Atenolol and Eprosartan: Differential Effects on Central Blood Pressure and Aortic Pulse Wave Velocity

• Published in: American journal of hypertension 2006-02, Vol.19 (2), p.214-219
• Main Authors: Dhakam, Zahid, McEniery, Carmel M., Yasmin, Cockcroft, John R., Brown, Morris J., Wilkinson, Ian B.
• Format: Article
• Language: English
• Subjects: Acrylates - therapeutic use; angiotensin receptor antagonist; Antihypertensive agents; Antihypertensive Agents - therapeutic use; Aorta, Thoracic - physiopathology; Arterial hypertension. Arterial hypotension; Atenolol - therapeutic use; augmentation index; Biological and medical sciences; Blood and lymphatic vessels; Blood Pressure - drug effects; Cardiology. Vascular system; Cardiovascular system; Clinical manifestations. Epidemiology. Investigative techniques. Etiology; Cross-Over Studies; Double-Blind Method; Electrocardiography; Female; Follow-Up Studies; Humans; Hypertension; Hypertension - drug therapy; Hypertension - physiopathology; Imidazoles - therapeutic use; Male; Medical sciences; Middle Aged; Pharmacology. Drug treatments; Prospective Studies; Pulsatile Flow - drug effects; pulse wave velocity; Receptor, Angiotensin, Type 1 - drug effects; Thiophenes - therapeutic use; Treatment Outcome; β-blockers
• ISSN: 0895-7061; 1879-1905; 1941-7225
• DOI: 10.1016/j.amjhyper.2005.08.007

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. 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. 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). 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.