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

• Published in: Journal of cardiac failure Vol. 7; no. 1; pp. 21 - 29
• Main Authors: Kazanegra, Radmila, Cheng, Van, Garcia, Alex, Krishnaswamy, Padma, Gardetto, Nancy, Clopton, Paul, Maisel, Alan
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01-03-2001
• Subjects: Aged; Atrial Natriuretic Factor - blood; Atrial Natriuretic Factor - pharmacology; Blood Urea Nitrogen; Heart Failure - blood; Heart Failure - mortality; Heart Failure - physiopathology; Humans; inotrope; left ventricular pressure; Male; Middle Aged; Natriuretic Peptide, Brain; neurohormonal; NYHA; Pilot Projects; Prognosis; Pulmonary Wedge Pressure - drug effects; Pulmonary Wedge Pressure - physiology; Survival Analysis; Swan-Ganz; Time Factors; vasodilator; NYHA; left ventricular pressure; Swan-Ganz; neurohormonal; vasodilator; inotrope
• ISSN: 1071-9164; 1532-8414
• DOI: 10.1054/jcaf.2001.23355

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 24 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 fall another 37% (937 ± 140 pg/mL at 24 hours to 605 ± 128 pg/mL). Patients who died (n = 4) 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.