6D.07

Objective: To evaluate the effects of amlodipine alone, compared to amlodipine + acetylsalicylic acid (ASA), on some inflammatory and endothelial damage markers in patients affected by essential hypertension. Design and method: We enrolled 213 hypertensive patients with mild to moderate hypertension. Patients were randomised to amlodipine 5 mg, or amlodipine 5 mg + ASA for three months; then, if adequate blood pressure control was not reached, amlodipine was up-titrated to 10 mg/day for further 3 months and compared to amlodipine 10 mg + ASA 100 mg. We evaluate, at baseline, after 3 and 6 months: high sensitivity C-reactive protein (Hs-CRP), adiponectin (ADN), tumor necrosis factor-alfa (TNF-alfa), interleukin-1beta (IL-1beta), myeloperoxidase (MPO), soluble CD40 ligand (sCDL40). Results: After 3 months of therapy, no variations of the above cited markers were recorded with amlodipine alone. Patients treated with amlodipine 5 mg + ASA 100 mg, instead, showed a reduction of Hs-CRP, TNF-alfa, MPO, and sCDL40, and an increase of ADN, both compared to baseline (p < 0.05 for all) and to amlodipine alone (p < 0.05 for all). Regarding IL-1beta, it decreased with amlodipine 5 mg + ASA 100 mg compared to baseline (p < 0.05 for all), but no differences were recorded compared to amlodipine alone. One hundred and seven patients continued the study, and were up-titrated to amlodipine 10 mg + ASA 100 mg or to amlodipine 10 mg alone. We observed a decrease of Hs-CRP, TNF-alfa, MPO, and sCDL40 and an increase of ADN in both groups compared to baseline (p < 0.05 for amlodipine alone, and p < 0.01 for amlodipine + ASA). Values recorded with amlodipine 10 mg + ASA were better than the ones recorded with amlodipine 10 mg alone (p < 0.05 for all). Regarding IL-1beta, it decreased compared to baseline only with amlodipine 10 mg + ASA. No significant serious adverse events were reported. Conclusions: The addition of ASA to anti-hypertensive therapy gave a better improvement of inflammatory parameters compared to amlodipine alone, suggesting a role of ASA in reducing inflammation and endothelial damage independently from the blood pressure reduction.