Regular paper
Functional Relevance of Aldosterone for the Determination of Left Ventricular Mass

https://doi.org/10.1016/S0002-9149(02)03158-2Get rights and content

Abstract

In experimental studies, the importance of aldosterone for the development of left ventricular (LV) hypertrophy has been demonstrated. In 120 healthy Caucasian men (aged 25 ± 3 years; blood pressure, 134 ± 15/86 ± 12 mm Hg), we determined LV mass (2-dimensionally guided M-mode echocardiography), urinary aldosterone concentration, and the response of aldosterone to angiotensin II infusion (3.0 ng/kg/min). Seventy-six volunteers took part in a follow-up visit after 2 years when urinary aldosterone concentration and LV mass were determined again. At follow-up, LV mass increased in 42 subjects (by 33 ± 26 g), whereas in 34 subjects LV mass decreased (by 27 ± 22 g). Between the 2 groups, only the change in urinary aldosterone concentration over time was significantly different (group with increased LV mass had an increase in urinary aldosterone concentration by 2.5 ± 5.4 μg/day; group with decreased LV mass had a decrease in urinary aldosterone concentration by 0.7 ± 4.6; p <0.01 between groups). In accordance, we found significant correlations between changes in LV mass and changes in urinary aldosterone concentration (r = 0.29, p <0.05) and between changes in LV mass and the response of aldosterone to angiotensin II at baseline (r = 0.25, p <0.05). Both changes in aldosterone concentration over time and the response of aldosterone to angiotensin II were related to changes in LV mass over time. These data underscore the importance of aldosterone for the development of LV hypertrophy. This process is already evident in young subjects with apparently small changes in LV mass over a mean follow-up period of 2 years.

Section snippets

Study population

Study participants were screened for normal or mildly elevated blood pressure at the campus of the University of Erlangen-Nürnberg. Subjects eligible for the study were asked to refer to our outpatient clinic where blood pressure readings were taken seated after 5 minutes at rest according to World Health Organization recommendations. All subjects underwent a thorough clinical and laboratory examination. Inclusion criteria were male gender, Caucasian race, and age between 20 and 40 years.

Changes in clinical, laboratory, and echocardiographic parameters over time

Clinical, laboratory, and echocardiographic parameters of the study cohort at baseline and follow-up are listed in Table 1. Baseline aldosterone concentration was independent of participants’ ages (data not shown). At follow-up, subjects gained 2.5 ± 3.5 kg in weight (p <0.001). Consequently, body mass index and body surface area were also significantly different from baseline at follow-up. In contrast, none of the other parameters were significantly different from baseline at follow-up.

Relation between changes in urinary aldosterone concentration and changes in LV mass

In the

Discussion

Experimental data in humans indicate the importance of aldosterone for the development of LV hypertrophy. For instance, Duprez et al3 observed a correlation between serum aldosterone concentration and LV mass in patients with mild to moderate essential hypertension. We recently demonstrated that inadequate suppression of aldosterone in response to an increase in salt intake is related to LV structural parameters (including LV mass).4 Moreover, we observed a different response of aldosterone to

Acknowledgements

We thank Anja Friedrich and Ortrun Alter for technical assistance throughout the study, and Angelika Kirpal, MD, for her help with some of the echocardiographic examinations.

References (15)

There are more references available in the full text version of this article.

Cited by (19)

  • Left ventricular hypertrophy in COPD without hypoxemia: The elephant in the room?

    2013, Chest
    Citation Excerpt :

    Indeed, ACE inhibition has been well documented in its ability to regress LVH,29,30 even demonstrating improvements in LV mass in patients with preserved ejection fraction > 40%,31 and most importantly in significantly reducing cardiovascular mortality.13 Raised aldosterone levels have also been shown to promote increased LV mass,32,33 with similar improvements in LVH by aldosterone suppression demonstrated previously.34 Genetically, an aldosterone synthase gene variant has been implicated with regard to increased LVH, particularly in hypertensives.35,36

View all citing articles on Scopus

This study was supported by grant DFG KFG 106-1 from the Deutsche Forschungsgemeinschaft, Bonn, Germany, to Dr. Schmieder.

View full text