Patients with the metabolic syndrome (MetSyn) are at increased risk for cardiovascular
mortality and morbidity.This increased cardiovascular risk is attributed to metabolic
dysregulations like impaired glucose tolerance or diabetes mellitus and dyslipidemia,
abdominal obesity and arterial hypertension, which promote oxidative stress and inflammation
with consecutive endothelial dysfunction causing an atherogenic environment.
Aldosterone promoted end organ damage is mainly found in the cardiovascular system and the
kidney. Inflammation and activation of different factors promotes fibroblast growth and
matrix production resulting in myocardial fibrosis, vascular remodelling and renal fibrosis.
MetSyn and aldosterone are cardiovascular risk factors and it is of crucial importance to
note that there is a connection between MetSyn and aldosterone. Other cross sectional studies
show a direct correlation of aldosterone levels and impaired glucose metabolism in patients
with and without the MetSyn. Taken together, aldosterone influences essential parameters of
the MetSyn. Coincidentally parameters of the MetSyn are stimulus for an increased aldosterone
synthesis, i.e. visceral adipocytes.
In large scale clinical trials - RALES, EPHESUS, 4E - inhibition of MR has proven to be
beneficial in patients with congestive heart failure and post myocardial infarction and this
result has been confirmed for diabetic patients, who are known to have an increased
There is only very limited data on the impact of MR inhibition on metabolic, endocrine, and
inflammatory parameters in patients with MetSyn, who have not yet suffered from