Cardiac Structure and Function in Hyperaldosteronism

Abstract

C hronic 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. However, left ventricular hypertrophy (LVH) is more common and more pronounced in PA than in either essential hypertension 2 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. 4 See Article by Cesari et alThe 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. 6 Secondary 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 lower peripheral vascular resistance than healthy controls, but the usual anatomic finding is a normal LV cavity diameter with increased LV wall thickness, 8,9 similar to that seen in PA. There is also echocardiographic evidence of diastolic dysfunction in patients with cirrhosis; most series report decreased early mitral inflow velocities and decreased left atrial contribution to ventricular filling. 8,9 Animal models of PA and SA have demonstrated that myocardial fibrosis occurs in both forms of hyperaldosteronism, whether or not hypertension is present. 10With this background, we will examine the interesting article by Cesari et al 11 in this issue of Circulation: Cardiovascular Imaging. Their purpose was to investigate whether PA and SA, which both feature high aldosterone levels, but different hemodynamic loads and plasma renin levels, are associated with different echocardiographic phenotypes. Accordingly they studied a remarkably large number of patients with PA, collected over 23 years from 1992 to 2015, and contrasted their LV structure and function with a large group of patients with SA, primarily because of liver cirrhosis, during the same time period. By contrasting echo findings i...