Assessment of myocardial oxidative metabolism in aortic valve disease using positron emission tomography with C-11 acetate

Hicks, Rodney J.; Savas, Vicky; Currie, Philip J.; Kalff, Victor; Starling, Mark R.; Bergin, Peter; Kirsch, Marvin; Schwaiger, Markus

doi:10.1016/0002-8703(92)90503-n

Cited by 15 publications

(4 citation statements)

References 35 publications

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“…Therefore, the apparent normalization of oxygen utilization per unit of weight induced by hypertrophy occurred at the expense of mechanical efficiency. It should be noted, however, that these observations could not be reproduced in hypertrophy caused by aortic valve stenosis 62,63 or in patients with hypertensive eccentric hypertrophy. 34 This underscores the complexity of various adaptive processes that occur in hypertrophy under different pathological loading conditions.…”

Section: Left Ventricular Hypertrophymentioning

confidence: 81%

Myocardial Energetics and Efficiency

et al. 2007

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T he 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 (MV O 2 ) 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 Ϸ25%, 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 MV O 2 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 MV O 2 (mL O2 · min Ϫ1 ) measurements according to the Fickprinciple by multiplying coronary sinus blood flow (mL · min Ϫ1 ) by the arteriovenous oxygen content difference. 7Blood 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 MV O 2 can be assessed, which also includes oxidative metabolism of the right ventricl...

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Section: Left Ventricular Hypertrophymentioning

confidence: 81%

Myocardial Energetics and Efficiency

et al. 2007

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“…Only a few minor studies have investigated MVO 2 in AS patients, and their conclusions are inconsistent 28, 29, 30, 31. These studies were also restricted by the absence of methods or by inaccurate methods to quantify stroke work, which evidently hampers any firm conclusion of how AS may affect myocardial efficiency.…”

Section: Discussionmentioning

confidence: 99%

Myocardial Oxygen Consumption and Efficiency in Aortic Valve Stenosis Patients With and Without Heart Failure

Hansson

Sørensen

Harms

et al. 2017

JAHA

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BackgroundMyocardial oxygen consumption (MVO2) and its coupling to contractile work are fundamentals of cardiac function and may be involved causally in the transition from compensated left ventricular hypertrophy to failure. Nevertheless, these processes have not been studied previously in patients with aortic valve stenosis (AS).Methods and ResultsParticipants underwent 11C‐acetate positron emission tomography, cardiovascular magnetic resonance, and echocardiography to measure MVO2 and myocardial external efficiency (MEE) defined as the ratio of left ventricular stroke work and the energy equivalent of MVO2. We studied 10 healthy controls (group A), 37 asymptomatic AS patients with left ventricular ejection fraction ≥50% (group B), 12 symptomatic AS patients with left ventricular ejection fraction ≥50% (group C), and 9 symptomatic AS patients with left ventricular ejection fraction <50% (group D). MVO2 did not differ among groups A, B, C, and D (0.105±0.02, 0.117±0.024, 0.129±0.032, and 0.104±0.026 mL/min per gram, respectively; P=0.07), whereas MEE was reduced in group D (21.0±1.6%, 22.3±3.3%, 22.1±4.2%, and 17.3±4.7%, respectively; P<0.05). Similarly, patients with global longitudinal strain greater than −12% and paradoxical low‐flow, low‐gradient AS had impaired MEE (P<0.05 versus controls). The ability to discriminate between symptomatic and asymptomatic patients was superior for global longitudinal strain compared with MVO2 and MEE (area under the curve 0.98, 0.48, and 0.61, respectively; P<0.05).ConclusionsAS patients display a persistent ability to maintain normal MVO2 and MEE (ie, the ability to convert energy into stroke work); however, patients with left ventricular ejection fraction <50%; global longitudinal strain greater than −12%; or paradoxical low‐flow, low‐gradient AS demonstrate reduced MEE. These findings suggest that mitochondrial uncoupling contributes to the dismal prognosis in patients with reduced contractile function or paradoxical low‐flow, low‐gradient AS.

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“…Myocardial oxidative metabolism measured 11 C-acetate PET is significantly increased by about 40 % in patients with moderate to severe aortic stenosis and preserved systolic volume index compared with healthy controls [36, 37••]. Estimated systolic left ventricular pressure measured by echocardiography was independently associated with the increased myocardial oxidative metabolism (Fig.…”

Section: Clinical Applications For Heart Failurementioning

confidence: 99%

Imaging of Myocardial Oxidative Metabolism in Heart Failure

Naya

Tamaki

2013

Curr Cardiovasc Imaging Rep

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Metabolic imaging has a potential for better understanding of pathophysiology of heart failure. C-11 acetate is taken up by the heart, rapidly converted to acetylCoA and readily metabolized to C-11 CO2 through TCA cycle with oxidative phosphorylation. Thus, the myocardial turnover rate of this tracer is tightly correlated with its clearance of C-11 CO2, reflecting overall oxidative metabolism. The heart relies on aerobic oxidative substrate for the generation of ATP, which is required to maintain its contractile function. The progression to heart failure is associated with a gradual decline in the activity of mitochondrial respiratory pathways, leading to diminished capacity for ATP production. The work metabolic index can also be estimated by the combination of C-11 acetate PET and hemodynamics by echocardiography, the metabolic index is a significant marker to understand the pathophysiology of heart failure as well as myocardial oxidative metabolism.

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Assessment of myocardial oxidative metabolism in aortic valve disease using positron emission tomography with C-11 acetate

Cited by 15 publications

References 35 publications

Myocardial Energetics and Efficiency

Myocardial Energetics and Efficiency

Myocardial Oxygen Consumption and Efficiency in Aortic Valve Stenosis Patients With and Without Heart Failure

Imaging of Myocardial Oxidative Metabolism in Heart Failure

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