title: Hypernatremia predicts adverse cardiovascular and neurological outcomes after SAH.
abstract: BACKGROUND
  Abnormalities of serum sodium are common after subarachnoid hemorrhage (SAH) and have been linked to poor outcome. This study analyzed whether abnormal serum sodium levels are associated with cardiac outcomes and mortality after subarachnoid hemorrhage (SAH).
  
  
  METHODS
  In a prospective cohort study of SAH patients, the primary predictor variable was subjects' sodium level. Hypernatremia was defined as sodium >143 mmol/L and hyponatremia was <133 mmol/L. Cardiac troponin I (cTi) was measured and echocardiography was performed on three study days. Dichotomous outcome variables were cTi > 1.0 microg/L, left-ventricular ejection fraction (LVEF) <50%, presence (vs absence) of regional wall motion abnormalities (RWMA) of the LV, pulmonary edema, and death. Additional analyses studied the degree of hypernatremia and sodium supplementation, and the temporal relationship between hypernatremia and cardiac outcomes.
  
  
  RESULTS
  The study included 214 subjects. Forty-eight subjects (22%) were hypernatremic on at least one study day, and 45 (21%) were hyponatremic. After multivariate adjustment, hypernatremia was an independent predictor of LVEF <50% (OR 4.7, CI 1.3-16.2, p = 0.015), elevated cTi (OR 3.7, CI 1.2-11.9, p = 0.028), and pulmonary edema (OR 4.1 CI 1.4-1.5, p = 0.008). It was not, however a statistically significant predictor of mortality (p = 0.075).
  
  
  CONCLUSIONS
  In the acute period after SAH, hypernatremia is associated with adverse cardiac outcomes and death. SAH patients with hypernatremia should be monitored for evidence of cardiac dysfunction.
authors.affiliation: Division of Cardiology, UCSF Medical Center, San Francisco, CA, USA.
authors.forename: Landis A
authors.initials: LA
authors.lastname: Fisher
authors.forename: Nerissa
authors.initials: N
authors.lastname: Ko
authors.forename: Jacob
authors.initials: J
authors.lastname: Miss
authors.forename: Poyee P
authors.initials: PP
authors.lastname: Tung
authors.forename: Alexander
authors.initials: A
authors.lastname: Kopelnik
authors.forename: Nader M
authors.initials: NM
authors.lastname: Banki
authors.forename: David
authors.initials: D
authors.lastname: Gardner
authors.forename: Wade S
authors.initials: WS
authors.lastname: Smith
authors.forename: Michael T
authors.initials: MT
authors.lastname: Lawton
authors.forename: Jonathan G
authors.initials: JG
authors.lastname: Zaroff
mesh_terms: D001925:Brain Damage, Chronic / Q000401:mortality* / Q000503:physiopathology*; D015331:Cohort Studies; D003422:Critical Care; D004452:Echocardiography; D005260:Female; D017052:Hospital Mortality; D006801:Humans; D006955:Hypernatremia / Q000401:mortality* / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D009460:Neurologic Examination; D011379:Prognosis; D011446:Prospective Studies; D011654:Pulmonary Edema / Q000401:mortality / Q000503:physiopathology; D012964:Sodium / Q000097:blood; D013318:Stroke Volume / Q000502:physiology; D013345:Subarachnoid Hemorrhage / Q000401:mortality* / Q000503:physiopathology*; D013564:Sympathetic Nervous System / Q000503:physiopathology; D018487:Ventricular Dysfunction, Left / Q000401:mortality / Q000503:physiopathology*
chemical_list: D012964:Sodium