title: Improvement of donor myocardial function after treatment of autonomic storm during brain death.
abstract: BACKGROUND
  In experimental brain death models, autonomic storm (AS) triggers severe myocardial dysfunction, which can be attenuated by pharmacologic treatment. The aim of this study was to determine the incidence of AS in a cohort of human organ donors and to evaluate the potential interest of AS treatment on myocardial function, cardiac harvesting and transplantation.
  
  
  METHODS
  The cohort consisted of 152 patients. Among them, 46 patients were initially considered as potential cardiac donors (main criteria: age < 60 years, no history of cardiac disease). AS diagnosis included increased systolic arterial pressure > 200 mm Hg associated with tachycardia >140 beats/min. Heart acceptance criteria were associated creatine kinase (CK), troponin Ic, and left ventricle ejection fraction (LVEF) estimated by echocardiography and visual inspection.
  
  
  RESULTS
  AS was observed in 29 patients (63%). Hypertension was treated in 12 patients (esmolol n = 6, urapidil n = 5, nicardipine). Cardiac harvesting was performed in 28 donors (61%). LVEFs were significantly higher after AS treatment (no AS: 55.4 +/- 13.4%, untreated AS: 49.0 +/- 18.8%, treated AS: 63.9+ +/- 10.3%, P = 0.049). AS treatment was found to be independently associated with LVEF in > 50% of the cases (P = 0.034). Treatment of AS or the lack of AS were associated with an increased probability of successful cardiac transplantation (OR = 8.8; 95% CI 2.1-38.3, P = 0.002).
  
  
  CONCLUSIONS
  Treatment of hypertension during AS may attenuate brain death-induced myocardial dysfunction and increase the number of available cardiac grafts.
authors.affiliation: Service d'Anesthésie-Réanimation, Centre Hospitalier Universitaire de Nancy, Nancy, France.
authors.forename: Gérard
authors.initials: G
authors.lastname: Audibert
authors.forename: Claire
authors.initials: C
authors.lastname: Charpentier
authors.forename: Carole
authors.initials: C
authors.lastname: Seguin-Devaux
authors.forename: Pierre-Alain
authors.initials: PA
authors.lastname: Charretier
authors.forename: Hélène
authors.initials: H
authors.lastname: Grégoire
authors.forename: Yvan
authors.initials: Y
authors.lastname: Devaux
authors.forename: Jean-François
authors.initials: JF
authors.lastname: Perrier
authors.forename: Dan
authors.initials: D
authors.lastname: Longrois
authors.forename: Paul-Michel
authors.initials: PM
authors.lastname: Mertes
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000328:Adult; D001926:Brain Death / Q000473:pathology*; D015331:Cohort Studies; D003402:Creatine Kinase / Q000378:metabolism; D004452:Echocardiography; D005260:Female; D016027:Heart Transplantation / Q000379:methods*; D006801:Humans; D006973:Hypertension / Q000628:therapy; D008297:Male; D008875:Middle Aged; D009529:Nicardipine / Q000494:pharmacology; D010879:Piperazines / Q000494:pharmacology; D011412:Propanolamines / Q000494:pharmacology; D012189:Retrospective Studies; D014665:Vasodilator Agents / Q000494:pharmacology; D016277:Ventricular Function, Left
chemical_list: D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D010879:Piperazines; D011412:Propanolamines; D014665:Vasodilator Agents; C015568:urapidil; D009529:Nicardipine; D003402:Creatine Kinase; C036604:esmolol