Arterial stiffness, intima-media thickness and carotid artery fibrosis in patients with primary aldosteronism.
OBJECTIVE
To evaluate vascular wall structure and conduit artery stiffness in patients with primary aldosteronism.


METHODS
This 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.


RESULTS
Intima-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).


CONCLUSIONS
Aldosterone excess is responsible per se for vascular morphological (wall thickening and carotid artery fibrosis) and functional (central stiffness) damage.
Bernini
Giampaolo
G
Department of Internal Medicine, University of Pisa, Pisa, Italy. g.bernini@med.unipi.it
Galetta
Fabio
F
Franzoni
Ferdinando
F
Bardini
Michele
M
Taurino
Chiara
C
Bernardini
Melania
M
Ghiadoni
Lorenzo
L
Bernini
Matteo
M
Santoro
Gino
G
Salvetti
Antonio
A
D001011:Aorta / Q000503:physiopathology; D002339:Carotid Arteries / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology*; D016022:Case-Control Studies; D004548:Elasticity / Q000502:physiology*; D005260:Female; D005263:Femoral Artery / Q000503:physiopathology; D005355:Fibrosis; D006801:Humans; D006929:Hyperaldosteronism / Q000473:pathology* / Q000503:physiopathology*; D006973:Hypertension / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D011673:Pulsatile Flow / Q000502:physiology; D017534:Radial Artery / Q000503:physiopathology; D012039:Regional Blood Flow / Q000502:physiology; D017539:Tunica Intima / Q000000981:diagnostic imaging / Q000473:pathology*; D017540:Tunica Media / Q000000981:diagnostic imaging / Q000473:pathology*; D014463:Ultrasonography