Kinetic Modeling of 18 F-FDG Myocardial Metabolism: Elucidating the Mechanistic Superiority of Insulin Loading in Viability Assessment

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Abstract

This study investigates the mechanism by which insulin loading enhances myocardial 18 F-fluorodeoxyglucose ( 18 F-FDG) uptake compared to glucose loading. Using dynamic positron emission tomography and two-compartment irreversible kinetic modeling, 18 patients with ischemic heart disease were analyzed. Results demonstrate that insulin significantly increases the net influx rate ( Ki ) by accelerating blood-to-tissue transport ( K1 ), while concurrently reducing tracer efflux ( k2 ) and phosphorylation ( k3 ). These findings provide a quantitative metabolic basis for the clinical superiority of insulin-enhanced imaging in detecting viable myocardium.

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