Long-term modifications in left ventricular structure and function after adrenalectomy or medical treatment in patients with primary aldosteronism

Background and aim: hyperaldosteronism has been related to collagen deposition, myocardial fibrosis, and ventricular remodeling in experimental studies. More recent evidence suggest that these detrimental effects can develop independently of blood pressure and a significant decrease in the mortality rate of patients with heart failure who were treated with aldosterone antagonists has been reported. Primary aldosteronism (PA) is a form of secondary arterial hypertension that offers an important clinical opportunity for assessing the effects of hyperaldosteronism on the left ventricular (LV) anatomy and function because, in this condition, its effects are isolated from those of the renin-angiotensin axis. In the literature, only few longitudinal studies have evaluated cardiac changes after treatment of hyperaldosteronism with either surgical or medical treatment. Hence, in the present study we have explored the relationship between aldosterone and the heart by assessing cardiac anatomic and functional evolution of a large number of patients with PA surgically or medically-treated. Methods and Results: fifty-five patients with PA were enrolled in a prospective study and were followed for a mean of 6.4 years (range: 4.5 to 8 years) after adrenalectomy (n=41) or medical treatment (n=14). The diagnosis of APA (aldosterone producing adenoma) was based on adrenal vein sampling and pathology results and on follow-up data. At baseline and at follow-up we performed Doppler echocardiography for estimation of LV wall thickness and dimensions and transmitral LV filling flow velocity indexes. At baseline, PA patients who subsequently underwent adrenalectomy were younger and had lower body mass index and lower diastolic blood pressure than PA patients medically-treated. The former showed an excess LV hypertrophy and concentric remodeling, but with a less degree of diastolic dysfunction compared with the latter. At follow-up, despite a greater reduction of antihypertensive drugs in surgically treated patients (number of drugs: 1.7±1.4 vs 2.6±0.8 in surgically and medically-treated, respectively, p= 0.024) in both groups there was a significant reduction of blood pressure levels. A significant (p< 0.001) reduction in LV end-diastolic diameter, a reduction in LV mass index but with an increase in the relative wall thickness was observed in both groups. However, the last two parameters were significant only in the surgically treated PA. As regards the diastolic function, no significant modification was observed in the surgically treated PA. At variance, a significant (p= 0.002) reduction in the atrial contribution to LV filling was observed in medically-treated PA, possibly because they showed a higher degree of diastolic dysfunction at baseline. In both groups LV mass decrease was independent from pre-treatment blood pressure, body mass index, age, known duration of hypertension, follow-up interval and medical treatment. Conclusions: in PA patients, the excess aldosterone is associated with both increased LV wall thickness and mass. Treatment of hyperaldosteronism with either surgical or medical treatment induce a reduction in blood pressure levels, LV end-diastolic diameter, a reduction in LV mass index and an increase in the relative wall thickness, particularly in the surgically treated PA. With a similar fall of blood pressure and despite a greater reduction of antihypertensive drugs, these changes were more prominent in the adrenalectomized patients. Treatment can improve the diastolic function, but this was observed only in the medically-treated PA patients, likely because they had a higher degree of diastolic dysfunction at baseline.