title: Haemolysis in patients with ventricular assist devices: major differences between systems.
abstract: BACKGROUND
  Implantation of a ventricular assist device (VAD) is a seminal therapeutic option for patients with terminal cardiac failure. However, haemolysis remains a clinically relevant adverse effect of several VAD types. Lysed erythrocytes release lactate dehydrogenase (LDH) and haemoglobin. Free haemoglobin in plasma is bound by haptoglobin with high affinity. The complex is internalised by monocytes/macrophages and degraded. Any more released free haemoglobin is captured by haemopexin. This complex also undergoes lysosomal degradation in various cells. Only now, the excessive free haemoglobin can be measured in plasma. Here, we investigated haemolysis in patients supported by different VAD types.
  
  
  METHODS
  Five patients with an intracorporeal centrifugal left ventricular VAD (LVAD), 10 patients with an axial LVAD and seven patients with a paracorporeal biventricular assist device (BVAD) were analysed preoperatively and 3 days (3.0+/-0.4 days, early), 2 weeks (14+/-1 days, intermediate) and 2 months (62+/-5 days, later) after VAD implantation for haptoglobin, haemopexin, free haemoglobin in plasma, LDH, total haemoglobin, haematocrit and transfusion requirements.
  
  
  RESULTS
  Patients with a centrifugal LVAD displayed normal haptoglobin and haemopexin, low free haemoglobin and moderately increased LDH. In comparison, axial LVADs were accompanied by lower haptoglobin and haemopexin and higher free haemoglobin and LDH values. In contrast, BVADs led to an almost complete loss of haptoglobin and haemopexin and to high levels of free haemoglobin and LDH at each analysed time point.
  
  
  CONCLUSIONS
  While severe haemolysis accompanies BVAD support, erythrocyte damage is less pronounced in the axial LVAD examined and only slight in the intracorporeal centrifugal LVAD. Haemopexin, a scavenger of free haemoglobin, can be used, in combination with haptoglobin and free haemoglobin, to assess erythrocyte damage.
authors.affiliation: Department of Cardiovascular Surgery, University Medical Center Freiburg, Hugstetter Str. 55, 79106 Freiburg, Germany.
authors.forename: Claudia
authors.initials: C
authors.lastname: Heilmann
authors.forename: Ulrich
authors.initials: U
authors.lastname: Geisen
authors.forename: Christoph
authors.initials: C
authors.lastname: Benk
authors.forename: Michael
authors.initials: M
authors.lastname: Berchtold-Herz
authors.forename: Georg
authors.initials: G
authors.lastname: Trummer
authors.forename: Christian
authors.initials: C
authors.lastname: Schlensak
authors.forename: Barbara
authors.initials: B
authors.lastname: Zieger
authors.forename: Friedhelm
authors.initials: F
authors.lastname: Beyersdorf
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D006242:Haptoglobins / Q000032:analysis; D006353:Heart-Assist Devices / Q000009:adverse effects; D006454:Hemoglobins / Q000032:analysis; D006461:Hemolysis; D006466:Hemopexin / Q000032:analysis; D006801:Humans; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008875:Middle Aged; D011184:Postoperative Period
chemical_list: D015415:Biomarkers; D006242:Haptoglobins; D006454:Hemoglobins; D006466:Hemopexin; D007770:L-Lactate Dehydrogenase