Abstract

Arterial stiffening is the most important cause of increasing systolic and pulse pressure, and for decreasing diastolic pressure beyond 40 years of age. Stiffening affects predominantly the aorta and proximal elastic arteries, and to a lesser degree the peripheral muscular arteries. While conceptually a Windkessel model is the simplest way to visualize the cushioning function of arteries, this is not useful clinically under changing conditions when effects of wave reflection become prominent. Many measures have been applied to quantify stiffness, but all are approximations only, on account of the nonhomogeneous structure of the arterial wall, its variability in different locations, at different levels of distending pressure, and with changes in smooth muscle tone.

This article summarizes the methods and indices used to estimate arterial stiffness, and provides values from a survey of the literature, followed by recommendations of an international group of workers in the field who attended the First Consensus Conference on Arterial Stiffness, which was held in Paris during 2000, under the chairmanship of M.E. Safar and E.D. Frohlich.

Arterial stiffness is emerging as the most important determinant of increased systolic and pulse pressure in our aging community, and therefore, the root cause of a host of cardiovascular complications and events, including left ventricular hypertrophy and failure, aneurysm formation and rupture, and a major contributor to atherosclerotic and small vessel disease and thus to stroke, myocardial infarction, and renal failure.

Although appreciated for years,1,2 it is only in recent times, after acceptance of ill effects of systolic pressure in the elderly, that serious attention has been directed at precise measurement of arterial stiffness. The issue, although superficially simple, is complex, as older treatises on the subject will attest.3–5 The purpose of this review is to introduce the different terms that are used to describe arterial stiffness, and note their pitfalls and limitations and to provide normal values, where possible, as a function of age. Because some terms, which refer to global properties, imply models of the circulation, it will be necessary initially to refer to these models.

Models

The oldest model of the arterial system is the Windkessel—the inverted air-filled dome of old fashioned fire engines that transformed pulsatile flow from a steam or hand-activated pump into a steady stream through the fire hose nozzle (Fig. 1 A). In this model, the dome represents the cushioning function of the arteries, and the nozzle, the peripheral resistance.6 Although conceptually useful, this model is unrealistic because elastic properties are not present at just one site but are distributed along the aorta and major arteries. The pressure wave has a finite wave velocity in arteries, and in addition, pressure waveforms are different in amplitude and contour in central and peripheral arteries.6 Physical properties of arteries are different as well, and different arteries at different sites respond differently to aging, to hypertension, and to drugs.7,8 Value of the Windkessel model is seriously limited as a comprehensive explanation of arterial behavior under different circumstances, although under some specific circumstances—the very elderly, the very hypertensive—it may appear realistic.

The cushioning and conduit functions of the arterial system may be represented separately by a proximal Windkessel with peripheral distributing tube (A) or by a single distensible tube in which both functions are combined (B). (Reprinted with permission from the publisher Churchill Livingstone for O’Rourke MF: Arterial Function in Health and Disease. Edinburgh, 1982).42 The left end of the tube represents the ascending aorta, and the right end, the summation of all arterial/arteriolar junctions.

The most realistic model of the arterial system is a simple tube with one end representing the peripheral resistance, and with the other end, receiving blood in spurts from the heart (Fig. 1).6 A wave generated by cardiac activity travels along the tube toward the periphery and is reflected back from the periphery. The pressure wave at any point along the tube is a resultant of incident and reflected wave. When the tube is distensible, as in youth, the wave velocity is slow, therefore reflection returns late to the heart, in diastole. When the tube wall is stiffened, as in the elderly, wave travel is fast, and the reflected wave merges with the systolic part of the incident wave, causing a high pressure in systole and corresponding low pressure in diastole throughout the tube (Fig. 2). 6

Pressure waves shown schematically in the ascending aorta and radial artery (delayed tracing) of a young adult (A) and older human subject (B).

Indices of arterial stiffness

A host of indices have been introduced to quantify arterial stiffness. As is usual when multiple indices exist, no one has proved superior, and all have problems in measurement and interpretation. The subject was addressed at the Satellite of the 1994 International Society of Hypertension (ISH) Meeting in Sydney, and this list of indices was put forward, and agreed to as an interim measure9,10 (Table 1). There are reservations on many of these indices, because they are influenced by one or more of the following: A. use of inappropriate arterial model (eg, Windkessel); B. assume values of cardiac output that are not, or poorly validated; C. relate proximal diameter change to pressure change at a distant site; and D. are influenced by heart rate or cardiac contractility.

Table 1

Definition and units of the various indices of arterial stiffness

 Relative diameter (or area) change for a pressure increment; the inverse of elastic modulus 
Arterial distensibility ΔD/ΔP · D) (mm Hg−1
 Absolute diameter (or area) change for a given pressure step at fixed vessel length 
Arterial compliance ΔD/ΔP (cm/mm Hg) or cm2/mm Hg) 
 Pressure step required for (theoretical) 100% increase in volume 
Volume elastic modulus ΔP/(ΔV/V) (mm Hg) = ΔP/(ΔD/D) (mm Hg) 
 where there is no change in length 
 The pressure step required for (theoretical) 100% stretch from resting diameter at fixed vessel length 
Elastic modulus (ΔP · D/ΔD) (mm Hg) 
 Elastic modulus per unit area; the pressure step per square centimeter required for (theoretical) 100% stretch from resting length 
Young's modulus ΔP · D/(ΔD · h) (mm Hg/cm) 
 Speed of travel of the pulse along an arterial segment 
Pulse wave velocity Distance/ Δt (cm/s) 
 Increase in aortic or carotid pressure after the peak of blood flow in the vessel 
Pressure augmentation (mm Hg or as % of pulse pressure) 
 Relationship between pressure change and flow velocity in the absence of wave reflections 
Characteristic impedance (ΔP/ΔV) [(mm Hg/cm)/s] 
 Ratio of logarithm (systolic/diastolic pressures) to (relative change in diameter) 
Stiffness index β = In (Ps/Pd) / [(Ds − Dd)/Dd] (nondimensional) 
 Relationship between pressure fall and volume fall in the arterial tree during the exponential component of diastolic pressure decay 
“Large artery elasticity index” ΔV/ΔP (cm3/mm Hg) 
 Relationship between oscillating pressure change and oscillating volume change around the exponential pressure decay during diastole 
Small artery elasticity index ΔV/ΔP (cm3/mm Hg) 
 Relative diameter (or area) change for a pressure increment; the inverse of elastic modulus 
Arterial distensibility ΔD/ΔP · D) (mm Hg−1
 Absolute diameter (or area) change for a given pressure step at fixed vessel length 
Arterial compliance ΔD/ΔP (cm/mm Hg) or cm2/mm Hg) 
 Pressure step required for (theoretical) 100% increase in volume 
Volume elastic modulus ΔP/(ΔV/V) (mm Hg) = ΔP/(ΔD/D) (mm Hg) 
 where there is no change in length 
 The pressure step required for (theoretical) 100% stretch from resting diameter at fixed vessel length 
Elastic modulus (ΔP · D/ΔD) (mm Hg) 
 Elastic modulus per unit area; the pressure step per square centimeter required for (theoretical) 100% stretch from resting length 
Young's modulus ΔP · D/(ΔD · h) (mm Hg/cm) 
 Speed of travel of the pulse along an arterial segment 
Pulse wave velocity Distance/ Δt (cm/s) 
 Increase in aortic or carotid pressure after the peak of blood flow in the vessel 
Pressure augmentation (mm Hg or as % of pulse pressure) 
 Relationship between pressure change and flow velocity in the absence of wave reflections 
Characteristic impedance (ΔP/ΔV) [(mm Hg/cm)/s] 
 Ratio of logarithm (systolic/diastolic pressures) to (relative change in diameter) 
Stiffness index β = In (Ps/Pd) / [(Ds − Dd)/Dd] (nondimensional) 
 Relationship between pressure fall and volume fall in the arterial tree during the exponential component of diastolic pressure decay 
“Large artery elasticity index” ΔV/ΔP (cm3/mm Hg) 
 Relationship between oscillating pressure change and oscillating volume change around the exponential pressure decay during diastole 
Small artery elasticity index ΔV/ΔP (cm3/mm Hg) 

P = pressure; D = diameter; V = volume; h = wall thickness; t = time; s = systolic; d = diastolic.

An example of C is that three articles in major cardiologic journals during 1999 relate diameter change in the aorta to systolic pressure in the brachial artery, thus ignoring the variable amplification of the pressure pulse wave between central and peripheral arteries.11–13

Likewise the widely quoted Heart Outcomes Prevention Evaluation study implies that brachial systolic pressure is an appropriate measure of central systolic pressure and of left ventricular load.14,15 These practical problems aside, there are fundamental problems in application of physical terms to arterial stiffness. The arterial media is a mix of collagen and elastin with consequent nonlinear relationship between pressure and diameter. Hence, stiffness can only be quantified at a given level of pressure as the tangent to a curve.6,16 Furthermore, collagen and elastin are linked by smooth muscle whose activity modulates the contribution of each to arterial stiffness; hence, measured stiffness varies with smooth muscle tone—as effected by nervous activity, by hormones, or locally produced vasoactive substances including nitric oxide released from the vascular endothelium or by drugs.8,17–19 Furthermore still, because the arterial wall is nonhomogenous, application of terms such as Young's modulus, which considers wall thickness, but assumes homogeneity of the wall, may be unrealistic. Finally, muscular arteries show spontaneous vasomotor changes that cause changes in diameter and wall stiffness.20,21 These play havoc with attempts to determine elastic properties in individual arteries. Such spontaneous changes, which are seen also in the arteriolar network, do not appear to the same extent in the aorta and large elastic arteries. Because they appear to be out of phase in different peripheral arterial beds, they appear to have little effect on global indices such as those derived from pulse wave contour.

The seminal studies on arterial stiffness were performed by Bergel3,4 on exteriorized arterial segments. These studies were extended by Gow and other researchers, with the field summarized by Gow in the Handbook of Physiology.5 In principle, these studies did not consider change in smooth muscle tone, as is seen clinically, on arterial stiffness,8,17–19 but did note the complicated interpretations of arterial stiffness with change in arterial caliber and in arterial pressure. Of particular difficulty was the issue of “initial length” of load-bearing elements, as used to determine elastic modulus and distensibility.

Direct measurement

Direct measurement of arterial stiffness relates measurement of change in arterial diameter and pressure at the same site. This can be accomplished invasively with the ultrasound/catheter tip manometer tip system introduced by Stefanadis et al.22 Similar approaches can be applied noninvasively at different sites. Diameter change, although small, can be measured accurately,17–19 but there are problems in estimation of pressure change at the same site. Amplification of the pressure pulse along the arterial tree is not the only problem.6 Inaccuracy of all cuff sphygmomanometer systems23,24 is another.

In measurements of pressure and diameter, stiffness (Table 1) can be expressed as: Distensibility, Compliance, Elastic modulus (Peterson), Elastic modulus (Young). Distensibility is the relative change in diameter with pressure, compliance is the absolute change in diameter (or volume) with pressure, elastic modulus is pressure change required for (theoretic) 100% increase in diameter, and Young's modulus is pressure change per square centimeter for (theoretic) 100% extension. The different indices, as discussed at the 1994 ISH Satellite Meeting are described in Table 1. Table 2 gives normal values as determined in multiple studies.

Table 2

Indices of arterial stiffness and reference values

INDEX Artery Condition Age Sex Pressure Value Reference Comments 
Elastic modulus* Ao arch Healthy Av. 33 M/F 118/76 0.526 Isnard et al 198948 Unit: Nxm−2 
 The pressure step required for (theoretical) 100% stretch from resting diameter at fixed vessel length (ΔP×D)/DD (mm Hg) Ao arch Healthy Av. 14 N/A 116/71 23.2 Ong et al 199249 Unit: kPa 
 Ao arch Healthy Av. 62 M/F 130/77 123 Gatzka et al 199850 Unit: kNxm−2 
 Ao arch CAD Av. 63 M/F 133/74 212 Gatzka et al 198550  
 Ao arch Hypertensives Av. 38 M/F 160/102 1.071 Isnard et al 198948 Unit: Nxm−2 
 Ao arch Postcoartectomy Av. 13 N/A 122/72 42.1 Ong et al 199249 Unit: kPa 
 Desc. thoracic Ao Various Av. 53 M/F 124/74 1.19 Pasierski et al 199451 Unit: dynes × 106/cm2 
 Desc. thoracic Ao Various Av. 55 M/F 91.5 (mean) 1.032 Lang et al 199452 Unit: dynes × 106/cm2 
 Desc. thoracic Ao Healthy Av. 47 125/78 0.76 Pearson et al 199453 Unit: dynes × 106/cm2 
 Desc. thoracic Ao Healthy Av. 43 123/75 0.68 Pearson et al 199453 Unit: dynes × 106/cm2 
 Desc. thoracic Ao Hypertensives Av. 47 M/F 150/92 0.98 Pearson et al 199453 Unit: dynes × 106/cm2 
 Abdominal Ao Healthy Av. 25 117/70 0.69 Lanne et al 199254 Unit: dynes × 106/cm2 
 Abdominal Ao Healthy Av. 27 120/76 0.52 Sonesson et al 199355 Unit: dynes × 105/cm2 
 Abdominal Ao Healthy 20–39 N/A 120/69 0.736 Kawasaki et al 198756 Unit: dynes × 106/cm2 
 Abdominal Ao Healthy Av. 60 N/A 124/74 1.1 Hirai et al 198926 Unit: dynes × 106/cm2 
 Abdominal Ao CAD Av. 55–59 M/F 128–140/79–83 1.62–3.08 Harai et al 198926 Unit: dynes × 106/cm2 
        4 subgroups: no stenosis 
        3-vessel disease 
 Healthy 20–39 N/A 117/70 0.7 Kawasaki et al 198756 Unit: dynes × 106/cm2 
 Normotensives Av. 56 M/F 113/69 124 Liao et al 199911 Unit: kPa 
 Normotensives Av. 47 M/F 115/71 0.71 (effective)/1.16 (intrinsic) Bussy et al 200057 Unit: kPa × 103 
 Healthy Av. 60 N/A 124/74 1.21 Hirai et al 198926 Unit: dynes × 106/cm2 
 CAD Av. 55–59 M/F 128–140/79–83 1.23–1.84 Hirai et al 198926 Unit: dynes × 106/cm2 
        4 subgroups: no stenosis 
        3-vessel disease 
 Hypertensives Av. 56 M/F 124/74 155 Liao et al 199911 Measured at baseline before development of hypertension 
        Unit kPa 
 Hypertensives Av. 50 M/F 153/99 1.04 (effective)/1.02 (intrinsic) Bussy et al 200057 Unit: kPa × 103 
 Healthy 20–39 N/A 116/69 0.94 Kawasaki et al 198756 Unit: dynes × 106/cm2 
 Fem Healthy 20–39 N/A 116/68 1.15 Kawasaki et al 198756 Unit: dynes × 106/cm2 
Arterial distensibility*Relative diameter (or area) change for a pressure increment; the inverse of elastic modulus ΔD/(ΔP×D) mm Hg−1 Asc. Ao Healthy Av. 45 120/70 3.96 Stefanadis et al 199058 Multiplication by 2 
        Unit: cm2 × dynes−1 × 10−6 
 Asc. Ao Healthy Av. 29 M/F 122/75 5.6 Hirata et al 199159 Multiplication by 2 
        Unit: cm2 × dynes−1 × 10−6 
 Asc. Ao Normotensive Av. 49 M/F 119/74 7.0 Resnick et al 199760 Unit: 10−3 × mm Hg−1 
 Asc. Ao CAD Av. 46 118/67 1.60 Stefanadis et al 199058 Multiplication by 2 
        Unit: cm2 × dynes−1 × 10−6 
 Asc. Ao Marfan S. Av. 26 M/F 126/81 2.9 Hirata et al 199159 Multiplication by 2 
        Unit: cm2 × dynes−1 × 10−6 
 Asc. Ao Chronic Ao Regurg. Av. 40 M/F 127/60 0.17 Wilson et al 199261 Unit: 10−2 × mm Hg−1 
 Asc. Ao Hypertensive Av. 50 M/F 149/93 2.5 Resnick et al 199760 Unit: 10−3 × mm Hg−1 
 Desc. thoracic Ao Healthy Av. 53 M/F 122/76 3.5 Stefanadis et al 199762 Multiplication by 2 
        Unit: cm2 × dynes−1 × 10−6 
 Desc. thoracic Ao Healthy Av. 50 119/75 3.95 Stefanadis et al 199522 Multiplication by 2 
        Unit: cm2 × dynes−1 × 10−6 
 Desc. thoracic Ao Normotensive Av. 49 M/F 119/74 5.1 Resnick et al 199760 Unit: 10−3 × mm Hg−1 
 Desc. thoracic Ao Hypertensive Av. 54 M/F 176/98 1.4 Stefanadis et al 199762 Multiplication by 2 
        Unit: cm2 × dynes−1 × 10−6 
 Desc. thoracic Ao Hypertensive Av. 50 M/F 149/93 2.2 Resnick et al 199760 Unit: 10−3 × mm Hg−1 
 Desc. thoracic Ao CAD Av. 55 125/74 1.73 Stefanadis et al 199522 Multiplication by 2 
        Unit: cm2 × dynes−1 × 10−6 
 Abdominal Ao Healthy Av. 29 M/F 122/75 7.7 Hirata et al 199159 Multiplication by 2 
        Unit: cm2 × dynes−1 × 10−6 
 Abdominal Ao Normotensive Av. 49 M/F 119/74 7.3 Resnick et al 199760 Unit: 10−3 × mm Hg−1 
 Abdominal Ao Healthy Av. 36 M/F 114/68 20.5 Jondeau et al 199963 Unit: 10−3 × kPa 
 Abdominal Ao Healthy Av. 34 M/F 128/77 ∼0.39 Giannattasio et al 199964 Multiplication by 2 
        Unit: 10−2 × mm Hg−1 
 Abdominal Ao Diabetics type I Av. 32 M/F 128/76 ∼0.335 Giannattasio et al 199964 Multiplication by 2 
  no complications      Unit: 10−2 × mm Hg−1 
 Abdominal Ao Diabetics type I Av. 38 M/F 145/782 ∼0.25 Giannattasio et al 199964 Multiplication by 2 
  complications      Unit: 10−2 × mm Hg−1 
 Abdominal Ao Marfan Av. 26 M/F 126/81 5.5 Hirata et al 199159 Multiplication by 2 
        Unit: cm2 × dynes−1 × × 10−6 
 Abdominal Ao Hypertensive Av. 50 M/F 149/93 2.3 Resnick et al 199760 Unit: 10−3 × mm Hg−1 
 Abdominal Ao Marfan Av. 37 M/F 110/64 12.7 Jondeau et al 199963 Unit: 10−3 × kPa 
 Healthy Av. 50 M/F 118/71 11.7 (effective)/9.0 (intrinsic) Laurent et al 199465 Unit: 10−3 × /kPa 
 Healthy Av. 28 M/F ∼108/63 ∼0.35 Faila et al 199766 Divided by 2 and multiplied by π 
        Unit: 10−3 × mm Hg−1 
 Healthy Av. 38 M/F — 22.8 Kool et al 199467 Multiplied by 2 π 
        Unit: 10−3 × /kPa−1 
 Healthy Av. 36 M/F 114/68 43.3 Jondeau et al 199963 Unit: 10−3 × /kPa 
 Hypertensive Av. 51 M/F 156/93 7.8 (effective)/10 (intrinsic) Laurent et al 199465 Unit: 10−3 × /kPa 
 Random population sample Av. 50 132/84 20.9 van der Heijden-Spek et al 200068 Unit: 10−3 × /kPa 
 Random population sample Av.50 128/81 24.4 van der Heijden-Spek et al 200068 Unit: 10−3 × /kPa 
 Healthy Av.38 — — 5.05 Bank & Kaiser 19988 at 95 mm Hg 
        Unit: mm Hg−1 
 Healthy Av. 38 M/F — 30.5 Kool et al 199467 Multiplied by 2πUnit: 10−3 × kPa−1 
 Normotensive Av.36–41 M/F 121–141/66–77 (0.67–1.00)*(0.50–0.90)† Laurent et al 199369 Multicenter study; *at mean pressure; †at 100 mm Hg 
        Unit: 10−3 × mm Hg−1 
 Healthy Av. 28 M/F ∼108/63 ∼0.84 Faila et al 199766 Divided by 2 and multiplied by π 
        Unit: 10−3 × mm Hg−1 
 Healthy Av. 55 M/F 127/68 ∼1.4 Giannattasio et al 199770 Langewouters formula 
        Unit: mm/mm Hg 10−3 
 Healthy Av. 36 M/F 114/68 5.0 Jondeau et al 199963 Unit: 10−3 kPa−1 
 Hypertensives Av. 43–50 M/F 163–172/81–103 (0.41–0.91)*(0.71–1.10)† Laurent et al 199369 Multicenter study; *at mean pressure; †at 100 mm Hg; unit: 10−3 × mm Hg−1 
 Hypothyroidism Av. 59 M/F 129/69 ∼1.85 Giannattasio et al 199770 Langewouters formula 
        Unit: mm/mm Hg 10−3 
 Healthy Av. 38 M/F — 21 Kool et al 199467 Multiplied by 2π 
        Unit: 10−3 × kPa−1 
 Healthy Av. 36 M/F 114/68 7.7 Jondeau et al 199963 Unit: 10−3 kPa−1 
Arterial compliance*Absolute diameter (or area) change for a given pressure step at a fixed vessel length ΔD/(ΔP) cm × mm Hg−1 Desc. thoracic Ao Various Av. 55 M/F 92 (mean) 0.010 Lang et al 199452 Unit: cm2/mm Hg 
 Abdominal Ao Healthy Av. 36 M/F 114/68 27.7 Jondeau et al 199963 Unit: m2 × kPa−1 × 10−7 
 Abdominal Ao Marfan Av. 37 M/F 110/64 21.6 Jondeau et al 199963 Unit: m2 × kPa−1 × 10−7 
 Healthy Av. 38 M/F — 0.84 Kool et al 199467 Multiplied by 2, divided by π 
        Unit: mm2 × kPa−1 
 Healthy Av. 50 M/F 118/71 8.72 (effective)/6.9 (intrinsic) Laurent et al 199465 Unit: m2 × kPa−1 × 10−7 
 Healthy Av. 36 M/F 114/68 8.55 Jondeau et al 199963 Unit: m2 × kPa−1 × 10−7 
 Hypertensive Av. 51 M/F 156/93 6.31 (effective)/7.8 (intrinsic) Laurent et al 199465 Unit: m2 × kPa−1 × 10−7 
 Healthy Av. 38 — — 0.010 Bank & Kaiser 19988 at 95 mm Hg 
        Unit: mm2/mm Hg 
 Healthy Av. 38 M/F — 0.47 Kool et al 199467 Multiplied by 2, divided by π 
        Unit: mm2 × kPa−1 
 Random population sample Av. 50 132/84 0.33 van der Heijden-Spek et al 200068 Unit: mm2/kPa 
 Random population sample Av. 50 128/81 0.25 van der Heijden-Spek et al 200068 Unit: mm2/kPa 
 Normotensive Av. 36–41 M/F 121–141/66–77 (3.23–4.58)* (2.8–3.4)† Laurent et al 199369 Multicenter study; *at mean pressure; †at 100 mm Hg 
        Unit: 10−3 × mm2 × mm Hg−1 
 Healthy Av. 53 M/F 117/64 ∼5.7 Giannattasio et al 199571 Langewouters formula 
        Unit: mm2/ mm Hg 10−3 
 Healthy Av. 48 M/F 121/73 1.81 Mourad et al 199872 Unit: m2 × kPa−1 × 10−8 
 Healthy Av. 36 M/F 114/68 0.22 Jondeau et al 199963 Unit: m2 × kPa−1 × 10−7 
 Hypertensives Av. 43–50 M/F 163–172/81–103 (2.61–4.81)† (3.4–6.8)† Laurent et al 199369 Multicenter study; *at mean pressure;†at 100 mm Hg 
        Unit: 10−3 × mm2 × mm Hg−1 
 Hypertensive Av. 57 M/F 179/100 ∼7 Giannattasio et al 199773 Langewouters formula 
        Isobaric 
        Unit: mm2/mm Hg 10−3 
 Hypertension (hypertrophied artery) Av. 50 M/F 163/99 1.82 Mourad et al 199872 Unit: m2 × kPa−1 × 10−8 
 Hypertension (remodeled artery) Av. 49 M/F 166/99 1.03 Mourad et al 199872 Unit: m2 × kPa−1 × 10−8 
 Hypercholesterolemia Av. 47 M/F 107/60 ∼2.5 Giannattasio et al 199774 Langewouters formula 
        Unit: mm2/mm Hg 10−3 
 Congestive heart failure Av. 57 M/F 106/62 ∼4.15 Giannattasio et al 199571 Langewouters formula 
        Unit: mm2/mm Hg 10−3 
 Healthy Av. 38 M/F — 1.28 Kool et al 199467 Multiplied by 2, divided by π 
        Unit: mm2 × kPa−1 
 Healthy Av. 36 M/F 114/68 5.3 Jondeau et al 199963 Unit: m2 × kPa−1 × 10−7 
Young's modulus*Elastic modulus per unit area; the pressure step per 4 square centimeter required for (theoretical) 100% strech from resting length ΔP × D/ (ΔD × h) (mm Hg/cm) Desc. thoracic Ao Healthy Av. 47 125/78 7.37 Pearson et al 199453 Unit: dynes × 106/cm2 
 Desc. thoracic Ao Healthy Av. 43 123/75 6.03 Pearson et al 199453 Unit: dynes × 106/cm2 
 Desc. thoracic Ao Hypertensives Av. 47 M/F 150/92 13.88 Pearson et al 199453 Unit: dynes × 106/cm2 
 Normotensives Av. 56 M/F 113/69 678 Liao et al 199911 Unit: kPa 
 Hypertensives Av. 56 M/F 124/74 822 Liao et al 199911 Measured at baseline before development of hypertension 
        Unit: kPa 
Pulse wave velocity*Speed of travel of the pulse along an arterial segment Distance/Δt (cm/s) Asc. Ao Healthy Av. 34 M/F 117/77 668 Murgo et al 198075  
 Asc. Ao Healthy (majority) Av. 38 M/F — 387 Merillon et al 197676  
 Asc. Ao Hypertensives Av. 32 M/F — 570 Merrillon et al 197676  
 Asc. Ao Healthy Av. 42 M/F Mean 91 440 Latham et al 198577  
 Thoracic Ao Healthy Av. 42 M/F Mean 91 530 Latham et al 198577  
 Abdominal Ao Healthy Av. 42 M/F Mean 91 570 Latham et al 198577  
 Iliac Healthy Av. 42 M/F Mean 91 880 Latham et al 198577  
 Healthy Av. 38 — — 1510 Bank & Kaiser 19988 at 95 mm Hg 
 Ao Arch to Fem Healthy/low prevalence of Hypertensive Av. 46 (approx) M/F — = 5.1 × age + 533 Avolio et al 198578 Site to site 
 Ao Arch to Fem Healthy/high prevalence of Hypertensive Av. 46 (approx) M/F — =9.2 × age + 615 Avolio et al 198578 Site to site 
 Asc. Ao or C-Fem Healthy Elderly Av. 70 M/F 140/73 906 Chen et al 199979 Suprastenal notch to femoral 
 Ao Arch or C-Fem End-stage renal disease Av. 52 M/F 157/85 1110 Blacher et al 199980 Site to site or distance subtraction 
 C-Fem Healthy Av. 33 M/F 118/76 890 Isnard et al 198948 Site to site 
 C-Fem Healthy whites Av. 25 120/78 815 Ferreira et al 199981 Site to site 
 C-Fem Healthy African Americans Av. 23 119/77 775 Ferreira et al 199981 Site to site 
 C-Fem Healthy Av. 24 118/68 620 Kingwell et al 199782 Distance subtraction 
 C-Fem Healthy Av. 29 M/F 122/75 950 Hirata et al 199159 Site to site 
 C-Fem Healthy Av. 52 M/F 141/82 930 London et al 19928 Distance subtraction 
 C-Fem Healthy Av. 62 M/F 143/89 980 Breithaupt-Grogler et al 199783 Site to site 
 C-Fem Random population sampleno cardiovasc. Treatment or complication Av. 46 M/F 98–222/62–130 =0.07 × SP+0.09 × age−4.3 Asmar et al 199584 Site to site 
 C-Fem Normotensives Av. 45 M/F 125/77 =0.06 × age+5.7 × 102 Asmar et al 199585 Site to site 
 C-Fem Random population sample Av. 50 132/84 700 van der Heijden-Spek et al 200068 Distance subtraction 
 C-Fem Random population sample Av. 50 128/81 670 van der Heijden-Spek et al 200068 Distance subtraction 
 C-Fem Hypertensive Av. 38 M/F 160/102 1180 Isnard et al 198948 Site to site 
 C-Fem Hypertensives treated Av. 59 M/F 144/82 =0.11 × age+3.5 × 102 Asmar et al 199585 Site to site 
 C-Fem Hypertensives untreated Av. 48 M/F 164/102 =0.12 × age+6.3 × 102 Asmar et al 199585 Site to site 
 C-Fem Hypertensive no vasc. Dis Av. 57 M/F 144/83 1240 Bortolotto et al 199986 Site to site 
 C-Fem Hypertensive no vasc. Dis. Av. 62 M/F 148/83 1430 Bortolotto et al 199986 Site to site 
 C-Fem Hypertensive whites Av. 28 151/94 880 Ferreira et al 199981 Site to site 
 C-Fem Hypertensive African Americans Av. 29 152/97 930 Ferreira et al 199981 Site to site 
 C-Fem Hypertensive no atherosclerosis Av. 57 M/F 144/84 1240 Blacher et al 199987 Site to site 
 C-Fem Hypertensive atherosclerosis Av. 67 M/F 149/80 1490 Blacher et al 199987 Site to site 
 C-Fem Marfan Av. 26 M/F 126/81 1160 Hirata et al 199159 Distance subtraction 
 C-Fem Chronic uremia Av. 53 M/F 153/81 1035 London et al 199228 Site to site 
 B-R Healthy Av. 39 132/78 880 Armentano et al 199188 Site to site 
 B-R Healthy/low prevalence of hypertension Av. 46 (approx) M/F — =0.61 × age+817 Avolio et al 198578 Site to site 
 B-R Healthy/high prevalence of hypertension Av. 46 (approx) M/F — =4.8×Age+998 Avolio et al 198578 Site to site 
 B-R Normotensives Av. 40 132/78 880 Simon et al 198589 Site to site 
 B-R Hypertensives Av. 43 168/98 1150 Simon et al 198589 Site to site 
 B-R Hypertensive Av. 43 168/98 1160 Armentano et al 199188 Site to site 
 Fem-foot Healthy/low prevalence of hypertension Av. 46 (approx) M/F — =4.43×Age+718 Avolio et al 198578 Site to site 
 Fem-foot Healthy/high prevalence of hypertension Av. 46 (approx) M/F — =5.6×Age+791 Avolio et al 198578 Site to site 
 Fem-foot Healthy Av. 24 118/68 830 Kingwell et al 199782 Site to site 
Characteristic impedance*Relationship between pressure change and flow velocity in the absence of wave reflections ΔP/Δv (mm Hg)(cm × s) Asc. Ao Healthy Av. 34 M/F 117/77 47 Murgo et al 198075 Unit: dyne · s · cm−5 
 Asc. Ao Healthy (majority) Av. 38 M/F — 73 Merillon et al 197676 Unit: dyne · s · cm−5 
 Asc. Ao CAD (majority) Av. 47 — 100 (mean) 97 O’Rourke and Avolio 198090 Unit: dyne · s · cm−5 
 Asc. Ao Healthy (majority) Av. 42 M/F 121/78 94 Ting et al 198634 Unit: dyne · s · cm−5 
 Asc. Ao Hypertensives Av. 35 M/F 168/99 146 Ting et al 198634 Unit: dyne · s · cm−5 
 Asc. Ao CAD Av. 56 M/F 126/71 136 Kelly and Fitchett 199291 Unit: dyne · s · cm−5 
 Asc. Ao Hypertensives Av. 32 M/F — 81 Merrillon et al 197676 Unit: dyne · s · cm−5 
 Asc. Ao Heart failure 21–70 M/F 89 (mean) 138 Binkley et al 199092 Unit: dyne · s · cm−5 
Stiffness index Ratio of logarithm (systolic/diastolic pressures) to (relative change in diameter) β=ln (Ps/Pd)/[(Ds−Dd)/Dd] nondimensional Asc. Ao Healthy Av. 29 M/F 112/75 5.9 Hirata et al 199159  
 Asc. Ao Marfan Av. 26 M/F 126/81 10.9 Hirata et al 199159  
 Ao arch Healthy Av. 14 N/A 116/71 2.17 Ong et al 199249 Did not divide by Dd
 Ao arch Healthy Av. 62 M/F 130/77 Gatzka et al 199850  
 Ao arch CAD Av. 63 M/F 133/74 16 Gatzka et al 199850  
 Ao arch Post coartectomy Av. 13 N/A 122/72 3.66 Ong et al 199249 Did not divide by Dd
 Desc. thoracic Ao Various Av. 53 M/F 124/74 3.77 Pasierski et al 199451  
 Desc. thoracic Ao Healthy Av. 47 125/78 5.71 Pearson et al 199453  
 Desc. thoracic Ao Healthy Av. 43 123/75 5.10 Pearson et al 199453  
 Desc. thoracic Ao Hypertensives Av. 47 M/F 150/92 13.88 Pearson et al 199453  
 Abdominal Ao Healthy 6-81 N/A Normotensive 4.29–9.83 Kawasaki et al 198756 4 different age groups 
 Abdominal Ao Healthy Av. 29 M/F 112/75 3.9 Hirata et al 199159  
 Abdominal Ao Healthy Av. 60 N/A 124/74 8.58 Hirai et al 198926  
 Abdominal Ao CAD Av. 55–59 M/F 128–140/79–83 12.25–22.37 Hirai et al 198926 4 subgroups: no stenosis 
        3-vessel disease 
 Abdominal Ao Marfan Av. 26 M/F 126/81 7.1 Hirata et al 199159  
 Healthy 6–81 N/A Normotensive 4.32–11.31 Kawasaki et al 198756 4 different age groups 
 Normotensives Av. 56 M/F 113/69 10.3 Liao et al 199911  
 Healthy Av. 60 N/A 124/74 9.17 Hirai et al 198926  
 CAD Av. 55–59 M/F 128–140/79–83 9.42–13.17 Hirai et al 198926 4 subgroups: no stenosis 
        3-vessel disease 
 Hypertensives Av. 56 M/F 124/74 11.87 Liao et al 199911 Measured at baseline before development of hypertension 
 Healthy 6–81 N/A Normotensive 8.56–13.73 Kawasaki et al 198756 4 different age groups 
 Healthy 6–81 N/A Normotensive 9.41–15.31 Kawasaki et al 198756 4 different age groups 
Capacitative compliance Relationship between pressure fall and volume fall in the arterial tree during the exponential component of diastolic pressure decay ΔV/ΔP (cm3/mm Hg) Proximal part of circulation Normotensive Av. 47 M/F 115/63 ∼2.2 Cohn et al 199524  
 Proximal part of circulation Healthy Av. 50 — 138/75 1.71 Duprez et al 199893  
 Proximal part of circulation Healthy 21–80 (M)/22–83 (F) M/F 125/68 & 120/66 ∼2(M)/1.7(F) McVeigh et al 199933  
 Proximal part of circulation Heart failure Av. 59 — 116/69 1.51 Duprez et al 199893  
 Proximal part of circulation Hypertensive Av. 54 M/F 152/86 ∼1.95 Cohn et al 199524  
 Proximal part of circulation No CAD Av. 53 123/68 ∼1.8 Cohn et al 199524  
 Proximal part of circulation CAD Av. 55 132/70 ∼1.8 Cohn et al 199524  
Oscillatory compliance Relationship between oscillating pressure change and oscillating volume change around the exponential pressure decay during diastole ΔV/ΔP (cm3/mm Hg) Distal part of circulation Normotensive Av. 47 M/F 115/63 ∼0.075 Cohn et al 199524  
 Distal part of circulation Healthy Av. 50 — 138/75 0.054 Duprez et al 199893  
 Distal part of circulation Healthy 21–80 (M)/22–83(F) M/F 125/68 & 120/66 ∼0.08(M)/0.056(F) McVeigh et al 199933  
 Distal part of circulation Heart failure Av. 59 — 116/69 0.050 Duprez et al 199893  
 Distal part of circulation Hypertensive Av. 54 M/F 152/86 ∼0.05 Cohn et al 199524  
 Distal part of circulation No CAD Av. 53 123/68 ∼0.065 Cohn et al 199524  
 Distal part of circulation CAD Av. 55 132/70 ∼0.05 Cohn et al 199524  
Total arterial compliance“Area method” Whole body Normotensive Av. 43 N/A 120/77 1.47 Liu et al 198994 At mean pressure 
        Units: mL/mm Hg 
 Whole body Hypertensive 37 N/A 166/99 0.80 Liu et al 198994 At mean pressure 
        Units: mL/mm Hg 
 Whole body Normotensive Av. 33 M/F 112/74 2.15 Ting et al 199595 At mean pressure 
        Units: mL/mm Hg 
 Whole body Hypertensive Av. 33 M/F 161/100 1.03 Ting et al 199595 At mean pressure 
        Units: mL/mm Hg 
 Whole body Healthy Av. 23 106/63 0.57 Rajkumar et al 199796 Arbitrary units dimensionally equivalent to mL/mm Hg 
 Whole body Healthy Av. 60 123/82 0.34 McGrath et al 199897 Arbitrary units dimensionally equivalent to mL/mm Hg 
 Whole body Healthy sedentary Av. 26 109/63 0.54 Bertovic et al 199998 Arbitrary units dimensionally equivalent to mL/mm Hg 
 Whole body Strength trained athletes Av. 26 120/59 0.40 Bertovic et al 199998 Arbitrary units dimensionally equivalent to mL/mm Hg 
 Whole body Postenenopausal Av. 59 126/71 0.26 Rajkumar et al 199796 Arbitrary units dimensionally equivalent to mL/mm Hg 
 Whole body Postenenopausal Av. 63 126/69 0.31 Waddell et al 199999 Arbitrary units dimensionally equivalent to mL/mm Hg 
INDEX Artery Condition Age Sex Pressure Value Reference Comments 
Elastic modulus* Ao arch Healthy Av. 33 M/F 118/76 0.526 Isnard et al 198948 Unit: Nxm−2 
 The pressure step required for (theoretical) 100% stretch from resting diameter at fixed vessel length (ΔP×D)/DD (mm Hg) Ao arch Healthy Av. 14 N/A 116/71 23.2 Ong et al 199249 Unit: kPa 
 Ao arch Healthy Av. 62 M/F 130/77 123 Gatzka et al 199850 Unit: kNxm−2 
 Ao arch CAD Av. 63 M/F 133/74 212 Gatzka et al 198550  
 Ao arch Hypertensives Av. 38 M/F 160/102 1.071 Isnard et al 198948 Unit: Nxm−2 
 Ao arch Postcoartectomy Av. 13 N/A 122/72 42.1 Ong et al 199249 Unit: kPa 
 Desc. thoracic Ao Various Av. 53 M/F 124/74 1.19 Pasierski et al 199451 Unit: dynes × 106/cm2 
 Desc. thoracic Ao Various Av. 55 M/F 91.5 (mean) 1.032 Lang et al 199452 Unit: dynes × 106/cm2 
 Desc. thoracic Ao Healthy Av. 47 125/78 0.76 Pearson et al 199453 Unit: dynes × 106/cm2 
 Desc. thoracic Ao Healthy Av. 43 123/75 0.68 Pearson et al 199453 Unit: dynes × 106/cm2 
 Desc. thoracic Ao Hypertensives Av. 47 M/F 150/92 0.98 Pearson et al 199453 Unit: dynes × 106/cm2 
 Abdominal Ao Healthy Av. 25 117/70 0.69 Lanne et al 199254 Unit: dynes × 106/cm2 
 Abdominal Ao Healthy Av. 27 120/76 0.52 Sonesson et al 199355 Unit: dynes × 105/cm2 
 Abdominal Ao Healthy 20–39 N/A 120/69 0.736 Kawasaki et al 198756 Unit: dynes × 106/cm2 
 Abdominal Ao Healthy Av. 60 N/A 124/74 1.1 Hirai et al 198926 Unit: dynes × 106/cm2 
 Abdominal Ao CAD Av. 55–59 M/F 128–140/79–83 1.62–3.08 Harai et al 198926 Unit: dynes × 106/cm2 
        4 subgroups: no stenosis 
        3-vessel disease 
 Healthy 20–39 N/A 117/70 0.7 Kawasaki et al 198756 Unit: dynes × 106/cm2 
 Normotensives Av. 56 M/F 113/69 124 Liao et al 199911 Unit: kPa 
 Normotensives Av. 47 M/F 115/71 0.71 (effective)/1.16 (intrinsic) Bussy et al 200057 Unit: kPa × 103 
 Healthy Av. 60 N/A 124/74 1.21 Hirai et al 198926 Unit: dynes × 106/cm2 
 CAD Av. 55–59 M/F 128–140/79–83 1.23–1.84 Hirai et al 198926 Unit: dynes × 106/cm2 
        4 subgroups: no stenosis 
        3-vessel disease 
 Hypertensives Av. 56 M/F 124/74 155 Liao et al 199911 Measured at baseline before development of hypertension 
        Unit kPa 
 Hypertensives Av. 50 M/F 153/99 1.04 (effective)/1.02 (intrinsic) Bussy et al 200057 Unit: kPa × 103 
 Healthy 20–39 N/A 116/69 0.94 Kawasaki et al 198756 Unit: dynes × 106/cm2 
 Fem Healthy 20–39 N/A 116/68 1.15 Kawasaki et al 198756 Unit: dynes × 106/cm2 
Arterial distensibility*Relative diameter (or area) change for a pressure increment; the inverse of elastic modulus ΔD/(ΔP×D) mm Hg−1 Asc. Ao Healthy Av. 45 120/70 3.96 Stefanadis et al 199058 Multiplication by 2 
        Unit: cm2 × dynes−1 × 10−6 
 Asc. Ao Healthy Av. 29 M/F 122/75 5.6 Hirata et al 199159 Multiplication by 2 
        Unit: cm2 × dynes−1 × 10−6 
 Asc. Ao Normotensive Av. 49 M/F 119/74 7.0 Resnick et al 199760 Unit: 10−3 × mm Hg−1 
 Asc. Ao CAD Av. 46 118/67 1.60 Stefanadis et al 199058 Multiplication by 2 
        Unit: cm2 × dynes−1 × 10−6 
 Asc. Ao Marfan S. Av. 26 M/F 126/81 2.9 Hirata et al 199159 Multiplication by 2 
        Unit: cm2 × dynes−1 × 10−6 
 Asc. Ao Chronic Ao Regurg. Av. 40 M/F 127/60 0.17 Wilson et al 199261 Unit: 10−2 × mm Hg−1 
 Asc. Ao Hypertensive Av. 50 M/F 149/93 2.5 Resnick et al 199760 Unit: 10−3 × mm Hg−1 
 Desc. thoracic Ao Healthy Av. 53 M/F 122/76 3.5 Stefanadis et al 199762 Multiplication by 2 
        Unit: cm2 × dynes−1 × 10−6 
 Desc. thoracic Ao Healthy Av. 50 119/75 3.95 Stefanadis et al 199522 Multiplication by 2 
        Unit: cm2 × dynes−1 × 10−6 
 Desc. thoracic Ao Normotensive Av. 49 M/F 119/74 5.1 Resnick et al 199760 Unit: 10−3 × mm Hg−1 
 Desc. thoracic Ao Hypertensive Av. 54 M/F 176/98 1.4 Stefanadis et al 199762 Multiplication by 2 
        Unit: cm2 × dynes−1 × 10−6 
 Desc. thoracic Ao Hypertensive Av. 50 M/F 149/93 2.2 Resnick et al 199760 Unit: 10−3 × mm Hg−1 
 Desc. thoracic Ao CAD Av. 55 125/74 1.73 Stefanadis et al 199522 Multiplication by 2 
        Unit: cm2 × dynes−1 × 10−6 
 Abdominal Ao Healthy Av. 29 M/F 122/75 7.7 Hirata et al 199159 Multiplication by 2 
        Unit: cm2 × dynes−1 × 10−6 
 Abdominal Ao Normotensive Av. 49 M/F 119/74 7.3 Resnick et al 199760 Unit: 10−3 × mm Hg−1 
 Abdominal Ao Healthy Av. 36 M/F 114/68 20.5 Jondeau et al 199963 Unit: 10−3 × kPa 
 Abdominal Ao Healthy Av. 34 M/F 128/77 ∼0.39 Giannattasio et al 199964 Multiplication by 2 
        Unit: 10−2 × mm Hg−1 
 Abdominal Ao Diabetics type I Av. 32 M/F 128/76 ∼0.335 Giannattasio et al 199964 Multiplication by 2 
  no complications      Unit: 10−2 × mm Hg−1 
 Abdominal Ao Diabetics type I Av. 38 M/F 145/782 ∼0.25 Giannattasio et al 199964 Multiplication by 2 
  complications      Unit: 10−2 × mm Hg−1 
 Abdominal Ao Marfan Av. 26 M/F 126/81 5.5 Hirata et al 199159 Multiplication by 2 
        Unit: cm2 × dynes−1 × × 10−6 
 Abdominal Ao Hypertensive Av. 50 M/F 149/93 2.3 Resnick et al 199760 Unit: 10−3 × mm Hg−1 
 Abdominal Ao Marfan Av. 37 M/F 110/64 12.7 Jondeau et al 199963 Unit: 10−3 × kPa 
 Healthy Av. 50 M/F 118/71 11.7 (effective)/9.0 (intrinsic) Laurent et al 199465 Unit: 10−3 × /kPa 
 Healthy Av. 28 M/F ∼108/63 ∼0.35 Faila et al 199766 Divided by 2 and multiplied by π 
        Unit: 10−3 × mm Hg−1 
 Healthy Av. 38 M/F — 22.8 Kool et al 199467 Multiplied by 2 π 
        Unit: 10−3 × /kPa−1 
 Healthy Av. 36 M/F 114/68 43.3 Jondeau et al 199963 Unit: 10−3 × /kPa 
 Hypertensive Av. 51 M/F 156/93 7.8 (effective)/10 (intrinsic) Laurent et al 199465 Unit: 10−3 × /kPa 
 Random population sample Av. 50 132/84 20.9 van der Heijden-Spek et al 200068 Unit: 10−3 × /kPa 
 Random population sample Av.50 128/81 24.4 van der Heijden-Spek et al 200068 Unit: 10−3 × /kPa 
 Healthy Av.38 — — 5.05 Bank & Kaiser 19988 at 95 mm Hg 
        Unit: mm Hg−1 
 Healthy Av. 38 M/F — 30.5 Kool et al 199467 Multiplied by 2πUnit: 10−3 × kPa−1 
 Normotensive Av.36–41 M/F 121–141/66–77 (0.67–1.00)*(0.50–0.90)† Laurent et al 199369 Multicenter study; *at mean pressure; †at 100 mm Hg 
        Unit: 10−3 × mm Hg−1 
 Healthy Av. 28 M/F ∼108/63 ∼0.84 Faila et al 199766 Divided by 2 and multiplied by π 
        Unit: 10−3 × mm Hg−1 
 Healthy Av. 55 M/F 127/68 ∼1.4 Giannattasio et al 199770 Langewouters formula 
        Unit: mm/mm Hg 10−3 
 Healthy Av. 36 M/F 114/68 5.0 Jondeau et al 199963 Unit: 10−3 kPa−1 
 Hypertensives Av. 43–50 M/F 163–172/81–103 (0.41–0.91)*(0.71–1.10)† Laurent et al 199369 Multicenter study; *at mean pressure; †at 100 mm Hg; unit: 10−3 × mm Hg−1 
 Hypothyroidism Av. 59 M/F 129/69 ∼1.85 Giannattasio et al 199770 Langewouters formula 
        Unit: mm/mm Hg 10−3 
 Healthy Av. 38 M/F — 21 Kool et al 199467 Multiplied by 2π 
        Unit: 10−3 × kPa−1 
 Healthy Av. 36 M/F 114/68 7.7 Jondeau et al 199963 Unit: 10−3 kPa−1 
Arterial compliance*Absolute diameter (or area) change for a given pressure step at a fixed vessel length ΔD/(ΔP) cm × mm Hg−1 Desc. thoracic Ao Various Av. 55 M/F 92 (mean) 0.010 Lang et al 199452 Unit: cm2/mm Hg 
 Abdominal Ao Healthy Av. 36 M/F 114/68 27.7 Jondeau et al 199963 Unit: m2 × kPa−1 × 10−7 
 Abdominal Ao Marfan Av. 37 M/F 110/64 21.6 Jondeau et al 199963 Unit: m2 × kPa−1 × 10−7 
 Healthy Av. 38 M/F — 0.84 Kool et al 199467 Multiplied by 2, divided by π 
        Unit: mm2 × kPa−1 
 Healthy Av. 50 M/F 118/71 8.72 (effective)/6.9 (intrinsic) Laurent et al 199465 Unit: m2 × kPa−1 × 10−7 
 Healthy Av. 36 M/F 114/68 8.55 Jondeau et al 199963 Unit: m2 × kPa−1 × 10−7 
 Hypertensive Av. 51 M/F 156/93 6.31 (effective)/7.8 (intrinsic) Laurent et al 199465 Unit: m2 × kPa−1 × 10−7 
 Healthy Av. 38 — — 0.010 Bank & Kaiser 19988 at 95 mm Hg 
        Unit: mm2/mm Hg 
 Healthy Av. 38 M/F — 0.47 Kool et al 199467 Multiplied by 2, divided by π 
        Unit: mm2 × kPa−1 
 Random population sample Av. 50 132/84 0.33 van der Heijden-Spek et al 200068 Unit: mm2/kPa 
 Random population sample Av. 50 128/81 0.25 van der Heijden-Spek et al 200068 Unit: mm2/kPa 
 Normotensive Av. 36–41 M/F 121–141/66–77 (3.23–4.58)* (2.8–3.4)† Laurent et al 199369 Multicenter study; *at mean pressure; †at 100 mm Hg 
        Unit: 10−3 × mm2 × mm Hg−1 
 Healthy Av. 53 M/F 117/64 ∼5.7 Giannattasio et al 199571 Langewouters formula 
        Unit: mm2/ mm Hg 10−3 
 Healthy Av. 48 M/F 121/73 1.81 Mourad et al 199872 Unit: m2 × kPa−1 × 10−8 
 Healthy Av. 36 M/F 114/68 0.22 Jondeau et al 199963 Unit: m2 × kPa−1 × 10−7 
 Hypertensives Av. 43–50 M/F 163–172/81–103 (2.61–4.81)† (3.4–6.8)† Laurent et al 199369 Multicenter study; *at mean pressure;†at 100 mm Hg 
        Unit: 10−3 × mm2 × mm Hg−1 
 Hypertensive Av. 57 M/F 179/100 ∼7 Giannattasio et al 199773 Langewouters formula 
        Isobaric 
        Unit: mm2/mm Hg 10−3 
 Hypertension (hypertrophied artery) Av. 50 M/F 163/99 1.82 Mourad et al 199872 Unit: m2 × kPa−1 × 10−8 
 Hypertension (remodeled artery) Av. 49 M/F 166/99 1.03 Mourad et al 199872 Unit: m2 × kPa−1 × 10−8 
 Hypercholesterolemia Av. 47 M/F 107/60 ∼2.5 Giannattasio et al 199774 Langewouters formula 
        Unit: mm2/mm Hg 10−3 
 Congestive heart failure Av. 57 M/F 106/62 ∼4.15 Giannattasio et al 199571 Langewouters formula 
        Unit: mm2/mm Hg 10−3 
 Healthy Av. 38 M/F — 1.28 Kool et al 199467 Multiplied by 2, divided by π 
        Unit: mm2 × kPa−1 
 Healthy Av. 36 M/F 114/68 5.3 Jondeau et al 199963 Unit: m2 × kPa−1 × 10−7 
Young's modulus*Elastic modulus per unit area; the pressure step per 4 square centimeter required for (theoretical) 100% strech from resting length ΔP × D/ (ΔD × h) (mm Hg/cm) Desc. thoracic Ao Healthy Av. 47 125/78 7.37 Pearson et al 199453 Unit: dynes × 106/cm2 
 Desc. thoracic Ao Healthy Av. 43 123/75 6.03 Pearson et al 199453 Unit: dynes × 106/cm2 
 Desc. thoracic Ao Hypertensives Av. 47 M/F 150/92 13.88 Pearson et al 199453 Unit: dynes × 106/cm2 
 Normotensives Av. 56 M/F 113/69 678 Liao et al 199911 Unit: kPa 
 Hypertensives Av. 56 M/F 124/74 822 Liao et al 199911 Measured at baseline before development of hypertension 
        Unit: kPa 
Pulse wave velocity*Speed of travel of the pulse along an arterial segment Distance/Δt (cm/s) Asc. Ao Healthy Av. 34 M/F 117/77 668 Murgo et al 198075  
 Asc. Ao Healthy (majority) Av. 38 M/F — 387 Merillon et al 197676  
 Asc. Ao Hypertensives Av. 32 M/F — 570 Merrillon et al 197676  
 Asc. Ao Healthy Av. 42 M/F Mean 91 440 Latham et al 198577  
 Thoracic Ao Healthy Av. 42 M/F Mean 91 530 Latham et al 198577  
 Abdominal Ao Healthy Av. 42 M/F Mean 91 570 Latham et al 198577  
 Iliac Healthy Av. 42 M/F Mean 91 880 Latham et al 198577  
 Healthy Av. 38 — — 1510 Bank & Kaiser 19988 at 95 mm Hg 
 Ao Arch to Fem Healthy/low prevalence of Hypertensive Av. 46 (approx) M/F — = 5.1 × age + 533 Avolio et al 198578 Site to site 
 Ao Arch to Fem Healthy/high prevalence of Hypertensive Av. 46 (approx) M/F — =9.2 × age + 615 Avolio et al 198578 Site to site 
 Asc. Ao or C-Fem Healthy Elderly Av. 70 M/F 140/73 906 Chen et al 199979 Suprastenal notch to femoral 
 Ao Arch or C-Fem End-stage renal disease Av. 52 M/F 157/85 1110 Blacher et al 199980 Site to site or distance subtraction 
 C-Fem Healthy Av. 33 M/F 118/76 890 Isnard et al 198948 Site to site 
 C-Fem Healthy whites Av. 25 120/78 815 Ferreira et al 199981 Site to site 
 C-Fem Healthy African Americans Av. 23 119/77 775 Ferreira et al 199981 Site to site 
 C-Fem Healthy Av. 24 118/68 620 Kingwell et al 199782 Distance subtraction 
 C-Fem Healthy Av. 29 M/F 122/75 950 Hirata et al 199159 Site to site 
 C-Fem Healthy Av. 52 M/F 141/82 930 London et al 19928 Distance subtraction 
 C-Fem Healthy Av. 62 M/F 143/89 980 Breithaupt-Grogler et al 199783 Site to site 
 C-Fem Random population sampleno cardiovasc. Treatment or complication Av. 46 M/F 98–222/62–130 =0.07 × SP+0.09 × age−4.3 Asmar et al 199584 Site to site 
 C-Fem Normotensives Av. 45 M/F 125/77 =0.06 × age+5.7 × 102 Asmar et al 199585 Site to site 
 C-Fem Random population sample Av. 50 132/84 700 van der Heijden-Spek et al 200068 Distance subtraction 
 C-Fem Random population sample Av. 50 128/81 670 van der Heijden-Spek et al 200068 Distance subtraction 
 C-Fem Hypertensive Av. 38 M/F 160/102 1180 Isnard et al 198948 Site to site 
 C-Fem Hypertensives treated Av. 59 M/F 144/82 =0.11 × age+3.5 × 102 Asmar et al 199585 Site to site 
 C-Fem Hypertensives untreated Av. 48 M/F 164/102 =0.12 × age+6.3 × 102 Asmar et al 199585 Site to site 
 C-Fem Hypertensive no vasc. Dis Av. 57 M/F 144/83 1240 Bortolotto et al 199986 Site to site 
 C-Fem Hypertensive no vasc. Dis. Av. 62 M/F 148/83 1430 Bortolotto et al 199986 Site to site 
 C-Fem Hypertensive whites Av. 28 151/94 880 Ferreira et al 199981 Site to site 
 C-Fem Hypertensive African Americans Av. 29 152/97 930 Ferreira et al 199981 Site to site 
 C-Fem Hypertensive no atherosclerosis Av. 57 M/F 144/84 1240 Blacher et al 199987 Site to site 
 C-Fem Hypertensive atherosclerosis Av. 67 M/F 149/80 1490 Blacher et al 199987 Site to site 
 C-Fem Marfan Av. 26 M/F 126/81 1160 Hirata et al 199159 Distance subtraction 
 C-Fem Chronic uremia Av. 53 M/F 153/81 1035 London et al 199228 Site to site 
 B-R Healthy Av. 39 132/78 880 Armentano et al 199188 Site to site 
 B-R Healthy/low prevalence of hypertension Av. 46 (approx) M/F — =0.61 × age+817 Avolio et al 198578 Site to site 
 B-R Healthy/high prevalence of hypertension Av. 46 (approx) M/F — =4.8×Age+998 Avolio et al 198578 Site to site 
 B-R Normotensives Av. 40 132/78 880 Simon et al 198589 Site to site 
 B-R Hypertensives Av. 43 168/98 1150 Simon et al 198589 Site to site 
 B-R Hypertensive Av. 43 168/98 1160 Armentano et al 199188 Site to site 
 Fem-foot Healthy/low prevalence of hypertension Av. 46 (approx) M/F — =4.43×Age+718 Avolio et al 198578 Site to site 
 Fem-foot Healthy/high prevalence of hypertension Av. 46 (approx) M/F — =5.6×Age+791 Avolio et al 198578 Site to site 
 Fem-foot Healthy Av. 24 118/68 830 Kingwell et al 199782 Site to site 
Characteristic impedance*Relationship between pressure change and flow velocity in the absence of wave reflections ΔP/Δv (mm Hg)(cm × s) Asc. Ao Healthy Av. 34 M/F 117/77 47 Murgo et al 198075 Unit: dyne · s · cm−5 
 Asc. Ao Healthy (majority) Av. 38 M/F — 73 Merillon et al 197676 Unit: dyne · s · cm−5 
 Asc. Ao CAD (majority) Av. 47 — 100 (mean) 97 O’Rourke and Avolio 198090 Unit: dyne · s · cm−5 
 Asc. Ao Healthy (majority) Av. 42 M/F 121/78 94 Ting et al 198634 Unit: dyne · s · cm−5 
 Asc. Ao Hypertensives Av. 35 M/F 168/99 146 Ting et al 198634 Unit: dyne · s · cm−5 
 Asc. Ao CAD Av. 56 M/F 126/71 136 Kelly and Fitchett 199291 Unit: dyne · s · cm−5 
 Asc. Ao Hypertensives Av. 32 M/F — 81 Merrillon et al 197676 Unit: dyne · s · cm−5 
 Asc. Ao Heart failure 21–70 M/F 89 (mean) 138 Binkley et al 199092 Unit: dyne · s · cm−5 
Stiffness index Ratio of logarithm (systolic/diastolic pressures) to (relative change in diameter) β=ln (Ps/Pd)/[(Ds−Dd)/Dd] nondimensional Asc. Ao Healthy Av. 29 M/F 112/75 5.9 Hirata et al 199159  
 Asc. Ao Marfan Av. 26 M/F 126/81 10.9 Hirata et al 199159  
 Ao arch Healthy Av. 14 N/A 116/71 2.17 Ong et al 199249 Did not divide by Dd
 Ao arch Healthy Av. 62 M/F 130/77 Gatzka et al 199850  
 Ao arch CAD Av. 63 M/F 133/74 16 Gatzka et al 199850  
 Ao arch Post coartectomy Av. 13 N/A 122/72 3.66 Ong et al 199249 Did not divide by Dd
 Desc. thoracic Ao Various Av. 53 M/F 124/74 3.77 Pasierski et al 199451  
 Desc. thoracic Ao Healthy Av. 47 125/78 5.71 Pearson et al 199453  
 Desc. thoracic Ao Healthy Av. 43 123/75 5.10 Pearson et al 199453  
 Desc. thoracic Ao Hypertensives Av. 47 M/F 150/92 13.88 Pearson et al 199453  
 Abdominal Ao Healthy 6-81 N/A Normotensive 4.29–9.83 Kawasaki et al 198756 4 different age groups 
 Abdominal Ao Healthy Av. 29 M/F 112/75 3.9 Hirata et al 199159  
 Abdominal Ao Healthy Av. 60 N/A 124/74 8.58 Hirai et al 198926  
 Abdominal Ao CAD Av. 55–59 M/F 128–140/79–83 12.25–22.37 Hirai et al 198926 4 subgroups: no stenosis 
        3-vessel disease 
 Abdominal Ao Marfan Av. 26 M/F 126/81 7.1 Hirata et al 199159  
 Healthy 6–81 N/A Normotensive 4.32–11.31 Kawasaki et al 198756 4 different age groups 
 Normotensives Av. 56 M/F 113/69 10.3 Liao et al 199911  
 Healthy Av. 60 N/A 124/74 9.17 Hirai et al 198926  
 CAD Av. 55–59 M/F 128–140/79–83 9.42–13.17 Hirai et al 198926 4 subgroups: no stenosis 
        3-vessel disease 
 Hypertensives Av. 56 M/F 124/74 11.87 Liao et al 199911 Measured at baseline before development of hypertension 
 Healthy 6–81 N/A Normotensive 8.56–13.73 Kawasaki et al 198756 4 different age groups 
 Healthy 6–81 N/A Normotensive 9.41–15.31 Kawasaki et al 198756 4 different age groups 
Capacitative compliance Relationship between pressure fall and volume fall in the arterial tree during the exponential component of diastolic pressure decay ΔV/ΔP (cm3/mm Hg) Proximal part of circulation Normotensive Av. 47 M/F 115/63 ∼2.2 Cohn et al 199524  
 Proximal part of circulation Healthy Av. 50 — 138/75 1.71 Duprez et al 199893  
 Proximal part of circulation Healthy 21–80 (M)/22–83 (F) M/F 125/68 & 120/66 ∼2(M)/1.7(F) McVeigh et al 199933  
 Proximal part of circulation Heart failure Av. 59 — 116/69 1.51 Duprez et al 199893  
 Proximal part of circulation Hypertensive Av. 54 M/F 152/86 ∼1.95 Cohn et al 199524  
 Proximal part of circulation No CAD Av. 53 123/68 ∼1.8 Cohn et al 199524  
 Proximal part of circulation CAD Av. 55 132/70 ∼1.8 Cohn et al 199524  
Oscillatory compliance Relationship between oscillating pressure change and oscillating volume change around the exponential pressure decay during diastole ΔV/ΔP (cm3/mm Hg) Distal part of circulation Normotensive Av. 47 M/F 115/63 ∼0.075 Cohn et al 199524  
 Distal part of circulation Healthy Av. 50 — 138/75 0.054 Duprez et al 199893  
 Distal part of circulation Healthy 21–80 (M)/22–83(F) M/F 125/68 & 120/66 ∼0.08(M)/0.056(F) McVeigh et al 199933  
 Distal part of circulation Heart failure Av. 59 — 116/69 0.050 Duprez et al 199893  
 Distal part of circulation Hypertensive Av. 54 M/F 152/86 ∼0.05 Cohn et al 199524  
 Distal part of circulation No CAD Av. 53 123/68 ∼0.065 Cohn et al 199524  
 Distal part of circulation CAD Av. 55 132/70 ∼0.05 Cohn et al 199524  
Total arterial compliance“Area method” Whole body Normotensive Av. 43 N/A 120/77 1.47 Liu et al 198994 At mean pressure 
        Units: mL/mm Hg 
 Whole body Hypertensive 37 N/A 166/99 0.80 Liu et al 198994 At mean pressure 
        Units: mL/mm Hg 
 Whole body Normotensive Av. 33 M/F 112/74 2.15 Ting et al 199595 At mean pressure 
        Units: mL/mm Hg 
 Whole body Hypertensive Av. 33 M/F 161/100 1.03 Ting et al 199595 At mean pressure 
        Units: mL/mm Hg 
 Whole body Healthy Av. 23 106/63 0.57 Rajkumar et al 199796 Arbitrary units dimensionally equivalent to mL/mm Hg 
 Whole body Healthy Av. 60 123/82 0.34 McGrath et al 199897 Arbitrary units dimensionally equivalent to mL/mm Hg 
 Whole body Healthy sedentary Av. 26 109/63 0.54 Bertovic et al 199998 Arbitrary units dimensionally equivalent to mL/mm Hg 
 Whole body Strength trained athletes Av. 26 120/59 0.40 Bertovic et al 199998 Arbitrary units dimensionally equivalent to mL/mm Hg 
 Whole body Postenenopausal Av. 59 126/71 0.26 Rajkumar et al 199796 Arbitrary units dimensionally equivalent to mL/mm Hg 
 Whole body Postenenopausal Av. 63 126/69 0.31 Waddell et al 199999 Arbitrary units dimensionally equivalent to mL/mm Hg 

Ao = aortic; Av. = average; B = brachial; C = carotid; CAD = coronary artery disease; Desc. = descending; F = female; Fem = femoral; M = male; N/A = not available; R = radial.

*

These indices are site specific and vary with distending pressure.

The most hallowed (and still probably the best) measure of arterial stiffness is pulse wave velocity (PWV).2,6,25 This quantity is related to the Young's modulus (E) of a thin-walled homogenous elastic tube by the formula: graphic, where ρ is the density of fluid within (blood is approximately 1.05) and h/2r is the wall thickness/diameter.6

Pulse wave velocity is measured as the difference between two recording sites in the line of pulse travel, and the delay between corresponding points on the wave (of pressure or of flow), which are not influenced by wave reflection. The wave front or initial upstroke is the usual point of reference in the two waveforms.25

Practical problems in measurement of pulse wave velocity arise when convenient points of measurement (eg, carotid and femoral artery) are not in the same line of travel, and in determining the actual arterial distance between recording sites from measurements on the surface of the body. Pulse wave velocity in large central elastic arteries such as the aorta increases markedly with age, whereas that in upper limb muscular arteries PWV does not increase (Fig. 3A).

Age-related changes in apparently normal populations. A) Brachial and aortic pulse wave velocity (Australian cohort). (Reprinted with permission from Ho K: Effects of ageing on arterial distensibility and left ventricular load in an Australian population. BSc(Med) thesis. University of New South Wales, Australia, 1982.)43B) Radial (left) and carotid (right) pressure waveforms, plotted as ensemble-averaged waveforms by decade, in a cohort of 1004 normal Australian subjects. (Reprinted with permission from Kelly R, et al: Non-invasive determination of age-related changes in the human arterial pulse. Circulation 1989;80:1652–1659.)27C) Ascending aortic augmentation index (augmentation pressure/pulse height) in a combined group of US and Japanese patients with chest pain syndrome and normal coronary arteries, undergoing cardiac catheterization. From Murgo et al44 and Takazawa.32D) Change in augmentation index (augmentation/pulse height) in the radial artery (bottom line) and carotid artery (center line), calculated from data in B, compared to the regression line for aortic augmentation index in C. E) Quartiles of systolic, diastolic, mean, and pulse pressure as a function of age in the original Framingham cohort. (Reprinted with permission from Franklin SS, et al: Hemodynamic pattern of age-related changes in blood pressure: the Framingham Heart Study. Circulation 1997;96:308–315.)40 PWV = pulse wave velocity; AG = augmentation; PH = pulse height.

Characteristic impedance is another valuable index of arterial stiffness, and relates absolute arterial pressure at a site to absolute velocity of flow at the same site in the absence of wave reflections.6 Characteristic impedance (Zc) is related to PWV by the formula Zc = PWV × ρ . Because ρ (density of blood) is approximately unity, these values are numerically almost identical when expressed as centimeters per second and as dyne second per cubic centimeters.6 It is difficult to measure characteristic impedance by noninvasive methods because of the difficulties in excluding effects of wave reflection, and the compounding of errors in measuring noninvasive flow and noninvasive pressure.

Because all values of arterial stiffness are pressure dependent, comparisons must relate to the same distending pressure. Attempts have been made to measure “isobaric” indices16 or to adjust for the (almost) logarithmic relationship between stiffness indices and pressure.26 Differences are often seen with differences in heart rate, but these are relatively small, at least in exteriorized arteries,4,5 and are not apparent in determinations of PWV or characteristic impedance.

Manifestations of arterial stiffness

Manifestations of arterial stiffness include effects of stiffness on the arterial pressure (or flow) wave. The influence of stiffness is apparent on the arterial pressure wave recorded noninvasively by applanation tonometry in the radial or carotid artery (Fig. 3B). Change in stiffness is responsible for the characteristic changes in the pressure waves with aging,27 and in the pressure wave that can be generated in the ascending aorta recorded directly (Fig. 2) or estimated from the radial waveform, using generalized transfer function techniques.6,19

The arterial pressure wave has two principal components—the wave generated by the heart, which travels away from the heart, and the reflected wave, which returns to the heart from peripheral sites, predominantly in the lower part of the body. Techniques exist for distinguishing these two components, and these are based on identification of the foot of the reflected wave, as this modifies the predicted initial wave contour. The time from the initial wave foot to reflected wave foot is generally less than the period of ventricular ejection, and therefore, is identifiable in systole. This time is related to aortic pulse wave velocity (Fig. 4), 25,28 and can be used as an index of aortic PWV. Also useful is the increase in pressure after the reflected wave foot—the pressure wave augmentation during systole.6,27 This is a manifestation rather than a measure of arterial stiffness, and represents the pressure boost with which the left ventricle must cope and which is caused by wave reflection. Aortic pressure wave augmentation can be measured from the transfer function process6 or can be gauged directly from the carotid artery pulse.6,19,27 It varies from less than zero at age 18 to a value approximating 50% of pulse pressure at age 80 years (Fig. 3C).6,19 At any age aortic pressure wave augmentation is greater than carotid augmentation, and carotid augmentation is greater than radial augmentation (Fig. 3D). Augmentation varies with heart rate,29 with heart failure,6,30,31 and with drug therapy.6,18 When factors are equivalent, it is a measure of arterial stiffness. When other factors are not equal, it is a manifestation of wave reflection. In the presence of heart failure due to systolic left ventricular dysfunction, any interpretation of pressure wave augmentation must consider the shape of the aortic flow wave.6,30,32

Relationship between time from wave foot to initial systolic inflection of the carotid pressure waveform (ordinate), and carotid–femoral pulse wave velocity (abcissa). (Reprinted with permission from London G, et al: Increased systolic pressure in chronic uremia: role of arterial wave reflections. Hypertension 1992;20:10–19.)28 Method of calculating time delay is illustrated as Δt. PP = pulse pressure.

Another method of pulse wave analysis concentrates exclusively on the diastolic part of the arterial pressure wave, and seeks to separate the exponential pressure wave decay in a modified Windkessel model from the effects of the damped sinusoidal wave caused by wave reflection.24,33 This is difficult when most of the wave reflection is in systole rather than in diastole, and when the position of the reflected wave can increase or lower pressure at the point where diastole is taken to start, and from which the exponential decay is calculated. Other problems with this approach include failure to consider the difference (usually about 12 mm Hg) between end-systolic pressure in central and peripheral arteries, and the need to estimate cardiac output from the pressure wave itself. (In validation studies of one device there was a better correlation between a line horizontal to the measured flow axis than the regression line to data points relating estimated and measured flow.24) With respect to pressure measurement, at high heart rates, the level of the incisura, which corresponds to aortic valve closure in the radial artery, may be actually lower than end-diastolic pressure, therefore the estimate of exponential decay and total arterial compliance may become negative (Takazawa K, personal communication).

The method for calculating total arterial compliance34 also requires noninvasive estimation of cardiac output and assumption of a Windkessel model of the arterial tree in which no wave reflection exists.

Pulse pressure increases with age (Fig. 3E). Brachial pulse pressure has recently been confirmed as a robust index of cardiovascular events in persons aged more than 50 years.35 In persons aged less than 40 years, this relationship ceases to be true, and in men less than 40 years there is an inverse relationship between brachial pulse pressure and coronary events (Table 3).36 Such an apparent anomaly is readily explained on the basis of different amplification of the pulse wave between the central aorta and the brachial artery with age, and this is a manifestation of pulse wave reflection (Fig. 5). 37 In major studies, there is a plateau in brachial systolic pressure between age 17 years (when the body is fully grown) and age 40 years. At less than 17 years and more than 40 years, brachial systolic pressure increases steeply with age (Fig. 5).

Change in brachial systolic pressure with age shows a steep rise from age 10 to a plateau when full body height is reached at age 18,41 then a subsequent rise after age 45 years. Data from National Heart Foundation of Australia,46 US National Health Survey (white males),46 Framingham,40 Staessen et al,45 and Uiterwaal et al,41 summarized in reference37.

Table 3

Relationship between components of arterial pressure and coronary heart disease risk at different ages; Framingham initial cohort and offspring study36

 Age <40 40–49 Years 50–59 Years 60 Years 
DBP 1.54 1.28 1.14* 1.12 
SBP 1.16* 1.15 1.09 1.17 
PP 0.84+ 1.16 1.12* 1.24 
 Age <40 40–49 Years 50–59 Years 60 Years 
DBP 1.54 1.28 1.14* 1.12 
SBP 1.16* 1.15 1.09 1.17 
PP 0.84+ 1.16 1.12* 1.24 

DBP = diastolic blood pressure; SBP = systolic blood pressure; PP = pulse pressure.

Hazard ratio/10 mm Hg.

*

P < .05.

P < .01.

P < .001.

+

in males 0.71 (negative relation P < .05).

This review is directed at arterial stiffness and its measurement, not at wave reflection and its implications. The two are related,6,19 and to a large extent can be separated. The therapeutic effects of vasodilator drugs on conduit arteries appear to be most pronounced on arteries smaller than those described here38,39 and are manifest as a reduction in wave reflection, with a decrease in pressure wave augmentation.6,19,32 This needs to be discussed in a separate consensus conference.

Recommendations

  1. As a generic term, stiffness is preferable, especially to compliance, which is more frequently used to describe adherence with therapy or advice, or adherence to protocol.

  2. For regional measurements, diameter and pressure should be measured at the same point. When this cannot be done, note should be made of possible confounders, such as age, drugs, or heart rate.

  3. For regional and other measurements, note should be made of distending pressure, and comparisons made at the same distending pressure. If technical correction for distending pressure is not possible, validated statistical “adjustment” should be carried out and clearly described.

  4. For indices that give absolute values, absolute initial size should always be given.

  5. For global measures of arterial mechanics, analysis of the arterial pressure waveform is often performed. Although various techniques (and underlying models) are used, they should all take into account anterograde and reflected waves as important components of the measured waveform.

  6. A preference is given to pure physical measures.

  7. Reference values for all arterial properties must be given as a function of age.

  8. Indices (Table 2) should be comprehensively applicable under different conditions.

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