Aortic stiffness, blood pressure and renal dysfunction

Abstract

In order to favor an optimal tissue oxygenation, a fundamental function of large arteries is the ability to modify a ‘‘pulsatile’’, i.e. systolic/diastolic, into a stable, continuous pressure [1]. The balance between contraction and relaxation is mainly responsible for rapid adaptation of lumen diameter. In contrast, changes in the structural properties of the vascular wall constitute a dynamic process occurring in response to long-term hemodynamic modifications [1, 2]. The above structural modifications are ‘‘adaptive’’. Nevertheless, successive changes become ‘‘maladaptive’’ and result in increased media thickness and decreased lumen diameter [2]. During systole, a part of the stroke volume flows directly toward the periphery, causing systolic perfusion. The other part of stroke volume is stored within the elastic thoracic aorta wall and restored during diastole, resulting in diastolic perfusion [3]. The more compliant the aorta, the smaller the pressure change during ventricular ejection (i.e., smaller pulse pressure), aorta modulating the alternative cyclic movement initiated by the heart [1–3]. Aging has been described to be associated with structural changes within the capacitance arteries resulting in increased pulse wave velocity (PWV) and consequent alterations in the pressure waveform and increases in systolic and pulse blood pressures (SBP and PP) [2, 4]. The Framingham Heart Study reported that aortic PWV is a potent driver of cardiovascular (CV) risk in middle-aged and older individuals, suggesting that age exerts a differential effect on arterial hemodynamics [5]. Indeed, the diastolic (D) BP is mostly dependent on peripheral arterial resistances, increases until middle age and then tends to fall. On the contrary, SBP and PP, largely influenced by the stiffness of large arteries, as well as peripheral PW reflection and the pattern of left ventricular ejection, increase progressively with age. In keeping with this, variations in the stiffness of large arteries, such as the aorta and its major branches, markedly account for the changes in SBP, DBP, and PP occurring in subjects [50 years old [1, 2, 5, 6]. Therefore, arterial stiffness describes the rigidity of the arterial walls and vascular stiffening is the consequence of complex interactions between the stable and dynamic modifications involving the structural and cellular elements of the vessel wall [1, 2]. Stiffness is not uniformly distributed throughout the vascular tree. It is often variable, occurring in central and conduit vessels while sparing more peripheral arteries [7, 8]. The structural and functional changes in the arterial circulation provide disturbances in regional blood flow, progression of atherogenesis, and microvascular changes occurring during senescence and in the presence of CV risk factors [1, 2, 7]. However, arterial stiffness and wave reflections are known to play a fundamental role in CV health and disease [1–7]. Indeed, in interplay with left ventricular ejection and the elastic properties of the aorta, wave reflections could specifically increase central PP, a recognized predictor of CV risk. These changes are attributed to the timing and amplitude of PW reflections from peripheral reflecting sites, where high resistance arterioles are considered to be the major sites of wave reflection in the circulation [1–7]. D. Grassi C. Ferri (&) Department of Internal Medicine and Public Health–Viale S. Salvatore, University of L’Aquila, Delta 6 Medicina, 67100, Coppito, L’Aquila, Italy e-mail: claudio.ferri@cc.univaq.it