Primary aldosteronism was associated with greater carotid intima-media thickness (0.84 vs 0.69 mm, P<0.01) and femoral pulse wave velocity (10.8 vs 9.1 m/s, P<0.03) than essential hypertension.
Observational (n=62)
No
Does primary aldosteronism increase arterial stiffness and carotid artery fibrosis compared to essential hypertension and healthy controls?
Aldosterone excess in primary aldosteronism is associated with significantly greater vascular wall thickening, carotid artery fibrosis, and central arterial stiffness compared to essential hypertension.
Absolute Event Rate: 0.84% vs 0.59%
p-value: p=<0.0001
OBJECTIVES: 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). CONCLUSION: Aldosterone excess is responsible per se for vascular morphological (wall thickening and carotid artery fibrosis) and functional (central stiffness) damage.
Bernini et al. (Fri,) conducted a observational in Primary aldosteronism (n=62). Primary aldosteronism vs. Essential hypertension and controls was evaluated on Intima-media thickness (p=<0.0001). Primary aldosteronism was associated with greater carotid intima-media thickness (0.84 vs 0.69 mm, P<0.01) and femoral pulse wave velocity (10.8 vs 9.1 m/s, P<0.03) than essential hypertension.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: