Abstract

Treatment with beta-blockers is characterized by inferior reduction of central versus peripheral blood pressure. We examined changes in blood pressure, cardiac function, and vascular resistance after 3 weeks of bisoprolol treatment (5 mg/day) during passive head-up tilt in 16 never-treated Caucasian males with grade I–II primary hypertension. A double-blind, randomized, placebo-controlled cross-over design was applied, and hemodynamics were recorded using continuous tonometric pulse wave analysis and whole-body impedance cardiography. Bisoprolol decreased blood pressure in the aorta (~8/10 mmHg, p ≤ 0.032) and radial artery (~10/9 mmHg, p ≤ 0.037), but upright aortic systolic blood pressure was not significantly reduced (p = 0.085). Bisoprolol reduced heart rate and left cardiac work, and increased subendocardial viability index in supine and upright positions (p ≤ 0.044 for all). Bisoprolol increased stroke volume in the supine (~11 ml, p = 0.02) but not in the upright position, while only upright (~1 l/min, p = 0.007) but not supine cardiac output was reduced. Upright elevation in systemic vascular resistance was increased 2.7-fold (p = 0.002), while upright pulse pressure amplification was decreased by ~20% (p = 0.002) after bisoprolol. Aortic augmentation index, augmentation pressure, and pulse pressure were not changed in the supine position but were increased in the upright position (from 9% to 17%, 3–6 mmHg, and 30–34 mmHg, respectively, p ≤ 0.016 for all). In conclusion, although bisoprolol treatment reduced peripheral blood pressure, central systolic blood pressure in the upright position was not decreased. Importantly, the harmful influences of bisoprolol on central pulse pressure and pressure wave reflection were manifested in the upright position.

Highlights

  • IntroductionBeta-blockers remain the first-line therapy in patients with heart failure or recent myocardial infarction [5]

  • Supplementary information The online version of this article contains supplementary material, which is available to authorized users.The use of beta-adrenoceptor blockers as first line treatment for hypertension has declined in recent years due to inferior efficacy in the prevention of cardiovascular events when compared with vasodilatory antihypertensive agents [1,2,3]

  • Augmentation index (AIx) is delineated as the proportion of the reflected pressure wave to pulse pressure (PP). It has been applied as a surrogate measure of arterial stiffness, but it is mainly a measure of wave reflections [7] that is influenced by systemic vascular resistance (SVR) [8]

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Summary

Introduction

Beta-blockers remain the first-line therapy in patients with heart failure or recent myocardial infarction [5]. The pathophysiological mechanism for the inferior reduction in central BP with betablockers could be the longer ejection period during slower heart rate which allows the reflected wave to arrive during systole and increase the systolic BP [6]. Augmentation index (AIx) is delineated as the proportion of the reflected pressure wave (augmentation pressure, AP) to pulse pressure (PP). It has been applied as a surrogate measure of arterial stiffness, but it is mainly a measure of wave reflections [7] that is influenced by systemic vascular resistance (SVR) [8]. Taking into account the aforementioned pathophysiology it can be readily understood why a beneficial effect of beta-blockers on AIx has not been demonstrated [10, 11]

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