Myocardial Energetics and Efficiency
2007; Lippincott Williams & Wilkins; Volume: 115; Issue: 7 Linguagem: Inglês
10.1161/circulationaha.106.660639
ISSN1524-4539
AutoresPaul Knaapen, Tjeerd Germans, Juhani Knuuti, Walter J. Paulus, Pieter A. Dijkmans, Cornelis P. Allaart, Adriaan A. Lammertsma, Frans C. Visser,
Tópico(s)Cardiac pacing and defibrillation studies
ResumoHomeCirculationVol. 115, No. 7Myocardial Energetics and Efficiency Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBMyocardial Energetics and EfficiencyCurrent Status of the Noninvasive Approach Paul Knaapen, MD, PhD, Tjeerd Germans, MD, Juhani Knuuti, MD, PhD, Walter J. Paulus, MD, PhD, Pieter A. Dijkmans, MD, Cornelis P. Allaart, MD, PhD, Adriaan A. Lammertsma, PhD and Frans C. Visser, MD, PhD Paul KnaapenPaul Knaapen From the Department of Cardiology (P.K., T.G., P.A.D., C.P.A., F.C.V.), the Laboratory of Physiology (W.J.P.), and the Department of Nuclear Medicine & PET Research (A.A.L.), VU University Medical Center, Institute for Cardiovascular Research, Amsterdam, The Netherlands, and the Turku PET Center (J.K.), University of Turku, Turku, Finland. , Tjeerd GermansTjeerd Germans From the Department of Cardiology (P.K., T.G., P.A.D., C.P.A., F.C.V.), the Laboratory of Physiology (W.J.P.), and the Department of Nuclear Medicine & PET Research (A.A.L.), VU University Medical Center, Institute for Cardiovascular Research, Amsterdam, The Netherlands, and the Turku PET Center (J.K.), University of Turku, Turku, Finland. , Juhani KnuutiJuhani Knuuti From the Department of Cardiology (P.K., T.G., P.A.D., C.P.A., F.C.V.), the Laboratory of Physiology (W.J.P.), and the Department of Nuclear Medicine & PET Research (A.A.L.), VU University Medical Center, Institute for Cardiovascular Research, Amsterdam, The Netherlands, and the Turku PET Center (J.K.), University of Turku, Turku, Finland. , Walter J. PaulusWalter J. Paulus From the Department of Cardiology (P.K., T.G., P.A.D., C.P.A., F.C.V.), the Laboratory of Physiology (W.J.P.), and the Department of Nuclear Medicine & PET Research (A.A.L.), VU University Medical Center, Institute for Cardiovascular Research, Amsterdam, The Netherlands, and the Turku PET Center (J.K.), University of Turku, Turku, Finland. , Pieter A. DijkmansPieter A. Dijkmans From the Department of Cardiology (P.K., T.G., P.A.D., C.P.A., F.C.V.), the Laboratory of Physiology (W.J.P.), and the Department of Nuclear Medicine & PET Research (A.A.L.), VU University Medical Center, Institute for Cardiovascular Research, Amsterdam, The Netherlands, and the Turku PET Center (J.K.), University of Turku, Turku, Finland. , Cornelis P. AllaartCornelis P. Allaart From the Department of Cardiology (P.K., T.G., P.A.D., C.P.A., F.C.V.), the Laboratory of Physiology (W.J.P.), and the Department of Nuclear Medicine & PET Research (A.A.L.), VU University Medical Center, Institute for Cardiovascular Research, Amsterdam, The Netherlands, and the Turku PET Center (J.K.), University of Turku, Turku, Finland. , Adriaan A. LammertsmaAdriaan A. Lammertsma From the Department of Cardiology (P.K., T.G., P.A.D., C.P.A., F.C.V.), the Laboratory of Physiology (W.J.P.), and the Department of Nuclear Medicine & PET Research (A.A.L.), VU University Medical Center, Institute for Cardiovascular Research, Amsterdam, The Netherlands, and the Turku PET Center (J.K.), University of Turku, Turku, Finland. and Frans C. VisserFrans C. Visser From the Department of Cardiology (P.K., T.G., P.A.D., C.P.A., F.C.V.), the Laboratory of Physiology (W.J.P.), and the Department of Nuclear Medicine & PET Research (A.A.L.), VU University Medical Center, Institute for Cardiovascular Research, Amsterdam, The Netherlands, and the Turku PET Center (J.K.), University of Turku, Turku, Finland. Originally published20 Feb 2007https://doi.org/10.1161/CIRCULATIONAHA.106.660639Circulation. 2007;115:918–927The heart is an aerobic organ that relies almost exclusively on the aerobic oxidation of substrates for generation of energy. Consequently, there is close coupling between myocardial oxygen consumption (MV̇o2) and the main determinants of systolic function: heart rate, contractile state, and wall stress.1 As in any mechanical pump, only part of the energy invested is converted to external power. In the case of the heart, the ratio of useful energy produced (ie, stroke work [SW]) to oxygen consumed is defined as mechanical efficiency, as originally proposed by Bing et al.2 Under normal conditions this ratio is ≈25%, and the residual energy mainly dissipates as heat.3 In pathophysiological disease states, such as heart failure, mechanical efficiency is reduced, and it has been hypothesized that the increased energy expenditure relative to work contributes to progression of the disease.4,5 Moreover, therapeutic interventions that enhance mechanical efficiency have proven to be beneficial with respect to outcome.6 It is therefore desirable to quantify efficiency of the heart to study disease processes and monitor interventions.Both cardiac oxidative metabolism and mechanical work, and thus efficiency, can be quantified through invasive measurements. Although these measurements are accurate and currently considered the gold standard, in clinical practice they are limited because of the need for dual-sided heart catheterization and selective catheterization of the coronary sinus. Recent advances in imaging techniques, however, offer the possibility to noninvasively estimate MV̇o2 and mechanical work by positron emission tomography and echocardiography or by magnetic resonance imaging, respectively.This review discusses the principles of mechanical efficiency, together with its invasive and noninvasive assessment, as well as their strengths and pitfalls. Finally, results from clinical pathophysiological studies are discussed.Invasive Measurement of Mechanical EfficiencyTo calculate the efficiency of the heart, input and output energy must be obtained. The first can be derived from MV̇o2 (mL O2 · min−1) measurements according to the Fick-principle by multiplying coronary sinus blood flow (mL · min−1) by the arteriovenous oxygen content difference.7 Blood flow can be estimated with the use of thermodilution or Doppler (electromagnetic flowmeter) methods after accessing the coronary sinus through right-sided heart catheterization. As oxygen dissolved in blood is negligible and hemoglobin concentrations in arterial and venous blood are similar, arteriovenous oxygen content difference can be obtained by determination of the differences in oxygen saturation levels between arterial and coronary sinus blood. This method to determine oxygen utilization is currently considered the gold standard, although it should be noted that it is limited by its invasive nature, susceptibility to sampling errors, and the fact that only global MV̇o2 can be assessed, which also includes oxidative metabolism of the right ventricle and both atria. Furthermore, thebesian left ventricular (LV) flow (≈1% to 2% of total coronary flow) is unaccounted for, and an additional noninvasive estimate of LV mass is required to calculate oxidative metabolism per gram of tissue.Output energy is defined as force · displacement and is expressed in joules (J). Energy generated by the heart can be divided into actual produced energy (ie, external work [EW] or SW) and potential energy.3 These parameters can best be estimated by generation of a pressure–volume (PV) loop of the cardiac cycle by use a conductance catheter placed in the left ventricle (Figure 1A). EW is defined by the area contained within the PV-loop. Potential energy can subsequently be estimated when a family of PV loops is acquired during different loading conditions, eg, by transient vena cava occlusion (Figure 1B). Connection of the end-systolic and end-diastolic points in the PV loops gives the end-systolic and end-diastolic PV relations, respectively. The slopes of these relations in turn function as indices of LV contractility and stiffness, respectively (Figure 1C). The area under the curve on the left side of EW and confined by the slopes of the end-systolic pressure–volume relation and the end-diastolic pressure–volume relation represents potential energy. The total pressure–volume area (PVA) (ie, the sum of EW and potential energy) equals total mechanical energy generated by the heart per beat.3Download figureDownload PowerPointFigure 1. A, Schematic graphic of a pressure–volume loop. With each heart beat a full loop is described. At end-diastole, isovolumic contraction occurs. When the aortic valve opens, ejection begins and during the ejection phase volume decreases, whereas pressure changes relatively little. After aortic valve closure, isovolumic relaxation takes place, characterized by a swift pressure drop. When the mitral valve opens, the chamber begins to fill, and volume increases with a very small increase in left ventricular pressure until the end-diastolic volume is reached. The area contained within the loop is external work (EW). B, A family of PV-loops under different loading conditions reveals the end-systolic pressure–volume relation (ESPVR) and the end-diastolic pressure–volume relation (EDPVR). C, The area on the left side of the PV-loop and confined by the ESPVR and EDPVR represents potential energy (PE). EW and PE together (pressure–volume area, PVA) represent total generated mechanical energy. D, Noninvasive estimate of the PV-loop based on stroke volume and end-systolic pressure estimation results in a rectangle. Areas of under- and overestimation compared with the original PV-loop are indicated. E, Diastolic dysfunction is characterized by an augmented pressure rise during the diastolic filling phase. F, Mitral regurgitation markedly influences the isovolumic contraction and ejection period characteristics of the PV-loop.It is important to realize that 2 stages can be distinguished in the process of MV̇o2 conversion to mechanical energy: (1) efficiency of energy transfer from MV̇o2 to total PVA-area and (2) efficiency of energy transfer from PVA area to EW. The product of the 2 stages yields the mechanical external efficiency and is most commonly used in clinical studies as it represents the conversion of MV̇o2 to "useful" EW. For the sake of clarity and brevity, only (noninvasive) assessment of mechanical external efficiency will be discussed in this review.To express efficiency in a dimensionless value or percentage, MV̇o2 and EW must be converted from units of mL O2 and mm Hg · mL, respectively, to units of energy (J). The caloric equivalent of 1 mL of O2 is ≈20 J, whereas 1 mm Hg · mL equals 1.33 · 10−4 J.8Figure 2 schematically illustrates the myocardial energy conversion process. Invasive studies in normal controls have demonstrated that ≈25% of consumed oxygen is finally converted to external work.2,9,10 The residual energy is used for nonmechanical activity of basal metabolism and excitation-contraction coupling, although the majority is converted to heat.3,11Download figureDownload PowerPointFigure 2. Energy flow diagram from O2 consumption to EW. Efficiency from O2 to ATP and PVA are ≈60% to 70%. Efficiency transfer from PVA to EW depends on contractile function and loading conditions. EC indicates excitation contraction coupling; BM, basal metabolism. Adapted from Suga.3 Used with permission of the publisher. Copyright © 1990, the American Physiological Society.Noninvasive Measurement of Mechanical EfficiencyInput Energy, Oxidative MetabolismNoninvasive assessment of MV̇o2 is currently limited to positron emission tomography.12 Two MV̇o2 tracers have been developed: carbon-11–labeled acetate (11C-acetate)13 and oxygen-15–labeled molecular oxygen (15O2).14,15 As shown in detail in Figure 3, acetate is a 2-carbon chain free fatty acid, which is taken up by the heart and subsequently rapidly converted to acetyl-coenzyme A in the mitochondrial matrix. The primary metabolic fate of acetyl-coenzyme A is via the tricarboxylic acid (TCA) cycle, where 11C-activity is transported to carbon-11–labeled carbon dioxide (11CO2), which readily diffuses from myocardial tissue.13,16Figure 4 shows an example of a dynamic cardiac 11C-acetate positron emission tomography acquisition and its corresponding myocardial time–activity curve. Within a few minutes after intravenous injection, tracer activity in myocardium reaches a maximum level that is directly proportional to myocardial blood flow. Thereafter, activity is cleared in a biexponential fashion, and the rate constants k1 and k2 can be assessed through curve fitting. The rapid phase, k1, represents the efflux of 11CO2 produced by the TCA cycle. Because of the tight coupling between the TCA cycle and oxidative phosphorylation, k1 correlates closely with MV̇o2, as has been demonstrated under a wide range of conditions, and therefore functions as an index of oxygen use.16 The slow phase, k2, represents clearance of 11C-activity, which is incorporated into amino acids and TCA cycle intermediates. This method of MV̇o2 estimation has been further simplified by monoexponential fitting of the linear part of the time–activity curve (kmono), which correlates well with k1.16 To reduce the length of the scanning protocol to <30 minutes, the slow wash-out phase k2 can be disregarded. Download figureDownload PowerPointFigure 3. Oxidative metabolism in myocardium. Oxidative phosphorylation is characterized by transferal of electrons to oxygen, producing water (H2O) in the final step, and is virtually the only source of ATP production in the human heart. Nicotinamide adenine dinucleotide (NADH+H+) and flavin adenine dinucleotide (FADH2), which are produced by glycolysis, beta-oxidation, and oxidation of acetyl-coenzyme A in the TCA cycle, act as carriers of these electrons. The TCA cycle flux is tightly coupled with oxidative phosphorylation and can therefore be used to estimate overall oxidative metabolism. 11C-acetate is rapidly converted to acetyl-coenzyme A, and its primary metabolic fate is via the TCA cycle where the 11C-activity is predominantly transported to 11CO2. The rate of 11CO2 efflux is directly correlated to the TCA cycle flux, which makes 11C-acetate suitable as a tracer to measure MV̇o2. Alternatively, because it is the final electron acceptor in all pathways of aerobic metabolism, 15O2 can be used as a MVO2 tracer. Fp indicates flavoprotein; Q, coenzyme. Reprinted from Klein et al,13 with kind permission of the publisher. Copyright © 2001, Springer Science and Business Media.Download figureDownload PowerPointFigure 4. Short axis view of a dynamic 11C-acetate PET acquisition displays transit of radioactivity through the right and left ventricular cavity after a bolus injection. Subsequently, 11C-acetate is readily taken up by the myocardium and reaches a maximum after ≈5 minutes. The matching myocardial time–activity curve demonstrates the bi- and monoexponential curve fitting of the wash-out phase of activity. The slope of the fitting curves k1 and kmono are correlated to MV̇o2.The use of the second available tracer to determine MV̇o2 (ie, 15O2 gas) expands on the well-defined measurements of myocardial blood flow by use of oxygen-15–labeled water (H215O).14,15 Inhalation of 15O2 causes 15O2 to bind to hemoglobin and, after transport to peripheral tissues, 15O2 is converted by cellular metabolism to H215O.17 A tracer kinetic model has been developed to account for recirculating H215O, which allows for oxygen extraction fraction to be estimated (Figure 5). Additional corrections, however, are required for substantial spillover effects from radioactivity in adjacent ventricular blood and lung tissue, which necessitates an additional blood pool scan with oxygen-15–labeled carbon monoxide (C15O) and a transmission image to calculate lung volume. Finally, the combination of a transmission, 15O2, H215O, and C15O scan, displayed in Figure 6, allows the quantification of both myocardial blood flow and oxygen extraction fraction. Subsequently, by multiplying arterial oxygen content of blood with myocardial blood flow and oxygen extraction fraction, MV̇o2 can be expressed in absolute terms per gram of myocardial tissue (mL O2 · g−1 · min−1). Download figureDownload PowerPointFigure 5. Simplified schematic representation of the compartment model to measure oxygen extraction fraction and MV̇o2 by use of PET and 15O2 inhalation. The defined region of interest (ROI) comprises radioactivity in the myocardial tissue as well as spillover activity from the LV cavity blood pool and lung. Spillover corrections can be made with the use of LV blood pool and lung volume imaging with C15O and a transmission image, respectively, as depicted in Figure 6. Hemoglobin-bound 15O2 is extracted from the intravascular space to the tissue space (myocardium) where it is instantaneously converted into H215O. The latter is freely diffusable across the capillary membrane and is washed out in proportion to myocardial blood flow. Therefore, shortly after 15O2 inhalation is started, radiolabeled water that is recirculating must be corrected for to measure the oxygen extraction fraction. This requires arterial blood sampling to determine the relative contribution of 15O2 and H215O to total arterial radioactivity. Alternatively, in steady-state conditions during continuous inhalation of 15O2, the proportion of recirculating H215O to total arterial radioactivity has been shown to be relatively constant at ≈18% and can therefore be fixed in the compartment model, which obviates the need for arterial blood sampling.17 Finally, a separate H215O scan is performed to measure myocardial blood flow. MV̇o2 equals the product of oxygen extraction fraction, myocardial blood flow, and the oxygen content of blood. MBF indicates myocardial blood flow; OEF, oxygen extraction fraction. Adapted from Iida et al14 with permission of the publisher. Copyright © 1996, the American Heart Association.Download figureDownload PowerPointFigure 6. Examples of a transmission (Tx), steady state oxygen (15O2), and blood pool (15CO) image obtained by positron emission tomography in a transaxial view. Through a weighted subtraction technique, lung volume and ventricular blood pool are subtracted from the 15O2 image. The lower panel, 15O2-myo, visualizes the myocardial 15O2 activity that can be used to calculate the oxygen extraction fraction. Courtesy of H. Laine, Turku PET Center, Turku, Finland.Output Energy, External Mechanical WorkIn contrast to oxidative metabolism, noninvasive assessment of mechanical EW is relatively straightforward. To estimate the area contained within the PV-loop, only knowledge of stroke volume (SV) (ie, LV end-diastolic and end-systolic volumes and end-systolic LV pressure [LV-Pes]) is required. LV volumes can routinely be derived by various imaging techniques, which include magnetic resonance imaging, echocardiography, and nuclear imaging.18 LV-Pes roughly corresponds to the mean arterial blood pressure of the brachial artery and can be assessed by a simple sphygmomanometer.19 The product of mean arterial blood pressure and SV yields a fairly accurate estimate of EW (Figure 1D).Mechanical EfficiencyThe combination of the noninvasive estimates of MV̇o2 and EW as described above allows for the assessment of mechanical efficiency according to the equation below,20equationDownload figurewhere HR is heart rate and LV mass (LVM) is measured in grams, the conversion factors to joules are as mentioned earlier. It needs to be emphasized that in this equation MV̇o2 is expressed in absolute terms. The most commonly employed method to estimate oxidative metabolism noninvasively, however, remains the exponentional curve-fitting procedure of 11C-acetate, which yields an index of MV̇o2. Therefore, Beanlands et al21 introduced an alternative efficiency index, the so called work metabolic index (WMI): equationDownload figurewhere SVI is stroke volume index and SBP is systolic blood pressure. This equation is a modification of the minute work-to-oxygen consumption relationship originally defined as mechanical efficiency by Bing et al.2 Traditionally, systolic blood pressure instead of mean arterial blood pressure is used to calculate the work metabolic index, although this is based solely on the personal preferences of the investigators who first proposed this index and is of little clinical significance.21Strengths and Limitations of the Noninvasive ApproachOxidative MetabolismDespite the fact that myocardial turnover of 11C-acetate is most commonly used to noninvasively assess MV̇o2, it has several limitations.12 First and most important, only a semiquantitative index of oxidative metabolism is obtained. Even though databases exist from animal experiments and studies in humans to convert the clearance rate constants (units · min−1) to equivalents of absolute units (mL · g−1 · min−1), the relationships found in those relatively small studies, which were performed under predominantly normal physiological conditions, may not hold true in a variety of pathological disease states. Second, the metabolic fate of 11C-acetate depends, at least in part, on pathological conditions such as ischemia and hibernation.16,22 In such conditions the initial myocardial 11C-acetate clearance rate k1 or kmono slightly overestimates actual MV̇o2 because of alterations in the TCA amino acid pool sizes. Third, fluctuations in the arterial input curve of tracer activity and spillover artifacts caused by alterations in cardiac output and recirculation of 11C-activity, respectively, can significantly affect tracer kinetics that are unrelated to oxygen utilization.23,24 Finally, selection of data points from the time–activity curve for subsequent analysis is susceptible to observer variability. To circumvent some of these drawbacks, compartment modeling approaches for myocardial 11C-acetate kinetics have been developed.13,24 The essence of these approaches lies in the correction of the arterial input curve of 11C-acetate for contaminating metabolites, predominantly 11CO2. The major advantage of this modeling approach is the fact that MV̇o2 is quantified in absolute terms. Furthermore, variability of the input curve and spillover artifacts are taken into account. However, the need for arterial cannulation, repetitive sampling of arterial blood to measure radiolabeled metabolites, and its subsequent implementation in the modeling procedure make this method cumbersome. In addition, corrections for the partial volume effect (underestimation of true radiotracer concentrations that is based on cardiac dimensions and motion) need to be carried out. As these corrections themselves may induce errors in the estimation of absolute MV̇o2, many groups return to the simple, but robust semiquantitative monoexponential or biexponential curve fitting method.15O2 is theoretically the most suitable tracer to assess oxidative metabolism, as oxygen is the final electron acceptor in all pathways of aerobic metabolism. This approach is independent of cellular metabolic changes that occur in pathological conditions and conveys absolute values of MV̇o2. Unfortunately, only a few centers worldwide are currently equipped to perform the combination of these specific 15O-scans, and the multiple tracer usage makes this method prone to motion artifacts. In addition, the data analysis, which includes the modeling procedure, is very challenging, and it has been applied only in small series of subjects. Nevertheless, it should be considered the gold standard for noninvasive quantification of MV̇o2.Regardless of the methodology used to assess MV̇o2, substrate metabolism affects the ratio of adenosine triphosphate (ATP) produced per oxygen molecule consumed. From Figure 3, one can calculate this ratio for various substrates and conclude that glucose metabolism yields 11% to 13% more ATP per unit of oxygen consumption compared with free fatty acid metabolism, irrespective of cardiac workload.13,25 Therefore, substrate metabolism affects mechanical efficiency and metabolic standardization (ie, during a fasting state, it is required when these measurements are performed).External Mechanical WorkAlthough external mechanical work calculation derived from SV and mean arterial blood pressure is elegant in its simplicity, some inaccuracies of this approach should be mentioned. First, the original PV-loop is represented as a rectangle, which results in some overestimation by including the area under the curve of the diastolic filling phase. Especially in patients with diastolic dysfunction, this effect can be substantial (Figure 1E). Furthermore, the parabolic shape of the systolic ejection phase of the loop is disregarded, which may result in over- or underestimation, depending on the characteristics of the individual PV-loop. Second, valvular disease significantly hampers noninvasive estimates of EW. In aortic stenosis, the systolic transvalvular pressure gradient results in underestimation of LV-Pes measured by a sphygmomanometer. Echocardiography-derived transvalvular pressure gradient estimation, however, can accurately correct for this underestimation.26 More complex are the discrepancies caused by mitral regurgitation. The systolic bidirectional flow of blood into the left atrium and aorta causes the isovolumic contraction phase to be shortened. For a given SV, this markedly diminishes EW by regurgitation of blood into the low-pressure atrium. Noninvasive assessment of EW will therefore be overestimated in proportion to the magnitude of regurgitating volume (Figure 1F). This problem can partly be resolved by substitution of total with forward SV determined by aortic flow measurements derived by echocardiography27 or magnetic resonance imaging.28 The subsequent calculation of the so-called forward SW, however, may not accurately reflect actual SW in these patients. Mitral regurgitation, therefore, remains an important source of error in noninvasive quantification of EW.A more general disadvantage lies in the fact that LV volumes are usually derived by echocardiography, which is hampered by a poor ultrasound window in a fairly large percentage of patients.18 Furthermore, geometric assumptions, made when 1- or 2-dimensional echocardiography is used, can lead to substantial inaccuracies in patients with, for example, severe LV remodeling and/or aneurysms. Magnetic resonance imaging overcomes these limitations but is less widely available, is contraindicated in patients with implanted devices, and ideally requires a regular heart beat for gating purposes, which excludes a reliable assessment in the presence of arrhythmias. More recently, 3-dimensional echocardiography has also proven to overcome some of the aforementioned limitations,29 particularly when images are enhanced with the use of contrast agents.30Mechanical EfficiencyTable 1 lists results of efficiency studies in healthy controls. A few remarks are in order. The noninvasively obtained mechanical efficiency values are somewhat lower than those found with invasive methods. This discrepancy is probably related to differences in loading conditions and contractile state, which affect mechanical efficiency,3 in combination with methodological issues as already discussed. It should be further noted that the number of both invasive2,9,10 and noninvasive20,31–35 studies in normal physiology is rather small and the accuracy and reproducibility of efficiency measurements have not yet been adequately demonstrated. Although validation studies are available for the assessment of noninvasive oxidative metabolism and external mechanical work separately, validation studies of noninvasive versus invasive efficiency estimation in human subjects are lacking. Clearly, more studies are warranted to more reliably define normal limits and reproducibility of mechanical efficiency in humans. TABLE 1. Mechanical Efficiency Studies in Normal ControlsStudyYearNo.MethodPET TracerMEME indicates mechanical efficiency (% ± SD); PET, positron emission tomography.Bing et al219494Invasive…22±2Nichols et al1019868Invasive…29±6Arnoult et al9199711Invasive…26±6Vanoverschelde et al3119938Noninvasive11C-acetate35±6Porenta et al20199911Noninvasive11C-acetate16±6Takala et al32199911Noninvasive15O214±4Laine et al33199910Noninvasive15O218±4Akinboboye et al34200410Noninvasive11C-acetate16±3Peterson et al35200412Noninvasive11C-acetate19±7Of interest, the noninvasive approach surpasses the invasive method in its unique possibility to quantify myocardial efficiency at a regional level, which is of specific relevance in coronary artery disease and cardiomyopathies that display marked regional disease expression as can be appreciated in the clinical studies described in the next section. Various noninvasively determined regional work parameters, which are based on regional wall stress estimation, systolic wall thickening, and myocardial deformation that can be related to regional oxidative metabolism, have been proposed (Figure 7).36–38Download figureDownload PowerPointFigure 7. End-diastolic (upper panels) and end-systolic (lower panels) cine (A to D) and tagging (E to F) magnetic resonance images in a short axis view of a patient with a previous myocardial infarction of the anterior wall. Endocardial and epicardial borders can be delineated to allow accurate estimation of wall thickness. In combination with measurements of LV diameter and end-systolic pressure, regional wall stress can be calculated in absolute terms (g · cm−2) according to Laplace's law.36 Relative work parameters can also be obtained by estimation of regional systolic wall thickening (C and D) and myocardial deformation (E and F).37 The magnetic resonance imaging tissue tagging technique to quantify systolic deformation alters the magnetic properties of the myocardial tissue for a short period of time and appears as black lines on the images.37 The relative change between these lines from end-diastole to end-systole can be quantified in 3 dimensions, and relative deformation (ie, strain) can be calculated (expressed in
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