Microvascular tissue perfusion is impaired in acutely decompensated heart failure and improves following standard...

Acutely decompensated heart failure (ADHF) leads to neurohumoral activation potentially affecting vascular tone and organ perfusion and may be linked to unfavourable outcome. Global haemodynamic, clinical, and laboratory parameters may severely underestimate tissue hypoperfusion. Therefore, the purpose of this study was to evaluate microvascular flow index (MFI) in patients with ADHF and to assess the effect of standard pharmacological therapy using Sidestream Dark Field (SDF) imaging.

Twenty-seven patients (mean age 75.5 ± 10.1 years, 48% male) with ADHF in New York Heart Association functional class ≥III were included. Serum markers of neurohumoral activation [brain natriuretic peptide (BNP)], endothelin-1 (ET-1), noradrenaline (NA), and echocardiographic parameters of left ventricle-function were determined at hospital admission and the day before discharge. Using SDF imaging, MFI was evaluated at both time-points in semi-quantitative vessel categories (small: 10-25 μm; medium: 26-50 μm; and large: 51-100 μm). At admission, increased serum levels of BNP, NA, and ET-1 and a severely reduced MFI were observed in association with ADHF. Serum levels of BNP, NA, and ET-1 decreased significantly with standard pharmacological therapy (BNP: 2163 ± 1577 vs.1006 ± 945 pg/mL, P< 0.05; NA: 349 ± 280 to 318 ± 265 pg/mL, P< 0.05; ET-1: 5.08 ± 0.72 to 4.81 ± 0.59 pg/mL; P< 0.01). Standard pharmacological treatment also had a profound impact on tissue perfusion by significantly improving median MFI in small [2.6; inter-quartile range (IQR) 2.3-2.9 vs. 2.9; IQR 2.8-3.0; P= 0.01) and medium-sized (2.0; IQR 1.9-2.5 vs. 2.7; IQR 2.5-2.8; P< 0.01) vessels.

In patients with ADHF, microvascular tissue perfusion is impaired even when global haemodynamic or laboratory signs of hypoperfusion are absent. Effective pharmacological treatment to decrease neurohumoral activation significantly improves microflow. Hypoperfusion in ADHF is potentially linked to neurohumoral activation with increased plasma levels of vasoconstrictors and sympatho-adrenergic activity.