Abstract
Background
Measuring the rate of clearance of carbon-11 labelled acetate from myocardium using positron emission tomography (PET) is an accepted technique for noninvasively assessing myocardial oxygen consumption. Initial myocardial uptake of [11C]acetate, however, is related to myocardial blood flow (MBF) and several tracer kinetic models for quantifying MBF using [11C]acetate have been proposed. The objective of this study was to assess these models.
Methods
Eighteen healthy subjects and 18 patients with hypertrophic cardiomyopathy (HCM) were studied under baseline conditions with [11C]acetate and [15O]water. Four previously reported methods, including single- and multi-tissue compartment models, were used to calculate MBF from the measured [11C]acetate rate of influx K 1 and the (previously) reported relationship between K 1 and MBF. These MBF values were then compared with those derived from corresponding [15O]water studies.
Results
For all models, correlations between [11C]acetate and [15O]water-derived MBF ranged from .67 to .86 (all P < .005) in the control group and from .73 to .85 (all P < .001) in the HCM group. Two out of four models systematically underestimated perfusion with [11C]acetate, whilst the third model resulted in an overestimation. The fourth model, based on a simple single tissue compartment model with spillover, partial volume and recirculating metabolite corrections, resulted in a regression equation with a slope of near unity and an Y-intercept of almost zero (controls, K 1 = .74[MBF] + .09, r = .86, SEE = .13, P < .001 and HCM, K 1 = .89[MBF] + .03, r = .85, SEE = .12, P < .001).
Conclusion
[11C]acetate enables quantification of MBF in fairly good agreement with actual MBF in both healthy individuals and patients with HCM. A single tissue compartment model with standardized correction for recirculating metabolites and with corrections for partial volume and spillover provided the best results.
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Timmer, S.A.J., Lubberink, M., Germans, T. et al. Potential of [11C]acetate for measuring myocardial blood flow: Studies in normal subjects and patients with hypertrophic cardiomyopathy. J. Nucl. Cardiol. 17, 264–275 (2010). https://doi.org/10.1007/s12350-009-9181-y
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DOI: https://doi.org/10.1007/s12350-009-9181-y