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REVIEW PAPER

Arterial stiffness and ventricular stiffness: a couple


of diseases or a coupling disease? A review from
the cardiologists point of view
Francesco Antonini-Canterin
1
*, Scipione Carerj
2
, Vitantonio Di Bello
3
, Giovanni Di Salvo
4
,
Salvatore La Carrubba
5
, Olga Vriz
6
, Daniela Pavan
7
, Alberto Balbarini
3
, and Gian Luigi Nicolosi
1
on behalf of the Research Group of the Italian Society of Cardiovascular Echography (SIEC)
1
Division of Cardiology, ARC, S. Maria degli Angeli Hospital, Via Montereale, 24, 33170 Pordenone, Italy;
2
Institute of
Cardiology, University of Messina, Messina, Italy;
3
Cardiac and Thoracic Department, University of Pisa, Pisa, Italy;
4
Department of Pediatric Cardiology, Second University of Naples, Monaldi Hospital, Naples, Italy;
5
Department of Internal
Medicine, Villa Soa Hospital, Palermo, Italy;
6
Division of Cardiology, San Daniele del Friuli Hospital, Udine, Italy; and
7
Division of Cardiology, S.Vito al Tagliamento Hospital, S.Vito al Tagliamento, Italy
Received 23 June 2008; accepted after revision 23 August 2008; online publish-ahead-of-print 16 September 2008
The assessment of arterial stiffness, a common feature of ageing, exacerbated by many common
disorders such as hypertension, diabetes mellitus, or renal diseases, has become an attractive tool
for identifying structural and functional abnormalities of the arteries in the preclinical stages of the
atherosclerotic disease. Arterial stiffness has been recognized as an important pathophysiological deter-
minant of systolic blood pressure and pulse pressure increases and therefore the cause of cardiovascular
complications, demonstrating also an independent predictive value for cardiovascular events. Although
there are many techniques and indices currently available, their large clinical application is limited by a
lack of standardization, with important difculties when one try effectively to measure, quantify, and
compare. Moreover, information on the heart-vessel coupling disease, in which combined stiffness of
both heart and arteries interact to limit cardiovascular performance and its possible implications in
different clinical conditions, is still not well known. We overviewed main methods and indices used
to estimate arterial stiffness and aimed to provide an insight into the knowledge of the ventricular
arterial coupling from the cardiologists point of view.
KEYWORDS
Arterial stiffness;
Ventricular stiffness;
Ventriculararterial coupling;
Echo-tracking
In recent years, arterial stiffness and wave reection
phenomenon were identied as the most important patho-
physiological determinants of systolic blood pressure (SBP)
and pulse pressure (PP) increases and therefore the cause
of cardiovascular (CV) complications and events.
1
Arterial
stiffness had also demonstrated an independent predictive
value for CV events in patients with hypertension,
2,3
dia-
betes mellitus,
4
end-stage renal disease,
5
in elderly sub-
jects
6
and in the general population.
7
However, for many
years, the concept of arterial stiffness was used in the
eld of pathophysiological and epidemiological studies and
not much regarded as being part of the clinical cardiologic
arena. For the rst time, the last (2007) European guidelines
for the diagnosis and treatment of hypertension
8
recommended the assessment of arterial stiffness, as an
evidence of target organ damage.
The pathophysiological and clinical implications of the
arterial stiffening should be considered together with the
cardiac function, as it is known that the interaction
between the heart and the arterial system, the ventricu-
lararterial coupling, could be a key determinant of CV per-
formance. It has been observed that age-related vascular
stiffening, which can seriously affect this coupling, is
accompanied by changes in the left ventricular (LV) stiff-
ness
9
and diastolic compliance. Furthermore, this combined
ventriculararterial stiffening, referred to as coupling
disease,
10
appears to be common in patients with heart
failure (HF) and preserved ejection fraction.
11
Also, it has
been shown that the accurate assessment of the haemo-
dynamic severity of aortic stenosis has to consider the
global LV afterload that include both the degree of the valv-
ular obstruction and the arterial system properties.
12,13
*
Corresponding author. Tel: 39 0434 399 462; fax: 39 0434 399 197.
E-mail address: cardiologia@aopn.fvg.it
Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2008.
For permissions please email: journals.permissions@oxfordjournals.org.
European Journal of Echocardiography (2009) 10, 3643
doi:10.1093/ejechocard/jen236

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Thus, the concept of ventriculararterial coupling or even
ventriculovalvuloarterial interaction is becoming an
issue of increasing interest with relevant clinical
implication.
This article reviews some of the indices and methods used
to estimate arterial stiffness, underlying the strengths and
weaknesses of each one. Also, it aims to discuss the
concept of ventriculararterial interaction and its possible
implications in different clinical conditions. It is a review
realized from the cardiologists point of view, emphasizing
the role of ultrasound and echo-tracking systems, since
these techniques allow an easy evaluation of both heart
and vessels during the same examination.
Characteristics of the arterial tree and their
clinical implications
The elastic properties of arteries vary along the arterial
tree, with more elastic proximal arteries and stiffer distal
arteries. The velocity of propagation of the pulse wave
increases with decreased arterial distensibility. Moreover,
wave reections, which amplify the pressure wave, are gen-
erated at the level of peripheral arterial bifurcations and
smaller muscular arteries. The net result is a progressive
increase in both SBP and PP from the heart to the periphery,
called amplication phenomenon.
14
Therefore, the bra-
chial blood pressure (BP) is not always a reliable measure
of the central aortic pressure. In young subjects, especially,
the brachial BP overestimates central pressure,
15
whereas in
older subjects there is a stiffening of central arteries and
consequently a lower amplication of PP from central to
peripheral blood vessels.
16
Central aortic pressure rep-
resents better the load imposed on the coronary and cere-
bral arteries and thereby should be better related to
vascular damage and prognosis. In the Strong Heart Study,
central PP was more strongly related to carotid artery
hypertrophy, extent of atherosclerosis, and incidence of
CV events than the brachial PP.
17
On the contrary, data
from the Second Australian National Blood Pressure Study,
in older hypertensive female patients, showed no benet
of central arterial waveform analysis (central SBP, central
PP, augmentation index, and systemic arterial compliance)
over brachial cuff BP in predicting CV events,
18
possibly
because of the lack of amplication of PP from the heart
to the periphery at this age.
Arterial stiffness: indices and methods of
assessment
Arterial stiffness can be assessed as local, regional, and
systemic stiffness. Although systemic arterial stiffness may
only be estimated, local and regional stiffness can also be
measured. Direct measurement of arterial stiffness implies
the measurements of change in arterial diameter and
pressure at the same site. This could be performed
invasively or non-invasively. Diameter changes can be deter-
mined accurately, especially with high-denition echo-
tracking systems (Figure 1), but the estimation of the
pressure changes at the same site may be difcult because
of the amplication of the PP and inaccuracy of all cuff
sphygmomanometer systems. Indices of local stiffness
19
are: distensibility (the relative change in diameter with
pressure), compliance (the absolute change in diameter or
area with pressure), Petersons elastic modulus (pressure
change required for theoretic 100% increase in diameter),
Youngs elastic modulus (pressure change per square centi-
metre for theoretic 100% extension). A non-dimensional
index of local arterial stiffness frequently used is the stiff-
ness index b [ratio of logarithm (systolic/diastolic pressures)
to relative change in diameter] (Table 1).
Figure 1 Examination of the common carotid artery with simultaneous display of waveforms derived from instantaneous changes in
diameter using echo-tracking technique.
Arterial stiffness and ventricular stiffness 37

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Pulse wave velocity
Pulse wave velocity (PWV) is accepted as the most simple,
robust, and reproducible method to determine the regional
arterial stiffness. There is a linear correlation between the
speed of travel of pulse along an arterial segment and arter-
ial stiffness. To calculate PWV, the distance between the
two sites at which the wave is being recorded is divided
by the time of travel of the wave from the rst to the
second site:
PWV
distance
time
It is usually measured using the foot-to-foot velocity
method from various waveforms at different sites (pressure,
distension, or Doppler waveforms) (Figure 2). The normal
values of PWV increase from 45 m/s in the ascending
aorta to 56 m/s in the abdominal aorta then 89 m/s in
the iliac and femoral arteries.
14
Carotid-femoral PWV is con-
sidered as the gold-standard
14
measurement of arterial
stiffness and has been largely used in epidemiological
studies demonstrating a strong independent predictive
value for CV events. The major limitation of this index
derives from the inaccuracy of distance measurement,
which could theoretically be overcome using methods
based on Doppler probes or echo-tracking systems with
measurements made at the root of the left subclavian
artery (suprasternal notch) and near the bifurcation of the
abdominal aorta (umbilical level).
14
Also, it could be dif-
cult to record the femoral pressure waveform in patients
with obesity, diabetes, and peripheral artery disease. In
addition, sometimes the thoraco-abdominal aorta is quite
straight, but often it is very curvilinear, so the external
measure could be inaccurate.
Echo-tracking systems allowthe assessment of local arterial
stiffness deriving the pressurediameter curve of the artery
(the measurements of stroke changes in diameter and local
PP should be determined simultaneously) and calculating the
local PWV from the time delay between the two adjacent
distension waveforms. With some echo-tracking systems
(Prosound Alfa 10; Aloka, Tokio, Japan), it is also possible to
determine the local PWV using on-line one-point measure-
ments.
20
The carotid artery is of special interest because
local carotid stiffness has a predictive value for CV events.
21
In addition, this system based on carotid ultrasounds provides
information about the presence of plaques and precise
measurement of intima-media thickness, which allows the
calculation of Youngs elastic modulus
14
and gives further
information about CVrisk. The exact assessment of these par-
ameters requires the measurement of the local BP, usually
obtained by applanation tonometry of the vessel and cali-
bration of the waveform to brachial mean and diastolic pres-
sures, assumed to be constant throughout the large arteries.
The use of a transfer function could be an alternative.
Anyway, the use of cuff brachial BP is accepted for clinical
use, especially in old people.
16
Regional aortic stiffness and carotid stiffness, although
providing similar information on the effect of ageing on
elastic arteries stiffening in normal subjects, are not
interchangeable predictors in high-risk patients, such as
hypertensive or diabetic subjects. It has to be considered
that in this type of patients, the aorta stiffened more than
the carotid artery, with age and other CV risk factors.
22
Central pulse wave analysis
The arterial pressure waveform is a composite of the
forward wave created by LV contraction and a reected
wave generated in the periphery, returning towards the
heart. The central pulse wave should be analysed through
three major parameters: central PP, central SBP, and aug-
mentation index (AIx).
14
In elastic vessels, PWV is low and the reected wave can
reach the ascending aorta after the aortic valve has
closed, in diastole, increasing central diastolic pressure
(DBP) and coronary perfusion, central SBP remaining
unchanged. Reduced compliance of the large arteries
increases the PWV and backwards wave from the periphery
returns early to the ascending aorta, during systole, increas-
ing central SBP (phenomenon quantied through the AIx)
Figure 2 The foot-to-foot velocity method for the measurement of
two points PWV.
Table 1 Indices of local arterial stiffness (modied after ORourke et al.
19
)
Index Denition Formula
Arterial distensibility Relative diameter (or area) change for a pressure increment (DD/DP D) (mmHg
21
)
Arterial compliance Absolute diameter (or area) change for a given pressure step at xed vessel
length
DD/DP (cm/mmHg) or (cm
2
/mmHg)
Elastic modulus The pressure step required for (theoretical) 100% stretch from resting
diameter at xed vessel length
(DP D/DD) (mmHg)
Youngs modulus The pressure step per square centimetre required for (theoretical) 100%
stretch from resting length
DP D/(DD h) (mmHg/cm)
Stiffness index b Ratio of logarithm (systolic/diastolic pressures) to relative change in
diameter
Ln(P
s
/P
d
)/[(D
s
2 D
d
)/D
d
]
(non-dimensional)
F. Antonini-Canterin et al. 38

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and decreasing central DBP and coronary perfusion pressure.
AIx (Figure 3) is calculated as the ratio between the aug-
mentation pressure (AP) and PP and is expressed in percen-
tage:
AIx
AP
PP
where AP is the difference between maximal pressure and
pressure at the rst peak (shoulder) on pulse waveform
and PP is the difference between SBP and DBP.
Thus, AIx is a complex composite measurement, derived
from many important dynamic variables. It is inuenced by
PWV, the reectance point, and LV ejection characteristics,
especially with respect to change in heart rate and ventricu-
lar contractility. It has been shown that AIx is also inuenced
by BP, age, gender, body height, and especially heart rate.
Central AIx and PP proved to be independent predictors of
mortality in end-stage renal disease,
23
in patients under-
going percutaneous coronary intervention
24
and in hyper-
tensive patients.
25
On the other hand, a recent study demonstrated that in
patients with systolic hypertension the pathogenesis of
increased PP seems to be due to increased wall stiffness
and reduced aortic diameter rather than to the premature
wave reection.
26
Arterial compliance
Arterial compliance can be either directly measured
(i.e. using an echo-tracking system) as an index of local
arterial compliance or calculated as systemic or total arter-
ial compliance (SAC), using the so-called area method
SAC
A
d
RP
s
P
d

where A
d
is the area under the BP diastolic decay curve from
end-systole to end-diastole, R the total peripheral resist-
ance, P
s
the end-systolic BP, and P
d
the end-diastolic BP.
Also, SAC can be estimated from the ratio of stroke
volume to PP, but this method is considered to be a crude
approximation.
14
It is known that SAC decreases with age
in both men and women.
18,27,28
The SAC has also been corre-
lated with disease status and common CV risk. It has been
shown that the changes in the central and/or peripheral
arteries can affect SAC in patients with hypertension, dia-
betes, and hyperlipidaemia. A very recent study
29
issued
that age and other irreversible risk factors (such as height
and weight) are the major determinants of SAC and thus
questioning its role as marker of arterial stiffness and
guide to therapy. Furthermore, until now, except for one
study,
30
there is no strong evidence that SAC has indepen-
dent predictive value for CV events.
Other indices of arterial stiffness
Characteristic impedance is another index that relates
absolute arterial pressure at a site to absolute velocity of
ow at the same site in the absence of wave reections.
19
Since the exclusion of the effects of wave reection is dif-
cult, when using non-invasive methods, another index was
proposed to adjust for the logarithmic relationship
between stiffness indices and pressurethe stiffness
index b:
b
lnP
s
=P
d

D
s
D
d
=D
d

where P
s
is the end-systolic BP, P
d
the end-diastolic BP, D
s
the end-systolic diameter and D
d
the end-diastolic diameter.
The stiffness index b is less affected by arterial pressure
changes and could be more useful than other parameters,
being easily determined using echo-tracking devices
31
(Figure 4). Carotid stiffness index b has been recently eval-
uated in CV diseases, such as myocardial infarction,
32
aortic
stenosis,
33,34
or various other clinical conditions (haemo-
dialysis,
35
hypothyroidism,
36
or hyperthyroid Graves
disease
37
).
The concept of ventriculararterial coupling
The ventriculararterial coupling, meaning the interaction
of the heart with the systemic vasculature, is a key deter-
minant of CV performance,
38
inuencing both magnitude
and efciency of transfer of LV stroke work to the circula-
tion.
39
The capacity of the body to increase cardiac
output, regulate systemic BP, and respond appropriately to
elevations in heart rate and preloads depends on both the
properties of the heart and the vessels into which the
heart ejects blood. Normal physiological ventricular
arterial coupling matches these properties, so that maximal
cardiac work, power, and chamber efciency are achieved
while maintaining BP and cardiac outputs within a physio-
logical range.
38
The ventriculararterial coupling can be
accurately quantied in the pressurevolume plane. Left
ventricular performance can be characterized by the slope
of the end-systolic pressurevolume relationend-systolic
elastance (E
es
). E
es
is a measure of end-systolic LV stiffness
and can be determined invasively or can be estimated non-
invasively by the formula:
40
E
es

P
d
E
Ndest
P
s
0:9
E
Ndest
SV
where P
s
and P
d
are systolic and diastolic arm-cuff pressures,
E
Nd(est)
is an estimated normalized ventricular elastance at
arterial end-diastole (or at the onset of ejection) and SV is
echo-Doppler stroke volume.
The arterial system can be similarly assessed using the
slope of the arterial P
es
stroke volume relationeffective
arterial elastance (E
a
). E
a
is a measure of impedance
(being inuenced by static and pulsatile afterload and by
Figure 3 Augmentation index (the ratio between the augmenta-
tion pressure and pulse pressure).
Arterial stiffness and ventricular stiffness 39

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heart rate)
41
and is calculated as:
42
E
a

P
es
SV
where P
es
is the end-systolic pressure, measured or esti-
mated non-invasively as P
s
0.9, and SV is stroke volume.
In this manner, both LV and arterial system could be con-
sidered elastic chambers with known volume elastances,
with the E
a
/E
es
ratio serving as a reliable index of ventricu-
lararterial coupling. Under normal conditions, the LV and
arterial system are nearly optimal coupled, operating at
an E
a
/E
es
ratio close to 1 (0.31.3)
41
resulting in maximal
stroke work and cardiac metabolic efciency. In contrast,
in HF due to LV systolic dysfunction, ventriculararterial
coupling is suboptimal, as E
es
is decreased (pump dysfunc-
tion) while E
a
is generally increased (increased impedance
and decreased compliance). Furthermore, there is some evi-
dence that ventriculararterial coupling defects occur prior
to signicant pump dysfunction.
39
The LV systolic and diastolic stiffness increases in tandem
with arterial stiffening in various conditions. Such combined
stiffening alters heartarterial system interactions at rest
and under stress by exertion, salt loading, and abrupt
changes in heart function. So, combined ventriculararterial
stiffness impacts on CV reserve, BP lability, diastolic func-
tion, coronary and peripheral ow regulation, and endo-
thelial function. In this context, the concept of stiff heart
artery coupling disease was proposed.
10
The most important
condition in which arterial stiffening is accompanied by
increasing LV stiffness is age.
9
In the elderly, the heart
appears to develop an increase in both diastolic and systolic
LV stiffness, with or without hypertrophy. The higher E
a
,
expected from arterial stiffening, is associated with an
increase in E
es
(reecting chamber geometry and structural
alterations in the myocardium with age). A rise in both ven-
tricular and arterial elastances means that the E
a
/E
es
ratio is
essentially preserved despite age-related changes in each
system. Although this matched increase of arterial and
cardiac stiffness can maintain ventriculararterial coupling
within a normal range, it impacts the haemodynamic stabi-
lity and cardiac reserve. As consequence, the systemic cir-
culatory compliance is reduced generating larger changes
in pressure for any given change in ejected volume, result-
ing in a greater BP lability. In addition, there is also limit-
ation of the reserve mechanisms. During exercise, E
a
typically rises because of the increased heart rate and arter-
ial pulsatility and E
es
also rises because of the contractile
increase. When basal E
a
and E
es
are already elevated,
there is less reserve and any increase in E
a
will only exacer-
bate systolic hypertension.
38
Furthermore, altered coupling
inuences myocardial perfusion by elevating the proportion
of coronary ow during systole (up to 50%). Another effect of
the change in coronary ow pattern due to ventricular
arterial stiffening is worsening the impact of regional cor-
onary ischaemia when a decline in ventricular systolic
performance and systolic pressure occurs.
38
The presence of ventriculararterial stiffening induces
higher BP sensitivity to circulating volume and diuretics,
thus rendering more difcult the treatment of HF, especially
of HF with a preserved cardiac ejection fraction. The role of
ventricular and arterial stiffness in the pathophysiology of
HF with preserved ejection fraction is beyond the associ-
ation with age and hypertension,
11
an increased ventricu-
lararterial stiffness worsening diastolic function,
augmenting BP lability, and elevating cardiac metabolic
demand under stress. Therefore, an increased systolic
ventriculararterial stiffness is one of the pathophysiological
mechanisms in HF with normal ejection fraction, together
with LV diastolic dysfunction (impaired relaxation and
increased passive diastolic stiffness) and cardiac volume
overload. A recent large, population-based study
43
showed
that, although patients with HF with normal ejection frac-
tion display arterial and LV systolic stiffening, the presence
and progression of diastolic dysfunction could be more
important, as conrmed by another study performed inva-
sively in patients with HF and normal ejection fraction.
44
Figure 4 Echo-tracking assessment of carotid stiffness parameters (b index, augmentation index, arterial compliance, and PWV).
F. Antonini-Canterin et al. 40

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An important aspect of ventriculararterial coupling is the
great impact of arterial stiffness on LV diastolic function in
different populations: in patients with CV risk factors,
45,46
hypertension,
4749
diabetes,
49,50
ESRD,
51
obstructive sleep
apnea,
52
in elderly subjects,
53
and in a population-based
cohort study.
54
Arterial stiffness was assessed using different
indices: PWV,
45,47,51,53
arterial compliance,
48,50
carotid stiff-
ness (b index,
46
Petersons elastic modulus,
50
Youngs elastic
modulus,
54
and distensibility coefcient
54
), central PP,
50,53
AP,
53
aortic strain, and distensibility.
49,52
Attempts have
been made to identify the most accurate arterial stiffness
index in detecting preclinical LV diastolic dysfunction:
aortic PP, brachial PP and PWV seem superior to AP,
53
and
PWV appears to be superior to central and brachial PP
55
in
older subjects. A correlation between arterial stiffness and
left atrial size, an index of ventricular diastolic function,
was described; being emphasized as a new possible patho-
physiological link between arterial stiffness and stroke, as
the left atrial dilatation is a risk factor for atrial brillation.
56
Arterial stiffness seems to impact also the regional ventricu-
lar function in patients with HF and normal ejection fraction:
LV longitudinal function
52,57
and LV circumferential strain.
54
Another rough measure of ventriculararterial coupling is
the ratio between LV force,
58
estimated as SBP divided by LV
systolic volume index, and E
a
, which proved to be inuenced
by pharmacological stress in normal subjects and patients
with coronary artery disease or dilated cardiomyopathy.
Given the implication of ventricularvascular coupling in
such pathological conditions, its assessment becomes of
clinical importance. The echo-tracking systems allow us to
obtain information about both ventricular and arterial func-
tions and their coupling during the same examination.
Wave intensity
Wave intensity (WI) is another haemodynamic index which
gives an image of ventriculararterial coupling. Its
advantages are the possibility of being measured non-
invasively with echo-tracking systems and the sensitivity to
changes in the working conditions of the heart interacting
with arterial system and conditions of the peripheral circu-
lation.
31
It also provides information about the forward
and the backward travelling waves, can be determined at
any site of the circulatory system, and was initially
dened as the product of DP and DU, where DP and DU
are the changes in BP and blood velocity during constant
short-time intervals. The original WI depends on the
sampling interval, Dt. The time-normalized WI is the
product of derivatives of P and U with respect to time:
31
WI
dP
dt


dU
dt

If WI is greater than zero, the changes in pressure and
velocity caused by the forward travelling wave from the
ventricle to the periphery are greater than those caused
by the backward travelling wave.
59
In normal subjects, carotid arterial WI has two positive
peaks (Figure 5). The rst peak W
1
appears during early
systole and its magnitude increases with cardiac contracti-
lity and correlates with the maximum rate of LV pressure
rise. The second peak W2 occurs towards the end of ejec-
tion, relates to the ability of the LV to actively stop aortic
blood ow, and correlates with the time constant of LV
relaxation. Between these two positive peaks, a negative
area signies reections from the cerebral circulation. WI
could be a useful parameter for the evaluation of LV systolic
and early diastolic performance simultaneously, as its rst
peak reects the LV contractile function, while the ampli-
tude of the second peak is determined by LV behaviour
during the period from late systole to isovolumic relax-
ation.
59
WI assessment was found to predict haemodynamic
deterioration in patients with end-stage dilated cardio-
myopathy referred for transplantation.
60
Figure 5 Automated assessment of carotid arterial wave intensity.
Arterial stiffness and ventricular stiffness 41

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Predictive value of arterial stiffness
An important body of evidence links increased PWV,
elevated PP, and premature/increased arterial wave reec-
tions with a higher risk of CV morbidity and mortality. Aortic
stiffness has independent predictive value for all-cause and
CV mortalities, fatal and non-fatal coronary events, and
fatal stroke in hypertensive,
2,3
diabetic,
4
or renal
5
patients,
in elderly
6
or healthy subjects
61
and in the general popu-
lation.
7
Data concerning the independent predictive value
of carotid stiffness, central Aix, and PP are scarce, as
mentioned above. An increased PP is associated with the
development of LV dysfunction and clinical HF in the
elderly and in hypertensives.
62
The independent predictive value of aortic stiffness has
also been demonstrated after adjustment to classical CV
risk factors.
14
In this context, it is important to understand
the prevalence and correlates of abnormally high aortic
stiffness. Recent data
63
from the Framingham Heart Study
show that the prevalence of abnormal aortic stiffness
increases steeply with advancing age in the community,
especially in the presence of obesity and diabetes.
In patients with asymptomatic LV dysfunction and systolic
HF, there is a positive correlation between the elevated PP
and an adverse outcome, a low PP being an independent
predictor of mortality. An explanation for these ndings
could be the ventriculararterial interaction. Because of
ventricularvascular coupling, central PP, SBP augmenta-
tion, and aortic PWVare altered in cardiomyopathy patients,
especially in those with very low ejection fraction.
62
Conclusion
Although arterial stiffness and wave reection provide
useful prognostic information concerning the CV events in
different populations, the clinical value of arterial stiffness
and wave reection attenuation for the reduction in CV
events under treatment remains largely to be demon-
strated. A major issue would be to determine whether a
reduction in PWV or wave reection is associated with a con-
comitant reduction in CV events, independently of the nor-
malization of classical risk factors. This is likely because
arterial stiffness decrease reects the true reduction of
arterial wall damage, whereas the reduction in BP, glycae-
mia, and lipids may not.
64
In this context, the measurement
of arterial stiffness, wave reection, and ventricular
arterial stiffness become of essential clinical interest. The
implementation of ultrasound systems, such as echo-
tracking devices embedded in echocardiographic machines,
can provide a precise, non-invasive determination of arterial
stiffness, and an assessment of ventriculararterial inter-
actions, determining a true impact in the clinical area of
cardiologists.
Conict of interest: none declared.
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Arterial stiffness and ventricular stiffness 43

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