Abstract
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.
Highlights
Metabolic imaging has a potential for better understanding of pathophysiology of heart failure
While metabolic studies with C-11 palmitate or FDG studies are quite dependent on plasma substrate levels, C-11 acetate metabolism is independent of concentration of energy substrates for the myocardium [4, 5]
Myocardial oxidative metabolism measured 11C-acetate positron emission tomography (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]
Summary
Metabolic imaging has a potential for better understanding of pathophysiology of heart failure. C-11 palmitate and F-18 fluorodeoxyglucose (FDG) are used to estimate myocardial metabolism with myocardial energy substrate such as fatty acid and glucose utilizations, respectively by PET. C-11 acetate has been proposed as a PET tracer to probe myocardial oxidative metabolism with PET. This tracer, a simple two-carbon carboxylic acid, can be rapidly prepared in high yields by the simple one step C-11 carboxylation of the appropriate Grinard reagent, methylmagnesium bromide [1]. C-11 acetate is taken up by the heart, rapidly converted to acetylCoA and readily metabolized to CO2 through TCA cycle with oxidative phosphorylation. The myocardial turnover rate of this tracer is tightly correlated with its clearance of C-11 CO2, reflecting overall oxidative metabolism. While metabolic studies with C-11 palmitate or FDG studies are quite dependent on plasma substrate levels, C-11 acetate metabolism is independent of concentration of energy substrates for the myocardium [4, 5]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
