Dietary sodium, aldosterone, and left ventricular mass changes during long-term inhibition of the renin-angiotensin

Guilhem du Cailar1, Pierre Fesler, Jean Ribstein

  • 1Department of Internal Medicine, Centre Hospitalier Universitaire, Montpellier, France.

Insights

High dietary salt intake exacerbates the negative effects of aldosterone on left ventricular hypertrophy regression in patients with essential hypertension. Reducing sodium intake is crucial for managing heart health in these individuals.

Area of Science:

  • Cardiology
  • Nephrology
  • Internal Medicine

Background:

  • Left ventricular hypertrophy (LVH) regression is a key treatment goal in essential hypertension.
  • Dietary factors, particularly sodium intake, may influence LVH regression alongside blood pressure control.
  • The interplay between aldosterone, sodium, and LVH requires further investigation.

Purpose of the Study:

  • To assess the impact of dietary sodium intake on left ventricular mass index (LVMI) regression in patients with essential hypertension treated with ACE inhibitors or ARBs.
  • To investigate the relationship between urinary sodium, plasma aldosterone, and LVMI changes over 3 years of antihypertensive treatment.
  • To determine if aldosterone's effect on LVH is modulated by dietary salt intake.

Main Methods:

  • Echographic LVMI was measured at baseline and after 3 years in 182 never-treated essential hypertension patients.
  • Patients received ACE inhibitors or ARBs with other antihypertensive agents, aiming for BP <140/90 mm Hg.
  • 24-hour urinary sodium excretion and supine plasma aldosterone concentration were assessed; LVMI changes were correlated with these and BP changes.

Main Results:

  • Treatment achieved satisfactory BP control (<140/90 mm Hg) in 64% of patients, reducing LVH prevalence from 56% to 39%.
  • 24-hour urinary sodium was positively related to LVMI at baseline and end-of-study, independent of age, sex, and systolic BP.
  • LVMI regression was positively correlated with changes in systolic BP, urinary sodium, and aldosterone. Aldosterone's detrimental effect on LVMI was evident only in patients with high urinary sodium.

Conclusions:

  • Aldosterone's unfavorable effect on cardiac structure (LVMI) in essential hypertension is dependent on high dietary salt intake.
  • Managing sodium intake is critical for optimizing LVH regression in hypertensive patients, particularly those with elevated aldosterone levels.
  • This study highlights the synergistic negative impact of salt and aldosterone on cardiac remodeling in hypertension.

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