Heart failure (HF) and cognitive impairment (CI) frequently coexist. The objective of this meta-analysis was to synthesize evidence on the association between circulating biomarkers of neurodegenerative diseases and (1) the incidence of HF; (2) cognitive dysfunction in patients with HF; and (3) adverse HF outcomes.

A comprehensive search of MEDLINE and EMBASE identified 17 studies assessing plasma levels of amyloid beta (Aβ), tau protein, neurofilament light chain (NfL), glial fibrillary acidic protein (GFAP), triggering receptor expressed on myeloid cells 2 (TREM2), ubiquitin C-terminal hydrolase L1 (UCHL1), and YKL-40 in relation to HF-related outcomes.

Elevated Aβ40 and YKL-40 levels were significantly associated with all-cause mortality in HF, with respective hazard ratios (HR) of 1.34 (95% CI: 1.01–1.79; P = 0.0434) and 1.081 (95% CI: 1.002–1.166; P = 0.0443). There was a positive, but not significant, trend between elevated plasma tau levels and HF hospitalization, with HR of 1.21 (95% CI: 0.94–1.55; P = 0.1383). A pooled analysis of all biomarkers across various adverse outcomes demonstrated a significant association, with a HR of 1.20 (95% CI: 1.10–1.30; P < 0.0001). pTau-181, NfL, GFAP, and TREM2 demonstrated associations with memory impairment in HF. Aβ40, pTau-181, NfL, and YKL-40 were linked to incident HF in individual studies.

Neurodegenerative biomarkers, particularly Aβ40 and YKL-40, are indicators of risk in HF populations. These data highlight the need to validate their clinical utility and elucidate shared potentially causative mechanistic pathways linking HF and neurodegenerative conditions, defining a neurodegenerative cardiomyopathy.

PD (PD) is associated with a twofold increase in the risk of death especially sudden death. A predisposing factor for cardiac sudden death is prolongation of the QT interval. This study evaluated the potential association between QT interval and PD.

A systematic search was conducted of Medline and EMBASE using the search terms “PD” AND “QT interval” OR “Cardiac Repolarization” to identify articles.

Seven studies with persons with PD (n = 981) and control groups were identified. There was a significant difference in QT interval comparing patients with PD and persons without PD. The odds ratio showed a significant (P < 0.001) 2.6-fold (random effect) greater QTc prolongation in PD compared to control. Overall, there was a significantly longer QT in patients with PD than controls of 10.7 ± 2.8 ms. Data analysis did not show much publication bias. Focusing only on studies that related the QT interval to the severity of PD as assessed by Hoehn–Yahr classification (n = 6), there was a significant (P = 0.004) overall correlation between QT interval and the severity of PD. There was little publication bias. The data directly examining patients with PD taking any drug than might prolong QT do not support an association between these mediations and QT prolongation.

Individuals with PD have a longer QT interval than individuals without PD. The QT interval is associated with a greater severity of PD and a greater probability of developing more severe PD. The QT interval should be considered in assessment of PD and possibly as a target for the treatment of PD.