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Pulmonary Arterial Stiffness
37
Lymphangioleiomyomatosis Biomarkers Linked to Lung Metastatic
Potential and Cell Stemness. PLoS One. 2015;10:e0132546.
Deep vein thrombosis and pulmonary embolism after solid organ
transplantation: an unresolved problem. Transplant Rev (Orlando).
2015;29:85-92.
Ventilator-associated respiratory infection following lung
transplantation. Eur Respir J. 2015;45:726-37.
Characteristics of candidates for lung transplantation due to chronic
obstructive pulmonary disease and alpha-1 antitrypsin deficiency
emphysema. Arch Bronconeumol. 2015;51:379-83.
Impairment of pulmonary vascular reserve and right ventricular
systolic reserve in pulmonary arterial hypertension. BMC Pulm Med.
2014;14:69.
High intra-individual variability of cyclosporine pharmacokinetics in
lung transplant recipients without cystic fibrosis. Clin Transplant.
2014;28:743-8.
The impact of the prevention strategies on the indirect effects of CMV
infection in solid organ transplant recipients. Transplant Rev
(Orlando). 2014;28:84-91.
Pharmacokinetic study of conversion from tacrolimus twice-daily to
tacrolimus once-daily in stable lung transplantation. Transplantation.
2014;97:358-62.
Pulmonary vascular abnormalities in chronic obstructive pulmonary
disease undergoing lung transplant. J Heart Lung Transplant.
2013;32:1262-9.
Biomarkers of pulmonary rejection. Transplant Proc. 2013;45:3163-9.
Inhaled iloprost plus oral sildenafil in patients with severe pulmonary
arterial hypertension delays the need for lung transplantation.
Transplant Proc. 2013;45:2347-50.
In vivo assessment of pulmonary arterial wall fibrosis by intravascular
optical coherence tomography in pulmonary arterial hypertension: a
new prognostic marker of adverse clinical follow-up. Open Respir
Med J. 2013;7:26-32.
Health-related quality of life in a national cohort of patients with
pulmonary arterial hypertension or chronic thromboembolic
pulmonary hypertension. Arch Bronconeumol. 2013;49:181-8.
Prophylaxis with nebulized liposomal amphotericin B for Aspergillus
infection in lung transplant patients does not cause changes in the
https://t.me/med1917
Juan C. Grignola, Antonio Roman and Enric Domingo
38
lipid content of pulmonary surfactant. J Heart Lung Transplant.
2013;32:313-9.
BIOGRAPHICAL SKETCH
Name: Enric Domingo Ribas
Affiliation: Unitat Hemodinàmica, Cardiologia, Hospital Universitari Vall
Hebron
Universitat Autònoma de Barcelona
MD, PhD
Research and Professional Experience:
Interventional Cardiologist 1984- today, Hospital Universitari Vall
Hebron
Full Professor Medical Physiology, Universitat Autonoma Barcelona
Research Fellow Physiology, Baylor College of Medicine, Houston, USA,
1981-1983
Professional Appointments:
Interventional Cardiologist 1984- today, Hospital Universitari Vall
Hebron
Full Professor Medical Physiology, Universitat Autonoma Barcelona
Honors:
Past President Societat Catalana Cardiologia
Publications Last 3 Years:
The emerging role of the contractile and vascular reserves in
pulmonary arterial hypertension. Eur Respir J 2015;45:1756-1758
Stress testing for the assessment of the right ventricular-pulmonary
vascular unit reserve in pulmonary arterial hypertension. E-journal of
Cardiology Practice 2015; 13:11.
Impairment of pulmonary vascular reserve and right ventricular
systolic reserve in pulmonary arterial hypertension. BMC Pulm Med
2014;14:69-79
Inhaled iloprost plus oral sildenafil in patients with severe pulmonary
arterial hypertension delays the need for lung transplantation.
Transplant Proc. 2013;45:2347-50.
Typical angina without significant coronary stenosis: comparison of
clinical profile, circadian presentation, and long-term follow-up
https://t.me/med1917
Pulmonary Arterial Stiffness
39
between patients with and patients without vasospastic angina. Coron
Artery Dis. 2013;24:374-80.
Methylated arginines and nitric oxide in end-stage renal disease:
impact of inflammation, oxidative stress and haemodialysis.
Biomarkers. 2013;18:357-64.
Acute absolute vasodilation is associated with a lower vascular
stiffness in pulmonary arterial hypertension. Int J Cardiol
2013;164:227-231
In vivo assessment of pulmonary arterial wall fibrosis by intravascular
optical coherence tomography in pulmonary arterial hypertension: a
new prognostic marker of adverse clinical follow-up. Open Respir
Med J 2013;7:26-32.
Pulmonary endarterectomy in Chronic Thromboembolic Pulmonary
Hypertension: How can patients be better selected?. World J Cardiol
2013;5:18-21
https://t.me/med1917
https://t.me/med1917
In: Advances in Arterial Stiffness Research ISBN: 978-1-63485-838-0
Editor: Becky Chavez © 2016 Nova Science Publishers, Inc.
Chapter 2
LOCAL AND REGIONAL ARTERIAL
STIFFNESS MEASUREMENT IN
CLINICAL PRACTICE
Iana Simova
1
, Maurizio Galderisi
2
, Tzvetana Katova
3
,
Dimitar Simov
4
and Nikolay Dimitrov
5
1
Cardiology Department, City Clinic – University Hospital, Sofia, Bulgaria
2
Intradepartimental Laboratory of Cardiac Imaging and
Department of Advanced Biomedical Sciences,
University of Naples Federico II, Naples, Italy
3
Department of Noninvasive Cardiovascular Imaging and
Functional Diagnostics, National Cardiology Hospital, Sofia, Bulgaria
4
Clinic of Cardiac Surgery,
City Clinic – University Hospital, Sofia, Bulgaria
5
Clinic of Cardiology, SHACT Kardiolife, Varna, Bulgaria
ABSTRACT
Arterial stiffness (AS) is an independent predictor of cardiovascular
morbidity and mortality and may be considered as a marker of
cardiovascular risk and a potential therapeutic target in selected
populations, in particular in patients with arterial hypertension. In clinical
setting an association of AS indices has been demonstrated with
established cardiovascular risk factors, such as age, male sex,
hypertension, diabetes, obesity and smoking. Increased AS (or decreased
https://t.me/med1917
Iana Simova, Maurizio Galderisi, Tzvetana Katova et al.
42
arterial elasticity) is a marker of subclinical organ damage, which is a
factor of great importance in patients with arterial hypertension – it helps
to establish cardiovascular risk and could re-classify a substantial
proportion of intermediate risk subjects into high or low risk categories.
Therefore, the measurement of AS is important (and recommended) in
hypertensive patients at moderate cardiovascular risk.
AS could be measured locally (usually with echo-tracking methods),
regionally (using tonoports, mechano-transducers and standard Doppler
probes) and through the analysis of central aortic pulse wave. The largest
amount of evidence that AS indices could serve as an independent
predictors of cardiovascular events exists for pulse wave velocity (PWV)
and carotid-femoral PWV (cfPWV) is considered as gold standard for
PWV measurement.
Recommended cut-off values for PWV are established for cfPWV
(regional arterial stiffness). Although regional and local PWV values
correlate well, we have found that regional PWV is significantly higher
than local PWV. These findings should be carefully taken into account
when using this technique in the clinical setting.
According to expert consensus documents local AS could be
measured either at the common carotid, brachial or femoral arteries. We
were able to demonstrate, however, that AS parameters measured at the
brachial artery do not correlate either with common carotid or with
femoral artery indices. We also found that there is good interobserver
correlation of AS parameters when they were measured at the carotid or
femoral artery. The values of AS indices at the brachial artery however
show considerably large interobserver variation.
On the basis of data provided by the scientific literature and our
personal experiences, we suggest that: 1. AS is a useful parameter for
evaluation of patients with arterial hypertension and to follow-up on the
effectiveness of therapy; 2. Reference cut-off values for cfPWV cannot
be applied to local PWV data; 3. Regarding local AS measurement –
brachial artery is not a suitable site for the evaluation of AS indices and
carotid or femoral arteries should be used instead.
INTRODUCTION
Arterial stiffness (AS) is an independent predictor of cardiovascular
morbidity and mortality in patients with AH and could be considered as a
potential therapeutic target [1]. It has been demonstrated in clinical setting that
AS indices are associated with established cardiovascular risk factors, such as
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Local and Regional Arterial Stiffness Measurement in Clinical …
43
age [2], male sex [3], hypertension [4], diabetes [5], obesity [6] and smoking
[7] has been.
Current European guidelines for the management of AH recommend for
identification of target organ damage, especially in patients at moderate
cardiovascular risk. The most popular arterial stiffness parameter - pulse wave
velocity (PWV) is an accepted marker of subclinical target organ damage and
the cut-off value of >10 m/s distinguishes the individuals with decreased
arterial compliance [8].
USEFULNESS OF AS MEASUREMENT IN
HYPERTENSIVE PATIENTS
Approximately 30-45% of the general population in Europe suffers from
arterial hypertension (AH) and its incidence is rapidly increasing with
advancing age. After the fifth decade of life nearly half of the population is
exposed to this risk factor. The majority of these people need treatment. The
effectiveness of monotherapy is rarely enough in order to achieve blood
pressure (BP) targets and in most instances there is a need to combine two or
more antihypertensive agents to lower adequately BP values [8].
AS may be considered as a marker of cardiovascular risk and a potential
therapeutic target in selected populations, for example in hypertensive
patients. In clinical setting an association of AS indices has been demonstrated
with established cardiovascular risk factors, such as age, male sex,
hypertension, diabetes, obesity and smoking. Increased AS (or decreased
arterial elasticity) is a marker of subclinical organ damage, which is a factor of
great importance in patients with arterial hypertension – it helps to establish
cardiovascular risk and could re-classify a substantial proportion of
intermediate risk subjects into high or low risk categories. Therefore, the
measurement of AS is important (and recommended) in hypertensive patients
at moderate cardiovascular risk [8].
Different antihypertensive agents affect AS indices differently,
irrespectively of their similar effect on the peripheral (brachial) BP [9]. For
example, there is clear evidence that inhibitors of angiotensin-converting
enzyme (ACEi) have a direct favorable effect on vessel wall structure by
decreasing the arterial stiffness, independently of their antihypertensive effect
[10, 11]. Calcium channel blockers (CCB), like amlodipine, could lead to a
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Iana Simova, Maurizio Galderisi, Tzvetana Katova et al.
44
regression of arterial hypertrophy and alteration of pulse wave reflection
pattern, leadings to favorable changes in the arterial stiffness indices [12].
We evaluated the effect of a fixed antihypertensive combination ramipril +
amlodipine (Egiramlon®, Egis) on BP values and AS parameters for a one-
month period of treatment, considering the fact that the large majority of
patients with AH would need a combined antihypertensive treatment with at
least two antihypertensive medications, and the combination between ACEi
and CCB is among the preferred combined therapies [13].
Thirty-one patients completed the study. The mean age in this group was
55+/-15 years; 12 patients (39%) were women; the baseline duration of AH
was eight years, 19 patients (61%) were treatment-naïve. The mean baseline
BP values were 166 ± 21 mmHg and 106 ± 11 mmHg for systolic and diastolic
blood pressure, respectively.
We performed patient evaluation in standard conditions according to the
Expert consensus document on arterial stiffness [14]. Evaluation of arterial
stiffness was performed with a scanner Aloka Prosound SDD- α 10, equipped
with a linear array 7.5 to 12 MHz transducer. We used the analytical
instrument Echo-tracking, manufactured by Aloka. For this analysis we used
different AS indices, among which – locally derived pulse wave velocity
(PWV) and augmentation index (AI) – a measure of pressure augmentation.
Our results showed that after one-month treatment with a fixed
combination ramipril + amlodipine office and 24-hour ambulatory BP values
(mmHg) decreased significantly (office systolic BP: from 164 ± 19 to 135 ±
12, diastolic BP: from 106 ± 12 to 86 ± 7, p < 0.001; 24-hour ambulatory
systolic BP: from 139 ± 14 to 125 ± 13, diastolic: from 84 ± 11 to 74 ± 12, p <
0.01). All arterial stiffness indices were significantly influenced in the course
of treatment. Comparing the values of these parameters at the end of the
first month of treatment with a fixed antihypertensive combination of ramipril
+ amlodipine and at baseline we found that there was a considerable
improvement of the elasticity parameters of the vessel wall. Pulse wave
velocity decreased from 7.6 to 6.4 m/s, p < 0.001 and augmentation index was
reduced from 16.7 to 10.9%, p = 0.007.
Arterial stiffness indices, especially PWV, are accepted markers of target
organ damage. According to previous experiences [10, 12], the results of our
study provide further confirmation that these parameters could also serve as a
therapeutic target.
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Local and Regional Arterial Stiffness Measurement in Clinical …
45
REGIONAL AND LOCAL AS MEASUREMENT
Arterial stiffness could be measured locally (usually with echo-tracking
methods), regionally (using tonoports, mechano-transducers and standard
Doppler probes) and through the analysis of central aortic pulse wave [14].
Locally measured arterial stiffness includes several parameters, such as
augmentation index, arterial compliance, local pulse wave velocity (PWV), β
stiffness index. Regional arterial stiffness is expressed as PWV. Central aortic
pulse wave analysis could provide useful parameters such as central aortic
pressure, augmentation pressure and augmentation index. The largest amount
of evidence that arterial stiffness indices could serve as an independent
predictors of cardiovascular events exists for PWV and carotid-femoral
PWV (cfPWV) is considered as gold standard for PWV measurement [15].
According to current guidelines, cfPWV values > 10 m/s indicate the presence
of asymptomatic vascular damage [8].
Some clinical studies analyzing both local PWV and cfPWV, showed that
these parameters increase in parallel in the presence of other evidence of
subclinical atherosclerosis, such as carotid plaque [16]. Although there is good
correlation between regional and local PWV values both in clinical [17, 18]
and experimental settings [19], regional PWV has been shown to be more
sensitive to detect changes in arterial stiffness than local PWV [20]. Before we
performed our analysis, the only available comparison between local (at the
abdominal aorta) and regional PWV in a small group of healthy subjects
describes significantly lower local PWV versus cfPWV in the subgroup with
PWV ≤ 7 m/s, and significantly higher local versus regional PWV in
individuals with PWV > 7 m/s [21].
Table 1. Comparison between cfPWV and local PWV according to
different cfPWV cut-off points
Subgroups
cfPWV (m/s)
– mean ± SD
Local PWV(m/s) –
mean ± SD
p
Cut-off 10
m/s
> 10 m/s (8 subjects)
13.4 ± 3.2
6.5 ± 1.3
< 0.001
≤ 10 m/s (14 subjects)
7.0 ± 1.1
5.7 ± 0.8
= 0.002
Cut-off 9
m/s
> 9 m/s (9 subjects)
12.9 ± 3.3
6.5 ± 1.2
< 0.001
≤ 9 m/s (13 subjects)
6.8 ± 0.9
5.6 ± 0.8
< 0.005
Cut-off 8
m/s
> 8 m/s (10 subjects)
12.4 ± 3.4
6.3 ± 1.3
< 0.001
≤ 8 m/s (12 subjects)
6.7 ± 0.8
5.7 ± 0.8
= 0.007
Cut-off 7
m/s
> 7 m/s (15 subjects)
10.8 ± 3.7
6.2 ± 1.2
< 0.001
≤ 7 m/s (7 subjects)
6.2 ± 0.6
5.6 ± 0.6
= 0.77
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Iana Simova, Maurizio Galderisi, Tzvetana Katova et al.
46
In a study with 22 prospectively enrolled healthy volunteers (mean age
38.7 ± 11.1 years, 50% male) we compared regional and local PWV values, in
order to determine the correlation between these two parameters and to
discriminate independent predictors for the variance in regional and local
PWV [22]. For regional PWV measurement we evaluated cfPWV with a
standard echo scanner and with a transthoracic Doppler probe, recording a
pulse wave signal at the right common carotid artery and at the right femoral
artery, measuring the time from the onset of QRS complex to the onset of
pulse wave at both sides, and dividing the distance between the points of
interrogation to the difference between these two time periods. Local
PWV was measured at the CCA bilaterally, around 10 mm proximal to
carotid bifurcation, with semi-automated dedicated software (MyLab, EsaOte,
Florence, Italy). We found a significant positive correlation in the pooled
population between regional and local PWV values which remained
significant after adjusting for possible confounding factors, such as age, body
mass index, systolic and diastolic blood pressure. Mean cfPWV values (9.29 ±
3.73 m/s) were significantly higher than mean local PWV values (5.96 ± 1.08
m/s), p < 0.001. This significant difference between regional and local PWV
values persisted in subgroups with different arterial elasticity defined by
cfPWV, except for the small group of subjects with very low cfPWV values (<
7 m/s) where regional and local PWV were similar – Table 1.
Our results allowed us to conclude that in a group of healthy volunteers
regional (cf) PWV values were significantly higher than local ones, although
the correlation between the two sets of PWV data was good. Therefore,
guideline-recommended cut-offs for cfPWV cannot be applied automatically
for local PWV values.
LOCAL AS IN DIFFERENT VASCULAR TERRITORIES
The elastic properties of conduit arteries are not constant along the arterial
tree, with proximal vessels tending to be more elastic than distal ones. For that
reason, the visco-elastic properties of each arterial segment are unique [23]
and the AS parameters measured at certain local site could not be applied to
the whole arterial system. According to the Expert consensus document on AS
[14] local AS could be measured either at the common carotid, brachial or
femoral arteries, with one of the basic methods for regional and local AS
measurement being Echo-tracking or E-tracking (ET) which measures the
variations in the diameter of the vessel in different cardiac cycle phases.
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