Inflammation has been shown to be activated in patients with heart failure (HF), especially in the setting of acute HF (AHF)1-4. Interestingly, first evidence that elevated C-reactive protein (CRP) was associated with more severe HF and signs of congestion in patients with HF appeared seventy years ago for AHF5 and was subsequently reconfirmed using different inflammatory markers6-11. Proinflammatory activation in HF has many potential adverse effects, such as worsening cardiac contractility, stimulation of fibrosis, renal and vascular dysfunction, fluid retention/redistribution, disruption of endothelial barrier with increased capillary permeability, and neuro-hormonal activation, all of which may promote congestion development4,12,13.

Patients with heart failure (HF) may experience debilitating symptoms and are at significant increased risk for disease progression, hospitalization, and death.1 Current HF guidelines strongly recommend treating patients with HF and a reduced left ventricular ejection fraction (LVEF ≤40%; HFrEF) with renin–angiotensin–aldosterone system inhibitors (RAASis) at the maximally tolerated or target doses that have been shown to reduce morbidity and mortality in randomized clinical trials.2,3 Guidelines provide weaker recommendations to consider RAASi therapy in patients with HF with mildly reduced ejection fraction (LVEF 41–49%; HFmrEF).

A novel implantable sensor has been designed to accurately measure inferior vena cava (IVC) area to allow daily monitoring of IVC area and collapse to predict congestion in heart failure (HF).