title: Subarachnoid hemorrhage induces an early and reversible cardiac injury associated with catecholamine release: one-week follow-up study.
abstract: BACKGROUND
  The occurrence of cardiac dysfunction is common after subarachnoid hemorrhage (SAH) and was hypothesized to be related to the release of endogenous catecholamines. The aim of this prospective study was to evaluate the relationship between endogenous catecholamine and cardiac dysfunction at the onset and during the first week after SAH.
  
  
  METHODS
  Forty consecutive patients admitted for acute SAH without known heart disease were included. Catecholamine plasma concentrations and transthoracic echocardiography (TTE) were documented on admission, on day 1 (D1), and day 7 (D7).
  
  
  RESULTS
  At baseline, 24 patients had a World Federation of Neurosurgical Societies score (WFNS) of one or two; the remaining 16 had a WFNS between three and five. Twenty patients showed signs of cardiac dysfunction on admission, including six with left ventricle (LV) systolodiastolic dysfunction and 14 with pure LV diastolic dysfunction. On admission, norepinephrine, epinephrine, dopamine, B-type Natriuretic Peptide (BNP) and Troponin Ic (cTnI) plasmatic levels were higher in patients with the higher WFNS score and in patients with altered cardiac function (all P <0.05). Among patients with cardiac injury, heart function was restored within one week in 13 patients, while seven showed persistent LV diastolic dysfunction (P = 0.002). Plasma BNP, cTnI, and catecholamine levels exerted a decrease towards normal values between D1 and D7.
  
  
  CONCLUSIONS
  Our findings show that cardiac dysfunction seen early after SAH was associated with both a rapid and sustained endogenous catecholamine release and WFNS score. SAH-induced cardiac dysfunction was regressive over the first week and paralleled the normalization of catecholamine concentration.
authors.forename: Reda
authors.initials: R
authors.lastname: Salem
authors.forename: Fabrice
authors.initials: F
authors.lastname: Vallée
authors.forename: François
authors.initials: F
authors.lastname: Dépret
authors.forename: Jacques
authors.initials: J
authors.lastname: Callebert
authors.forename: Jean Pierre Saint
authors.initials: JP
authors.lastname: Maurice
authors.forename: Philippe
authors.initials: P
authors.lastname: Marty
authors.forename: Joaquim
authors.initials: J
authors.lastname: Matéo
authors.forename: Catherine
authors.initials: C
authors.lastname: Madadaki
authors.forename: Emmanuel
authors.initials: E
authors.lastname: Houdart
authors.forename: Damien
authors.initials: D
authors.lastname: Bresson
authors.forename: Sebastien
authors.initials: S
authors.lastname: Froelich
authors.forename: Christian
authors.initials: C
authors.lastname: Stapf
authors.forename: Didier
authors.initials: D
authors.lastname: Payen
authors.forename: Alexandre
authors.initials: A
authors.lastname: Mebazaa
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D009202:Cardiomyopathies / Q000097:blood / Q000209:etiology*; D002395:Catecholamines / Q000097:blood*; D004452:Echocardiography / Q000379:methods; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D013345:Subarachnoid Hemorrhage / Q000097:blood / Q000150:complications*; D013997:Time Factors; D019210:Troponin I / Q000097:blood; D018487:Ventricular Dysfunction, Left / Q000097:blood
chemical_list: D015415:Biomarkers; D002395:Catecholamines; D019210:Troponin I; D020097:Natriuretic Peptide, Brain