1223-H1230 ◽  
Author(s):  
Fadi G. Akar ◽  
Robert D. Nass ◽  
Samuel Hahn ◽  
Eugenio Cingolani ◽  
Manish Shah ◽  
...  
Keyword(s):  
Heart Failure ◽  
Conduction Velocity ◽  
Connexin 43 ◽  
Time Course ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Early Event ◽  
Mechanical Function ◽  
Dynamic Changes ◽  
End Stage

End-stage heart failure (HF) is characterized by changes in conduction velocity (CV) that predispose to arrhythmias. Here, we investigate the time course of conduction changes with respect to alterations in connexin 43 (Cx43) properties and mechanical function during the development of HF. We perform high-resolution optical mapping in arterially perfused myocardial preparations from dogs subjected to 0, 3, 7, 14, and 21 days of rapid pacing to produce variable degrees of remodeling. CV is compared with an index of mechanical function [left ventricular end-diastolic pressure (LVEDP)] and with dynamic changes in the expression, distribution, and phosphorylation of Cx43. In contrast to repolarization, CV was preserved during early stages of remodeling (3 and 7 days) and significantly reduced at later stages, which were associated with marked increases in LVEDP. Measurements of differentially phosphorylated Cx43 isoforms revealed early, sustained downregulation of pan-Cx43 that preceded changes in CV and LVEDP, a gradual rise in a dephosphorylated Cx43 isoform to over twofold baseline levels in end-stage HF, and a late abrupt increase in pan-Cx43, but not dephosphorylated Cx43, lateralization. These data demonstrate that 1) CV slowing occurs only at advanced stages of remodeling, 2) total reduction of pan-Cx43 is an early event that precedes mechanical dysfunction and CV slowing, 3) changes in Cx43 phosphorylation are more closely associated with the onset of HF, and 4) Cx43 lateralization is a late event that coincides with marked CV reduction. These data reveal a novel paradigm of remodeling based on the timing of conduction abnormalities relative to changes in Cx43 isoforms and mechanical dysfunction.

scholarly journals Mechanics of intraventricular filling: study of LV early diastolic pressure gradients and flow velocities

1998 ◽  
Vol 275 (3) ◽  
pp. H1062-H1069 ◽  
Author(s):  
Otto A. Smiseth ◽  
Kjetil Steine ◽  
Gunnar Sandbæk ◽  
Marie Stugaard ◽  
Tor Ø. Gjølberg
Keyword(s):  
Pressure Gradient ◽  
Diastolic Pressure ◽  
Time Derivative ◽  
Left Ventricular ◽  
Outflow Tract ◽  
Transmitral Flow ◽  
Intraventricular Flow ◽  
Artery Disease ◽  
Lv Volume ◽  
Flow Velocities

This study investigates mechanisms of left ventricular (LV) intracavitary flow during early, rapid filling. In eight coronary artery disease patients with normal LV ejection fraction we recorded simultaneous LV apical and outflow tract pressures and intraventricular flow velocities by color M-mode Doppler echocardiography. In five anesthetized dogs we also recorded left atrial pressure and LV volume by sonomicrometry. In patients, as the early diastolic mitral-to-apical filling wave arrived at the apex, we observed an apex-outflow tract pressure gradient of 3.5 ± 0.3 mmHg (mean ± SE). This pressure gradient correlated with peak early apex-to-outflow tract flow velocity ( r = 0.75, P < 0.05). The gradient was reproduced in the dog model and decreased from 3.1 ± 0.3 to 1.7 ± 0.5 mmHg ( P < 0.05) with caval constriction and increased to 4.2 ± 0.5 mmHg ( P < 0.001) with volume loading. The pressure gradient correlated with peak early transmitral flow (expressed as time derivative of LV volume; r = 0.95) and stroke volume ( r = 0.97). In conclusion, arrival of the early LV filling wave at the apex was associated with a substantial pressure gradient between apex and outflow tract. The pressure gradient was sensitive to changes in preload and correlated strongly with peak early transmitral flow. The significance of this gradient for intraventricular flow propagation in the normal and the diseased heart remains to be determined.

Asynchrony and ryanodine modulate load-dependent relaxation in the canine left ventricle

1995 ◽  
Vol 268 (1) ◽  
pp. H17-H24 ◽  
Author(s):  
W. Y. Lew
Keyword(s):  
Left Ventricle ◽  
Time Constant ◽  
Cardiac Cycle ◽  
Left Ventricular ◽  
Pressure Load ◽  
Single Cardiac Cycle ◽  
Anesthetized Dogs ◽  
Pressure Fall

Load-dependent relaxation was studied in six anesthetized dogs by inflating an intra-aortic balloon to increase peak left ventricular (LV) pressure by 1–20 mmHg within a single cardiac cycle. A series of timed and graded pressure loads was produced by inflating the balloon either during diastole (early loads) or midsystole (midsystolic pressure loads). The rate of LV pressure fall was measured with the time constant (tau). There was a significant increase in tau with 63 midsystolic pressure load [tau increased 1.4 +/- 0.1% (SE)/mmHg increase in peak LV pressure] but not with 67 early pressure loads (-0.5 +/- 0.1%/mmHg). This difference remained with LV pacing-induced asynchrony (tau increased 1.8 +/- 0.1%/mmHg with 54 midsystolic pressure loads compared with -0.2 +/- 0.1%/mmHg with 56 early pressure loads) and after 5 micrograms/kg of intravenous ryanodine (tau increased 1.0 +/- 0.2%/mmHg with 58 midsystolic pressure loads compared with -0.7 +/- 0.1%/mmHg with 59 early pressure loads). When compared with control, asynchrony significantly augmented and ryanodine significantly attenuated the effects of midsystolic pressure loads. In conclusion, asynchrony and ryanodine modulate the extent of load-dependent relaxation in the intact left ventricle.

Temporal sequence of endotoxin-induced systolic and diastolic myocardial depression in rabbits

1993 ◽  
Vol 265 (3) ◽  
pp. H810-H819 ◽  
Author(s):  
J. Hung ◽  
W. Y. Lew
Keyword(s):  
Time Course ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Progressive Increase ◽  
Left Ventricular ◽  
Temporal Sequence ◽  
Lv Function ◽  
Myocardial Depression ◽  
Systolic Volume ◽  
End Systolic Volume

Twelve anesthetized rabbits received endotoxin (175 +/- 38 micrograms/kg i.v., mean +/- SD) to evaluate the temporal sequence of alterations in left ventricular (LV) function. LV volume was calculated from LV minor- and long-axis diameters, and wall thickness was measured with sonomicrometers. Hypotension, acidosis, and hypoxia were immediately corrected to eliminate these causes of myocardial depression. LV dilation developed early (1.2 +/- 0.5 h) with a significant (21 +/- 23%) increase in end-diastolic volume measured at a LV end-diastolic pressure of 5 +/- 6 mmHg. The LV stiffness did not change, and the LV dilation did not progressively worsen. Significant systolic depression developed later (2.8 +/- 1.0 h) with a 32 +/- 22% increase in end-systolic volume measured at a LV end-systolic pressure of 69 +/- 9 mmHg. The late preterminal phase (4.1 +/- 0.8 h) was characterized by a progressive increase in end-systolic volume (73 +/- 41% above control) and a significant (53 +/- 34%) increase in tau, the time constant of LV pressure fall. Diastolic abnormalities (LV dilation and increased tau) were not attributable to depressed contractility or altered hemodynamics. We conclude that endotoxin impairs systolic and diastolic LV function with distinct differences in time course. This suggests that contractility, relaxation, and passive LV properties are impaired by different endotoxin-mediated pathways and/or have different sensitivities to endotoxin.

Mechanism of elevated left ventricular end-diastolic pressure after ischemic arrest and reperfusion

1981 ◽  
Vol 240 (2) ◽  
pp. H300-H307 ◽  
Author(s):  
H. V. Schaff ◽  
V. L. Gott ◽  
R. A. Goldman ◽  
J. W. Frederiksen ◽  
J. T. Flaherty
Keyword(s):  
Time Constant ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Muscle Stiffness ◽  
Ventricular Relaxation ◽  
Ischemic Period ◽  
Pressure Volume Relationship ◽  
Heart Preparation ◽  
Developed Pressure ◽  
Contractile Performance

The effects of ischemic arrest and reperfusion on isovolumic end-diastolic pressure, diastolic pressure-volume curves, and indices of ventricular relaxation and contractility were studied in an isolated feline heart preparation. In hearts subjected to 60 min of normothermic (37 degrees C) ischemic arrest, isovolumic developed pressure, and dP/dtmax during reperfusion returned to only approximately 60% of prearrest control levels. Isovolumic end-diastolic pressure (Ped) increased 37.0 +/- 4.3 mmHg and the time constant of ventricular relaxation was prolonged. Hearts maintained at 27 degrees C hypothermia during the 60-min ischemic period demonstrated improved contractile performance (approximately 100% of control), less elevation of Ped (21.4 +/- 4.5 mmHg), and no significant increase in the time constant of relaxation. In both groups of hearts, postarrest end-diastolic pressure-volume curves were shifted up and to the left, whereas indices of ventricular stiffness and muscle stiffness remained unchanged. These data suggest that the rise in isovolumic end-diastolic pressure observed after 1 h of ischemic arrest and reperfusion is the result of an upward and to the left shift of the entire diastolic pressure-volume relationship of the left ventricle. This shift does not appear to be related to diminished contractile performance or incomplete relaxation. Furthermore, the shift is not due to a change in muscle compliance, but to a reduction in the unstressed volume of the ventricle, which most likely results from myocardial contracture and edema.

Effect of PDE5 inhibition on coronary hemodynamics in pacing-induced heart failure

2003 ◽  
Vol 284 (5) ◽  
pp. H1513-H1520 ◽  
Author(s):  
YingJie Chen ◽  
Jay H. Traverse ◽  
Mingxiao Hou ◽  
Yunfang Li ◽  
Ruisheng Du ◽  
...  
Keyword(s):  
Heart Failure ◽  
Diastolic Pressure ◽  
Time Derivative ◽  
Systolic Pressure ◽  
Coronary Vessels ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Pde5 Inhibition ◽  
Rapid Ventricular Pacing ◽  
Phosphodiesterase Type

Inhibition of phosphodiesterase type 5 (PDE5) can relax systemic and coronary vessels by causing accumulation of cGMP. Both the endothelial dysfunction with decreased nitric oxide production and increased natriuretic peptide levels in congestive heart failure (CHF) have the potential to alter cGMP production, thereby influencing the response to PDE5 inhibition. Consequently, this study examined the effects of PDE5 inhibition with sildenafil in dogs with CHF produced by rapid ventricular pacing. CHF resulted in decreases of left ventricular (LV) systolic pressure, coronary blood flow, and the maximal first time derivative of LV pressure (LV dP/d t max) at rest and during treadmill exercise compared with normal, whereas resting LV end-diastolic pressure increased from 10 ± 1.4 to 23 ± 1.4 mmHg. Sildenafil (2 and 10 mg/kg per os) caused a 5- to 6-mmHg decrease of aortic pressure ( P < 0.05), with no change of heart rate, LV systolic pressure, or LV dP/d t max. Sildenafil caused no change in coronary flow or myocardial oxygen consumption in animals with CHF at rest or during exercise. In contrast to findings in normal animals, sildenafil did not augment endothelium-dependent coronary vasodilation in response to acetylcholine in animals with CHF. Furthermore, Western blotting showed decreased PDE5 protein expression in myocardium from failing hearts. These findings demonstrate that PDE5 contributes little to regulation of coronary hemodynamics in CHF.

Impact of mitral regurgitation on left ventricular anatomic and molecular remodeling and systolic function: implication for outcome

2009 ◽  
Vol 296 (6) ◽  
pp. H1727-H1732 ◽  
Author(s):  
Min Pu ◽  
Zhaohui Gao ◽  
Xueqian Zhang ◽  
Duanping Liao ◽  
Daniel K. Pu ◽  
...  
Keyword(s):  
Mitral Regurgitation ◽  
Time Course ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Sham Operation ◽  
Proportional Hazard ◽  
Long Term Outcome ◽  
Lv Remodeling ◽  
And Function ◽  
The Impact

The aim of the study was to assess the impact of mitral regurgitation (MR) on left ventricular (LV) anatomic and molecular remodeling and function and to determine whether early LV remodeling and function predict long-term outcome in experimental organic MR. A new rodent model of chronic MR was created. Twenty-eight rats had surgically induced MR, twelve rats had a sham operation, and twelve rats had no operation. LV diameters, volume, and mass and LV ejection fraction (LVEF) and LV fractional shortening (LVFS) were assessed using echocardiography in the early stage of MR (6 and 12 wk after induction of MR). LV hemodynamics was assessed invasively. Cardiac α- and β-myosin heavy chains and sarco(endo)plasmic reticulum Ca2+-ATPase 2 (SERCA2) were measured to assess molecular remodeling and contractility. Cox's proportional hazard ratios (HR) were used to identify outcome predictors. Early LV dilation was demonstrated in rats with MR when LVEF and LVFS were still normal. LV remodeling was associated with an increase in LV end-diastolic pressure and decrease in maximal change in pressure over time. Shifting of α- to β-myosin and reduced SERCA2 were observed in rats with MR. Cox's proportional hazard analysis showed that LV end-diastolic diameters (HR, 1.2–2.4; P = 0.007) and LV end-diastolic volume (HR, 1.1–1.4; P = 0.005) at 6 wk and LV mass index (HR, 1.1–2.0; P = 0.004) at 12 wk after induction of MR were significantly associated with 1-yr mortality. However, LVEF (HR, 0.7–6.8 for the 6 wk, P > 0.05; and HR, 0.4–3.2 for the 12 wk, P > 0.05) and LVFS (HR, 0.4–1.4 for the 6 wk; and 0.4–3.1 for the 12 wk, P > 0.05) did not predict late death. Chronic MR leads to LV anatomic and cellular remodeling and impaired contractility. The time course of LV remodeling and function changes in the rat model of MR is similar to humans. Prediction of outcome may be achieved by assessments of early LV remodeling.

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