Endocrine Abstracts

Background

Aldosterone excess causes volume retention and cardiovascular damage. We evaluated the long-term haemodynamic changes in patients with targeted treatment of primary aldosteronism (PA) (n = 40) in comparison with essential hypertension (EH) (n = 40) and untreated normotensive controls (n = 40).

Methods

PA patients were subjected to adrenal vein sampling and allocated to adrenalectomy (n = 20) or spironolactone-based treatment (n = 20) and followed for 2.8 years (median). In the PA and EH groups, age (55 and 50 years, respectively), sex distribution (30 and 31 males), body mass index (BMI) (31 and 29 kg/m²), and smoking status (6 and 3 present, 25 and 23 never, respectively) were corresponding. The normotensive controls had similar sex distribution and smoking status but were younger (44 years) with lower mean BMI (26 kg/m²). Supine haemodynamics were recorded using whole-body impedance cardiography and continuous radial tonometric pulse wave analysis.

Results

The average initial number of antihypertensive medications in the PA and EH groups was 3 vs 1, and the final number was 3 vs 2, respectively, with all major classes of antihypertensives in use. Aortic systolic and diastolic blood pressures (BP) were similarly elevated in the PA and EH groups, and the values were correspondingly reduced by treatment. However, BP remained higher in both hypertensive groups than in normotensive controls. The PA and EH groups presented with similar treatment-induced reductions in systemic vascular resistance without changes in cardiac output. The foremost initial haemodynamic change in the PA patients was about 1 litre (10%) excess of extracellular water volume versus the EH and NT groups (P < 0.001) that was completely normalised by treatment. Before treatment aortic forward wave amplitude (FWA) and backward wave amplitude were correspondingly elevated in the two hypertensive groups. However, when compared with normotensive controls, the treatment-induced decrease in FWA was more pronounced in PA patients (4.1±1.4 vs 0.2±1.4 mmHg, P = 0.043) but not in EH patients (–2.1±1.2 vs 0.2±1.4 mmHg, P = 0.170). In two models of linear regression analysis, extracellular water volume (β=0.255, P = 0.007, R² of the model 0.338) and PA (β=0.289, P = 0.013, R²0.353) were independent explanatory factors for FWA.

Conclusions

Patients with PA presented with corresponding BP, systemic vascular resistance, and cardiac output, but clearly higher extracellular water volume than patients with EH. Targeted treatment of PA eliminated the volume excess and reduced aortic forward wave amplitude. These findings support the view that systematic evaluation of the volume status would benefit the clinical diagnostics and treatment of PA.