Cardiac Remodeling in Patients With Primary and Secondary Aldosteronism

Abstract

P rimary aldosteronism (PA) is a common curable cause of high blood pressure (BP) characterized by undetectable renin and angiotensin II, and an excess rate of metabolic syndrome, 1 cardiovascular damage, 2,3 and events. 4,5 Secondary aldosteronism (SA) is a common feature of conditions characterized by effective circulating volume, causing cardiovascular underfilling as heart failure, nephrotic syndrome, and liver cirrhosis. 6 The latter also features low systemic vascular resistance owing to splanchnic vasodilatation, which might suggest that in liver cirrhosis patients, the left ventricle (LV) does not need to undergo remodeling to cope with the low afterload. Although PA and SA share the hyperaldosteronism, from the pathophysiological standpoint, these conditions are antithetical in that in PA, the aldosterone secretion is inappropriate for the prevailing sodium and volume status, whereas in SA, it reflects a physiological response to reduced intravascular volume/sodium status. An independent association of high levels of plasma aldosterone or renin with increased LV mass (LVM) 2,3,7 and development of LV hypertrophy (LVH) 2,3,8 has been reported. Whether hyperaldosteronism in the setting of low-to-normal BP, as found in conditions characterized by underfilling, 6 also causes morphological and functional changes of the LV is unknown. See Editorial by Parker and Aurigemma See Clinical PerspectiveThe long axis-oriented fibers in the luminal part of the myocardium are more susceptible to changes in cardiomyocyte function than the midwall radial-oriented fibers. Hence, tissue Doppler imaging (TDI) technique in the long-axis plane allows accurate detection even of subtle changes of systolic and diastolic function. Moreover, because TDI-derived indexes (early diastolic peak velocity of mitral annulus [septal E′], early and late diastolic strain rate [SR] parameters [SRe and SRa], and their ratio [SR e/a]) are held to be less Background-Primary aldosteronism (PA) causes excess left ventricular (LV) hypertrophy and diastolic dysfunction;whether this occurs also in secondary aldosteronism (SA) without hypertension is unknown. We investigated the cardiac modifications in patients with preserved LV ejection fraction who had PA or SA. Methods and Results-We measured several Doppler echocardiography-derived variables, including tissue Doppler imaging (TDI) parameters and strain rate analysis, in 262 patients with PA, 117 with SA because of liver cirrhosis, and in 61 control healthy subjects. SA and PA patients showed markedly elevated aldosterone levels (67 versus 39 ng/ dL, respectively; normal values <15 ng/dL) but contrasting values of plasma renin activity (15.00 versus 0.56 ng/mL/h; P<0.001). Compared with PA, SA patients showed higher heart rate, and lower blood pressure and vascular resistance values. Both PA and SA showed increased LV diameters, LV volumes, stroke volume, stroke work, and septal peak systolic tissue velocity, and had more LV hypertrophy (61% and 39%, respectively) and diastolic dysfunction (...

Aldosterone and renin in cardiac patients referred for catheterization

“…Furthermore, it is also in accordance with the report of a relationship of excess PAC with LV hypertrophy, regardless of the elevation of blood pressure. [14] …”

Arterial Hypertension, Atrial Fibrillation, and Hyperaldosteronism

“…64 The PA patients had increased LV mass, high prevalence of LVH, inappropriate LV mass, subclinical LV systolic and diastolic dysfunction. The patients with secondary hyperaldosteronism (due to liver cirrhosis) also show increased LV mass, high prevalence of LVH and diastolic dysfunction, but not subclinical systolic dysfunction.…”

“…The work overload caused by a hyper-dynamic circulatory state and the high renin with ensuing hyperaldosteronism could be driving these changes in patients with liver cirrhosis. 64 Thus, in both PA and secondary hyperaldosteronism, aldosterone contributes to LVH and also cardiac fibrosis, causing LV diastolic dysfunction, increased atrial afterload, with ensuing atrial stretching, and wall stress, favoring AF onset. 64,65 …”

Cardiac Structure and Function in Hyperaldosteronism

“…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. 10 With 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.…”

“…A plot of midwall shortening (FSmw, %) on the y axis vs end-systolic circumferential stress, an index of afterload, on the y axis, using methodology described in the study by Narayanan et al 19 The values for FSmw and circumferential stress were computed based on mean values for cardiac dimensions and blood pressure supplied by the authors 11 (NB: our methodology computes FSmw as values that are systematically higher than the authors' results for FSmw, but should be directionally similar. ); 95% confidence limits were derived from normal controls in our laboratory.…”