¹⁸F‐FDG PET/CT brain glucose metabolism as a marker of different types of depression comorbidity in chronic heart failure patients with impaired systolic function

Abstract

Aims Depression is an important issue in heart failure (HF). The study investigated whole‐brain and regional brain glucose metabolism in HF patients and its association with depression comorbidity. Methods and results Twenty‐nine hospitalized patients with symptomatic systolic HF (left ventricular ejection fraction <40%), New York Heart Association (NYHA) class II–IV and mean age of 55.5 ± 12.0 years, had psychometric questionnaires before discharge and an 18F‐FDG PET/CT brain scan after discharge. Semi‐automated image analysis was performed on all cases and 30 matched controls. The metabolic parameter mean standardized uptake value (SUVmean) was calculated for the whole brain and three brain regions implicated in depression pathogenesis. A standardized SUVmean was also estimated by dividing regional brain SUVmean with whole‐brain SUVmean. Cases had lower average whole‐brain SUVmean (3.90 ± 1.49 vs. 5.10 ± 1.35, P = 0.001) and average regional brain SUVmean (4.57 ± 2.31 vs. 9.96 ± 3.58, P < 0.001) compared to controls. Whole‐brain SUVmean had a significant correlation with patient age, NYHA class, diabetes, creatinine levels, depression, and cognitive impairment. Regional brain SUVmean was correlated with whole‐brain SUVmean and depression. The standardized SUVmean, in particular, was found to be a robust index that could differentiate HF patients with ‘epiphenomenal’ (>0.93) or ‘real’ (≤0.93) depression. Conclusion Heart failure patients with more severe disease showed whole‐brain and regional brain hypometabolism in 18F‐FDG PET/CT. Depressed HF patients (Beck Depression Inventory score >13) exhibited different metabolic patterns that could be used to differentiate between ‘epiphenomenal’ and ‘real’ depression. Namely, presence of whole‐brain hypometabolism suggested ‘epiphenomenal’ depression, whereas absence suggested ‘real’ depression. Presence of significant relative regional brain hypometabolism enhanced the likelihood of ‘real’ depression diagnosis.

Potential of 18F-FDG PET to evaluate the cardiocerebral interaction

“…1 Recently, Lyra et al investigated brain glucose metabolism in patients with HF using FDG PET/CT. 18 In their study, patients with HF showed whole-brain and regional brain hypometabolism compared to that in matched controls, similar to the findings of the study by Yun and colleagues. Furthermore, patients with HF and epiphenomenal or real depression showed different metabolic patterns with significant relative regional brain hypometabolism in the amygdala, hippocampus, and ventral prefrontal cortex implicated in the pathogenesis of depression.…”

“…Although biochemical markers have received considerable attention for Alzheimer's disease in recent years, Kresge et al found an interaction between the left ventricular ejection fraction (LVEF) and cerebrospinal fluid biomarkers in participants with normal cognition, whereas lower LVEF is associated with increased total tau and phosphorylated tau. 11 In this issue of the Journal of Nuclear Cardiology, Yun and colleagues report their investigation of the metabolic heart-brain interaction in patients with HF with a reduced ejection fraction using 18 F-fluorodeoxyglucose (FDG) positron emission tomography (PET)/computed tomography (CT). The importance of this study is in determining if there is a relationship between cardiac function and the cerebral metabolic activity derived from FDG PET/CT in comparison with that in healthy volunteers.…”

Prognostic value of post-discharge depression in patients recently hospitalized with acute heart failure

“…Theoretically, patients with stable and chronic HF may be more similar to the general population ( 31 ). Conversely, in patients recently hospitalized with acute HF, secondary depression due to severe somatic disorders ( 32 ) may surpass the effects of a higher BMI and younger age. In this study, COPD and diabetes mellitus were independent predictors of post-discharge depression.…”

Stable Isotope-Resolved Metabolomics Reveals the Abnormal Brain Glucose Catabolism in Depression Based on Chronic Unpredictable Mild Stress Rats

“…In addition, the deficiency of energy substrates forces the brain to make adaptive changes in the utilization of glucose. A great number of studies have reported that depression impaired brain energy metabolism, ,, but the detailed mechanism is not clear. Therefore, the supply of energy substrates is indispensable for revealing brain energy metabolism disorders in depression.…”