Central arterial function in refractory hypertensives treated with versus without β-adrenoreceptor blockers

Abstract

Although atenolol is not recommended for first line therapy in the treatment of hypertension, it is commonly used to control blood pressure particularly in resource limited settings and where blood pressure control is resistant or refractory to therapy. However, for a given decrease in brachial blood pressure, atenolol does not reduce central arterial blood pressure as effectively as alternative antihypertensive agents. The mechanisms of this effect are nevertheless, poorly understood. Hence, using advanced approaches to the assessment of aortic function (central arterial pressure and simultaneous aortic velocity and diameter assessments in the left ventricular outflow tract [echocardiography]) in 61 resistant or refractory hypertensive participants I therefore compared the peripheral and central hemodynamic correlates of BP between 28 participants receiving atenolol and 33 not receiving atenolol, but who were receiving similar alternative agents. Atenolol therapy was associated with similar peripheral blood pressure values, but a lower heart rate (p<0.01), and hence cardiac output (p<0.05), prolonged ejection duration (p<0.05), and an increase in total peripheral resistance (p<0.01). Atenolol-treated hypertensives showed an increased slope of the relationship between maximal compression (forward travelling) wave pressures (determined from the product of peak aortic flow and aortic characteristic impedance) and aortic pulse pressure (p<0.01). Thus, at higher compression wave pressures, atenolol-treated participants had increased pulse pressure values. The higher pulse pressure at increased compression wave pressures was attributed to an enhanced reflected wave magnitude and wave reflection and re-reflection pressures at lower heart rates (p<0.01), but not to an increased TPR or to an increased overlap of the compression with the reflected wave mediated by a prolonged ejection duration. In conclusion, the adverse effects of heart rate reducing agents such as atenolol on central arterial pulsatile load is a class effect likely to be mediated by harmonic effects on oscillating waves at lower frequencies. Indeed, these relations between atenolol use and central aortic haemodynamics were not through atenolol’s limited vasoactive properties or through an increased overlap of backward with forward waves (following extended ejection duration). The adverse effects are therefore, likely to be common to all heart rate reducing agents, but are only observed when the amplitude of forward travelling compression waves are high.