A rapid test for B-type natriuretic peptide correlates with falling wedge pressures in patients treated for decompensated heart failure: A pilot study

被引:310
作者
Kazanegra, R
Cheng, V
Garcia, A
Krishnaswamy, P
Gardetto, N
Clopton, P
Maisel, A
机构
[1] VAMC Cardiol 111A, Div Cardiol, San Diego, CA 92161 USA
[2] Vet Affairs Med Ctr, Dept Med, San Diego, CA 92161 USA
[3] Univ Calif San Diego, San Diego, CA 92103 USA
关键词
neurohormonal; Swan-Ganz; left ventricular pressure; NYHA; inotrope; vasodilator;
D O I
10.1054/jcaf.2001.23355
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objectives: To determine if changes in B-type natriuretic peptide (BNP) levels can accurately reflect acute changes in pulmonary capillary wedge pressure during treatment of decompensated heart failure. Background: Tailored therapy of decompensated congestive heart failure with hemodynamic monitoring is controversial. Other than the expense and complications of Swan-Ganz catheters, its use in titration of drug therapy has no conclusive end point. Because BNP reflects both elevated left ventricular pressure and neurohormonal modulation and has a short half-life, we hypothesized that levels of BNP would decline in association with falling wedge pressures. Final BNP levels would perhaps signify a new set point of neuromodulation. Methods and Results: Twenty patients with decompensated New York Heart Association (NYHA) class: III-IV congestive heart failure (CHF) undergoing tailored therapy were studied. BNP levels were drawn every 2 to 4 hours for the first 24 hours (active treatment phase) and then every 4 hours for the next 24 to 48 hours (stabilization period). Hemodynamic data was recorded simultaneously. In 15 patients whose wedge pressure responded to treatment in the first 21 hours. there was a significant drop in BNP levels (55%) versus nonresponders (8%). There was a significant correlation between percent change in wedge pressure from baseline per hour and the percent change of BNP from baseline per hour (r = 0.79, P < .05). When the wedge pressure was kept at a stable, low level during the stabilization phase. BNP levels continued to frill another 37% (937 <plus/minus> 140 pg/mL at 24 hours to 605 +/- 128 pg/mL). Patients who died (n = 1) had higher final BNP levels (1,078 +/- 123 pg/mL v 701 +/- 107 pg/mL). Conclusions: The data suggest that rapid testing of BNP may be an effective way to improve the in-hospital management of patients admitted with decompensated CHF. Although BNP levels will not obviate the need for invasive hemodynamic monitoring, it may be a useful adjunct in tailoring therapy to these patients.
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页码:21 / 29
页数:9
相关论文
共 67 条
[21]  
Grantham JA, 1997, CIRCULATION, V96, P388
[22]   RAPID VENTRICULAR INDUCTION OF BRAIN NATRIURETIC PEPTIDE GENE-EXPRESSION IN EXPERIMENTAL ACUTE MYOCARDIAL-INFARCTION [J].
HAMA, N ;
ITOH, H ;
SHIRAKAMI, G ;
NAKAGAWA, O ;
SUGA, S ;
OGAWA, Y ;
MASUDA, I ;
NAKANISHI, K ;
YOSHIMASA, T ;
HASHIMOTO, Y ;
YAMAGUCHI, M ;
HORI, R ;
YASUE, H ;
NAKAO, K .
CIRCULATION, 1995, 92 (06) :1558-1564
[23]   An experimental study of cardiac natriuretic peptides as markers of development of congestive heart failure [J].
Klinge, R ;
Hystad, M ;
Kjekshus, J ;
Karlberg, BE ;
Djoseland, O ;
Aakvaag, A ;
Hall, C .
SCANDINAVIAN JOURNAL OF CLINICAL & LABORATORY INVESTIGATION, 1998, 58 (08) :683-691
[24]   CLONING AND SEQUENCE-ANALYSIS OF CDNA-ENCODING A PRECURSOR FOR RAT-BRAIN NATRIURETIC PEPTIDE [J].
KOJIMA, M ;
MINAMINO, N ;
KANGAWA, K ;
MATSUO, H .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1989, 159 (03) :1420-1426
[25]   Differential atrial and ventricular expression of myocardial BNP during evolution of heart failure [J].
Luchner, A ;
Stevens, TL ;
Borgeson, DD ;
Redfield, M ;
Wei, CM ;
Porter, JG ;
Burnett, JC .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1998, 274 (05) :H1684-H1689
[26]   Plasma brain natriuretic peptide as a biochemical marker of high left ventricular end-diastolic pressure in patients with symptomatic left ventricular dysfunction [J].
Maeda, K ;
Tsutamoto, T ;
Wada, A ;
Hisanaga, T ;
Kinoshita, M .
AMERICAN HEART JOURNAL, 1998, 135 (05) :825-832
[27]  
MAEDA K, 1999, J AM COLL CARDIOL A, V192, P1140
[28]   Mechanisms and models in heart failure - A combinatorial approach [J].
Mann, DL .
CIRCULATION, 1999, 100 (09) :999-1008
[29]   Evaluation of plasma natriuretic peptides as markers for left ventricular dysfunction [J].
Muders, F ;
Kromer, EP ;
Griese, DP ;
Pfeifer, M ;
Hense, HW ;
Riegger, GAJ ;
Elsner, D .
AMERICAN HEART JOURNAL, 1997, 134 (03) :442-449
[30]   Titration of vasodilator therapy in chronic heart failure according to plasma brain natriuretic peptide concentration: Randomized comparison of the hemodynamic and neuroendocrine effects of tailored versus empirical therapy [J].
Murdoch, DR ;
McDonagh, TA ;
Byrne, J ;
Blue, L ;
Farmer, R ;
Morton, JJ ;
Dargie, HJ .
AMERICAN HEART JOURNAL, 1999, 138 (06) :1126-1132