Reconsideration of normalization of Emax for heart size

Suga, Hiroyuki; Goto, Yoichi; Igarashi, Yuichi; Yasumura, Yoshio; Nozawa, Takashi

doi:10.1007/bf02059958

Cited by 17 publications

(2 citation statements)

References 20 publications

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“…Pressure-volume loops combined with variations of preload permit the assessment of the ESPVR, end-diastolic pressure-volume relationship, dead volume, and, in general, the varying elastance curves. Suga and colleagues have shown that the E(t) is fairly independent of loading conditions, contractile state, and HR (31). However, subsequent studies revealed limitations to this simplified theory, such as ESPVR curvilinearity, afterload dependence under certain conditions, and that V o may change during contraction (18,26,29).…”

Section: The Use Of Time-varying Elastance For Assessing Cardiac Funcmentioning

confidence: 99%

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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Section: The Use Of Time-varying Elastance For Assessing Cardiac Funcmentioning

confidence: 99%

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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“…Weber et al [13] observed that systolic stiffness increases with contractility, and they proposed end-systolic stiffness as a contractility index. Suga et al [14,15] proposed a similar index of systolic vigor which might be called hydraulic stiffness, calculated as the slope of the raw end-systolic pressure-volume relation (Era,x) multiplied by the dead space (Va). They remarked [14] that this index (EmaxWo) would not be valid if dead space were acutely variable or if dead space could be negative.…”

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confidence: 99%

Estimation of left-ventricular systolic performance and its determinants in man from pressures and dimensions of one beat: Effects of aortic valve stenosis and replacement

1990

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Within a thick heart-chamber wall, there is a midwall element or layer whose displacements best express systolic performance. The volume enclosed by that midwall element (Vm) and the average stress in that element (sigma m) can be calculated accurately by simple formulae. From simultaneous left-side pressure tracings and contrast cine-ventriculograms, Vm and sigma m were calculated at 20-ms intervals for an entire cardiac cycle in five normal subjects and in eight patients before and one year after replacement of stenotic aortic valves. Prior to surgery, the overloaded left ventricles were not hypertrophied enough to restore normal mid- and end-ejection stresses. Four had subnormal cavity ejection fractions, but all had subnormal midwall ejection fractions. All had subnormal fractional midwall ejection rates and prolonged active intervals (from the beginning of activation to the end of deactivation). Judging from pre-ejection pressure-development rates, the pressure-developing ability was not consistently elevated by concentric hypertrophy, because the stress-developing ability (contractility) was usually subnormal. The ability to shorten in the absence of afterload appeared to be subnormal in about half of the cases. The subnormal midwall ejection fractions appeared to be due to various combinations of increased mid- and late-ejection stresses, reduced contractility, and reduced shortening ability. On average and in several cases, reduced shortening ability appeared to be the main cause of the reduced performance. The effect of the slowed fractional midwall ejection rate to reduce the midwall ejection fraction was partially compensated by a prolonged active interval, by prolonged ejection time relative to the active interval, and by a more sustained ejection rate. Valve replacement partially restored all values except contractility towards normal, but the restorations of wall/cavity ratio and active interval were slight.

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The Measurement of Systolic Function in the Mammalian Heart

Carabello

Stem Cell Therapy and Tissue Engineering for Cardiovascular Repair

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Reconsideration of normalization of Emax for heart size

Cited by 17 publications

References 20 publications

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

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

Estimation of left-ventricular systolic performance and its determinants in man from pressures and dimensions of one beat: Effects of aortic valve stenosis and replacement

The Measurement of Systolic Function in the Mammalian Heart

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