Hypertension is a major cardiovascular risk factor that affects between 10–40% of
the general population in an age dependent manner. The
renin-angiotensin-aldosterone system (RAAS) regulates blood pressure, fluid
volume, and the vascular response to injury and inflammation [1]. Chronic RAAS activation in the presence
of sufficient sodium consumption leads to persistent hypertension, setting off a
cascade of inflammatory, thrombotic, and atherogenic effects eventually leading
to end-organ damage [2]
[3]. Accordingly, numerous studies have
demonstrated that elevated renin and/or aldosterone levels are predictors of
adverse outcome in hypertension [4], heart
failure [5]
[6], myocardial infarction [7], and renal insufficiency [8] and influence insulin resistance [9]. Primary aldosteronism (PA) is the most
common secondary form of hypertension with an estimated prevalence between 4 and
12% of hypertensives [10]
[11]
[12] and 11–20% in patients that are resistant to combined
antihypertensive medication [13]
[14]. Given the severe cardiovascular
adverse effects of aldosterone excess that are independent of high blood
pressure levels [15]
[16]
[17]
[18] detection and treatment
of PA has important impact on clinical outcome and survival.
