title: B-type natriuretic peptide release and left ventricular filling pressure assessed by echocardiographic study after subarachnoid hemorrhage: a prospective study in non-cardiac patients.
abstract: BACKGROUND
  Serum B-type natriuretic peptide (BNP) is frequently elevated after subarachnoid hemorrhage (SAH), but whether this high BNP level is related to transient elevation of left ventricular filling pressure (LVFP) is unknown. However, in patients with preexistent cardiac pathologies, it is impossible to differentiate between BNP elevation caused by chronic cardiac abnormalities and BNP related to acute neurocardiac injury.
  
  
  METHODS
  All adult patients with SAH admitted to our intensive care unit were eligible. Patients were excluded for the following reasons: admission >48 hours after aneurysm rupture, pre-existing hypertension, or cardiac disease. Levels of BNP and cardiac troponin Ic were measured daily for 7 days. Echocardiography was performed by a blinded cardiologist on days 1, 2, and 7. Doppler signals from the mitral inflow, tissue Doppler, and the color M-mode-derived flow propagation velocity (FPV) were obtained to assess echo-estimated LVFP.
  
  
  RESULTS
  During a 3-year period, sixty-six consecutive patients with SAH were admitted. Thirty one patients were studied. The BNP level was >100 ng/L in 25 patients (80%) during the first 3 days, with a peak on day 2 (median, 126 ng/L) followed by a gradual decrease (median variation days 1 to 7, 70%). All patients had an ejection fraction >50%. Early transmitral velocity/tissue Doppler mitral annular early diastolic velocity was low: 5.4 (+/- 1.5) on day 1, 5.8 (+/- 1.2) on day 2, and 5.1 (+/- 0.9) on day 7. Early transmitral velocity/FPV was also low: 1.27 (+/- 0.4), 1.25 (+/- 0.3), and 1.1 (+/- 0.2) on days 1, 2, and 7, respectively. Cardiac troponin Ic levels ranged from 0 to 3.67 microg/L and were correlated with BNP (r = 0.63, P < 0.01).
  
  
  CONCLUSIONS
  BNP rises gradually over two days and return to normal within a week after SAH. Its release is associated with myocardial necrosis, but is unrelated to elevated LVFP assessed by echocardiography.
authors.affiliation: Department of Anesthesiology and Critical Care, Hôpital d'Instruction des Armées Sainte-Anne, Boulevard Sainte-Anne, Toulon, BP 20545 - 83041 Cedex 9, France. meaudre@club-internet.fr
authors.forename: Eric
authors.initials: E
authors.lastname: Meaudre
authors.forename: Christophe
authors.initials: C
authors.lastname: Jego
authors.forename: Nadia
authors.initials: N
authors.lastname: Kenane
authors.forename: Ambroise
authors.initials: A
authors.lastname: Montcriol
authors.forename: Henry
authors.initials: H
authors.lastname: Boret
authors.forename: Philippe
authors.initials: P
authors.lastname: Goutorbe
authors.forename: Gilbert
authors.initials: G
authors.lastname: Habib
authors.forename: Bruno
authors.initials: B
authors.lastname: Palmier
mesh_terms: D000208:Acute Disease; D000328:Adult; D009202:Cardiomyopathies / Q000097:blood / Q000473:pathology; D015150:Echocardiography, Doppler; D005260:Female; D006439:Hemodynamics; D006801:Humans; D008297:Male; D020097:Natriuretic Peptide, Brain / Q000097:blood*; D009336:Necrosis / Q000097:blood; D011446:Prospective Studies; D013345:Subarachnoid Hemorrhage / Q000097:blood*; D019210:Troponin I / Q000097:blood; D018487:Ventricular Dysfunction, Left / Q000097:blood* / Q000000981:diagnostic imaging
chemical_list: D019210:Troponin I; D020097:Natriuretic Peptide, Brain