Kazanegra R, Cheng V, Garcia A, Krishnaswamy P, Gardetto N, Clopton P, Maisel A
Division of Cardiology, Department of Medicine, Veteran's Affairs Medical Center, San Diego, California 92161, USA.
J Card Fail. 2001 Mar;7(1):21-9. doi: 10.1054/jcaf.2001.23355.
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.
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.
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).
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.
确定B型利钠肽（BNP）水平的变化能否准确反映失代偿性心力衰竭治疗期间肺毛细血管楔压的急性变化。
通过血流动力学监测对失代偿性充血性心力衰竭进行个体化治疗存在争议。除了Swan-Ganz导管的费用和并发症外，其在药物治疗滴定中的应用没有明确的终点。由于BNP既反映左心室压力升高又反映神经激素调节，且半衰期短，我们假设BNP水平会随着楔压下降而降低。最终的BNP水平可能意味着神经调节的新设定点。
对20例接受个体化治疗的纽约心脏协会（NYHA）III-IV级失代偿性充血性心力衰竭（CHF）患者进行研究。在最初24小时（积极治疗阶段）每2至4小时检测一次BNP水平，随后在接下来的24至48小时（稳定期）每4小时检测一次。同时记录血流动力学数据。在15例楔压在最初24小时对治疗有反应的患者中，BNP水平显著下降（55%），而无反应者为8%。每小时楔压相对于基线的变化百分比与每小时BNP相对于基线的变化百分比之间存在显著相关性（r = 0.79，P <.05）。在稳定期，当楔压保持在稳定的低水平时，BNP水平继续下降37%（24小时时为937±140 pg/mL降至605±128 pg/mL）。死亡患者（n = 4）的最终BNP水平更高（1,078±123 pg/mL对701±107 pg/mL）。
数据表明，快速检测BNP可能是改善失代偿性CHF入院患者院内管理的有效方法。虽然BNP水平不能消除有创血流动力学监测的必要性，但它可能是为这些患者制定治疗方案的有用辅助手段。
