Eprosartan reduced central systolic BP significantly more than atenolol (16 vs 11 mm Hg; P=0.03), despite similar peripheral BP reductions, due to atenolol's failure to reduce wave reflection.
RCT (n=21)
Double-blind
cross-over
Does atenolol compared to eprosartan differentially affect central blood pressure and aortic pulse wave velocity in subjects with never-treated hypertension?
Despite similar peripheral blood pressure lowering, eprosartan reduces central systolic blood pressure more effectively than atenolol, potentially explaining atenolol's inferior cardiovascular outcomes in older hypertensive patients.
Absolute Event Rate: 11% vs 16%
p-value: p=0.03
BACKGROUND: Recent data suggest that atenolol may be inferior to other antihypertensive drugs in reducing cardiovascular risk in older individuals with hypertension, despite lowering peripheral blood pressure (BP). We hypothesized that that atenolol fails to reduce central BP as much as other agents. The aim of the present study was to compare the hemodynamic effects of atenolol and eprosartan in a double-blind, randomized, cross-over study. METHODS: After a 2-week placebo run-in, 21 subjects with never-treated hypertension underwent 6 weeks of therapy with atenolol (50 mg) and eprosartan (600 mg). Central BP and augmentation index were assessed using pulse wave analysis, and aortic pulse wave velocity was measured, at baseline and at the end of each treatment. RESULTS: Both drugs reduced peripheral BP to the same degree. However, there was a significantly greater reduction in central systolic BP with eprosartan (means +/- SEM: 16 +/- 3 v 11 +/- 2 mm Hg; P = .03). Despite identical reductions in mean pressure, atenolol reduced aortic pulse wave velocity more than eprosartan (0.8 +/- 0.1 v 0.5 +/- 0.1 m/sec; P = .005). Conversely, augmentation index and N-terminal pro-brain natiuretic peptide levels were reduced significantly after eprosartan (6% +/- 2% and 11 +/- 5 pg/mL, respectively) but were increased after atenolol (7% +/- 2% and 67 +/- 24 pg/mL, respectively). CONCLUSIONS: These data indicate that despite similar effects on peripheral BP and a greater effect on aortic stiffness, atenolol had less impact on central systolic BP than eprosartan because it failed to reduce wave reflection. This provides one potential explanation for the failure of atenolol to improve outcome in older patients with essential hypertension.
Dhakam et al. (Tue,) conducted a rct in never-treated hypertension (n=21). Atenolol vs. Eprosartan (600 mg) was evaluated on Reduction in central systolic BP (mm Hg) (p=0.03). Eprosartan reduced central systolic BP significantly more than atenolol (16 vs 11 mm Hg; P=0.03), despite similar peripheral BP reductions, due to atenolol's failure to reduce wave reflection.