Volpe M, Tritto C, DeLuca N, Rubattu S, Rao M A, Lamenza F, Mirante A, Enea I, Rendina V, Mele A F
First Clinica Medica, Facoltà di Medicina e Chirurgia, Università di Napoli Federico II, Italy.
Circulation. 1993 Oct;88(4 Pt 1):1620-7. doi: 10.1161/01.cir.88.4.1620.
Sodium retention and hormonal activation are fundamental hallmarks in congestive heart failure. The present study was designed to assess the ability of patients with asymptomatic to mildly symptomatic heart failure and no signs or symptoms of congestion to excrete ingested sodium and to identify possible early abnormalities of hormonal and hemodynamic mechanisms related to sodium handling.
The effects of a high salt diet (250 mEq/day for 6 days) on hemodynamics, salt-regulating hormones, and renal excretory response were investigated in a balanced study in 12 untreated patients with idiopathic or ischemic dilated cardiomyopathy and mild heart failure (NYHA class I-II, ejection fraction < 50%) (HF) and in 12 normal subjects, who had been previously maintained a 100 mEq/day NaCl diet. In normal subjects, high salt diet was associated with significant increases of echocardiographically measured left ventricular end-diastolic volume, ejection fraction, and stroke volume (all P < .001) and with a reduction of total peripheral resistance (P < .001). In addition, plasma atrial natriuretic factor (ANF) levels increased (P < .05), and plasma renin activity and aldosterone concentrations fell (both P < .001) in normals in response to salt excess. In HF patients, both left ventricular end-diastolic and end-systolic volumes increased in response to high salt diet, whereas ejection fraction and stroke volume failed to increase, and total peripheral resistance did not change during high salt diet. In addition, plasma ANF levels did not rise in HF in response to salt loading, whereas plasma renin activity and aldosterone concentrations were as much suppressed as in normals. Although urinary sodium excretions were not significantly different in the two groups, there was a small but systematic reduction of daily sodium excretion in HF, which resulted in a significantly higher cumulative sodium balance in HF than in normals during the high salt diet period (P < .001).
These results show a reduced ability to excrete a sodium load and early abnormalities of cardiac and hemodynamic adaptations to salt excess in patients with mild heart failure and no signs or symptoms of congestion.
钠潴留和激素激活是充血性心力衰竭的基本特征。本研究旨在评估无症状至轻度症状性心力衰竭且无充血体征或症状的患者排泄摄入钠的能力，并确定与钠处理相关的激素和血流动力学机制可能存在的早期异常。
在一项对照研究中，对12例未经治疗的特发性或缺血性扩张型心肌病且轻度心力衰竭（纽约心脏协会心功能分级I-II级，射血分数<50%）（HF）患者和12例正常受试者进行了高盐饮食（250 mEq/天，共6天）对血流动力学、盐调节激素和肾脏排泄反应影响的研究。这些正常受试者之前维持100 mEq/天的氯化钠饮食。在正常受试者中，高盐饮食与超声心动图测量的左心室舒张末期容积、射血分数和每搏量显著增加相关（均P<.001），并伴有总外周阻力降低（P<.001）。此外，正常受试者因盐摄入过多，血浆心房利钠因子（ANF）水平升高（P<.05），血浆肾素活性和醛固酮浓度下降（均P<.001）。在HF患者中，高盐饮食导致左心室舒张末期和收缩末期容积均增加，而射血分数和每搏量未能增加，且高盐饮食期间总外周阻力未改变。此外，HF患者盐负荷后血浆ANF水平未升高，而血浆肾素活性和醛固酮浓度与正常受试者一样受到抑制。尽管两组的尿钠排泄无显著差异，但HF患者每日钠排泄有小幅但系统性的减少，这导致在高盐饮食期间HF患者的累积钠平衡显著高于正常受试者（P<.001）。
这些结果表明，轻度心力衰竭且无充血体征或症状的患者排泄钠负荷的能力降低，且对盐过多的心脏和血流动力学适应性存在早期异常。
