title: Prevalence and implications of diastolic dysfunction after subarachnoid hemorrhage.
abstract: BACKGROUND
  Electrocardiographic changes, troponin release, and reduced left ventricular ejection fraction have been described after subarachnoid hemorrhage (SAH). Little is known about the occurrence of diastolic dysfunction in this setting. The purpose of this study was to determine the prevalence of diastolic dysfunction and its association with cardiac outcomes after SAH.
  
  
  METHODS
  SAH patients were prospectively enrolled into the study, and echocardiographic, clinical, chest X-ray, and cardiac troponin I data were obtained on days 1, 3, and 6 after enrollment. Each echocardiogram included Doppler recordings of mitral inflow and pulmonary venous flow. For each study, diastolic function was categorized as normal, impaired relaxation, pseudonormal, or restrictive. The relationships between diastolic dysfunction and pulmonary edema-elevated cardiac troponin I and left ventricular contractile dysfunction were quantified using both univariate and multivariate statistical methods. Clinical predictors of diastolic dysfunction were defined by multivariate logistic regression.
  
  
  RESULTS
  Of 223 enrolled subjects, 207 had technically adequate Doppler data. Diastolic dysfunction was observed in 71% of subjects. The prevalence of diastolic versus systolic dysfunction in 44 patients with pulmonary edema was 91 versus 37%, respectively (p=0.001). After multivariate statistical adjustment, diastolic dysfunction remained a significant predictor of pulmonary edema (odds ratio [OR] 3.34, 95% CI=1.05-10.59). Diastolic dysfunction also was associated with troponin release (p=0.02). A history of hypertension and increasing age were predictive of diastolic dysfunction.
  
  
  CONCLUSIONS
  Diastolic dysfunction is common after SAH. It is associated with history of hypertension and older age and may explain the development of pulmonary edema in many SAH patients.
authors.affiliation: Division of Cardiology, University of California San Francisco Medical Center, San Francisco, CA 94143-0124, USA.
authors.forename: Alexander
authors.initials: A
authors.lastname: Kopelnik
authors.forename: Landis
authors.initials: L
authors.lastname: Fisher
authors.forename: Jacob C
authors.initials: JC
authors.lastname: Miss
authors.forename: Nader
authors.initials: N
authors.lastname: Banki
authors.forename: Poyee
authors.initials: P
authors.lastname: Tung
authors.forename: Michael T
authors.initials: MT
authors.lastname: Lawton
authors.forename: Nerissa
authors.initials: N
authors.lastname: Ko
authors.forename: Wade S
authors.initials: WS
authors.lastname: Smith
authors.forename: Barbara
authors.initials: B
authors.lastname: Drew
authors.forename: Elyse
authors.initials: E
authors.lastname: Foster
authors.forename: Jonathan
authors.initials: J
authors.lastname: Zaroff
mesh_terms: D000328:Adult; D000368:Aged; D001794:Blood Pressure; D003327:Coronary Disease / Q000453:epidemiology; D003971:Diastole / Q000502:physiology*; D017548:Echocardiography, Transesophageal; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010656:Phenylephrine; D015995:Prevalence; D012307:Risk Factors; D013345:Subarachnoid Hemorrhage / Q000453:epidemiology / Q000503:physiopathology*; D019210:Troponin I / Q000097:blood; D016277:Ventricular Function, Left / Q000187:drug effects / Q000502:physiology
chemical_list: D019210:Troponin I; D010656:Phenylephrine