title: Microvascular tissue perfusion is impaired in acutely decompensated heart failure and improves following standard treatment.
abstract: OBJECTIVE
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Internal Medicine I (Cardiology, Angiology, Pneumology), Friedrich-Schiller University, Erlanger Allee 101, Jena, Germany. alexander.lauten@med.uni-jena.de
authors.forename: Alexander
authors.initials: A
authors.lastname: Lauten
authors.forename: Markus
authors.initials: M
authors.lastname: Ferrari
authors.forename: Bjoern
authors.initials: B
authors.lastname: Goebel
authors.forename: Wilma
authors.initials: W
authors.lastname: Rademacher
authors.forename: Julia
authors.initials: J
authors.lastname: Schumm
authors.forename: Olivia
authors.initials: O
authors.lastname: Uth
authors.forename: Michael
authors.initials: M
authors.lastname: Kiehntopf
authors.forename: Hans R
authors.initials: HR
authors.lastname: Figulla
authors.forename: Christian
authors.initials: C
authors.lastname: Jung
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000368:Aged; D057911:Angiotensin Receptor Antagonists / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D018450:Disease Progression; D019332:Endothelin-1 / Q000097:blood; D005260:Female; D006333:Heart Failure / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D008297:Male; D008833:Microcirculation / Q000502:physiology; D055414:Myocardial Perfusion Imaging / Q000295:instrumentation / Q000379:methods*; D020097:Natriuretic Peptide, Brain / Q000097:blood; D009638:Norepinephrine / Q000097:blood; D011379:Prognosis; D012039:Regional Blood Flow; D049994:Sodium Potassium Chloride Symporter Inhibitors / Q000627:therapeutic use; D013148:Spironolactone / Q000627:therapeutic use; D018709:Statistics, Nonparametric; D013318:Stroke Volume; D016277:Ventricular Function, Left
chemical_list: D000319:Adrenergic beta-Antagonists; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D019332:Endothelin-1; D049994:Sodium Potassium Chloride Symporter Inhibitors; D020097:Natriuretic Peptide, Brain; D013148:Spironolactone; D009638:Norepinephrine