{'fraction_non_alphanumeric': 0.02513747054202671, 'fraction_numerical': 0.024351924587588374, 'mean_word_length': 5.434343434343434, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Effect of carbon-11-acetate recirculation on estimates of myocardial oxygen consumption by PET.

Mono- and biexponential fitting of myocardial 11C-acetate kinetics does not account for the effect of recirculating 11C activity following intravenous injection of the tracer. A tracer kinetic model comprising two and three compartments was developed to describe intravascular and myocardial 11C-acetate kinetics defined by PET. This model approach including a correction for 11C-metabolites in blood was validated by correlating the model parameter estimates with directly measured oxygen consumption (MVO2) in 11 closed-chest dog experiments over a wide range of cardiac work. The model parameter k2 closely correlated with oxygen consumption (r = 0.94). This approach was subsequently applied to human studies and k2-related to rate-pressure product (PRP). In comparison to conventional monoexponential fitting of 11C-acetate tissue kinetics, the model approach improved the correlation coefficients of scintigraphic MVO2 estimates and PRP values from 0.61 to 0.91. Thus, analysis of myocardial 11C-acetate and clearance kinetics with a tracer kinetic model corrects for recirculating 11C-activity and may provide more consistent estimates of myocardial oxygen consumption.