Journal of the American Heart Association · 2026
Cerebral Injury and Impaired Brain Metabolism in Patients With Left Ventricular Assist Device and Chronic Heart Failure -An Interdisciplinary Cognition, Blood-Based Biomarker and Brain Metabolism Assessment.
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Jungclaus Martin S, Barba Lorenzo, Otto Markus, Wilke Florian, Ruhparwar Arjang, Hanke Jasmin S, Schmitto Jan D, Berliner Dominik, Derlin Thorsten, Werner Rudolf A, Bengel Frank M, Weissenborn Karin, Kahl Kai G, Hoffmeister Julia, Berding Georg, Worthmann Hans, Weiberg Desiree, Gabriel Maria M
Аннотация
BACKGROUND: Chronic heart failure is linked to cognitive dysfunction. Left ventricular assist devices (LVAD) potentially ameliorate cognition, but continuous flow profiles might result in long-term progression. In this cross-sectional pilot study, we aimed to investigate the association between LVAD therapy and neuronal impairment measured by cognitive performance, blood-based biomarkers of neuronal injury and 18F-fluorodeoxyglucose-positron emission tomography/computed tomography-derived brain metabolism.
METHODS: We prospectively enrolled 19 patients with LVAD and 13 patients with advanced chronic heart failure receiving best medical treatment. Cognitive performance was assessed using the Montreal Cognitive Assessment and Frontal Assessment Battery. Serum levels of NfL (neurofilament light chain), pTau181 (phosphorylated Tau protein at threonine 181), and GFAP (glial fibrillary acidic protein) were measured by immunoassay. Brain metabolism was assessed using 18F-fluorodeoxyglucose-positron emission tomography/computed tomography by statistical parametric mapping analyses compared with 16 healthy controls (P<0.001 uncorrected).
RESULTS: Of all patients, 69% showed cognitive dysfunction, 5 patients had evidence for frontotemporal impairment. Median neurochemical biomarker concentrations were elevated in the whole cohort (NfL 45.7 pg/mL [26.9-80.2]; pTau181 23.1 pg/mL [18.1-40.1]; GFAP 191.3 pg/mL [126.3-251.7]). Both groups did not differ regarding cognitive performance and biomarker levels. The uncorrected statistical parametric mapping analyses indicated frontotemporally accentuated hypometabolism in both groups compared with healthy controls. Patients with LVAD revealed more hypometabolic volumes in single-subject analyses (LVAD 1.03 mL (0-7.34); chronic heart failure 0 mL (0-0.01), P<0.003).
CONCLUSIONS: In this exploratory study, patients with chronic heart failure and patients with LVAD exhibited impaired cognitive performance and elevated biomarker levels of neuronal injury. 18F-fluorodeoxyglucose-positron emission tomography/computed tomography results of uncorrected thresholds suggested subtle frontal hypometabolism. Neurochemical biomarkers and 18F-fluorodeoxyglucose-positron emission tomographyappear promising for further investigation of cerebral health in patients with heart failure.
METHODS: We prospectively enrolled 19 patients with LVAD and 13 patients with advanced chronic heart failure receiving best medical treatment. Cognitive performance was assessed using the Montreal Cognitive Assessment and Frontal Assessment Battery. Serum levels of NfL (neurofilament light chain), pTau181 (phosphorylated Tau protein at threonine 181), and GFAP (glial fibrillary acidic protein) were measured by immunoassay. Brain metabolism was assessed using 18F-fluorodeoxyglucose-positron emission tomography/computed tomography by statistical parametric mapping analyses compared with 16 healthy controls (P<0.001 uncorrected).
RESULTS: Of all patients, 69% showed cognitive dysfunction, 5 patients had evidence for frontotemporal impairment. Median neurochemical biomarker concentrations were elevated in the whole cohort (NfL 45.7 pg/mL [26.9-80.2]; pTau181 23.1 pg/mL [18.1-40.1]; GFAP 191.3 pg/mL [126.3-251.7]). Both groups did not differ regarding cognitive performance and biomarker levels. The uncorrected statistical parametric mapping analyses indicated frontotemporally accentuated hypometabolism in both groups compared with healthy controls. Patients with LVAD revealed more hypometabolic volumes in single-subject analyses (LVAD 1.03 mL (0-7.34); chronic heart failure 0 mL (0-0.01), P<0.003).
CONCLUSIONS: In this exploratory study, patients with chronic heart failure and patients with LVAD exhibited impaired cognitive performance and elevated biomarker levels of neuronal injury. 18F-fluorodeoxyglucose-positron emission tomography/computed tomography results of uncorrected thresholds suggested subtle frontal hypometabolism. Neurochemical biomarkers and 18F-fluorodeoxyglucose-positron emission tomographyappear promising for further investigation of cerebral health in patients with heart failure.