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Aldosterone and Left Ventricular Remodeling.

C Catena1, G Colussi1, G Brosolo1

  • 1Hypertension Unit, Internal Medicine, Department of Experimental and Clinical Medical Science, University of Udine, Udine, Italy.

Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et Metabolisme
|November 14, 2015
PubMed
Summary
This summary is machine-generated.

High aldosterone levels can harm heart structure and function, especially with high salt intake. Aldosterone

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Area of Science:

  • Cardiology
  • Endocrinology
  • Nephrology

Background:

  • Protracted exposure to elevated aldosterone levels significantly alters left ventricular (LV) structure and function.
  • Aldosterone induces myocardial inflammation and fibrosis, particularly with high salt intake, as shown in animal studies.
  • Clinical conditions like heart failure, hypertension, and primary aldosteronism provide insights into aldosterone's cardiac effects.

Purpose of the Study:

  • To review clinical studies on aldosterone's role in LV remodeling and diastolic function.
  • To investigate the influence of salt intake on aldosterone-induced cardiac changes in humans.
  • To clarify the direct and indirect effects of aldosterone on cardiac structure and function.

Main Methods:

  • Review of experimental and clinical evidence on aldosterone's cardiac effects.
  • Analysis of studies in conditions with elevated aldosterone, including primary aldosteronism.
  • Examination of data from mineralocorticoid receptor blocker trials.

Main Results:

  • Aldosterone significantly impacts LV mass and geometry.
  • No direct effect of aldosterone on LV diastolic function is evident; improvements may stem from reduced LV mass.
  • The necessity of high salt intake for aldosterone's cardiac effects in humans requires further investigation.

Conclusions:

  • Aldosterone plays a significant role in LV remodeling.
  • The direct impact of aldosterone on diastolic function is minimal, with improvements likely secondary to mass reduction.
  • The synergistic role of salt in aldosterone-mediated cardiac damage in humans warrants further research.