Abstract

Objective: Primary aldosteronism (PA) has been associated with excess left ventricular (LV) hypertrophy, but whether this is also a feature of secondary aldosteronism (SA) without hypertension is uncertain. We therefore investigated the cardiac changes in patients with PA and SA, who had preserved LV ejection fraction, but had contrasting levels of blood pressure (BP) and plasma renin activity (PRA). Design and method: PA patients (n 278) were compared to SA (n 117) patients with liver cirrhosis for PRA, aldosterone, and multiple Doppler echocardiography-derived variables. Healthy subjects (HS, n 60) were used as controls. LV systo/diastolic function was assessed also by use of tissue Doppler imaging and strain-rate analysis. Results: HS and SA patients showed normal BP values, but SA showed increased heart rate, reduced peripheral vascular resistance and increased cardiac index, output and work (p < 0.0001). PA showed higher BP values than SA and HS (p < 0.0001). SA and PA showed high and low PRA values (15 ng/ml/hr vs 0.56 ng/ml/hr, p < 0.0001) respectively, in spite of similarly elevated aldosterone levels (66 ng/dl vs 42 ng/dl, respectively). Of interest, in both PA and SA the LV mass index (51.4 and 54.3 g/m2,7) was higher than in HS (41 g/m2,7). Peak systolic septal strain (21% vs 24% and 23%, p = 0.02) and midwall fractional shortening (16% vs 17% and 17%, p = 0.004) were significantly reduced in PA compared to both the other groups. No differences emerged as regards LV ejection fraction, peak longitudinal systolic septal tissue velocity and septal systolic strain rate. The indexes of diastolic filling (E/A ratio, DT and E/E’) did not differ between PA and SA. Conclusions: Hyperaldosteronism is associated with a prominent increase in LV mass and with related diastolic dysfunction. These changes imply a subclinical systolic dysfunction and appear to be related to raised total peripheral resistance in PA. At variance, in SA patients with liver cirrhosis, who have normal BP and reduced total peripheral resistance, they are related to the increased cardiac work deriving from underfilling. Whether the increased PRA contribute to this, remains to be clarified.

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