Department of Internal Medicine, Section of Cardiovascular Medicine, Yale University School of Medicine, New Haven, CT, United States of America.
Department of Critical Care Medicine, Stanford University School of Medicine, Palo Alto, CA, United States of America.
Int J Cardiol. 2023 Jun 15;381:57-61. doi: 10.1016/j.ijcard.2023.04.002. Epub 2023 Apr 5.
Previous studies have suggested venous congestion as a stronger mediator of negative cardio-renal interactions than low cardiac output, with neither factor having a dominant role. While the influence of these parameters on glomerular filtration have been described, the impact on diuretic responsiveness is unclear. The goal of this analysis was to understand the hemodynamic correlates of diuretic response in hospitalized patients with heart failure.
We analyzed patients from the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE) dataset. Diuretic efficiency (DE) was defined as the average daily net fluid output per doubling of the peak loop diuretic dose. We evaluated a pulmonary artery catheter hemodynamic-guided cohort (n = 190) and a transthoracic echocardiogram (TTE) cohort (n = 324) where DE was evaluated with hemodynamic and TTE parameters. Metrics of "forward flow" such as cardiac index, mean arterial pressure and left ventricular ejection fraction were not associated with DE (p > 0.2 for all). Worse baseline venous congestion was paradoxically associated with better DE as assessed by right atrial pressure (RAP), right atrial area (RAA), and right ventricular systolic and diastolic area (p < 0.05 for all). Renal perfusion pressure (capturing both congestion and forward flow) was not associated with diuretic response (p = 0.84).
Worse venous congestion was weakly associated with better loop diuretic response. Metrics of "forward flow" did not demonstrate any correlation with diuretic response. These observations raise questions about the concept of central hemodynamic perturbations as the primary drivers of diuretic resistance on a population level in HF.
先前的研究表明，静脉淤血比低心输出量更能介导负面的心肺相互作用，而这两个因素都没有主导作用。虽然已经描述了这些参数对肾小球滤过的影响，但它们对利尿剂反应性的影响尚不清楚。本分析的目的是了解充血性心力衰竭住院患者利尿剂反应的血流动力学相关性。
我们分析了来自充血性心力衰竭和肺动脉导管有效性评估研究（ESCAPE）数据集的患者。利尿剂效率（DE）定义为每加倍峰值环利尿剂剂量的平均每日净液体输出。我们评估了肺动脉导管血流动力学指导组（n=190）和经胸超声心动图（TTE）组（n=324），其中通过血流动力学和 TTE 参数评估 DE。心输出量、平均动脉压和左心室射血分数等“前向流动”指标与 DE 无关（所有 p>0.2）。基线静脉淤血更严重，反而与右心房压（RAP）、右心房面积（RAA）和右心室收缩和舒张面积更好相关（所有 p<0.05）。肾灌注压（同时捕捉淤血和前向流动）与利尿剂反应无关（p=0.84）。
更严重的静脉淤血与更好的环利尿剂反应呈弱相关。“前向流动”指标与利尿剂反应性无相关性。这些观察结果对充血性心力衰竭人群中中心血流动力学紊乱作为利尿剂抵抗主要驱动因素的概念提出了质疑。
