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Effect of spironolactone on plasma brain natriuretic peptide and left ventricular remodeling in patients with

T Tsutamoto1, A Wada, K Maeda

  • 1First Department of Internal Medicine, Shiga University of Medical Science, Seta, Otsu, Japan. tutamoto@belle.shiga-med.ac.jp

Journal of the American College of Cardiology
|April 13, 2001
PubMed

Insights

Spironolactone treatment significantly reduced left ventricular volume and mass in patients with congestive heart failure (CHF). This aldosterone antagonist also decreased neurohumoral factors and myocardial fibrosis markers, improving cardiac remodeling.

Area of Science:

  • Cardiology
  • Pharmacology
  • Heart Failure Research

Background:

  • Aldosterone (ALD) is implicated in cardiac collagen synthesis and structural remodeling.
  • Spironolactone, an ALD receptor antagonist, is known to reduce mortality in congestive heart failure (CHF).
  • The specific impact of spironolactone on left ventricular remodeling in CHF requires further elucidation.

Purpose of the Study:

  • To assess the efficacy of spironolactone in modulating neurohumoral factors.
  • To evaluate the effects of spironolactone on left ventricular remodeling.
  • To investigate the role of aldosterone in the cardiac remodeling process in CHF patients.

Main Methods:

  • A randomized controlled trial involving 37 patients with mild-to-moderate nonischemic CHF.
  • Patients were assigned to receive either spironolactone (n=20) or placebo (n=17) for four months.
  • Measurements included left ventricular volume, mass, ejection fraction, and plasma levels of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and procollagen type III aminoterminal peptide (PIIINP).

Main Results:

  • Spironolactone treatment led to significant reductions in left ventricular volume and mass, alongside an increase in ejection fraction.
  • Plasma levels of ANP, BNP, and PIIINP were significantly decreased in the spironolactone group but not in the placebo group.
  • Positive correlations were observed between PIIINP changes and left ventricular volume/mass index changes with spironolactone treatment.

Conclusions:

  • Spironolactone treatment for four months effectively improved left ventricular structure and function in nonischemic CHF patients.
  • The drug significantly reduced neurohumoral factors and myocardial fibrosis markers, indicating a beneficial effect on cardiac remodeling.
  • These findings underscore the critical role of endogenous aldosterone in driving left ventricular remodeling in CHF.
Abstract

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