Abstract

Objective: We studied the influence of rosuvastatin added to a standard therapy on endothelial dependent vasodilatation (EDVD) and arterial stiffness markers in patients with uncontrolled hypertension. Design and method: 56 patients (40 men and 16 women aged 51.19.1) with uncontrolled hypertension were randomized into two groups. Group 1 included 30 patients who received a fixed combination of 10 mg/day lisinopril and 5 mg/day amlodipine. Group 2 consisted of 26 patients who followed the same regimen of therapy with addition of 20 mg/day of rosuvastatin. The office and central (aortic) BP, augmentation index (AIx), carotid-femoral and carotid-radial pulse wave velocity (PWV) as well as EDVD by cuff occlusion test were evaluated before and after a 24-week follow-up period. Results: The office systolic/diastolic BP decreased in both groups from 172.424.3/105.413.5 to 136.712,8/88.19.4 mmHg (p < 0.001) in the 1st group and from 170.820.0/104.014.3 to 131.09.1/83.37.7 mmHg (p < 0.001) in the 2nd one. Central BP also decreased in both groups from 153.622.1/100.513.2 to 118.610.5/82.48.5 mmHg (p < 0.001) in the 1st group and from 154.220.3/98.810.0 to 118.311.9/81.26.8 mmHg (p < 0.001) in the other. The extent of office and central BP decline did not differ. AIx decreased from 30.614.0 to 25.814.6% (p = 0.05) in the 1st group and from 34.38.3% to 24.712.6% in the 2nd group (p < 0.001) with more prominent AIx decrease in the latter (-4.8% and -9.6% respectively, p = 0.035). Mean carotid-femoral PWV decreased statistically only in the 1st group from 9.22.0 to 8.11.3 m/s (p < 0.005). The carotid-radial PWV did not change in both groups. The level of EDVD was equally more pronounced in the 1st group from −1.35.2% to 4.24.9% (p < 0.001) vs -0.56.4% to 3.95.9% (p = 0.01) in the 2nd group. Conclusions: Addition of rosuvastatin to a fixed lisinopril/amlodipine combination in treatment of patients with uncontrolled hypertension resulted in a more pronounced decline of augmentation index, but was beneficial neither for decrease of carotid-femoral pulse wave velocity nor endothelial dependent vasodilatation increase.

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