Cardiac Structure and Function in Hyperaldosteronism

Chronic activation of the renin–angiotensin–aldosterone system is known to be associated with cardiovascular injury. Primary aldosteronism (PA), either from bilateral adrenal hyperplasia or an aldosterone-secreting tumor, is one of the principal causes of secondary hypertension. The combined vascular resistance and sodium retention lead to increased afterload and result in increased left ventricular (LV) wall thickness, most often with minimal change in LV diameter.1 However, left ventricular hypertrophy (LVH) is more common and more pronounced in PA than in either essential hypertension2 or in other secondary forms of hypertension, such as pheochromocytoma or Cushing disease.3 Tissue Doppler studies have also demonstrated a higher prevalence of subclinical abnormalities of systolic and diastolic dysfunction in patients with this condition compared with age-matched patients with essential hypertension.4See Article by Cesari et al The hormonal effects of aldosterone seem to amplify the hemodynamic effects of aldosterone-related hypertension by changing the composition of the cardiac extracellular matrix,5 a pathophysiology that has proven to be an important therapeutic target.6Secondary aldosteronism (SA), commonly associated with cirrhosis of the liver but also present in renal vascular disease, often results in higher circulating levels of aldosterone than is seen in PA but is not necessarily associated with hypertension. Specifically in cirrhosis, blood pressure and systemic vascular resistance are low because of obligatory splanchnic dilatation. The cardiac effects of SA in cirrhosis including LV remodeling, proarrhythmia, and reduced contractile reserve, are collectively referred to as cirrhotic cardiomyopathy.7 The principal hemodynamic finding is that of a high-output state, with higher systolic performance and …