Bio-Humoral and Haemodynamic Correlates of Renal Venous Congestion in the Heart Failure Spectrum

Objective: Increased central venous pressure worsens systemic congestion in heart failure (HF); this has a particular pathophysiological significance in the renal vascular bed, which can be evaluated by Doppler analysis of renal venous flow (RVF). RVF is continuous in healthy subjects and becomes discontinuous with increased fluid retention; thus, RVF evaluation allows for refined pathophysiological characterisation in HF. We sought to analyse the relationship between different RVF patterns, echocardiography-derived haemodynamics and laboratory parameters in patients at risk of or with overt HF. Design and method: The study enrolled 304 patients. 63 patients were at risk of developing HF, while 241 had overt HF. Among the latter, 61 patients had preserved left ventricular ejection fraction (LVEF >=50%), and 180 had reduced LVEF (<50%). All subjects underwent a baseline echocardiographic examination, lung ultrasound, Doppler-derived RVF evaluation, and laboratory evaluation of blood and urine samples. Results: The most prevalent cardiovascular risk factor was arterial hypertension (AH), which was present in 60% of patients at risk of developing HF and in 72% of those with overt HF. RVF was continuous in 230 patients (76%), and discontinuous in 74 (24%; dRVF). Among the latter, 39 showed pulsatile dRVF, 18 showed biphasic dRVF (i.e., two separate phases of venous flow), and 17 showed monophasic dRVF (i.e., only during diastole). dRVF was more prevalent in patients with overt HF. Monophasic dRVF was associated with more severe haemodynamic impairment and impaired renal function, as evaluated by estimated glomerular filtration rate and urinary albumin-to-creatinine ratio. After adjusting for clinical confounders, worsening RVF patterns were associated with increased natriuretic peptide levels, worse right ventricular-pulmonary arterial uncoupling, increased inferior vena cava diameter, and increased estimated pulmonary capillary wedge pressure (Figure). These results were confirmed in the subgroup of patients with overt HF, even after adjusting for LVEF. Conclusions: The evaluation of RVF patterns improves the characterisation of patients with HF. The pathophysiological significance of impaired RVF is independent of common cardiovascular risk factors and LVEF. Implementing RVF analysis in clinical practice could allow for timely identification of patients at greater risk for developing or worsening HF.