Increased arterial stiffness in end-stage renal failure: why is it of interest to the clinical nephrologist?

Hypertension is a cardiovascular risk factor whose adverse effects have been attributed to a reduction in the calibre and/or number of small arteries and arterioles, resulting in increased peripheral vascular resistance. Peripheral vascular resistance and cardiac output are determinants of the mean blood pressure. These indices refer to steady-state phenomena, i.e. pressure and flow are considered as constant over time. This definition does not take into account the fact that blood pressure and flow fluctuate during the cardiac cycle and that, in clinical practice, blood pressure is defined in terms of systolic pressure (SBP) and diastolic pressure (DBP), representing the oscillatory extremes of pulsatile pressure around a mean blood pressure. A more realistic approach is to consider arterial pressure as having a steady component, i.e. mean blood pressure, and a pulsatile component, i.e. pulse pressure [1]. Mean blood pressure is the pressure head for steady flow distribution to the tissues and organs. For a given cardiac output it is determined by the cross-sectional area and the number of arterioles and small arteries. Because ventricular ejection is intermittent, pulse pressure is determined by (i) the pattern of left ventricular ejection, (ii) the viscoelastic properties of large conduit arteries (arterial stiffness), and (iii) the timing of arterial wave reflections.