NGAL and ST2 levels in ambulatory patients with chronic heart failure. Clinical and echocardiographic correlates.

AIM: Neutrophil gelatinase-associated lipocalin (NGAL) and ST2 receptor, a member of the interleukin-1 receptor family, are novel biomarkers with a potential role in the diagnosis and risk stratification of patients with chronic heart failure (CHF). There is however scarce data on their relation with clinical characteristics and cardiac function in patients with CHF. METHODS: Consecutive ambulatory patients with CHF were studied. All patients underwent clinical and echocardiographic assessment, and blood samples were collected for the estimation of ST2 and NGAL serum levels during the same assessment. RESULTS: A total of 76 patients (79% male, mean age: 63 ± 14 years), with CHF and left ventricular ejection fraction of 28 ± 7% were included. Median NGAL was 0.16 (0.09-0.275) mg/L and median ST2 was 0.0125 (0.0071-0.0176) mg/L. No association between NGAL and ST2 was observed. Multivariate analysis revealed tissue Doppler-derived right ventricular systolic velocity as an independent predictor of ST2, and the duration of HF and serum creatinine levels as independent predictors of NGAL. CONCLUSIONS: NGAL levels depend on the renal function and the duration of HF, while ST2 levels are affected by the right but not the left ventricular function and show no association with clinical indices of HF.

TMS-induced brain connectivity modulation in Genetic Generalized Epilepsy.

OBJECTIVE: In epilepsy patients, Transcranial Magnetic Stimulation (TMS) may result in the induction and modulation of epileptiform discharges (EDs). We hereby investigate the modulatory effects of TMS on brain connectivity in Genetic Generalized Epilepsy (GGE) and explore their potential as a diagnostic biomarker in GGE. METHODS: Patients with GGE (n=18) and healthy controls (n=11) were investigated with a paired-pulse TMS-EEG protocol. The brain network was studied at local and at global levels using Coherence as an EEG connectivity measure. Comparison of patients vs controls was performed in a time-resolved manner by analyzing comparatively pre- vs post-TMS brain networks. RESULTS: There was statistically significant TMS-induced modulation of connectivity at specific frequency bands within groups and difference in TMS-induced modulation between the two groups. The most significant difference between patients and controls related to connectivity modulation in the γ band at 1-3 sec post-TMS (p=0.004). CONCLUSIONS: TMS modulates the healthy and epileptic brain connectivity in different ways. Our results indicate that TMS-EEG connectivity analysis can be a basis for a diagnostic biomarker of GGE. SIGNIFICANCE: The analysis identifies specific time periods and frequency bands of interest of TMS-induced connectivity modulation and elucidates the effect of TMS on the healthy and epileptic brain connectivity.