title: Autotransfusion system or integrated automatic suction device in minimized extracorporeal circulation: influence on coagulation and inflammatory response.
abstract: OBJECTIVE
  To measure surrogate markers of coagulation activation as well as of the systemic inflammatory response in patients undergoing primary elective coronary artery bypass grafting (CABG) using either the so-called Smart suction device or a continuous autotransfusion system (C.A.T.S.®).
  
  
  METHODS
  Fifty-eight patients being operated with a miniaturized circuit (minimal extracorporeal circuit, MECC) were prospectively randomized to using a so-called Smart suction device or a routine continuous autotransfusion system (C.A.T.S.®) for collection of mediastinal shed blood. The coagulation response was measured by thrombin-antithrombin complex (TAT) and D-dimer. The inflammatory response was measured by Interleukin 6 (IL-6) and complement factor 3a (C3a) at three different time points, before surgery, 2h after surgery, as well as 18 h after surgery.
  
  
  RESULTS
  No serious adverse cardiovascular event was observed. Serum levels of TAT significantly differed between both groups 2h after surgery (Smart suction 16.12 ± 13.51 μg l⁻¹ vs C.A.T.S® 9.83 ± 7.81 μg l⁻¹, p = 0.040) and returned to baseline values after 18 h in both groups. Serum levels of D-dimer showed a corresponding pattern with a peak 2h after surgery (Smart suction 1115 ± 1231 ng ml⁻¹ vs C.A.T.S.® 507 ± 604 ng ml⁻¹, p = 0.025). IL-6 levels also significantly differed between both groups 2h after surgery (Smart suction 186 ± 306 pg ml⁻¹ vs C.A.T.S.® 82 ± 71 pg ml⁻¹, p = 0.072). No significant changes in serum levels of C3a over time could be observed.
  
  
  CONCLUSIONS
  Despite no differences in the clinical course of patients with either Smart suction or C.A.T.S.® being observed, surrogate markers of coagulation and inflammation seem to be less pronounced in patients where cardiotomy blood is not being directly reinfused. As such, C.A.T.S.® should be preferred in routine CABG, as long as no extensive volume substitution is anticipated.
authors.affiliation: Clinic of Cardiovascular Surgery, University Hospital, Freiburgstrasse, 3010 Bern, Switzerland.
authors.forename: Hansjörg
authors.initials: H
authors.lastname: Jenni
authors.forename: Julia
authors.initials: J
authors.lastname: Rheinberger
authors.forename: Martin
authors.initials: M
authors.lastname: Czerny
authors.forename: Erich
authors.initials: E
authors.lastname: Gygax
authors.forename: Robert
authors.initials: R
authors.lastname: Rieben
authors.forename: Eva
authors.initials: E
authors.lastname: Krähenbühl
authors.forename: Thierry
authors.initials: T
authors.lastname: Carrel
authors.forename: Mario
authors.initials: M
authors.lastname: Stalder
mesh_terms: D000368:Aged; D000990:Antithrombin III; D015415:Biomarkers / Q000097:blood; D001777:Blood Coagulation / Q000502:physiology*; D001804:Blood Transfusion, Autologous; D015926:Complement C3a / Q000378:metabolism; D001026:Coronary Artery Bypass / Q000009:adverse effects / Q000295:instrumentation* / Q000379:methods; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D015850:Interleukin-6 / Q000097:blood; D008875:Middle Aged; D010447:Peptide Hydrolases / Q000097:blood; D011446:Prospective Studies; D013396:Suction; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood / Q000209:etiology*
chemical_list: D015415:Biomarkers; D005338:Fibrin Fibrinogen Degradation Products; D018836:Inflammation Mediators; D015850:Interleukin-6; C046193:antithrombin III-protease complex; C036309:fibrin fragment D; D015926:Complement C3a; D000990:Antithrombin III; D010447:Peptide Hydrolases