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Purpose <p>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&#xa0;h of fasting in infectious compared with noninfectious disease studies.</p> Methods <p>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.</p> Results <p>Myocardial ¹⁸F-FDG uptake correlated negatively with CRP only in the infectious subgroup (ρ = − 0.179), with a stronger correlation at CRP ≥ 4.21&#xa0;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.</p> Conclusion <p>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.</p>

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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

  • 期刊论文

  • 发表日期：

    2026年3月10日

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  • Hyojung Kim,
  • Joonhee Gook,
  • Seokkyu Jeong,
  • Jeonghoon Kim,
  • Hyunjong Lee,
  • Seung Hyup Hyun,
  • Young Seok Cho,
  • Joon Young Choi,
  • Kyung-Han Lee,
  • Seung Hwan Moon

摘要

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.