Fig. 1

Neuro-Endocrino-Immuno-Pathophysiology Of Heart Failure. HF: Heart failure (HF) is initiated by various mechanisms. HF leads to lower mean arterial pressure (BP-) and compensatory upregulation of sympathetic nervous system (SNS) and renin-angiotensin-aldosterone system (RAAS) in an attempt to maintain BP, cardiac output (CO) and oxygen delivery (O2). Further myocardial injury leads to HF progression and reduced CO (CO-) and O2–delivery (O2-) to organs/tissues. This triggers, hypothetically via organ-specific endothelial cell/platelet/peripheral blood mononuclear cell (PBMC) interactions, compensatory immune system activation that serves to provide shortterm compensation for the failing heart. This increasing immune system activation coincides with worsening organ dysfunction of the kidneys (higher creatinine, Cr+), liver (higher bilirubin, Bili+), bone marrow (lower platelets, Plt-) and brain (worse Glasgow Coma Scale, GCS-). In this milieu, the surgical implantation of therapies such as mechanical circulatory support (MCS) restore normal CO and O2–delivery to the organs yet are associated with an unpredictable inflammatory state transition. This makes the prediction of a future survivor/non-survivor outcome challenging. We hypothesize that time-dependent NGS-based PBMC-biology analysis, when added to current clinical predictors, improve prediction precision of future survivor/non-survivor outcome