1. health and fitness
2. disease

Nephrol Dial Transplant (2010) 25: 3815–3823
doi: 10.1093/ndt/gfq614
Advance Access publication 14 October 2010
Editorial Reviews
Arterial functions: how to interpret the complex physiology
Gerard M. London and Bruno Pannier
INSERM U970, Hopital Européen Georges Pompidou, Paris, France
Correspondence and offprint requests to: Gérard M. London; E-mail: [email protected]
Epidemiological studies have emphasized the close relationship between blood pressure (BP) and the incidence
of cardiovascular diseases with mean BP (MBP) being
considered as a major factor of left ventricular (LV) afterload. This interpretation resulted from the view that MBP
was the product of cardiac (cardiac output, CO) and vascular factors (peripheral resistance, PR) reflected by the
equation MBP = CO × PR. Peripheral resistance as a determinant of mean BP sets the general level at which the
pressure wave will fluctuate, and represents the opposition
to steady component of blood flow, i.e. cardiac output. Peripheral resistance is mainly determined by vasomotor tone
and the number of perfused arterioles and blood viscosity.
This model has however several limitations, the principal
being that blood pressure and blood flow are considered as
constant over time, and the second that it does not take the
arterial factors opposing left ventricular ejection into consideration. Arterial pressure is a cyclic phenomenon characterized by a pressure wave oscillating around the mean
BP. The limits of these oscillations are the systolic and diastolic pressures whose determinants are different from
those of mean BP, and who play also important roles as
determinants of LV afterload and coronary perfusion. Initially, the stroke volume is accommodated in the proximal
aorta where the rise in pressure creates a pressure gradient
from aorta towards peripheral arteries, initiating blood
movement/flow. The relationships between these cyclic
flow and pressure changes are best characterized by aortic
input impedance [1]. Aortic input impedance is a measure
of the opposition of the circulation to an oscillatory flow
input (i.e. stroke volume). Aortic input impedance integrates factors opposing LV ejection, i.e. (i) peripheral resistance; (ii) viscoelastic properties and dimensions of
the aorta and large central arteries; (iii) and the intensity
and timing of the pressure wave reflections. Finally, the opposition to LV ejection is also influenced by inertial forces
represented by the mass of blood in the aorta and LV that
must be mobilized during cardiac cycle [1].
The arterial wall has both elastic and viscous properties.
The difference is related to the time-dependent response
to stress–strain relationship (pressure change–diameter
change). In a purely elastic artery, this relationship is
time-independent, and after removal of stress, the arterial
diameter dimensions would return to initial dimensions. In
the presence of wall viscosity, the arterial wall retains part of
the deformation. The arterial viscous properties are responsible for part of the LV energy dissipation characterized by
hysteresis of the pressure–diameter loop [2] (Figure 1). Difficult to measure and to evaluate in humans, the role of arterial ‘viscosity’ has not been evaluated as extensively as the
‘elastic’ properties of arteries expressed as compliance, distensibility, stiffness or elastic modulus.
Prospective epidemiologic studies have drawn the attention to the arterial elastic properties as independent and
strong cardiovascular risk factor and predictor of all-cause
and cardiovascular death [3–5]. Several different para-
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Abstract
Arterial pressure is a cyclic phenomenon characterized by a
pressure wave oscillating around the mean blood pressure,
from diastolic to systolic blood pressure, defining the pulse
pressure. Aortic input impedance is a measure of the opposition of the circulation to an oscillatory flow input (stroke
volume generated by heart work). Aortic input impedance
integrates factors opposing LV ejection, such as peripheral
resistance, viscoelastic properties and dimensions of the
large central arteries, and the intensity and timing of the
pressure wave reflections, associated with the opposition
to LV ejection influenced by inertial forces. The two most
frequently used methods of arterial stiffness are measurement of PWV and central (aortic or common carotid artery)
pulse wave analysis, recorded directly at the carotid artery
or indirectly in the ascending aorta from radial artery
pressure curve. The arterial system is heterogenous and characterized by the existence of a stiffness gradient with progressive stiffness increase (PWV) from ascending aorta and
large elastic proximal arteries to the peripheral muscular
conduit arteries. Analysis of aortic or carotid pressure waveform and amplitude concerns the effect of reflected waves
on pressure shape and amplitude, estimated in absolute
terms, augmented pressure in millimetre of mercury, or, in
relative terms, ‘augmentation index’ (Aix in percentage of
pulse pressure). Finally, if the aortic PWV has the highest
predictive value for prognosis, the aortic or central artery
pressure waveform should be recorded and analysed in parallel with the measure of PWV to allow a deeper analysis of
arterial haemodynamics.
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Arterial diameter-pressure curve
Diameter (mm)
Diameter (mm)
Local pressure
7.30
7.3
150
Diastole
125
7.2
7.15
Systole
100
7.1
7
75
0
1
Time (sec)
7.00
70
90
110
130
150
0
1
Time (sec)
Pressure (mm Hg)
meters can be evaluated for the measurements of arterial
stiffness, but they do not always have the same significance and are frequently the source of misinterpretation.
The aim of the present short review is to briefly detail
how to interpret all these arterial parameters in order to
better understand the arterial haemodynamics.
Arterial functions
The arterial system has two intimately interrelated haemodynamic functions: (i) they behave as pipes to deliver an
adequate blood supply from the heart to peripheral tissues,
as dictated by metabolic activity—‘the conduit function’;
and (ii) they also behave as a ‘windkessel’ (hydraulic filter) to dampen blood flow and pressure oscillations
caused by the intermittent character of the LV ejection
ensuring peripheral organ perfusion at steady flow and
pressure—‘cushioning or dampening function’ [6].
The efficiency of the conduit function is the consequence of the width of the arterial diameters and the very
low resistance of large arteries offered to flow (under normal conditions, the MBP drops between the ascending
aorta and arteries in the forearm or leg by not more than
2–4 mmHg in supine position). Atherosclerosis, characterized by the presence of plaques and arterial narrowing, is
the most common occlusive vascular disease that disturbs
the conduit function.
The second role of arteries is to dampen the pressure
oscillations and to ensure an almost steady flow of the peripheral tissues and organs. Owing to the peripheral resistance to flow, only part of the stroke volume is forwarded
directly to the peripheral tissues. About 50% of stroke volume would be momentarily stored in the aorta and large
elastic arteries stretching the arterial walls and raising the
blood pressure (Figure 2). In normal conditions, ~10% of
the energy produced by the heart is diverted for the distension of arteries and is ‘accumulated’ in the vessel walls.
During diastole, the ‘accumulated’ energy recoils the
aorta, squeezing the stored blood forward into the peripheral tissues, ensuring a continuous flow (Figure 2). When
the arterial system is rigid and cannot be stretched, the entire stroke volume will flow through the arterial system and
peripheral tissues only during systole. For the dampening
function to be efficient, it is essential that the energy necessary for arterial distension and recoil be as low as possible, i.e. for a given stroke volume, the pulse pressure
should be as low as possible. The efficiency of this function depends on the elastic properties of the arterial walls
and the geometry of the arteries, including their diameter
and length. The ability of arteries to accommodate the volume ejected by the LV instantaneously can be described in
terms of ‘compliance’, ‘distensibility’, or ‘stiffness’ of the
aorta, an individual artery or the systemic arterial system
(systemic compliance). These terms express the contained
volume of the vasculature (total or segmental) as a function
of a given transmural pressure over the physiological pressure range. Compliance (C) is a term that describes the absolute change in volume (ΔV, strain) due to a change in
pressure (ΔP, stress): C = ΔV/ΔP. The reciprocal value
of compliance is elastance (E = ΔP/ΔV), or stiffness. To
facilitate comparisons of elastic properties of structures
with different initial dimensions, compliance can be expressed relative to the initial volume as a coefficient of distensibility Di, defined as Di = ΔV/ΔPV, where ΔV/ΔP is
compliance and V is the initial volume. 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 direct information on the intrinsic elastic properties of the materials that compose the arterial wall independent of vessel geometry. The pressure–volume relationship is
non-linear; at low distending pressure, the tension is borne
by elastin-distensible fibres, whereas at a high distending
pressure, the tension is predominantly transferred to and
borne by less extensible collagen fibres, and the arterial wall
becomes stiffer [6]. Thus, the stiffness can only be defined
in terms of a given pressure since stiffness increases with
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Fig. 1. Common carotid artery pressure–diameter loop from simultaneous recording of arterial diameter and local pulse pressure. The surface between
ascending and descending parts of the loop is hysteresis representing the energy dissipation due to viscous properties of arterial wall. Red line is the
averaged pressure–diameter relationship.
Nephrol Dial Transplant (2010): Editorial Reviews
3817
Arterial
Compliance
A. Systole
In normally compliant arterial system
important part of the stroke volume
is stored in the arteries during ventricular
systole stretching the arterial walls
Left
ventricle
Peripheral
Resistance
Arterial
Compliance
B. Diastole
Left
ventricle
Peripheral
Resistance
Fig. 2. Schematic representation of the role of arterial compliance on assuring continuous blood flow through the peripheral circulation.
increases in BP. Arterial stiffness can be measured with several methods depending on the clinical use or experimental
situation. In clinical practice, arterial stiffness can be noninvasively estimated by three principal methodologies: (i)
pulse transit time for evaluation of the pulse wave velocity
(PWV), (ii) the analysis of the arterial pressure wave contour, and (iii) the direct stiffness estimation using measurements of diameter or arterial luminal cross-sectional area
and distending pressure measured at the site of diameter
changes (Figure 1) [7–9]. The two most frequently used
methods are measurement of PWV and central (aortic or
common carotid artery) pulse wave analysis, recorded directly at the carotid artery or indirectly in the ascending aorta,
and computed from the radial artery pulse wave using a
transfer function [9]. PWV is an assessment of stiffness of
an artery as a hollow structure, and it depends on the geometry of the artery (thickness, h; and radius, r) as well as the
intrinsic elastic properties of the arterial wall (i.e. elastic incremental modulus, E) and the blood density (ρ). According
to the Moens and Korteweg formula, PWV2 = Eh/2rρ [6].
The assessment of PWV involves measurement of two parameters: transit time of the arterial pulse along the analysed
arterial segment (t), and distance between recording sites
(D) measured over the body surface: PWV = D/t. The measurement of carotid–femoral (‘aortic’) PWV is considered
the gold standard [8]. PWV is measured along the aortic
and aorto-iliac pathway. PWV can also be measured at the
level of peripheral arteries, but ‘aortic’ PWV is the most
relevant because the aorta is the principal ‘cushioning’ artery and is responsible for the pathophysiological effects
of arterial stiffening and its association with cardiovascular
events (Figure 3) [10]. The arterial system is heterogenous
and characterized by the existence of a stiffness gradient
with progressive stiffness (PWV) increase from ascending
aorta and large elastic arteries towards the peripheral muscular conduit arteries [10,11] (Figure 4).
PWV must not be confounded with blood velocity.
PWV varies according to age and pressure between 4
and 12 m/s, while blood velocity is in order of centimetres/second. PWV relates to transmission of energy
through the arterial wall, while blood velocity relates to
displacement of mass through the incompressible blood
column. This difference in speed propagation is physiologically advantageous for the LV and the arterial flow. When
the left ventricle starts to eject incompressible blood, it is
faced with a blood column occupying the aorta and the arterial tree. During the first milliseconds, the ejected blood
has to find space, and this is done partly by distending the
proximal aorta and pushing forward the blood column
already present. All these changes are confined to a short
segment of the proximal aorta. These local alterations are
to be transmitted downstream since the incompressible
blood displaced from the proximal aorta must also find
place in downstream segments. Relying only on the
‘pushing’ force of blood entering the proximal aorta,
the movement of all the arterial blood would necessitate
a very high cardiac energy expenditure due to the high
inertial forces of the blood column. In parallel to the
blood entering the aorta, the proximal aortic pressure
starts to rise creating a local small pressure gradient with
pressures higher in the proximal part than in the downstream segments. This pressure gradient is moving downstream to distal arterial segments at a high speed (PWV
in metres/second) propagating rapidly the pressure gradient from segment to segment, i.e. displacing blood in
these segments downstream (Figure 4). As PWV increases from the aorta towards the peripheral arteries,
this rapidly propagated ‘shunting effect’ along the arterial
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During ventricular diastole the previously
stretched arterial walls recoils with
the stored volume insuring continuous
perfusion of tissues and organs
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Nephrol Dial Transplant (2010): Editorial Reviews
Aortic PWV
Brachial PWV
1.00
<9.7m/s
0.75
0.50
>9.7 m/s
0.25
χ2=72.8
P<0.00001
CV Survival
CV Survival
1.00
50
0.50
χ2=1.78
P=0.411
0.25
>12 m/s
0.00
0.0
0.75
100
150
200
250
0.00
0.0
50
Follow-up (months)
CV Survival
3rd tertile
200
250
0.75
0.50
χ2=2.34
P=0.310
0.25
0.00
0.0
50
100
150
200
250
Follow-up (months)
Fig. 3. Probability of cardiovascular survival of ESRD patients according to the levels of aortic, brachial and femoral PWVs [10].
Fig. 4. Schematic illustration of the pressure wave transmission along the arterial system. Vertical thick arrows indicate the position of the pulse
pressure ‘head’. Dotted filling represent the ‘local’ blood column movement. Pulse pressure travels along the arterial tree in 0.3 sec., while blood
ejected from the left ventricle only 20 cm per beat (small arrow) (adapted from [13]).
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2nd tertile
150
Femoral PWV
1.00
1st tertile
100
Follow-up (months)
Nephrol Dial Transplant (2010): Editorial Reviews
A
3819
Δt
B
Aix
PP
Time
Tr
LVET
Forward-wave
Reflected wave
Actual measured wave
Reflected wave
Forward-wave
Actual wave
‘direct mechanism’, involves the generation of a higher
pressure wave by the left ventricle ejecting into a stiff arterial system. This direct mechanism is complemented by a
second, which is an ‘indirect mechanism’ via the influence
of increased arterial stiffness on increased PWV and the
timing of forward and reflected pressure waves. Indeed,
the pressure wave generated in the aorta (forward or incident wave) is propagated to arteries throughout the body.
amplification
Aorta
Peripheral
Artery
Tsh
(mm Hg)
tree results in almost immediate (in milliseconds) downstream mobilization of blood in the arterial system [12].
This occurs still during the ventricular ejection time, and
the downstream displacement of arterial blood ‘liberates’
space for the stroke volume. At the end of LV ejection,
the stroke volume now occupies the blood column whose
length (stroke distance) is in centimetres—mean velocity
of blood (Figure 4) [12]. The fact that PWV exceeds
largely the blood velocity in the aorta is important;
otherwise, the peak aortic flow velocity exceeding
PWV would create conditions for generation of longitudinal shock waves (like those generated by an airplane
passing the speed of sound) potentially provoking arterial
injury [6].
Aortic stiffness together with stroke volume and ejection velocity is a determinant of arterial pressure wave
amplitude, influencing systolic, diastolic and pulse pressures in the aorta (PP). Analysis of aortic or carotid pressure waveform and amplitude is another frequently used
method to assess large artery properties and eventually arterial stiffness. The principal ‘stiffness’ parameter assessed
concerns the effect of reflected waves on pressure shape
and amplitude, estimated in absolute terms, i.e. augmented
pressure in millimeter of mercury (mmHg), or in relative
terms, i.e. ‘augmentation index’ (Aix in percentage of PP)
[9,13] (Figures 5 and 6). Considered to be a stiffness
index, relationships of Aix with arterial stiffness are more
complex, depending on the overlap between forward and
reflected pressure waves. The overlap is influenced by
the relationships between transit time of pressure waves
from the aorta to reflecting sites and back (Figure 7A)
(Tr, depending on PWV and travelling distance—body
size) (Figure 7B), and duration of LV ejection (heart rate)
[6,13,14] (Figure 7C).
Arterial stiffening determines the arterial pressure shape
and amplitude by two mechanisms. The first, which is a
150
100
50
Fig. 6. (A) Schematic representation of arterial pressure waves travelling
from the aorta towards the periphery and back. In the peripheral arteries,
the reflected wave occurs at the impact of forward wave—the waves are in
phase (Tr = 0) and summed up. Reflected wave returns towards the aorta
with a delay corresponding to Tr. The forward and reflected waves are not
in phase—aortic PP and systolic pressures are lower than in periphery (B).
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Fig. 5. (A) Recorded aortic pulse pressure waveform and its composing waves. PP, pulse pressure; Aix, augmentation index (effect of reflected wave
expressed in percentage of PP); Tr, travelling time of pressure wave from the aorta to reflecting sites and back (milliseconds); LVET, left ventricular
ejection time (milliseconds). (B) Representation of wave propagation using the model of a rope with fixed end.
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Nephrol Dial Transplant (2010): Editorial Reviews
A 180
P<0.0001
Tr (ms)
145
110
75
40
5
10
15
20
Aortic PWV (m/s)
35
B 180
110
75
P<0.0001
40
1.30
Aortic augmentation inex (%)
C
1.45
1.60
1.75
Body height (m)
1.90
60
35
10
P<0.0001
-15
-40
1.00
2.25
3.50
4.75
LVET/Tr (ratio)
6.00
Fig. 7. (A) Relationship between Tr and aortic pulse wave velocity
(PWV). (B) Relationship between Tr and body height (influencing the
travelling distance L = [Tr/2] × PWV). (C) Relationship between aortic
augmentation index (Aix) and the ratio between left ventricular ejection
time (LVET) and Tr (i.e. the overlap).
The progressive increase of arterial stiffnesses, together
with changes in aortic geometry (tapering), local arterial
branchings and lumen narrowing, creates an impedance
mismatch causing partial reflections (‘echo’) of forward
progressing incident pressure waves, i.e. a reflected wave,
travelling back to the central aorta, and participating to
changes in the amplitude of systolic and pulse pressure
along the arterial tree [6,9,13–16] (Figure 6).
Forward and reflected pressure waves are overlapping and
are summed up in the measured pressure wave (Figures 5
and 6). The final amplitude and shape of the measured
pulse pressure wave are determined by the phase relationship (the timing) between the component waves, i.e. the
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Tr (ms)
145
overlap between the two waves which depends on the site
of pressure recording in the arterial tree. Peripheral arteries
are close to reflection sites, and the reflected wave occurs
immediately at the impact of forward wave, i.e. the waves
are in phase (Tr = 0, where Tr is transit time of pressure
wave from the aorta to reflecting sites and back), producing an additive effect (Figure 6). The ascending aorta
and central arteries are distant from reflecting sites, and
the return of the reflected wave is variably delayed. In central arteries (aorta and carotid), the forward and reflected
waves are not in phase, and the shape and amplitude of
pressure wave depend on the overlap between forward
wave and reflected wave. The overlap between forward
and reflected pressure waves depends on the PWV and
travelling distance of pressure waves to reflection sites (determinants of Tr) and the left ventricular ejection time
(LVET) duration as a determinant of the overlap possibility. In subjects with low PWV (low stiffness), the Tr is
long, and reflected waves impact on central arteries during
diastole, after ventricular ejection has ceased (Figure 8A),
increasing the aortic pressure in early diastole and not during systole. This is physiologically advantageous since the
increase in early diastolic pressure has a boosting effect on
the coronary perfusion without increasing the left ventricular afterload. This decreased overlap between component pressure waves results in lower aortic systolic and
pulse pressures compared with peripheral arteries (central-to-peripheral systolic and PP amplification) (Figure 6).
The higher peripheral pressure is not only due to a high
overlap between incident and reflected wave but also due
to higher stiffness of the peripheral arteries, i.e. the higher
local pressure effect of the displaced blood column [6].
The desirable timing is disrupted by an increased PWV
due to arterial stiffening. With increased PWV, the reflected waves return earlier impacting on the central arteries during systole rather than diastole, amplifying aortic
and ventricular pressures during systole and reducing aortic
pressure during diastole (Figure 8B). With ageing or in the
presence of high PWV, the Tr is very short, and even in the
aorta, the forward and reflected waves are almost in phase,
the central aortic pressure is close to the peripheral pressure
and the amplification tends to disappear or to be attenuated.
The overlap (timing) between forward and reflected wave
depends also on the LVET. In the presence of tachycardia,
the duration of LVET could be too short for the ‘reception’
of the reflected wave, and the latter will impact on the diastole and not on the systole (Figure 8C and D ). Short LVET
is associated with increased central-to-peripheral pressure
amplification. In contrast, long LVET is favourable for ‘reception’ of the reflected wave still during generation of the
forward wave, increasing the overlap between these pressure
waves and reducing the central-to-peripheral systolic and
pulse pressure amplification (Figure 8C).
Finally, the partial reflection of the forward wave depends on the existence of impedance mismatches of the
successive arterial segments [11,15,16]. The impedance
mismatch is pronounced in young subjects characterized
by a low aortic PWV and higher PWV of the peripheral
arteries. The impedance mismatch of successive arterial
Nephrol Dial Transplant (2010): Editorial Reviews
A
3821
B
Positive
Aix
Negative
Aix
PWV = 6 ms
PWV = 12 ms
Tr
Tr
C
D
Positive
Aix
Negative
Aix
Shortened LVET
tachycardia
Baseline
Tr
LVET
Fig. 8. (A, B) Influence of PWV on aortic pulse pressure shape and Tr. (A) Low PWV reflected wave impacts during late systole and diastole (long Tr),
and Aix is negative. (B) High PWV reflected wave impacts during systole (shorter Tr), and Aix is positive. (C, D) Influence of left ventricular ejection
time (LVET) on aortic pulse pressure shape and Aix. With long LVET, reflected wave gets back during systole (C); when LVET shortens (tachycardia),
reflected wave is more likely to impact during diastole (in conditions of unchanged PWV) (D).
segments originates local partial reflections which are distant from the peripheral vascular bed and limiting the
transmission of pulsatile energy to microcirculation and
capillaries. As it is coupled with low aortic PWV, the reflected wave still returns in diastole (Figure 9, upper
panel). With ageing, the aortic stiffness (PWV) increases
to a far greater extent than the peripheral artery stiffnesses,
dissipating progressively the stiffness gradient [11,15,16].
This limits and progressively decreases the partial reflection, increasing the transmission of the pulsatile energy
into the peripheral microcirculation [16] (Figure 9, lower
panel). This ‘non-protection’ is especially pronounced in
the brain and the kidney, two organs highly perfused with
low resistance. At the systemic level, the impedance mismatch depends on the relationships between the characteristic impedance (depending on ascending aortic diameter
and stiffness) and peripheral resistances, and will determine the systemic reflection coefficient [1,2].
Local arterial stiffness, e.g. aortic, carotid, brachial or radial artery, can be determined by local PP changes (aortic,
carotid, radial or brachial) coupled with local changes in arterial diameter or luminal cross-sectional area (ultrasound
echo-tracking, MRI) (Figure 1). As PP and systolic BP are
amplified from the aorta towards peripheral arteries, only
local PP can be used to measure local stiffness. Local PP
changes can be recorded non-invasively by applanation tonometry [9]. A major advantage of local stiffness is that it is
derived directly from pressure–diameter changes without
using any model of the circulation. The ultrasound technique has the advantages of allowing simultaneous mea-
surements of intima − media thickness and is the only
method able to determine non-invasively the elastic properties of the arterial wall material (Young's elastic modulus).
Arterial stiffness interpretation
All studies dealing with arterial stiffness should consider
the two principal factors influencing stiffness and necessitating careful matching when comparing different populations. These factors are age and ‘operating’ BP. It was
already mentioned that stiffness is pressure-dependent
and increases with higher BP. Decrease of stiffness in the
presence of decreased BP cannot be interpreted only as an
improvement of arterial wall properties, while increased
stiffness in the presence of decreased or unchanged BP
could be interpreted as a worsening condition [17].
The second factor is age. With ageing, the arterial wall
thickens, and the arteries become stiffer. The principal
changes occur in the media and intima, where the orderly
arrangement of elastic laminae disappears, being replaced
by thinning, splitting and fragmentation of the elastic fibres
[6]. The degeneration of the elastic fibres is associated with
an increase in collagen fibres and ground substance, and depositions of calcium. The loss of distensibility is partly compensated by dilatation of the arteries. A major manifestation
of these changes is the rise in systolic and pulse pressures,
an increase in aortic PWV, and the disappearance of pressure
amplification between the aorta and peripheral arteries due
to the earlier return wave reflections [11,16].
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LVET
Tr
3822
Nephrol Dial Transplant (2010): Editorial Reviews
Pressure mm Hg
120
100
80
15
Incident pressure
Terminal pressure
Reflected pressure
Aorta
PWV 6 m/s
Large arteries
PWV=10 m/s
Resistance Microcirculatory
arteries
network
Pressure mm Hg
120
80
5
Incident pressure
Reflected pressure
Aorta
PWV 11 m/s
Terminal pressure
Large arteries
PWV=10 m/s
Resistance Microvascular
arteries
network
Fig. 9. Upper panel. In the presence of arterial stiffness gradient (aortic PWV <peripheral PWV), partial reflections occur distant from microcirculation
and return at low PWV to the aorta in diastole maintaining central-to-peripheral amplification. Partial reflections limit the transmission of pulsatile
pressure energy to the periphery and protect the microcirculation. Lower panel. In the disappearance or inversion of stiffness gradient (aortic PWV >
peripheral PWV), pulsatile pressure is not sufficiently dampened and is transmitted and damaging the microcirculation. In parallel, the central-toperipheral pressure amplification is attenuated.
Arterial stiffening is typically observed in several pathological conditions, including isolated systolic hypertension,
atherosclerosis, diabetes and chronic kidney disease. Several studies demonstrated that arterial stiffening (increased
aortic PWV) and increased wave reflections are per se independent predictors of all-cause and cardiovascular death in
ESRD and diabetic patients as well as in the general population [3–5,10]. For clinical or epidemiological studies, the
aortic PWV is the most useful measurement of stiffness, and
in comparison with other surrogate markers of cardiovascular risk, the aortic PWV has the highest predictive value
(Figure 3). The aortic or central artery pressure waveform
should be recorded and analysed in parallel with the measure of PWV. This allows a deeper analysis of the pathogenesis and significance of arterial pressure waves and arterial
haemodynamics.
Conflict of interest statement. None declared.
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Endorsement of the Kidney Disease Improving Global Outcomes
(KDIGO) Chronic Kidney Disease–Mineral and Bone Disorder
(CKD-MBD) Guidelines: a European Renal Best Practice (ERBP)
commentary statement
David J.A. Goldsmith1, Adrian Covic2, Denis Fouque3, Francesco Locatelli4, Klaus Olgaard5,
Mariano Rodriguez6, Goce Spasovski7, Pablo Urena8, Carmine Zoccali9, Gérard Michel London10
and Raymond Vanholder11
1
King’s Health Partners, Guy’s Campus, London SE1 9RT, UK, 2Nephrology, Dialysis and Transplantation, C. I. Parhon University
Hospital, University of Medicine Gr. T. Popa, Iasi, Romania, 3Division of Nephrology, Hôpital Edouard Herriot and Inserm U870,
University Claude Bernard Lyon1, Lyon, France, 4Department of Nephrology, Dialysis and Transplantation, “A. Manzoni” Hospital,
Lecco, Italy, 5Department of Nephrology P2132, University of Copenhagen, Rigshospitalet, Copenhagen, Denmark, 6Servicio de
Nefrologia (redinren), Unidad de Investigación, Hospital Universitario Reina Sofia, Cordoba, Spain, 7Department of Nephrology,
Medical Faculty, University of Skopje, Skopje, F.Y.R. of Macedonia, 8Clinique du Landy. Service de Néphrologie et Dialyse, Saint
Ouen; Hôpital Necker-Enfants Malades, Service d’Explorations Fonctionnelles, Paris; and Centre de Recherche Croissance et
Signalisation. Université Paris Descartes, Faculté de Médecine, Paris, France, 9Unità Operativa di Nefrologia, Dialisi e Trapianto e
CNR-IBIM, Ospedali Riuniti, Reggio Calabria, Italy, 10INSERM U970, Paris, France and 11Nephrology Section, Department of
Internal Medicine, University Hospital, Ghent, Belgium
Correspondence and offprint requests to: David J.A. Goldsmith; E-mail: [email protected]
Abstract
Under the auspices of the European Renal Best Practice, a
group of European nephrologists, not serving on the Kidney Disease Improving Global Outcomes (KDIGO) work-
ing group, but with significant clinical and research
interests and expertise in these areas, was invited to examine and critique the Chronic Kidney Disease–Mineral and
Bone Disorder KDIGO document published in August
© The Author 2010. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.
For Permissions, please e-mail: [email protected]
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doi: 10.1093/ndt/gfq513
Advance Access publication 9 September 2010