Plasma B-type natriuretic peptide levels are associated with early cardiac dysfunction after subarachnoid hemorrhage

被引:92
作者
Tung, PP
Olmsted, E
Kopelnik, A
Banki, NM
Drew, BJ
Ko, N
Lawton, MT
Smith, W
Foster, E
Young, WL
Zaroff, JG
机构
[1] Univ Calif San Francisco, Div Cardiol, San Francisco, CA 94143 USA
[2] Univ Calif San Francisco, Gen Clin Res Ctr, San Francisco, CA 94143 USA
[3] Univ Calif San Francisco, Dept Physiol Nursing, San Francisco, CA 94143 USA
[4] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA
[5] Univ Calif San Francisco, Dept Neurol Surg, San Francisco, CA 94143 USA
关键词
aneurysm; echocardiography; natriuretic peptides; atrial; stroke; sympathetic nervous system;
D O I
10.1161/01.STR.0000170699.59783.d6
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Background and Purpose - Serum B-type natriuretic peptide (BNP) is elevated after subarachnoid hemorrhage (SAH), as well as in the setting of congestive heart failure and myocardial infarction. The aim of this study was to prospectively quantify the relationship between BNP levels and cardiac outcomes after SAH. Methods - Plasma was collected for BNP measurements as soon as possible after enrollment; a mean of 5 +/- 4 days after SAH symptom onset. On days 1, 3, and 6 after enrollment, troponin I (cTi) was measured and 2-dimensional echocardiography was performed. The following cardiac variables were collected and treated dichotomously: left ventricular ejection fraction (LVEF), regional wall motion abnormalities (RWMA), diastolic dysfunction, pulmonary edema, and cTi. Results - There were 57 subjects. The median BNP level was 141 pg/mL (range, 0.8 to 3330 pg/mL). Higher mean BNP levels were present in those with RWMA (550 versus 261 pg/mL; P = 0.012), diastolic dysfunction (360 versus 44; P = 0.011), pulmonary edema (719 versus 204; P = 0.016), elevated cTi (662 versus 240; P = 0.004), and LVEF < 50 % ( 644 versus 281; P = 0.015). Conclusion - Early after SAH, elevated BNP levels are associated with myocardial necrosis, pulmonary edema, and both systolic and diastolic dysfunction of the left ventricle. These findings support the hypothesis that the heart releases BNP into the systemic circulation early after SAH.
引用
收藏
页码:1567 / 1569
页数:3
相关论文
共 11 条
[1]   Secretion of brain natriuretic peptide in patients with aneurysmal subarachnoid haemorrhage [J].
Berendes, E ;
Walter, M ;
Cullen, P ;
Prien, T ;
VanAken, H ;
Horsthemke, J ;
Schulte, M ;
vonWild, K ;
Scherer, R .
LANCET, 1997, 349 (9047) :245-249
[2]   Differential secretion of atrial and brain natriuretic peptide in critically ill patients [J].
Berendes, E ;
Van Aken, H ;
Raufhake, C ;
Schmidt, C ;
Assmann, G ;
Walter, M .
ANESTHESIA AND ANALGESIA, 2001, 93 (03) :676-682
[3]   The prognostic value of B-type natriuretic peptide in patients with acute coronary syndromes [J].
de Lemos, JA ;
Morrow, DA ;
Bentley, JH ;
Omland, T ;
Sabatine, MS ;
McCabe, CH ;
Hall, C ;
Cannon, CP ;
Braunwald, E .
NEW ENGLAND JOURNAL OF MEDICINE, 2001, 345 (14) :1014-1021
[4]   The neuro-cardio-endocrine response to acute subarachnoid haemorrhage [J].
Espiner, EA ;
Leikis, R ;
Ferch, RD ;
MacFarlane, MR ;
Bonkowski, JA ;
Frampton, CM ;
Richards, AM .
CLINICAL ENDOCRINOLOGY, 2002, 56 (05) :629-635
[5]  
Kantor Howard L., 1995, Cardiology Clinics, V13, P179
[6]   A practical approach to the echocardiographic evaluation of diastolic function [J].
Khouri, SJ ;
Maly, GT ;
Suh, DD ;
Walsh, TE .
JOURNAL OF THE AMERICAN SOCIETY OF ECHOCARDIOGRAPHY, 2004, 17 (03) :290-297
[7]  
Maisel Alan, 2001, Cardiology Clinics, V19, P557, DOI 10.1016/S0733-8651(05)70243-5
[8]   Correlation of serum brain natriuretic peptide with hyponatremia and delayed ischemic neurological deficits after subarachnoid hemorrhage [J].
McGirt, MJ ;
Blessing, R ;
Nimjee, SM ;
Friedman, AH ;
Alexander, MJ ;
Laskowitz, DT ;
Lynch, JR .
NEUROSURGERY, 2004, 54 (06) :1369-1373
[9]  
Schiller N B, 1989, J Am Soc Echocardiogr, V2, P358
[10]   Plasma concentrations of brain natriuretic peptide in patients with subarachnoid hemorrhage [J].
Tomida, M ;
Muraki, M ;
Uemura, K ;
Yamasaki, K .
STROKE, 1998, 29 (08) :1584-1587