title: Lactic acidosis after cardiac transplantation: foe or common innocent bystander?
abstract: BACKGROUND
  Lactic acidosis (LA) frequently occurs after heart transplantation (HTx). It is hypothesized to be related to inotropic support or metabolic derangements from chronic heart failure. As such, restoring hemodynamic stability with mechanical circulatory support before HTx should mitigate this problem. Our aim was to evaluate the incidence and outcomes of LA after HTx.
  
  
  METHODS
  We evaluated HTx recipients January 2000 to May 2011. Post-HTx outcomes included graft dysfunction, length of intensive care unit stay, length of hospital stay, inotropic support, and survival.
  
  
  RESULTS
  Of 143 eligible patients, 98.6% had LA, 67% severe, after HTx. Data were analyzed based on the severity of LA. Time to peak lactate, intensive care unit stay, length of hospital stay, peak glucose, inotropic dose, graft dysfunction, and survival after HTx were similar between groups. Statistically significant differences included pretransplant support (25.6% mechanical circulatory support in nonsevere vs. 44.9% severe LA), hospitalization at the time of HTx (37.2% vs. 21.4%), glucose at the time of peak lactate (182.88 ± 69.80 vs. 221.31 ± 56.91), ischemic time (187.4 ± 63.1 vs. 215.5 ± 68.1), and duration of inotrope.
  
  
  CONCLUSIONS
  Severe LA is common after HTx, though it appears to be transient and benign. Mechanical circulatory support after HTx does not prevent LA. High lactate levels are associated with longer ischemic times, longer duration of inotrope, and correspond with higher glucose levels. The underlying mechanism is yet to be satisfactorily elucidated.
authors.affiliation: 1 Heart Failure and Transplant Program, Intermountain Heart Institute, Salt Lake City, UT.
authors.forename: Jennifer L
authors.initials: JL
authors.lastname: Nixon
authors.forename: Abdallah G
authors.initials: AG
authors.lastname: Kfoury
authors.forename: Raymond
authors.initials: R
authors.lastname: McCubrey
authors.forename: Kim
authors.initials: K
authors.lastname: Brunisholz
authors.forename: Tami
authors.initials: T
authors.lastname: Bair
authors.forename: Kyle D
authors.initials: KD
authors.lastname: Balling
authors.forename: Deborah
authors.initials: D
authors.lastname: Budge
authors.forename: John
authors.initials: J
authors.lastname: Doty
authors.forename: Brad
authors.initials: B
authors.lastname: Rasmusson
authors.forename: Bruce
authors.initials: B
authors.lastname: Reid
authors.forename: Hildegard
authors.initials: H
authors.lastname: Smith
authors.forename: George
authors.initials: G
authors.lastname: Thomsen
authors.forename: Mark
authors.initials: M
authors.lastname: Goddard
authors.forename: Rami
authors.initials: R
authors.lastname: Alharethi
mesh_terms: D000140:Acidosis, Lactic / Q000453:epidemiology / Q000209:etiology* / Q000628:therapy; D000328:Adult; D001243:Assisted Circulation; D002316:Cardiotonic Agents / Q000627:therapeutic use; D005260:Female; D006085:Graft Survival; D016027:Heart Transplantation / Q000009:adverse effects*; D006801:Humans; D015994:Incidence; D019344:Lactic Acid / Q000097:blood; D008297:Male; D008875:Middle Aged; D009926:Organ Preservation; D012307:Risk Factors; D016896:Treatment Outcome; D014589:Utah / Q000453:epidemiology
chemical_list: D002316:Cardiotonic Agents; D019344:Lactic Acid