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Published on: July 3, 2013
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.
Abstract:
In essential hypertension, the regression of left ventricular hypertrophy is an important goal of treatment. In addition to treatment-associated changes in blood pressure (BP), the roles of other determinants of left ventricular hypertrophy regression, including dietary sodium intake, deserve investigation. In the present study, the change in echographic left ventricular mass index (LVMI) was assessed in 182 patients with never-treated essential hypertension at baseline and after 3 years of treatment by angiotensin converting enzyme inhibitors or angiotensin II receptor antagonists given at recommended doses and associated with other antihypertensive agents. Treatment was associated with satisfactory control of BP (<140/90 mm Hg) in 64% of patients, and left ventricular hypertrophy prevalence decreased from 56% to 39%. Twenty-four-hour urinary sodium was positively related to LVMI at baseline and at the end of the study, independently of age, sex, and systolic BP. Supine plasma aldosterone concentration was correlated with LVMI only at baseline but not in multivariate analysis. In response to treatment, the percentage of change in LVMI was positively correlated with the absolute changes in systolic BP, urinary sodium, and plasma aldosterone concentration, independently of baseline LVMI. The population was divided into 3 tertiles according to final values of gender-specific urinary sodium. When, within each urinary sodium tertile, patients were divided into those with plasma aldosterone concentration below and above the median (11.6 ng/dL), LVMI progressively increased across sodium tertiles only in patients with high plasma aldosterone concentration. Systolic BP was similar across all of the groups. In conclusion, aldosterone requires the presence of high dietary salt for the expression of its unfavorable effect on the heart.
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