Sofia Chatziioannou and colleagues recently published a paper in European Journal of Heart Failure

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.

The prevalence of depression in heart failure (HF) is high compared to other chronic diseases. Depression comorbidity represents a well-established independent prognostic factor for poor functional status and quality of life (QoL), as well as high mortality and hospitalization rates in HF patients. Anxiety and cognitive disorders (memory and attention deficits mainly) are also common comorbidities and may coexist in HF patients with depression. The frequency and clinical-economic impact of these neuropsychiatric comorbidities on HF disease are significant. They remain, however, underdiagnosed, due to overlook or atypical symptomatology and consequently and more importantly, without specific treatment. Moreover, there are controversies about appropriate treatment of these neuropsychiatric comorbidities. Antidepressants, such as selective serotonin reuptake inhibitors (SSRIs), can be safely included in multidrug treatment of HF patients. However, recent randomized trials did not clearly demonstrate any benefit on clinical outcome in depressed HF patients treated with SSRIs.

The development of depression in HF patients is multifactorial. Psychological, behavioural and pathophysiological factors, acting through the neuroendocrine and immune-inflammatory system, are considered responsible for the onset of depression and the worse outcome in depressed HF patients. Dysfunction of autoregulatory cerebral blood flow (CBF) mechanism and hypoperfusion due to reduced cardiac output, could also have a specific pathogenetic role in the dysregulation of mood and cognitive neural circuits in HF patients, as suggested by various neuroimaging studies. Moreover, global CBF measured by functional magnetic resonance imaging (MRI) and other imaging methods, was found correlated with clinical outcome in HF patients. As cerebral hypoperfusion means essentially hypometabolism and vice versa, a recent study investigated brain glucose metabolism in HF patients, by ¹⁸F-fluorodeoxyglucose positron emission tomography/computed tomography (¹⁸F-FDG PET/CT) imaging. HF patients with severely reduced ejection fraction (<25%) presented lower mean standardized uptake value (SUVmean) in PET images, indicating whole-brain hypometabolism, compared to HF patients with less severely reduced ejection fraction. Our study aimed to investigate whole-brain and regional brain glucose metabolism in HF patients compared to control subjects with ¹⁸F-FDG PET/CT imaging. Metabolic indices derived from the processing and analysis of the data were correlated to: (i) the severity of HF, assessed by clinical markers and HF-adapted questionnaires; (ii) the severity of psychiatric and cognitive comorbidities, assessed by psychometric tests and questionnaires; and (iii) the clinical outcome, assessed by all composite events during follow-up.

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. Vassiliki Lyra, John Parissis, Maria Kallergi, Emmanouil Rizos, Gerasimos Filippatos, Dimitrios Kremastinos, and Sofia Chatziioannou. Eur J Heart Fail 2020 Jun 12. doi: 10.1002/ejhf.1866.

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