Rapid Reversal of Left Ventricular Hypertrophy and Intracardiac Volume Overload in Patients With Resistant Hypertension and Hyperaldosteronism

Abstract

Abstract-We have shown previously that patients with resistant hypertension and hyperaldosteronism have increased brain natriuretic peptide suggestive of increased intravascular volume. In the present study, we tested the hypothesis that hyperaldosteronism contributes to cardiac volume overload. Thirty-seven resistant hypertensive patients with hyperaldosteronism (urinary aldosterone Ն12 g/24 hours and plasma renin activity Յ1.0 ng/mL per hour) and 71 patients with normal aldosterone status were studied. Both groups had similar blood pressure and left ventricular mass, whereas left and right ventricular end-diastolic volumes measured by cardiac MRI were greater in high versus normal aldosterone subjects (PϽ0.05). Spironolactone treatment (19 patients in the high aldosterone group and 15 patients from the normal aldosterone group participated in the follow-up) resulted in a significant decrease in clinic systolic blood pressure, right and left ventricular end diastolic volumes, left atrial volume, left ventricular mass, and brain natriuretic peptide at 3 and 6 months of follow-up in patients with high aldosterone, whereas in those with normal aldosterone status, spironolactone decreased blood pressure and left ventricular mass without changes in ventricular or atrial volumes or plasma brain natriuretic peptide. Hyperaldosteronism causes intracardiac volume overload in patients with resistant hypertension in spite of conventional thiazide diuretic use. Mineralocorticoid receptor blockade induces rapid regression of left ventricular hypertrophy irrespective of aldosterone status. In subjects with high aldosterone, mineralocorticoid receptor blockade induces a prominent diuretic effect compared with a greater vasodilatory effect in subjects with normal aldosterone status. (Hypertension. 2010;55:1137-1142.)Key Words: resistant hypertension Ⅲ hyperaldosteronism Ⅲ cardiac volume Ⅲ cardiac hypertrophy A ldosterone excess is increasingly recognized as a common cause of hypertension. [1][2][3][4][5][6][7][8][9][10][11] Compared with patients with similar levels of hypertension, patients with hyperaldosteronism have greater left ventricular (LV) hypertrophy, worse diastolic function, and an increased rate of cardiovascular complications including myocardial infarction, stroke, and atrial fibrillation. [12][13][14][15] In such patients, echocardiographic/Doppler studies provide support for aldosterone-induced myocardial fibrosis and hypertrophy separate from changes in blood pressure (BP). 16 -19 A large body of experimental literature, including landmark studies by Brilla and Weber, 20 clearly demonstrates that aldosterone excess in the presence of high dietary salt intake induces LV hypertrophy and fibrosis. [21][22][23] These effects are attributable, at least in part, to aldosterone-induced urinary and fecal loss of Ca 2ϩ and Mg 2ϩ , with consequent hypocalcemia, hypomagnesia, and secondary hyperparathyroidism. This secondary increase in parathyroid hormone promotes intracellular Ca 2ϩ overloading in various tissues, ...

Long-term effects of adrenalectomy or spironolactone on blood pressure control and regression of left ventricle hypertrophy in patients with primary aldosteronism

“…This interpretation seems to be supported by studies of the LV pressure-volume curves in rats after aldosterone infusion 38 and also by human studies showing an increase in brain natriuretic peptide (BNP) levels in patients with PA. 39 Increased LV volumes compared with essential hypertension were confirmed also in a smaller group of patients with PA examined by magnetic resonance imaging (MRI) as a potentially more accurate method than commonly used echocardiography. 40 The present study shows that both adrenalectomy and mineralocorticoid receptor blockers can reverse the enlargement of the LV cavity during long-term follow-up, probably through the reduction of plasma volume and LV preload. In spite of the significant and similar blood pressure drop in both groups, however, only surgery led to a successful reduction in the thickness of LV walls.…”

Outcomes of Drug-Based and Surgical Treatments for Primary Aldosteronism

“…28 Many studies have shown that left ventricular mass decreases and that aortic pulse wave velocity and carotid intima-media thickness improve after adrenalectomy. [29][30][31][32][33][34][35] A prospective study compared cardiovascular events in 54 PA patients treated by adrenalectomy (unilateral disease) or with spironolactone (unilateral or bilateral disease) with 323 patients with essential hypertension. 36 The composite endpoint was myocardial infarction, stroke, any type of revascularization procedure, and sustained arrhythmia.…”

Primary aldosteronism — recent progress and current concepts

“…Fluid retention in cardiomyocytes influenced by aldosterone, and intracardiac volume increase, accompanied by increased intramural stress -in-wall-stress -should also be taken into consideration [17,34].…”