Energy conversion efficiency in human left ventricle.

Kameyama, Tomoki; Asanoi, Hidetsugu; Ishizaka, Shigeaki; Yamanishi, Kazuto; Fujita, Masatoshi; Sasayama, Shígetake

doi:10.1161/01.cir.85.3.988

Cited by 65 publications

(39 citation statements)

References 37 publications

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“…In contrast to the above, mechanical conversion efficiency remained unaltered between groups and was fairly consistent with investigations in healthy adults [34,35]. This indicates that, despite impaired PVA due to inefficient energetics, the transferral ratio from energy production to effective work is preserved.…”

Section: Myocardial Efficiencysupporting

confidence: 87%

Determinants of myocardial energetics and efficiency in symptomatic hypertrophic cardiomyopathy

Timmer

Germans

Götte

et al. 2010

Eur J Nucl Med Mol Imaging

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Purpose Next to hypertrophy, hypertrophic cardiomyopathy (HCM) is characterized by alterations in myocardial energetics. A small number of studies have shown that myocardial external efficiency (MEE), defined by external work (EW) in relation to myocardial oxidative metabolism (MVO 2 ), is reduced. The present study was conducted to identify determinants of MEE in patients with HCM by use of dynamic positron emission tomography (PET) and cardiovascular magnetic resonance imaging (CMR). Methods Twenty patients with HCM (12 men, mean age: 55.2 ± 13.9 years) and 11 healthy controls (7 men, mean age: 48.1 ± 10 years) were studied with [ 11 C]acetate PET to assess MVO 2 . CMR was performed to determine left ventricular (LV) volumes and mass (LVM). Univariate and multivariate analyses were employed to determine independent predictors of myocardial efficiency.Results Between study groups, MVO 2 (controls: 0.12 ± 0.04 ml·min −1 ·g −1 , HCM: 0.13 ± 0.05 ml·min −1 ·g −1 , p = 0.64) and EW (controls: 9,139 ± 2,484 mmHg·ml, HCM: 9,368 ± 2,907 mmHg·ml, p = 0.83) were comparable, whereas LVM was significantly higher (controls: 99 ± 21 g, HCM: 200 ± 76 g, p < 0.001) and MEE was decreased in HCM patients (controls: 35 ± 8%, HCM: 21 ± 10%, p < 0.001). MEE was related to stroke volume (SV), LV outflow tract gradient, NH 2 -terminal pro-brain natriuretic peptide (NT-proBNP) and serum free fatty acid levels (all p < 0.05). Multivariate analysis revealed that SV (ß = 0.74, p < 0.001) and LVM (ß = −0.43, p = 0.013) were independently related to MEE. Conclusion HCM is characterized by unaltered MVO 2 , impaired EW generation per gram of myocardial tissue and subsequent deteriorated myocardial efficiency. Mechanical external efficiency could independently be predicted by SV and LVM.

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Section: Myocardial Efficiencysupporting

confidence: 87%

Determinants of myocardial energetics and efficiency in symptomatic hypertrophic cardiomyopathy

Timmer

Germans

Götte

et al. 2010

Eur J Nucl Med Mol Imaging

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“…Therefore, the kinematic filling efficiency (KFEI) of early filling is higher than that of the whole cardiac cycle. Also, the total work efficiency of the whole cardiac cycle has been reported to be 69%, which is comparable in magnitude with the kinematic filling efficiency (Kameyama et al 1992).…”

Section: Discussionmentioning

confidence: 55%

“…A volume-based efficiency of around 50% is not physiologically unreasonable. As mentioned in Kameyama et al (Kameyama et al 1992), the mechanical efficiency during the cardiac cycle among normal subjects is about 22%. Therefore, the kinematic filling efficiency (KFEI) of early filling is higher than that of the whole cardiac cycle.…”

Section: Discussionmentioning

confidence: 77%

“…It is well-known that in certain dysfunctional hearts, the Doppler E-wave exhibits a 'delayed relaxation' pattern (Kameyama et al 1992,Riordan et al 2005. The concomitant alterations of chamber physiology, which generate this 'delayed relaxation' pattern, result in a reduction of the volume of blood aspirated by the left ventricle (LV) during early rapid filling.…”

Section: Introductionmentioning

confidence: 99%

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The Kinematic Filling Efficiency Index of the Left Ventricle: Contrasting Normal vs. Diabetic Physiology

Zhang

Chung

Riordan

et al. 2007

Ultrasound in Medicine & Biology

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An index of filling efficiency incorporating stiffness and relaxation (S&R) parameters has not been derived or validated although numerous studies have focused on the effects of altered relaxation or stiffness on early rapid filling and diastolic function. Previous studies show that S&R parameters can be obtained from early rapid filling (Doppler E-wave) via kinematic modeling. E-wave contours are governed by harmonic oscillatory motion, modeled via the parameterized diastolic filling (PDF) formalism. The previously validated model determines three (unique) oscillator parameters from each E-wave having established physiologic analogues: x o (load), c (relaxation/viscoelasticity), and k (chamber stiffness). We define the dimensionless, filling-volume based kinematic filling efficiency index (KFEI) as the ratio of the velocity-time integral (VTI) of the actual clinical E-wave contour fit via PDF to the VTI of the PDF model-predicted ideal E-wave contour having the same x o and k, but with no resistance to filling (c=0). To validate the new index, Doppler E-waves from 36 subjects with normal ventricular function, 17 diabetic and 19 well-matched non-diabetic controls, were analyzed. E-wave parameters x o , c, and k and KFEI were computed for each subject and compared. In concordance with prior human and animal studies in which c differentiated between normal and diabetic hearts, KFEI differentiated (p<0.001) between non-diabetics (55.8±3.3%) and diabetics (49.1±3.3%). Thus, the new index introduces and validates the concept of filling efficiency, and using diabetes as a working example, provides quantitative and mechanistic insight into how S&R affects ventricular filling efficiency.

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“…The finding of an increase in oxygen consumption per unit stress developed by hypertrophied myocardium has been reported in humans with pressure overload hypertrophy due to aortic valve disease. 28 In other studies of human hearts, 29 the relation between oxygen consumption and pressure-volume area was found to be relatively independent of inotropic state in hearts with normal to mildly impaired systolic function. On the other hand, a reduction in mechanical efficiency with ejection fractions <40% has been reported.…”

mentioning

confidence: 83%

Oxygen cost of stress development in hypertrophied and failing hearts from the spontaneously hypertensive rat.

Brooks¹,

Healey²,

Sen³

et al. 1993

Hypertension

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Left ventricular isovolumic stress development and metabolic parameters were studied in 18-24-monthold spontaneously hypertensive rats (SHRs) and age-matched Wistar-Kyoto (WKY) rat controls using the isolated, isovolumic (balloon in left ventricle) buffer-perfused rat heart preparation. After WKY rats and all SHRs were compared, SHRs were divided into two groups: those animals with (SHR-F) and without (SHR-NF) evidence of heart failure. Hearts were perfused at 100 mm Hg using a constant pressure system at a temperature of 37°C. In the baseline state, peak systolic pressure was greatest in the SHR-NF group and lowest in the SHR-F group. Peak midwall stress was greatest in the WKY group and, again, lowest in the SHR-F group. Oxygen consumption was lowest in the SHR-F group. When the oxygen cost of stress development was estimated by normalizing myocardial oxygen consumption by peak developed midwall stress, values were lowest in the WKY, greater in the SHR-NF, and greatest in the SHR-F group. Lactate production did not occur in the baseline state in any of the groups. Functional and metabolic responses to graded hypoxia, induced by changing the gas mixture of the perfusate from 95% to 50%, 25%, and 0% oxygen at perfusion pressures of 100 and 130 mm Hg, were studied. Increasing perfusion pressure generally resulted in small increases in peak systolic pressure and myocardial oxygen consumption but did not substantially reverse the contractile or metabolic deficit present in the SHR-F group. Graded hypoxia resulted in declines in peak midwall stress and myocardial oxygen consumption, and increases in lactate production in all groups; the oxygen cost of stress development continued to be greatest in the SHR-F group. Thus, peak systolic stress development is progressively impaired during the transition from hypertrophy to failure in the SHR. Although the oxygen cost of stress development appears to be increased in hypertrophied and to a greater degree in failing myocardium, the present isolated heart data provide no evidence to suggest that the baseline depression of isovolumic stress development in the SHR-F is due to hypoxia. (Hypertension 1993;21:56-64) KEY WORDS • hypertrophy • rats, inbred SHR • heart failure, congestive • oxygen consumption H ypertrophy represents an adaptive response of the myocardium to an increased work load. 12Studies of experimental pressure overload have largely examined relatively short-term models of compensated hypertrophy, in which mechanical or pharmacological interventions impose a relatively abrupt load on the heart (e.g., see References 3-5).There are relatively few studies of long-term stable hypertrophy, which then progresses to heart failure. The spontaneously hypertensive rat (SHR) provides a laboratory model of chronic hypertension.6 Hemodynamic studies in the SHR demonstrate a compensated state of

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Energy conversion efficiency in human left ventricle.

Cited by 65 publications

References 37 publications

Determinants of myocardial energetics and efficiency in symptomatic hypertrophic cardiomyopathy

Determinants of myocardial energetics and efficiency in symptomatic hypertrophic cardiomyopathy

The Kinematic Filling Efficiency Index of the Left Ventricle: Contrasting Normal vs. Diabetic Physiology

Oxygen cost of stress development in hypertrophied and failing hearts from the spontaneously hypertensive rat.

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