title: Long-term cardiac effects of adrenalectomy or mineralocorticoid antagonists in patients with primary aldosteronism.
abstract: Exposure to excess aldosterone results in cardiac damage in hypertensive states. We evaluated the long-term cardiac structural and functional evolution in patients with primary aldosteronism after surgical or medical treatment. Fifty-four patients with primary aldosteronism were enrolled in a prospective study and were followed for a mean of 6.4 years after treatment with adrenalectomy (n=24) or spironolactone (n=30). At baseline, echocardiographic measurements of patients with primary aldosteronism were compared with those of 274 patients with essential hypertension. Patients with primary aldosteronism had greater left ventricular mass, more prevalent left ventricular hypertrophy, lower early:late-wave diastolic filling velocities ratio, and longer deceleration time than patients with essential hypertension but no differences in relative wall thickness and systolic function. During follow-up, average blood pressure was 135/82 and 137/82 mm Hg in patients treated with adrenalectomy and spironolactone, respectively. In the initial 1-year period, left ventricular mass decreased significantly only in adrenalectomized patients. Subsequent changes in left ventricular mass were greater in patients treated with spironolactone, with an overall change from baseline to the end of follow-up that was comparable in the 2 groups. Prevalence of hypertrophy decreased in both treatment groups, whereas diastolic parameters had only mild and nonsignificant improvement. Changes in blood pressure and pretreatment plasma aldosterone were independent predictors of left ventricular mass decrease in both treatment groups. Thus, in the long-term, both adrenalectomy and spironolactone are effective in reducing left ventricular mass in patients with primary aldosteronism, with effects that are partially independent of blood pressure changes.
authors: Division of Internal Medicine, Hypertension and Cardiovascular Unit, Department of Experimental and Clinical Pathology and Medicine, University of Udine, Udine, Italy.
authors: Cristiana
authors: C
authors: Catena
authors: GianLuca
authors: G
authors: Colussi
authors: Roberta
authors: R
authors: Lapenna
authors: Elisa
authors: E
authors: Nadalini
authors: Alessandra
authors: A
authors: Chiuch
authors: Pasquale
authors: P
authors: Gianfagna
authors: Leonardo A
authors: LA
authors: Sechi
mesh_terms: D000236:Adenoma / Q000601:surgery*; D000310:Adrenal Gland Neoplasms / Q000601:surgery*; D000315:Adrenalectomy; D000450:Aldosterone / Q000097:blood; D000959:Antihypertensive Agents / Q000627:therapeutic use; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006929:Hyperaldosteronism / Q000150:complications / Q000503:physiopathology* / Q000628:therapy; D006973:Hypertension / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D000451:Mineralocorticoid Receptor Antagonists; D011188:Potassium / Q000097:blood; D011446:Prospective Studies; D012083:Renin / Q000097:blood; D013148:Spironolactone / Q000627:therapeutic use; D013995:Time
chemical_list: D000959:Antihypertensive Agents; D000451:Mineralocorticoid Receptor Antagonists; D013148:Spironolactone; D000450:Aldosterone; D012083:Renin; D011188:Potassium