Pressure-volume-based single-beat estimations cannot  predict left ventricular contractility in vivo

Kjørstad, Kjell E.; Korvald, Christian; Myrmel, Truls

doi:10.1152/ajpheart.00638.2001

Cited by 50 publications

(38 citation statements)

References 22 publications

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“…Notice that some curves corresponding to hypertrophy appear more enhanced than in the normal group as can be expected from Eqns (10)(11)(12).…”

Section: Areas Under the Espvrsupporting

confidence: 55%

“…Near end-systole, when the cardiac muscle reaches its maximum state of activation, the relation between the ventricular pressure P m and the ventricular volume V m is known as the end-systolic pressurevolume relation ESPVR. 1,[3][4][5][6][8][9][10][11][12][13][14][15][16][28][29][30][31] In the study of the linear approximation of the ESPVR special attention has been given to the way the slope E max of the ESPVR and the intercept V om of the ESPVR with the volume axis can be applied for the purpose of clinical diagnosis. One of the difficulties in applying the ESPVR in clinical diagnosis is the difficulty to calculate the parameters of the ESPVR in a non-invasive way from several PVR loops, and more recently attempts have been made to determine these parameters from single loop measurements (for a critical review, see Kjorstad, et al).…”

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confidence: 99%

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Ejection Fraction and ESPVR

Shoucri

2013

Int. Heart J.

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SummaryA formula derived by using large elastic deformation for the contraction of the myocardium is used to describe the pressure-volume relation (PVR) in the heart left ventricle, it is also used to calculate a mathematical expression for the non-linear end-systolic pressure-volume relation (ESPVR) in the left ventricle. An important feature of the mathematical formalism used is the inclusion of the isovolumic pressure P iso (equal active pressure generated by the myocardium) in the formalism describing the PVR. Relations between the ejection fraction (EF) and parameters describing the non-linear ESPVR are presented. It is shown that the non-linear ESPVR offers a rich collection of parameters that can be used to study the performance of the ventricles, like the areas under the ESPVR (units of energy) or the ordinates of the ESPVR (units of pressure), slopes and intercepts of the curves involved. The mathematical procedure can be easily implemented in a non-invasive way in routine clinical work when ratios of variables are calculated, it necessitates only the non-invasive measurement of the dimensions of the ventricles. Applications to clinical data published in the literature are presented, and they give results that show the consistency of the mathematical formalism used. The implications of the results of this research work on the study of the problem of heart failure with normal or preserved ejection fraction (HFpEF) are discussed. (Int Heart J 2013; 54: 318-327) Key words: Cardiac mechanics, Mathematical physiology of the heart, Pressure volume relation in ventricles, Active pressure of myocardium, Peak isovolumic pressure, End-systolic pressure-volume relation, Heart failure with preserved ejection fraction HFpEF T he study of the pressure-volume relation (PVR) in the left or right ventricle has been the object of intensive attention in the scientific literature. Near end-systole, when the cardiac muscle reaches its maximum state of activation, the relation between the ventricular pressure P m and the ventricular volume V m is known as the end-systolic pressurevolume relation ESPVR. 1,[3][4][5][6][8][9][10][11][12][13][14][15][16][28][29][30][31] In the study of the linear approximation of the ESPVR special attention has been given to the way the slope E max of the ESPVR and the intercept V om of the ESPVR with the volume axis can be applied for the purpose of clinical diagnosis. One of the difficulties in applying the ESPVR in clinical diagnosis is the difficulty to calculate the parameters of the ESPVR in a non-invasive way from several PVR loops, and more recently attempts have been made to determine these parameters from single loop measurements (for a critical review, see Kjorstad, et al). 11)The introduction of the active pressure generated by the myocardium on its inner surface (endocardium) (also called isovolumic pressure P iso by physiologists) in the formalism describing the PVR or the ESPVR in the ventricles has been the main idea of a series of studies published by the author. [17][18][19]...

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“…Notice that some curves corresponding to hypertrophy appear more enhanced than in the normal group as can be expected from Eqns (10)(11)(12).…”

Section: Areas Under the Espvrsupporting

confidence: 55%

mentioning

confidence: 99%

Ejection Fraction and ESPVR

Shoucri

2013

Int. Heart J.

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“…However, their study did not include patients with aortic stenosis. Moreover, their results are also in disagreement with those recently published by Kjørstad et al (15), where a considerable variability of the normalized elastance was observed among the patients. Further studies in a larger number of patients with aortic stenosis are thus needed to assess the interindividual variability of normalized elastance in these patients.…”

Section: ϫ3contrasting

confidence: 92%

A ventricular-vascular coupling model in presence of aortic stenosis

Garcia¹,

Barenbrug²,

Pîbarot³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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In patients with aortic stenosis, the left ventricular afterload is determined by the degree of valvular obstruction and the systemic arterial system. We developed an explicit mathematical model formulated with a limited number of independent parameters that describes the interaction among the left ventricle, an aortic stenosis, and the arterial system. This ventricularvalvular-vascular (V 3 ) model consists of the combination of the time-varying elastance model for the left ventricle, the instantaneous transvalvular pressure-flow relationship for the aortic valve, and the three-element windkessel representation of the vascular system. The objective of this study was to validate the V 3 model by using pressure-volume loop data obtained in six patients with severe aortic stenosis before and after aortic valve replacement. There was very good agreement between the estimated and the measured left ventricular and aortic pressure waveforms. The total relative error between estimated and measured pressures was on average (standard deviation) 7.5% (SD 2.3) and the equation of the corresponding regression line was y ϭ 0.99x Ϫ 2.36 with a coefficient of determination r 2 ϭ 0.98. There was also very good agreement between estimated and measured stroke volumes (y ϭ 1.03x ϩ 2.2, r 2 ϭ 0.96, SEE ϭ 2.8 ml). Hence, this mathematical V 3 model can be used to describe the hemodynamic interaction among the left ventricle, the aortic valve, and the systemic arterial system. mathematical modeling; cardiovascular system; cardiac catheterization; left ventricle LEFT VENTRICULAR (LV) pressure, aortic pressure, and cardiac output result from a matching among the oxygen demand of the body, the LV performance, and the LV afterload. The presence of an aortic valve stenosis causes an obstruction to LV outflow, thus resulting in an increase in LV afterload (20). Patients with aortic stenosis also often have concomitant diseases, including hypertension, hyperlipidemia, diabetes, and atherosclerosis (1,6,22,25). These diseases have been shown to alter the structural and functional properties of the systemic arterial system (8,40). More specifically, they may reduce arterial elasticity and/or increase arteriolar resistance. Hence in patients with aortic stenosis, the left ventricle is often facing a double load: a valvular load imposed by the aortic stenosis and an arterial load caused by a decrease in systemic arterial compliance (C) and/or an increase in systemic vascular resistance (R). Briand et al. (3) have recently shown that reduced C is a frequent occurrence in patients with aortic stenosis where it independently contributes to increase afterload and decrease LV function. In addition, Antonini-Canterin et al. (1) have reported that symptoms of aortic stenosis develop at a lesser degree of valvular obstruction in hypertensive compared with normotensive patients. It is thus important to assess the respective contributions of the aortic valve and the systemic arterial system to the LV workload in such patients. This information could be ...

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“…Shisido et al (29) found that this ratio was significantly attenuated during reduced contractility and vasoconstriction but augmented during vasodilatation. Kjorstad et al (16) showed significant differences in ␤ values between controls Fig. 4.…”

Section: Uniqueness Of the Normalized Time-varying Elastance Curvementioning

confidence: 91%

“…*Significantly different from CTRL (P Ͻ 0.05). (16). When scrutinizing the results of Senzaki et al, one reveals large differences (standard deviations) on the E n (t n ), especially during the ejection and diastolic phases in the presence of aneurysms, dilated cardiomyopathy, and coronary artery disease with conserved LV function (28).…”

Section: Uniqueness Of the Normalized Time-varying Elastance Curvementioning

confidence: 98%

The effect of a myocardial infarction on the normalized time-varying elastance curve

Jochheim¹,

Mallik²,

Nasratullah³

et al. 2007

Journal of Applied Physiology

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Jegger D, Mallik AS, Nasratullah M, Jeanrenaud X, da Silva R, Tevaearai H, von Segesser LK, Stergiopulos N. The effect of a myocardial infarction on the normalized time-varying elastance curve. J Appl Physiol 102: [1123][1124][1125][1126][1127][1128][1129] 2007. First published December 7, 2006; doi:10.1152/japplphysiol.00976.2006.-It has been suggested that the shape of the normalized time-varying elastance curve [E n (t n )] is conserved in different cardiac pathologies. We hypothesize, however, that the E n (t n ) differs quantitatively after myocardial infarction (MI). Sprague-Dawley rats (n ϭ 9) were anesthetized, and the left anterior descending coronary artery was ligated to provoke the MI. A sham-operated control group (CTRL) (n ϭ 10) was treated without the MI. Two months later, a conductance catheter was inserted into the left ventricle (LV). The LV pressure and volume were measured and the E n (t n ) derived. Slopes of E n (t n ) during the preejection period (␣PEP), ejection period (␣EP), and their ratio (␤ ϭ ␣EP/␣PEP) were calculated, together with the characteristic decay time during isovolumic relaxation () and the normalized elastance at end diastole (E min n ). MI provoked significant LV chamber dilatation, thus a loss in cardiac output (Ϫ33%), ejection fraction (Ϫ40%), and stroke volume (Ϫ30%) (P Ͻ 0.05). Also, it caused significant calcium increase (17-fold), fibrosis (2-fold), and LV hypertrophy. End-systolic elastance dropped from 0.66 Ϯ 0.31 mmHg/l (CTRL) to 0.34 Ϯ 0.11 mmHg/l (MI) (P Ͻ 0.05). Normalized elastance was significantly reduced in the MI group during the preejection, ejection, and diastolic periods (P Ͻ 0.05). The slope of E n (t n ) during the ␣PEP and ␤ were significantly altered after MI (P Ͻ 0.05). Furthermore, and end-diastolic E min n were both significantly augmented in the MI group. We conclude that the E n (t n ) differs quantitatively in all phases of the heart cycle, between normal and hearts post-MI. This should be considered when utilizing the single-beat concept.compliance; ischemia; contractility; ventricular function; hemodynamics; conductance volumetry THE END-SYSTOLIC PRESSURE-VOLUME RELATION (ESPVR) provides a useful measure of contractile function of the heart in health and disease (23,30). At the basis of the ESPVR stands the time-varying elastance [E(t)] concept, whereby the E(t) gives a time-domain description of the heart pump function (30). The shape of the normalized time-varying elastance curve [E n (t n )] has been shown to be similar in different animal species (10). It has been reported that, when E(t) is normalized with respect to peak value and peak time, the shape (wave form) of the E n (t n ) is independent of different cardiac pathologies, afterload, preload, and contractility (28). The single-beat estimation method of ESPVR was proposed, based on the assumption that human E n (t n ) were indeed identical under various physiopathological conditions (28). However, to date, detailed quantification of the difference in E n (t n ) between healthy ...

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Pressure-volume-based single-beat estimations cannot predict left ventricular contractility in vivo

Cited by 50 publications

References 22 publications

Ejection Fraction and ESPVR

Ejection Fraction and ESPVR

A ventricular-vascular coupling model in presence of aortic stenosis

The effect of a myocardial infarction on the normalized time-varying elastance curve

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