Minimal Additional Effect of Heparin Bolus Beyond Prolonged Fasting on Cardiac 18F-FDG Suppression in Infectious Disease PET/CT Evaluation: Inverse Association Between Myocardial 18F-FDG Uptake and CRP
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Hyojung Kim1, Joonhee Gook1, Seokkyu Jeong1
1Department of Nuclear Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Gangnam-gu, Seoul, 06351 Republic of Korea.
Insights
In infectious states, C-reactive protein (CRP) correlates with reduced myocardial uptake, and unfractionated heparin (UFH) offers no additional benefit. In noninfectious conditions, UFH further reduces myocardial uptake, independent of CRP levels.
Area of Science:
- Nuclear medicine
- Cardiovascular imaging
- Metabolic imaging
Background:
- Stress-induced metabolic shifts in infectious states may affect cardiac imaging protocols.
- Understanding myocardial fatty acid utilization is crucial for interpreting PET/CT scans.
- The role of unfractionated heparin (UFH) in modulating myocardial uptake needs further investigation.
Purpose of the Study:
- To investigate the relationship between myocardial ¹⁸F-FDG uptake and C-reactive protein (CRP) in infectious versus noninfectious conditions.
- To assess the impact of UFH on myocardial uptake after fasting in different disease states.
- To determine if UFH provides additional metabolic suppression beyond fasting in infectious and noninfectious diseases.
Main Methods:
- Retrospective analysis of 275 cardiac ¹⁸F-FDG PET/CT studies using a standardized suppression protocol.
- Evaluation of myocardial uptake using averaged SUVmax values and normalization to blood pool and liver SUVmean.
- Stratification of studies into infectious and noninfectious subgroups for comparative analysis.
Main Results:
- Myocardial ¹⁸F-FDG uptake showed a negative correlation with CRP in the infectious subgroup (ρ = -0.179), particularly at higher CRP levels (≥4.21 mg/dL, ρ = -0.430).
- UFH administration resulted in significant additional myocardial uptake suppression only in the noninfectious subgroup.
- CRP was a negative predictor of myocardial uptake in infectious studies, while UFH was the primary factor in noninfectious studies.
Conclusions:
- Elevated CRP is associated with reduced myocardial uptake in infectious diseases, with UFH offering no added benefit post-fasting.
- In noninfectious conditions, myocardial uptake is independent of CRP and can be further suppressed by UFH.
- These findings highlight differential metabolic responses influencing cardiac imaging interpretation in various disease states.
Purpose:
In infectious states, stress-induced metabolic shifts toward fatty acid utilization may limit the additional effect of unfractionated heparin (UFH) bolus administration. This study aimed to evaluate the relationship between myocardial ¹⁸F-FDG uptake suppression and systemic inflammatory marker C-reactive protein (CRP) and to assess the differential effect of UFH beyond 12 h of fasting in infectious compared with noninfectious disease studies.
Methods:
Three hundred ¹⁸F-FDG PET/CT studies under the institutional cardiac ¹⁸F-FDG suppression protocol (December 2015-May 2025) were reviewed. Outlier removal yielded 275 pooled, 147 infectious, and 127 noninfectious studies in the multi-device cohort and 225, 116, and 110 studies in the single-device cohort. Cardiac suppression was assessed with averaged SUVmax values in each wall of the left ventricle (LVavg) and LVavg normalized to SUVmean of blood pool and liver.
Results:
Myocardial ¹⁸F-FDG uptake correlated negatively with CRP only in the infectious subgroup (ρ = - 0.179), with a stronger correlation at CRP ≥ 4.21 mg/dL (ρ = - 0.430). UFH produced significant additional suppression beyond that achieved by fasting in the non-infectious subgroup only. Moreover, while CRP was a consistent negative predictor of myocardial uptake in both univariate and multivariable analyses of infectious studies, UFH was the sole significant factor reducing uptake in the univariate analysis of noninfectious cases. All results were consistent across single- and multi-device cohorts.
Conclusion:
In infectious diseases, elevated CRP was associated with reduced myocardial uptake, and UFH provided no additional suppression beyond fasting. In noninfectious conditions, myocardial uptake was independent of CRP and further reduced by UFH bolus injection.
Supplementary Information:
The online version contains supplementary material available at 10.1007/s13139-026-00996-8.
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