Abstract

The variability of physiologic 18F-FDG uptake in the myocardium has hampered the accurate evaluation of cardiac glucose metabolism. We investigated the effects of multiple factors, including fasting duration and physical activity, on the physiologic uptake of 18F-FDG by the myocardium in healthy participants. A total of 446 participants (predominantly male, 91%) in a health screening program were included in this retrospective study. For the visual analysis of myocardial 18F-FDG uptake, the participants were categorized into three groups according to qualitative visual scales (QVS). For the quantitative analysis, the maximum SUV of the left ventricular myocardium was measured. Significant differences were observed in fasting duration (p < 0.001), SUVmax (p < 0.001), aspartate aminotransferase (AST) (p < 0.001), alanine aminotransferase (ALT) (p < 0.001), gamma-glutamyl transpeptidase (γ-GTP) (p = 0.001), and uric acid (p = 0.015) among the QVS groups. Participants who regularly exercised with vigorous activity (p = 0.032) and HbA1c > 6% (p = 0.005) showed significant association with myocardial FDG uptake in the Chi-squared test. The median value of fasting duration decreased significantly as the QVS of the myocardium increased. Twenty-nine of the 31 participants (93.5%) who fasted for 21.5h or more showed a suppressed FDG uptake (mean SUVmax = 2.1). In multivariate logistic regression analysis, fasting duration (OR = 0.74, 95% CI 0.69-0.80, p < 0.001), HbA1c > 6% (OR = 0.29, 95% CI: 0.12 - 0.66, p = 0.004), uric acid (OR = 0.82, 95% CI 0.68-1.00, p = 0.049) and regular exercise with vigorous activity (OR = 1.75, 95% CI 1.13-2.70, p = 0.012) were significant factors for physiologic myocardial FDG uptake. Reduced physiologic 18F-FDG uptake of the myocardium was associated with longer fasting duration, higher level of HbA1c, and less frequency of regular exercise with vigorous activity. For the preparation of cardiac 18F-FDG PET, inclusion of longer fasting duration (more than 18h) might be necessary for the adequate suppression of physiologic 18F-FDG myocardial uptake.

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