Aronson Doron, Burger Andrew J
Department of Cardiology, Rambam Medical Center, Haifa, Israel; Rappaport Faculty of Medicine, Technion, Israel Institute of Technology, Haifa, Israel.
Division of Cardiovascular Disease, University of Cincinnati, Cincinnati, Ohio.
J Card Fail. 2016 Mar;22(3):193-200. doi: 10.1016/j.cardfail.2015.07.006. Epub 2015 Jul 21.
The aims of this work were to investigate the clinical and hemodynamic profile underlying the response to loop diuretics in acute decompensated heart failure (ADHF), and to compare the relative usefulness of measures of diuretic resistance for predicting mortality.
We studied 475 patients with ADHF, of whom 241 underwent right heart catheterization. Linear regression models were used to identify factors that affected urine output. Loop diuretics response was estimated as (1) net fluid loss per 40 mg furosemide equivalents and (2) urine output produced per 40 mg furosemide equivalents. In a multivariable regression model, key independent predictors of urine output included diuretic dose (partial r = 0.44), baseline renal function (partial r = 0.38), systolic blood pressure (partial r = 0.26), and fluid intake (partial r = 0.31; all P < .0001). Among hemodynamic variables, elevated right atrial pressure was associated with greater urine output (partial r = 0.19; P = .002). The partial correlation attributable to diuretic dose (partial R2 = 0.19) accounted for approximately one-half of the variance in urine output explained by the model (model R2 = 0.40).Cox regression models demonstrated inverse relationships between quartiles of net fluid loss (P = .004) and quartiles of urine output (P = .04) per 40 mg furosemide and 6-month mortality. When comparing nested models, the model based on net fluid loss was better than the model based on urine output for the prediction of mortality (χ2 = 8.1; 3 df; P = .04).
In patients with ADHF, beyond diuretic dose, other parameters including renal function, hemodynamic status, the degree of volume overload, and fluids intake also affect urine output. Measures of loop diuretic response are associated with short-term mortality.
本研究旨在探讨急性失代偿性心力衰竭(ADHF)患者对襻利尿剂反应的临床和血流动力学特征,并比较利尿剂抵抗指标对预测死亡率的相对效用。
我们研究了475例ADHF患者,其中241例接受了右心导管检查。采用线性回归模型确定影响尿量的因素。襻利尿剂反应评估为:(1)每40mg呋塞米等效剂量的净液体丢失量;(2)每40mg呋塞米等效剂量产生的尿量。在多变量回归模型中,尿量的关键独立预测因素包括利尿剂剂量(偏相关系数r = 0.44)、基线肾功能(偏相关系数r = 0.38)、收缩压(偏相关系数r = 0.26)和液体摄入量(偏相关系数r = 0.31;均P <.0001)。在血流动力学变量中,右心房压力升高与尿量增加相关(偏相关系数r = 0.19;P =.002)。利尿剂剂量所致的偏相关系数(偏R2 = 0.19)约占模型解释的尿量方差的一半(模型R2 = 0.40)。Cox回归模型显示,每40mg呋塞米的净液体丢失四分位数(P =.004)和尿量四分位数(P =.04)与6个月死亡率呈负相关。比较嵌套模型时,基于净液体丢失的模型在预测死亡率方面优于基于尿量的模型(χ2 = 8.1;3自由度;P =.04)。
在ADHF患者中,除利尿剂剂量外,其他参数包括肾功能、血流动力学状态、容量超负荷程度和液体摄入量也会影响尿量。襻利尿剂反应指标与短期死亡率相关。