Sodium retention in heart failure and cirrhosis

Shweta Bansal, Jo Ann Lindenfeld, Robert W. Sdirier

Research output: Contribution to journalArticle

75 Citations (Scopus)

Abstract

Patients with cirrhosis and heart failure (HF) share the pathophysiology of decreased effective arterial blood volume because of splanchnic vasodilatation in cirrhosis and decreased cardiac output in HF, with resultant stimulation of the renin-angiotensin-aldosterone system. Hyperaldosteronism plays a major role in the pathogenesis of ascites and contributes to resistance to loop diutics. Therefore, the use of high doses of aldosterone antagonist (spironolactone up to 400 mg/day) is the main therapy to produce a negative sodium balance in cirrhotic patients with ascites. Hyperaldosteronism also has increasingly been recognized as a risk factor for myocardial and vascular fibrosis. Therefore, low-dose aldosterone antagonists are being used in patients with HF for cardioprotective action. However, the doses (25 to 50 mg/day) at which they are being used in cardiac patients as reported in the Randomized Aldactone Evaluation Study are not natriuretic. It is likely, therefore, that the mortality benefit relates primarily from their effect on cardiac and vascular fibrosis. Resistance to commonly used loop diuretics is frequently present in patients with advanced HF. In patients with decompensated HF with volume overload who are loop diuretic resistant, ultrafiltration may be the only available option. This is, however, an invasive procedure. For these patients, natriuretic doses of aldosterone antagonists (spironolactone >50 mg/day) may be a potential option. The competitive natriuretic response of aldosterone antagonists is related to activity of the renin-angiotensin-aldosterone system: the higher the renin-an-giotensin-aldosterone system activity, the higher the dose of aldosterone antagonist required to produce natriuresis. This article will discuss the potential use of natriuretic doses of aldosterone antagonists in patients with HF, including the potential side effect of hyperkalemia.

Original languageEnglish (US)
Pages (from-to)370-376
Number of pages7
JournalCirculation: Heart Failure
Volume2
Issue number4
DOIs
StatePublished - Jul 2009
Externally publishedYes

Fingerprint

Mineralocorticoid Receptor Antagonists
Fibrosis
Heart Failure
Sodium
Spironolactone
Sodium Potassium Chloride Symporter Inhibitors
Hyperaldosteronism
Renin-Angiotensin System
Ascites
Blood Vessels
Natriuresis
Hyperkalemia
Viscera
Ultrafiltration
Blood Volume
Aldosterone
Renin
Vasodilation
Cardiac Output
Mortality

Keywords

  • Cardiorenal syndrome
  • Edematous states
  • Neurohumoral axis
  • Spironolactone

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Sodium retention in heart failure and cirrhosis. / Bansal, Shweta; Lindenfeld, Jo Ann; Sdirier, Robert W.

In: Circulation: Heart Failure, Vol. 2, No. 4, 07.2009, p. 370-376.

Research output: Contribution to journalArticle

Bansal, Shweta ; Lindenfeld, Jo Ann ; Sdirier, Robert W. / Sodium retention in heart failure and cirrhosis. In: Circulation: Heart Failure. 2009 ; Vol. 2, No. 4. pp. 370-376.
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