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• W2047367002 abstract "We recognize that increased systolic pressure is the most challenging form of hypertension today and that pulse pressure as an independent cardiovascular risk factor has focused attention on arterial stiffness and wave reflections as the most important factors determining these pressures. In recent years, many studies emphasized the role of arterial rigidity in the development of cardiovascular diseases, and it was shown that stiffening of arteries is associated with increased cardiovascular mortality and morbidity. Moreover, arterial stiffening is linked to decreased glomerular filtration rate, and is predictive of kidney disease progression and the patient's cardiovascular outcome. Premature vascular aging and arterial stiffening are observed with progression of chronic kidney disease (CKD) and in end-stage renal disease (ESRD). This accelerated aging is associated with outward remodeling of large vessels, characterized by increased arterial radius not totally compensated for by artery wall hypertrophy. Arterial stiffening in CKD and ESRD patients is of multifactorial origin with extensive arterial calcifications representing a major covariate. With aging, the rigidity is more pronounced in the aorta than in peripheral conduit arteries, leading to the disappearance or inversion of the arterial stiffness gradient and less protection of the microcirculation from high-pressure transmission. Various non-pharmacological or pharmacological interventions can modestly slow the progression of arterial stiffness, but arterial stiffness is, in part, pressure dependent and treatments able to stop the process mainly include antihypertensive drugs. We recognize that increased systolic pressure is the most challenging form of hypertension today and that pulse pressure as an independent cardiovascular risk factor has focused attention on arterial stiffness and wave reflections as the most important factors determining these pressures. In recent years, many studies emphasized the role of arterial rigidity in the development of cardiovascular diseases, and it was shown that stiffening of arteries is associated with increased cardiovascular mortality and morbidity. Moreover, arterial stiffening is linked to decreased glomerular filtration rate, and is predictive of kidney disease progression and the patient's cardiovascular outcome. Premature vascular aging and arterial stiffening are observed with progression of chronic kidney disease (CKD) and in end-stage renal disease (ESRD). This accelerated aging is associated with outward remodeling of large vessels, characterized by increased arterial radius not totally compensated for by artery wall hypertrophy. Arterial stiffening in CKD and ESRD patients is of multifactorial origin with extensive arterial calcifications representing a major covariate. With aging, the rigidity is more pronounced in the aorta than in peripheral conduit arteries, leading to the disappearance or inversion of the arterial stiffness gradient and less protection of the microcirculation from high-pressure transmission. Various non-pharmacological or pharmacological interventions can modestly slow the progression of arterial stiffness, but arterial stiffness is, in part, pressure dependent and treatments able to stop the process mainly include antihypertensive drugs. Cardiovascular disease is a major cause of morbidity and mortality in patients with chronic kidney disease (CKD) or end-stage renal disease (ESRD). Epidemiological and clinical studies showed that structural and functional changes of central and large conduit arteries are major contributing factors associated with these complications.1.Lindner A. Charra B. Sherrard D. et al.Accelerated atherosclerosis in prolonged maintenance hemodialysis.N Engl J Med. 1974; 290: 697-702Crossref PubMed Google Scholar, 2.Pascazio L. Bianco F. Giorgini A. et al.Echo color Doppler imaging of carotid vessels in hemodialysis patients: evidence of high levels of athrosclerotic lesions.Am J Kidney Dis. 1996; 28: 713-720Abstract Full Text PDF PubMed Google Scholar, 3.Cheung A.K. Sarnak M.J. Yan G. et al.Atherosclerotic cardiovascular disease risks in chronic hemodialysis patients.Kidney Int. 2000; 58: 353-362Abstract Full Text Full Text PDF PubMed Scopus (504) Google Scholar These changes concern the two interrelated arterial functions: delivering adequate blood flow to tissues and organs, as dictated by their metabolic activity (conduit function), and transforming cyclic high-flow and pressure oscillations in the aorta into continuous and low-pressure capillary flow (cushioning or dampening function).4.O'Rourke M.F. Mechanical principles in arterial disease.Hypertension. 1995; 26: 2-9Crossref PubMed Google Scholar,5.Nichols W.W. O’Rourke M.F. Vascular impedance.in: Arnold H. McDonald’s Blood Flow in Arteries: Theoretical, Experimental and Clinical Principles. 5th edn. Hodder Arnold, London2005: 299-337Google Scholar Atherosclerosis, characterized by atheromatous plaques with restriction of blood flow and ischemia or infarction of downstream tissues, is the principal long-term alteration of conduit function, and a frequent cause of ischemic heart disease, strokes, and peripheral artery diseases. Dampening function disorders reflect changes of arterial wall viscoelastic properties and dimensions, and are more typically associated with left ventricular hypertrophy, congestive heart failure, and sudden death.6.Marchais S.J. Guérin A.P. Pannier B.M. et al.Wave reflections and cardiac hypertrophy in chronic uremia: influence of body size.Hypertension. 1993; 22: 876-883Crossref PubMed Google Scholar, 7.Chang K.C. Tseng Y.Z. Kuo T.S. et al.Impaired left ventricular relaxation and arterial stiffness in patients with essential hypertension.Clin Sci. 1994; 8: 641-647Crossref Google Scholar, 8.Nitta K. Akiba T. Uchida K. et al.Left ventricular hypertrophy is associated with arterial stiffness and vascular calcification in hemodialysis patients.Hypertens Res. 2004; 27: 47-52Crossref PubMed Scopus (100) Google Scholar, 9.Robinson R.F. Nahata M.C. Sparks E. et al.Abnormal left ventricular mass and aortic distensibility in pediatric dialysis patients.Pediatr Nephrol. 2005; 20: 64-68Crossref PubMed Scopus (25) Google Scholar, 10.Boutouyrie P. Laurent S. Girerd X. et al.Common carotid artery stiffness and patterns of left ventricular hypertrophy in hypertensive patients.Hypertension. 1995; 25: 651-659Crossref PubMed Google Scholar, 11.London G.M. Guérin A.P. Marchais S.J. et al.Cardiac and arterial interactions in end-stage renal disease.Kidney Int. 1996; 50: 600-608Abstract Full Text PDF PubMed Google Scholar, 12.Zoungas S. Cameron J.D. Kerr P.G. et al.Association of intima–media carotid thickness and indices of arterial stiffness with cardiovascular disease outcome in CKD.Am J Kidney Dis. 2007; 50: 622-630Abstract Full Text Full Text PDF PubMed Scopus (51) Google Scholar Results of cross-sectional studies emphasized the role of arterial stiffness as an independent cardiovascular risk factor and predictor of all-cause and cardiovascular death in many populations, as well as of diseases such as coronary atherosclerosis, diabetes, ESRD, aging, coronary events, and stroke.13.Blacher J. Pannier B. Guérin A.P. et al.Carotid arterial stiffness as a predictor of cardiovascular and all-cause mortality in end-stage renal disease.Hypertension. 1998; 32: 570-574Crossref PubMed Google Scholar, 14.Blacher J. Guérin A.P. Pannier B. et al.Impact of aortic stiffness on survival in end-stage renal disease.Circulation. 1999; 99: 2434-2439Crossref PubMed Google Scholar, 15.Shoji T. Emoto M. Shinohara K. et al.Diabetes mellitus, aortic stiffness, and cardiovascular mortality in end-stage renal disease.J Am Soc Nephrol. 2001; 12: 2117-2124PubMed Google Scholar, 16.Laurent S. Boutouyrie P. Asmar R. et al.Aortic stiffness is an independent predictor of all-cause and cardiovascular mortality in hypertensive patients.Hypertension. 2001; 37: 1236-1241Crossref PubMed Google Scholar, 17.Guérin A. Blacher J. Pannier B. et al.Impact of aortic stiffness attenuation on survival of patients in end-stage renal disease.Circulation. 2001; 103: 987-992Crossref PubMed Google Scholar, 18.Meaume S. Benetos A. Henry O.F. et al.Aortic pulse wave velocity predicts cardiovascular mortality in subjects >70 years of age.Arterioscler Thromb Vasc Biol. 2001; 21: 2046-2050Crossref PubMed Google Scholar, 19.Cruickshank K. Riste L. Anderson S.G. et al.Aortic pulse-wave velocity and its relationship to mortality in diabetes and glucose intolerance: an index of vascular function.Circulation. 2002; 106: 2085-2090Crossref PubMed Scopus (882) Google Scholar, 20.Boutouyrie P. Tropeano A.I. Asmar R. et al.Aortic stiffness is an independent predictor of primary coronary events in hypertensive patients: a longitudinal study.Hypertension. 2002; 39: 10-15Crossref PubMed Scopus (1070) Google Scholar, 21.Laurent S. Katsahian S. Fassot C. et al.Aortic stiffness is an independent predictor of fatal stroke in essential hypertension.Stroke. 2003; 34: 1203-1206Crossref PubMed Scopus (585) Google Scholar, 22.Najjar S.S. Scuteri A. Lakatta E.G. Arterial aging: is it an immutable cardiovascular risk factor?.Hypertension. 2005; 46: 454-462Crossref PubMed Scopus (336) Google Scholar The arterial wall has elastic and viscous properties. Their difference reflects the time-dependent response of the stress–strain relationship (arterial pressure–arterial diameter changes). In a purely elastic artery, this relationship is time independent and, after stress removal, the arterial diameter returns to its initial dimensions. In the presence of wall viscosity, the arterial wall retains part of the deformation, meaning that part of the left ventricular energy responsible for strain is dissipated, characterized by hysteresis of the pressure–diameter loop.23.Nichols W.W. O’Rourke M.F. Vascular impedance.in: McDonald’s Blood Flow in Arteries: Theoretical, Experimental and Clinical Principles. 5th edn. Hodder Arnold, London2005: 11-64Google Scholar As it is difficult to measure and evaluate in humans, the role of arterial ‘viscosity’ has not been evaluated as extensively as the ‘elastic’ properties of arteries. In contrast, a vast body of literature on elastic properties is available. The ability of arteries to accommodate the stroke volume can be described in terms of compliance or arterial stiffness.24.O'Rourke M.F. Principles and definitions of arterial stiffness, wave reflections and pulse pressure amplification.in: Safar M.E. O'Rourke M.F. Handbook of Hypertension (series edts Birkenhäger WH, Reid JL). Vol. 23.. Elsevier, Amsterdam2006: 3-20Google Scholar These terms express the contained volume of the vasculature (total or segmental), as a function of a given transmural pressure. Compliance (C) describes the absolute volume change (ΔV=strain) due to a pressure change (ΔP=stress): C=ΔV/ΔP. The reciprocal value of compliance is elastance (E=ΔP/ΔV) or stiffness. Compliance can be expressed relative to the initial volume (V) as a coefficient of distensibility Di, defined as Di=ΔV/V × ΔP. In contrast to compliance or elastance/stiffness, which provides information about the ‘elasticity’ of the artery as a hollow structure, the elastic incremental modulus (Einc, Young's modulus) provides information on the intrinsic elastic properties of the biomaterials constituting the arterial wall independent of vessel geometry. The pressure–volume relationship is nonlinear: at low distending pressure the tension is borne by distensible elastin fibers, whereas at a high distending pressure the tension is transferred and borne by less extensible collagen fibers. Thus, the arterial wall gets stiffer and more ‘resistant’ to distension, limiting arterial blood pooling during left ventricular ejection. The most typical clinical consequence of arterial stiffening is a steep pressure–volume relationship, with increased systolic pressure during ventricular ejection and decreased diastolic pressure during diastolic runoff, resulting in high pulse pressure.24.O'Rourke M.F. Principles and definitions of arterial stiffness, wave reflections and pulse pressure amplification.in: Safar M.E. O'Rourke M.F. Handbook of Hypertension (series edts Birkenhäger WH, Reid JL). Vol. 23.. Elsevier, Amsterdam2006: 3-20Google Scholar Arterial dampening has two aspects: transformation of cyclic blood flow in the aorta into a continuous capillary flow and dampening of arterial pressure oscillations, thereby limiting their transmission to the microcirculation. The efficiency of these functions depends on the stiffness and geometry of the aorta and central arteries, and rigidity of successive arterial segments (stiffness gradient).24.O'Rourke M.F. Principles and definitions of arterial stiffness, wave reflections and pulse pressure amplification.in: Safar M.E. O'Rourke M.F. Handbook of Hypertension (series edts Birkenhäger WH, Reid JL). Vol. 23.. Elsevier, Amsterdam2006: 3-20Google Scholar, 25.Mitchell G.F. Parise H. Benjamin E.J. et al.Changes in arterial stiffness and wave reflections with advancing age in healthy men and women: The Framingham Heart Study.Hypertension. 2004; 43: 1239-1245Crossref PubMed Scopus (621) Google Scholar, 26.London G.M. Pannier B. Arterial functions: how to interpret the complex physiology.Nephrol Dial Transplant. 2010; 25: 3815-3823Crossref PubMed Scopus (38) Google Scholar During ventricular contraction, part of the stroke volume is forwarded directly to the peripheral tissues, and part of it is momentarily stored in the aorta and central arteries, stretching the arterial walls and raising local blood pressure. Part of the energy produced by the heart is diverted for the distension of arteries and is ‘stored’ in the vessel walls. During diastole, the ‘stored’ energy recoils the aorta, propelling the accumulated blood forward into the peripheral tissues, ensuring continuous flow (Figure 1). To limit the cardiac work required during ventricular ejection, the energy necessary for arterial distension and recoil should be low, i.e., for a given stroke volume, the pressure increase should be as small as possible. The efficiency of this function depends on artery stiffness and geometry. When rigidity is mild, the arterial wall opposes low resistance to distension and the pressure effect is minimized. When the arterial system is rigid and cannot be stretched, the entire stroke volume flows through the arterial system and peripheral tissues only during systole with two consequences: intermittent flow and short capillary transit time, with reduced metabolic exchanges (Figure 1).24.O'Rourke M.F. Principles and definitions of arterial stiffness, wave reflections and pulse pressure amplification.in: Safar M.E. O'Rourke M.F. Handbook of Hypertension (series edts Birkenhäger WH, Reid JL). Vol. 23.. Elsevier, Amsterdam2006: 3-20Google Scholar,26.London G.M. Pannier B. Arterial functions: how to interpret the complex physiology.Nephrol Dial Transplant. 2010; 25: 3815-3823Crossref PubMed Scopus (38) Google Scholar In addition to influencing the ‘resistance to distension’, arterial stiffness determines the propagation velocity of the pressure wave from the proximal aorta toward peripheral vessels; i.e., pulse wave velocity (PWV).4.O'Rourke M.F. Mechanical principles in arterial disease.Hypertension. 1995; 26: 2-9Crossref PubMed Google Scholar, 23.Nichols W.W. O’Rourke M.F. Vascular impedance.in: McDonald’s Blood Flow in Arteries: Theoretical, Experimental and Clinical Principles. 5th edn. Hodder Arnold, London2005: 11-64Google Scholar, 24.O'Rourke M.F. Principles and definitions of arterial stiffness, wave reflections and pulse pressure amplification.in: Safar M.E. O'Rourke M.F. Handbook of Hypertension (series edts Birkenhäger WH, Reid JL). Vol. 23.. Elsevier, Amsterdam2006: 3-20Google Scholar The arterial system is heterogenous, with PWV increasing progressively from the ascending aorta to the peripheral muscular conduit arteries, generating a stiffness gradient 25.Mitchell G.F. Parise H. Benjamin E.J. et al.Changes in arterial stiffness and wave reflections with advancing age in healthy men and women: The Framingham Heart Study.Hypertension. 2004; 43: 1239-1245Crossref PubMed Scopus (621) Google Scholar, 26.London G.M. Pannier B. Arterial functions: how to interpret the complex physiology.Nephrol Dial Transplant. 2010; 25: 3815-3823Crossref PubMed Scopus (38) Google Scholar, 27.Avolio A.O. Chen S.G. Wang R.P. et al.Effects of aging on changing arterial compliance and left ventricular load in a northern Chinese urban community.Circulation. 1983; 68: 50-58Crossref PubMed Google Scholar, 28.Pannier B. Guérin A.P. Marchais S.J. et al.Stiffness of capacitive and conduit arteries: prognostic significance for end-stage renal disease patients.Hypertension. 2005; 45: 592-596Crossref PubMed Scopus (209) Google Scholar, 29.Mitchell G.F. Effects of central artery aging on the structure and function of the peripheral vasculature: implication for end-organ damage.J Appl Physiol. 2008; 105: 1652-1660Crossref PubMed Scopus (185) Google Scholar that is important for the regulation of cardiac work and pulsatile pressure transmission to the microcirculation.25.Mitchell G.F. Parise H. Benjamin E.J. et al.Changes in arterial stiffness and wave reflections with advancing age in healthy men and women: The Framingham Heart Study.Hypertension. 2004; 43: 1239-1245Crossref PubMed Scopus (621) Google Scholar, 26.London G.M. Pannier B. Arterial functions: how to interpret the complex physiology.Nephrol Dial Transplant. 2010; 25: 3815-3823Crossref PubMed Scopus (38) Google Scholar, 29.Mitchell G.F. Effects of central artery aging on the structure and function of the peripheral vasculature: implication for end-organ damage.J Appl Physiol. 2008; 105: 1652-1660Crossref PubMed Scopus (185) Google Scholar, 30.O'Rourke M.F. Safar M.R. Relationship between aortic stiffening and microvascular disease in brain and kidney: cause and logic of therapy.Hypertension. 2005; 46: 200-204Crossref PubMed Scopus (480) Google Scholar PWV is a convenient way to measure arterial stiffness. Briefly, the speed of pressure wave propagation in a solid is proportional to its rigidity. PWV assesses the stiffness of an artery as a hollow structure and according to the Moens and Korteweg's formula: PWV2=Einc × h/2r × ρ. It depends on artery geometry (wall thickness, h; radius, r), intrinsic elastic properties of the arterial wall biomaterials (Einc), and density (ρ).4.O'Rourke M.F. Mechanical principles in arterial disease.Hypertension. 1995; 26: 2-9Crossref PubMed Google Scholar,24.O'Rourke M.F. Principles and definitions of arterial stiffness, wave reflections and pulse pressure amplification.in: Safar M.E. O'Rourke M.F. Handbook of Hypertension (series edts Birkenhäger WH, Reid JL). Vol. 23.. Elsevier, Amsterdam2006: 3-20Google Scholar PWV must not be confounded with blood velocity. Indeed, although PWV varies between 4 and 5m/s in the ascending aorta and between 9 and 12m/s in peripheral conduit arteries,4.O'Rourke M.F. Mechanical principles in arterial disease.Hypertension. 1995; 26: 2-9Crossref PubMed Google Scholar, 27.Avolio A.O. Chen S.G. Wang R.P. et al.Effects of aging on changing arterial compliance and left ventricular load in a northern Chinese urban community.Circulation. 1983; 68: 50-58Crossref PubMed Google Scholar, 28.Pannier B. Guérin A.P. Marchais S.J. et al.Stiffness of capacitive and conduit arteries: prognostic significance for end-stage renal disease patients.Hypertension. 2005; 45: 592-596Crossref PubMed Scopus (209) Google Scholar blood velocity is in the order of cm/s.5.Nichols W.W. O’Rourke M.F. Vascular impedance.in: Arnold H. McDonald’s Blood Flow in Arteries: Theoretical, Experimental and Clinical Principles. 5th edn. Hodder Arnold, London2005: 299-337Google Scholar, 23.Nichols W.W. O’Rourke M.F. Vascular impedance.in: McDonald’s Blood Flow in Arteries: Theoretical, Experimental and Clinical Principles. 5th edn. Hodder Arnold, London2005: 11-64Google Scholar, 31.Levick J.R. Haemodynamics: pressure, flow and resistance.An Introduction to Cardiovascular Physiology. Butterworths Ltd, London1991: 90-116Crossref Google Scholar PWV represents the transmission of energy through the arterial wall, whereas blood velocity represents the displacement of mass through the incompressible blood column. This difference in speed propagation is physiologically advantageous for left ventricular work and arterial blood flow. At the start of ventricular ejection, the incompressible blood faces a blood column occupying the aorta and arterial tree. The ejected blood has to find space, which is achieved principally by distending the proximal aorta and propelling the blood column forward. Concomitant to blood entering the aorta, the proximal aortic pressure increase creates a pressure wave with higher proximal pressures than in downstream segments (pressure gradient). All these changes are confined to a short segment of the proximal aorta. These local alterations are transmitted downstream, because the incompressible blood displaced from the proximal aorta must also find its place in downstream segments. The pressure wave moves downstream to distal arterial segments, rapidly propagating the pressure gradient from segment to segment, i.e., displacing blood downstream. The PWV increase from the aorta to the peripheral arteries quickly propelling the pressure gradient along the arterial tree, resulting in a rapid (in milliseconds) downstream mobilization of blood in the arterial system. This transmission occurs during ventricular ejection, and the downstream displacement of arterial blood ‘frees up’ space for the stroke volume. Relying only on the ‘thrusting’ force of blood entering the proximal aorta, the movement of all arterial blood would require very high cardiac energy expenditure to counter the high inertial forces of the blood column. At the end of ventricular ejection, the stroke volume is now occupying the blood column whose length (stroke distance) is measured in centimeters, i.e., mean blood velocity in cm/s.31.Levick J.R. Haemodynamics: pressure, flow and resistance.An Introduction to Cardiovascular Physiology. Butterworths Ltd, London1991: 90-116Crossref Google Scholar The fact that PWV largely exceeds blood velocity in the aorta is important; otherwise, peak aortic flow velocity exceeding PWV would create conditions for the generation of longitudinal shock waves (similar to those generated by an airplane passing the speed of sound), potentially provoking arterial injury. The arterial stiffness gradient regulates pressure transmission along the arterial tree and to the microcirculation. The arterial pressure wave generated in the aorta (forward or incident wave) is propagated to arteries throughout the body. The stiffness gradient, together with aortic geometry changes (tapering), local arterial branchings, and lumen-narrowing, creates an impedance mismatch, causing partial reflections of forward pressure waves traveling back to the central aorta (reflected waves).24.O'Rourke M.F. Principles and definitions of arterial stiffness, wave reflections and pulse pressure amplification.in: Safar M.E. O'Rourke M.F. Handbook of Hypertension (series edts Birkenhäger WH, Reid JL). Vol. 23.. Elsevier, Amsterdam2006: 3-20Google Scholar, 32.Murgo J.P. Westerhof N. Giolma J.P. et al.Aortic input impedance in normal man: relationship to pressure wave forms.Circulation. 1980; 62: 105-116Crossref PubMed Google Scholar, 33.Latham R.D. Westerhof N. Sipkema P. et al.Regional wave travel and reflections along the human aorta: a study with six simultaneous micromanometric pressures.Circulation. 1985; 72: 1257-1269Crossref PubMed Google Scholar, 34.O'Rourke M.F. Kelly R.P. Wave reflections in systemic circulation and its implications in ventricular function.J Hypertens. 1993; 11: 327-337Crossref PubMed Google Scholar Wave reflections considerably influence the pressure wave amplitude and shape along the arterial tree.32.Murgo J.P. Westerhof N. Giolma J.P. et al.Aortic input impedance in normal man: relationship to pressure wave forms.Circulation. 1980; 62: 105-116Crossref PubMed Google Scholar, 33.Latham R.D. Westerhof N. Sipkema P. et al.Regional wave travel and reflections along the human aorta: a study with six simultaneous micromanometric pressures.Circulation. 1985; 72: 1257-1269Crossref PubMed Google Scholar, 34.O'Rourke M.F. Kelly R.P. Wave reflections in systemic circulation and its implications in ventricular function.J Hypertens. 1993; 11: 327-337Crossref PubMed Google Scholar, 35.Karamanoglu M. O'Rourke M.F. Avolio A.P. et al.An analysis of the relationship between central aortic and peripheral upper limb pressure waves in man.Eur Heart J. 1993; 14: 160-167Crossref PubMed Google Scholar Forward and reflected pressure waves overlap, and the final amplitude and shape of the pulse pressure wave are determined by the phase relationship (timing) between these component waves. The overlap between the two waves depends on the site of pressure recording along the arterial tree. Peripheral arteries are close to reflection sites, and the reflected wave occurs at the impact of forward wave, i.e., the waves are in phase producing an additive effect. The ascending aorta and central arteries are distant from reflecting sites, and the return of the reflected wave is variably delayed (Tsh, time to shoulder) (Figure 2), depending on PWV and traveling distances.36.London G.M. Guérin A.P. Pannier B. et al.Increased systolic pressure in chronic uremia: role of arterial wave reflections.Hypertension. 1992; 20: 10-19Crossref PubMed Google Scholar In the aorta or central arteries, forward and reflected waves are not in phase. In subjects with low PWV, reflected waves impact on central arteries during end-systole and diastole, increasing the aortic pressure in early diastole but not during systole.24.O'Rourke M.F. Principles and definitions of arterial stiffness, wave reflections and pulse pressure amplification.in: Safar M.E. O'Rourke M.F. Handbook of Hypertension (series edts Birkenhäger WH, Reid JL). Vol. 23.. Elsevier, Amsterdam2006: 3-20Google Scholar, 32.Murgo J.P. Westerhof N. Giolma J.P. et al.Aortic input impedance in normal man: relationship to pressure wave forms.Circulation. 1980; 62: 105-116Crossref PubMed Google Scholar, 33.Latham R.D. Westerhof N. Sipkema P. et al.Regional wave travel and reflections along the human aorta: a study with six simultaneous micromanometric pressures.Circulation. 1985; 72: 1257-1269Crossref PubMed Google Scholar, 34.O'Rourke M.F. Kelly R.P. Wave reflections in systemic circulation and its implications in ventricular function.J Hypertens. 1993; 11: 327-337Crossref PubMed Google Scholar, 35.Karamanoglu M. O'Rourke M.F. Avolio A.P. et al.An analysis of the relationship between central aortic and peripheral upper limb pressure waves in man.Eur Heart J. 1993; 14: 160-167Crossref PubMed Google Scholar This situation is physiologically advantageous, as the higher diastolic pressure boosts coronary perfusion without increasing the left ventricular pressure load. This difference in the overlap between component pressure waves in the aorta and peripheral arteries results in lower aortic systolic and pulse pressures, compared with peripheral arteries (central-to-peripheral systolic and pulse pressure amplification) 33.Latham R.D. Westerhof N. Sipkema P. et al.Regional wave travel and reflections along the human aorta: a study with six simultaneous micromanometric pressures.Circulation. 1985; 72: 1257-1269Crossref PubMed Google Scholar, 34.O'Rourke M.F. Kelly R.P. Wave reflections in systemic circulation and its implications in ventricular function.J Hypertens. 1993; 11: 327-337Crossref PubMed Google Scholar, 35.Karamanoglu M. O'Rourke M.F. Avolio A.P. et al.An analysis of the relationship between central aortic and peripheral upper limb pressure waves in man.Eur Heart J. 1993; 14: 160-167Crossref PubMed Google Scholar, 36.London G.M. Guérin A.P. Pannier B. et al.Increased systolic pressure in chronic uremia: role of arterial wave reflections.Hypertension. 1992; 20: 10-19Crossref PubMed Google Scholar (Figure 2). The higher peripheral pressure is also due to the higher peripheral artery stiffness, i.e., the higher local pressure effect of the displaced blood column. Arterial stiffening disrupts the desirable timing. With increased PWV, the reflected waves return earlier, thus impacting the central arteries during systole rather than diastole, amplifying aortic and ventricular pressures during systole, and reducing aortic pressure during diastole. With arterial stiffening (high PWV), the forward and reflected waves in the aorta are almost in phase, and central aortic pressure is close to the peripheral pressure, and the central-to-peripheral systolic and pulse pressure amplification tends to disappear or be attenuated.4.O'Rourke M.F. Mechanical principles in arterial disease.Hypertension. 1995; 26: 2-9Crossref PubMed Google Scholar, 23.Nichols W.W. O’Rourke M.F. Vascular impedance.in: McDonald’s Blood Flow in Arteries: Theoretical, Experimental and Clinical Principles. 5th edn. Hodder Arnold, London2005: 11-64Google Scholar, 35.Karamanoglu M. O'Rourke M.F. Avolio A.P. et al.An analysis of the relationship between central aortic and peripheral upper limb pressure waves in man.Eur Heart J. 1993; 14: 160-167Crossref PubMed Google Scholar, 36.London G.M. Guérin A.P. Pannier B. et al.Increased systolic pressure in chronic uremia: role of arterial wave reflections.Hypertension. 1992; 20: 10-19Crossref PubMed Google Scholar By favoring early wave reflections, arterial rigidity in" @default.
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• W2047367002 date "2012-08-01" @default.
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• W2047367002 title "Arterial stiffness and pulse pressure in CKD and ESRD" @default.
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