Arterial stiffness, intima-media thickness and carotid artery fibrosis in patients with primary aldosteronism

OBJECTIVESTo evaluate vascular wall structure and conduit artery stiffness in patients with primary aldosteronism. METHODSThis observational study, conducted in a University Hypertension Center, evaluated the carotid wall by 2-D ultrasonography and ultrasonic tissue characterization, and analyzed arterial stiffness by applanation tonometer. Twenty-three consecutive patients with primary aldosteronism, 24 matched patients with essential hypertension and 15 controls were studied. Intima-media thickness and corrected integrated backscatter signal of the carotid arteries were evaluated. Radial and femoral pulse wave velocity and aortic augmentation index were also investigated. RESULTSIntima-media thickness in patients with essential hypertension (0.69 ± 0.03 mm) was higher (P < 0.04) than that in controls (0.59 ± 0.02 mm). This finding was more evident in primary aldosteronism patients (0.84 ± 0.03 mm), in whom intima-media thickness was greater than that in controls (P < 0.0001) or in patients with essential hypertension (P < 0.01). Similarly, corrected integrated backscatter signal in patients with essential hypertension (−23.6 ± 0.35 dB) was higher (P < 0.0001) than that in controls (−26.2 ± 0.44 dB), but it was even more elevated in patients with primary aldosteronism (−22.1 ± 0.46 dB), who showed greater corrected integrated backscatter signal than was the case in patients with essential hypertension (P < 0.009) or in controls (P < 0.0001). Femoral pulse wave velocity was higher in primary aldosteronism patients (10.8 ± 0.57 m/s) than in patients with essential hypertension (9.1 ± 0.34 m/s, P < 0.03) or in controls (7.1 ± 0.51 m/s, P < 0.0001). Femoral pulse wave velocity was lower in controls than in patients with essential hypertension (P < 0.0001). The same pattern was observed for radial pulse wave velocity. Aortic augmentation index was higher in primary aldosteronism patients (28.2 ± 2.1%) than in patients with essential hypertension (26.0 ± 1.8%) or in controls (16.8 ± 2.0%, P < 0.001). Patients with essential hypertension likewise exhibited higher aortic augmentation index than controls (P < 0.001). CONCLUSIONAldosterone excess is responsible per se for vascular morphological (wall thickening and carotid artery fibrosis) and functional (central stiffness) damage.