Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4012_Библиотеки_им_академика_М_И_Перельмана
.pdf
Local and Regional Arterial Stiffness Measurement in Clinical …
47
Table 2. ANOVA data for between group and within group p values
for every pair of comparison of AS indices between different
vascular territories
Parameter
Between
group
Within
group
Carotid
Femoral
Brachial
β
р < 0.001
Carotid
-
p = 0.09
р < 0.001
Femoral
p = 0.09
-
р < 0.001
Brachial
р < 0.001
р < 0.001
-
Ер (kPa)
р < 0.001
Carotid
-
p = 0.2
р < 0.001
Femoral
p = 0.2
-
р < 0.001
Brachial
р < 0.001
р < 0.001
-
АС
(mm
2
/kPa)
р < 0.001
Carotid
-
p = 0.79
р < 0.001
Femoral
p = 0.79
-
р < 0.001
Brachial
р < 0.001
р < 0.001
-
АІ (%)
p = 0.19
Carotid
-
p = 0.48
p = 0.42
Femoral
p = 0.48
-
p = 0.34
Brachial
p = 0.42
p = 0.34
-
PWV (m/s)
р < 0.001
Carotid
-
p = 0.15
р < 0.001
Femoral
p = 0.15
-
р < 0.001
Brachial
р < 0.001
р < 0.001
-
ΔD (%)
р < 0.001
Carotid
-
p = 0.18
р < 0.001
Femoral
p = 0.18
-
p = 0.23
Brachial
р < 0.001
p = 0.23
-
β – β index of AS; Ep – pressure-strain elasticity modulus; AC – arterial compliance;
AI – augmentation index; PWV – pulse wave velocity; ΔD – change in vessel
diameter between systole and diastole.
There is, however, a controversy in the literature about the reproducibility
and prognostic value of AS indices in different vascular territories [24-27]. We
therefore set ourselves the task to measure the correlation between AS indices
in the carotid, brachial and femoral territories and to obtain interobserver
variability for each of these arterial segments [28].
The initial study population included 75 patients (40 ± 14.5 years, 45%
males) with a variable distribution of cardio-vascular risk factors and without
clinical evidence of coronary artery disease. In this patient group we compared
the values of ET-derived AS parameters measured in different vascular
territories. AS parameters were measured bilaterally at the common carotid,
brachial and femoral arteries in all patients using Echo-tracking (ET)
technique. In a selected subgroup of 36 patients (with a decreased age
variation and almost no risk factors except some smokers) we tested
https://t.me/med1917
Iana Simova, Maurizio Galderisi, Tzvetana Katova et al.
48
interobserver variability in the three vascular territories. Three investigators
with a considerable experience of cardiovascular ultrasound were engaged in
the study. Usually we started our evaluation with a bilateral visualization of
the common carotid arteries (1 cm proximal to the bulbus caroticus), followed
by the brachial arteries and common femoral arteries. All arterial segments
were evaluated in longitudinal view in a segment with optimal vessel wall
visualization. For interobserver variability evaluation two investigators blinded
for each other’s results performed twice the entire AS measurement study (i.e.,
true “test-retest” agreement) over one and the same patient and during one and
the same session. We found that there was a significant correlation between
AS indices measured at the common carotid and femoral artery (with the only
exception for augmentation index) and that AS parameters measured at the
brachial artery did correlate neither with common carotid nor with femoral
artery indices - Table 2.
The interobserver variability of ET derived AS parameters was good when
they were measured at the carotid or femoral artery. The values of AS indices
at the brachial artery however differed significantly when measured from two
independent observers. Performing multivariable analysis, we found that there
were good fitting models, predicting most of AS indices’ values, measured at
the carotid and femoral arteries. For the brachial artery there was once again a
difference when compared with the other two vascular beds - none of the
models (which included demographic characteristics, risk factors and maximal
and minimal diameters of the vessel) performed well enough to predict AS
parameters’ values. Considering our results, we were able to demonstrate that
the reproducibility of ET derived AS parameters was good when AS was
measured at the common carotid or femoral arteries, and that brachial artery
was probably not a reliable site for AS measurement. Therefore, we did not
recommend AS measurement at the brachial artery.
CONCLUSION
AS measurement is a very useful tool in clinical practice as a marker of
subclinical organ damage, and therefore helping to re-classify a substantial
proportion of intermediate risk subjects into high or low risk categories, and as
an independent predictor of cardiovascular morbidity and mortality.
On the basis of our personal experience and results we were able to
demonstrate that: 1. AS indices are important for the evaluation of patients
with arterial hypertension and are useful in order to follow-up on the
https://t.me/med1917
Local and Regional Arterial Stiffness Measurement in Clinical …
49
effectiveness of therapy; 2. Regional (cf) PWV values were significantly
higher than local ones and, therefore, reference guideline-recommended cut-
off values for cfPWV cannot be applied automatically for local PWV values;
3. Regarding local AS measurement – brachial artery is not a reliable site for
the evaluation of AS parameters and carotid or femoral arteries should be used
instead.
REFERENCES
[1] Koumaras, C; Tzimou, M; Stavrinou, E; Griva, T; Gossios, T; et al. Role
of Antihypertensive Drugs in Arterial ‘De-Stiffening’ and Central
Pulsatile Hemodynamics. Am J Cardiovasc Drugs., 2012, 2(3), 143-156.
[2] Lee, HY; Oh, BH. Aging and arterial stiffness. Circ J, 2010, 74, 2257-
62.
[3] Rossi, P; Francès, Y; Kingwell, BA; et al. Gender differences in artery
wall biomechanical properties throughout life. J Hypertens, 2011, 29,
1023-33.
[4] McEniery, CM; Wilkinson, IB; Avolio, AP. Age, hypertension and
arterial function. Clin Exp Pharmacol Physiol, 2007, 34, 665-71.
[5] Kalkan, GY; Gur, M; Haydardedeoğlu, FE; et al. The Association
between Aortic Distensibility and Coronary Flow Reserve in Newly
Diagnosed Diabetic Patients. Echocardiography, 2015, 32 (2), 205-212.
[6] Seifalian, AM; Filippatos, TD; Joshi, J; et al. Obesity and arterial
compliance alterations. Curr Vasc Pharmacol, 2010, 8, 155-68.
[7] Doonan, RJ; Hausvater, A; Scallan, C; et al. The effect of smoking on
arterial stiffness. Hypertens Res, 2010, 33, 398-410.
[8] Mancia, G; Fagard, R; Narkiewicz, K; Redon, J; Zanchetti, A; et al.
2013 ESH/ESC Guidelines for the management of arterial hypertension.
European Heart Journal, 2013, 34 (28), 2159-2219.
[9] Koumaras, C; Tzimou, M; Stavrinou, E; Griva, T; Gossios, T; et al. Role
of Antihypertensive Drugs in Arterial ‘De-Stiffening’ and Central
Pulsatile Hemodynamics. Am J Cardiovasc Drugs., 2012, 2(3), 143-156.
[10] Jankowski, P; Safar, M; Benetos, A. Pleiotropic effects of drugs
inhibiting the renin-angiotensin-aldosterone system. Curr Pharm Des,
2009, 15 (5), 571–84.
[11] Ahimastos, A; Natoli, A; Lawler, A; Blombery, P; Kingwell, B.
Ramipril reduces large artery stiffness in peripheral arterial disease and
https://t.me/med1917
Iana Simova, Maurizio Galderisi, Tzvetana Katova et al.
50
promotes elastogenic remodeling in cell culture. Hypertension, 2005, 45
(6), 1194 –9.
[12] Safar, M; Jankowski, P. Antihypertensive therapy and de-stiffening of
the arteries. Expert Opin Pharmacother, 2010, 11(16), 2625–34.
[13] Simova, I; Katova, T; Kostova, V. Effects of combined antihypertensive
treatment with ramipril and amlodipine on blood pressure and arterial
stiffness parameters. Experimental and Clinical Cardiology, 2014, 20
(1), 3495-3502.
[14] Laurent, S; Cockcroft, J; Bortel, LV; Boutouyrie, P; Giannattasio, C;
et al. on behalf of the European Network for Non-invasive Investigation
of Large Arteries. Expert consensus document on arterial stiffness:
methodological issues and clinical applications. European Heart
Journal, 2006, 27(21), 2588-2605.
[15] Van Bortel, L; Laurent, S; Boutouyrie, P; et al. Expert consensus
document on the measurement of aortic stiffness in daily practice using
carotid-femoral pulse wave velocity. J Hypertens, 2012, 30, 445-448.
[16] Hallab, M; Collette, M; Terrier-Barbeau, C; et al. Regional and
peripheral arterial stiffness measured by pOpmetre® in patients with
Cvx risk factor, link with carotid plaques. Ann Cardiol Angeiol (Paris),
2013, 62, 189-92.
[17] Collette, M; Humeau, A; Chevalier, C; et al. Assessment of aortic
stiffness by local and regional methods. Hypertens Res, 2011, 34, 578-
83.
[18] Gaszner, B; Lenkey, Z; Illyés, M; et al. Comparison of aortic and carotid
arterial stiffness parameters in patients with verified coronary artery
disease. Clin Cardiol, 2012, 35, 26-31.
[19] Williams, R; Needles, A; Cherin, E; et al. Noninvasive ultrasonic
measurement of regional and local pulse-wave velocity in mice.
Ultrasound Med Biol, 2007, 33, 1368-75.
[20] Liu, J; Zhang, Y; Cao, TS; et al. Preferential macrovasculopathy in
systemic sclerosis detected by regional pulse wave velocity from wave
intensity analysis: comparisons of local and regional arterial stiffness
parameters in cases and controls. Arthritis Care Res (Hoboken), 2011,
63, 579-87.
[21] Vappou, J; Luo, J; Okajima, K; et al. Aortic pulse wave velocity
measured by pulse wave imaging (PWI): a comparison with applanation
tonometry. Artery Res, 2011, 5, 65-71.
[22] Simova, I; Katova, T; Santoro, C; Galderisi, M. Comparison between
regional and local pulse wave velocity data. Echocardiography – A
https://t.me/med1917
Local and Regional Arterial Stiffness Measurement in Clinical …
51
Journal of Cardiovascular Ultrasound and Alied technoques, 2016, 33
(1), 77-81.
[23] Nichols, WW; O’Rourke, MF. McDonald’s blood flow in arteries.
Theoretical, Experimental and Clinical Principles 5th ed. Oxford
University Press 2005, p. 624.
[24] Kawasaki, T; Sasayama, S; Yagi, S; et al. Non-invasive assessment of
the age related changes in stiffness of major branches of the human
arteries. Cardiovasc Res., 1987, 21(9), 678-87.
[25] Buntin, CM; Silver, FH. Noninvasive assessment of mechanical
properties of peripheral arteries. Ann Biomed Eng., 1990, 18(5), 549-66.
[26] Kimoto, E; Shoji, T; Shinohara, K; et al. Regional arterial stiffness in
patients with type 2 diabetes and chronic kidney disease. J Am Soc
Nephrol, 2006, 17(8), 2245-52.
[27] Giannattasio, C; Failla, M; Lucchina, S; et al. Arterial
stiffening influence of sympathetic nerve activity: evidence from hand
transplantation in humans. Hypertension, 2005, 45, 608–611.
[28] Simova, I; Katova, T; Kostova, V; Hristova, K; Dimitrov,
N. Reproducibility of arterial stiffness indices in different vascular
territories and between different observers. Echocardiography, 2011,
28, 448-56.
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 3
ARTERIAL STIFFNESS IN CHRONIC
OBSTRUCTIVE PULMONARY DISEASE:
IS THERE A COMMON PATHWAY
FOR VASCULAR
AND PULMONARY INVOLVEMENT?
Adriana Albu
2
nd
Department of Internal Medicine, University of Medicine
and Pharmacy “Iuliu Hatieganu” Cluj-Napoca, Romania
ABSTRACT
Cardiovascular diseases represent an important cause of mortality in
patients with chronic obstructive pulmonary disease (COPD). The
increased prevalence of cardiovascular diseases is partly linked to
common risk factors, such as smoking and ageing. Patients with COPD
have an increased risk of cardiovascular morbidity and mortality, which
is independent of classical risk factors. Moreover, reduced FEV1
independently predicts cardiovascular risks in general population and in
patients with COPD.
Corresponding author: Adriana Albu, PhD MD, Associate professor, 2
nd
Department of Internal
Medicine, University of Medicine and Pharmacy, “Iuliu Hatieganu” Cluj-Napoca,Clinicilor
Str. 2-4, E-mail address: adriana.albu@umfcluj.ro.
https://t.me/med1917
Adriana Albu
54
Arterial stiffness is an independent predictor of cardiovascular
risk, and aortic PWV provides strong evidence concerning the prognostic
significance of large artery stiffening. In COPD patients, arterial stiffness
is increased compared to controls matched for classical cardiovascular
risk factors. The mechanisms responsible for the association between
pulmonary and vascular diseases are not completely understood. Age
related degradation of elastin in lungs is involved in emphysema, but
ageing may also cause disruption of elastin in arterial walls with
excess collagen production and stiffening of arteries. Besides
modifications determined by age, some other mechanisms, such as
systemic inflammation, oxidative stress or neurohormonal activation,
may be responsible for both pulmonary and arterial diseases. This chapter
reviews the processes involved in pathogenesis of arterial stiffness in
COPD, and the possible role of COPD therapy in vascular alterations.
Keywords: arterial stiffness, chronic obstructive pulmonary disease, systemic
inflammation, premature vascular ageing
INTRODUCTION
Cardiovascular diseases represent an important cause of mortality in
patients with COPD [1, 2, 3]. The increased prevalence of cardiovascular
disease is partly linked to common risk factors, such as smoking and ageing.
However, patients with COPD have an increased risk of cardiovascular
morbidity and mortality, which is independent of classical risk factors [1].
Moreover, reduced FEV1 independently predicts cardiovascular risk in general
population and in patients with COPD [4]. The reduction of predicted FEV1%
is associated with cardiovascular risk, even in never smokers [5].
The mechanisms responsible for the association between COPD and
cardiovascular diseases are not completely clarified. Several interesting
hypotheses based on common pathogenic pathways, have been developed,
such as systemic inflammation, oxidative stress, activation of sympathetic
nervous system or connective tissue degradation, which are stimulated in
COPD and may also contribute to vascular structure and function alterations
[6].
Arterial stiffness is an independent predictor of cardiovascular events in
healthy people and in various pathological conditions [7, 8, 9]. Carotid-
femoral (aortic) pulse wave velocity (PWV), which is a direct reflection of
wall stiffness, has the best predictive value, an easy and reproducible
https://t.me/med1917
Arterial Stiffness in Chronic Obstructive Pulmonary Disease
55
measurement, and it is considered the “gold standard” of arterial stiffness
assessment [7].
Arterial stiffness has been correlated with air flow limitation and COPD
[6, 10], and it may be responsible for the residual cardiovascular risk non-
explained by the classical risk factors.
CLINICAL AND EPIDEMIOLOGICAL DATA RELATING
AIR FLOW LIMITATION AND COPD
TO ARTERIAL STIFFNESS
Arterial stiffness was positively correlated with the air flow reduction in
healthy people. Zureik et al. in a study that included 196 healthy middle-aged
men, found that PWV was associated with FEV1, independently of age, sex
and smoking status [11]. It has been shown that, mid-life lung function is a
stronger risk factor than later-life lung function for arterial stiffness in men,
even after taking traditional risk factors into account. This finding was
explained by possible developmental factors that influence both lung function
and arterial stiffness [12]. Correlations between decreased lung function and
arterial stiffness have also been found if arterial stiffness was assessed as pulse
pressure [13] or, in another study, as cardio-ankle vascular index [14].
In patients with COPD, Sabit et al. reported an increased aortic PWV,
peripheral pulse pressure and augmentation index (AIx), compared to controls
matched for age, sex, height and body mass index [15]. Arterial stiffness was
associated with the severity of airway obstruction, but it was increased even in
patients with mild severity stages, suggesting that arterial stiffness occurs early
in the disease process [15]. Arterial stiffness was more severe in COPD
patients with concomitant osteoporosis, supporting the hypothesis that arterial
stiffness may be one feature of the systemic involvement in COPD [15]. The
increased arterial stiffness in patients, within each decade, was similar to
changes in type 1 diabetes mellitus [16], and it suggests a premature vascular
ageing in COPD [15]. Cinarka et al. showed that carotid-femoral PWV was
increased in patients with COPD than in controls, and it was higher in patients
with more severe disease [17]. In an observational study, that included 102
patients with COPD who were compared to healthy controls matched for age
and smoking status, arterial stiffness was assessed by central pressure wave
analysis [18]. The authors reported an increased aortic stiffness in COPD
patients, who had increased central augmentation pressure, and a reduced time
https://t.me/med1917
Adriana Albu
56
of wave reflection [18]. The average age of patients was 67 years, and the
augmentation pressures were similar to those from a group of healthy 80 year-
olds, suggesting that COPD may result in premature ageing of the vasculature
[18, 19]. McAllister et al. found that emphysema severity is associated
with arterial stiffness, independent of age, sex, blood pressure, dyslipidemia,
inflammation, hypoxemia and airflow obstruction [20]. Based on these results,
the authors speculated that in some individuals with COPD, there may be an
acquired or inherited tendency to develop both emphysema and arterial
stiffness [20].
In a study that enrolled 153 patients with moderate and severe COPD,
patients in the highest quartile of aortic PWV, compared to the lowest quartile,
were older, had higher systolic blood pressure, were more likely to be current
smokers, and had greater burden of thoracic aortic calcification [21]. The
results of this research suggest that in COPD, increased arterial stiffness can
be predicted using age, blood pressure and thoracic aortic calcification, and
this may identify patients who may have the most beneficial effect from
the pharmacological treatment of COPD [20], as inhaled pharmacologic
intervention appears limited to those patients with more severe arterial
stiffness [22].
In a population based cohort study, central arterial stiffness was compared
between subjects with or without COPD, and also in relation with the disease
severity and with the presence of productive cough [23]. Subjects with severe
and very severe COPD had increased arterial stiffness, when compared with
non COPD subjects. In COPD patients, productive cough was associated with
an increased arterial stiffness, when compared with COPD patients without
productive cough. However, after the adjustment for age, sex, smoking,
arterial blood pressure, history of cardiovascular disease, GOLD stage 3and 4,
but not productive cough, remained associated with an increased arterial
stiffness [23]. The association of vascular alterations with productive cough
may suggest that bronchitis phenotype of COPD is more susceptible to
develop arterial stiffness [23]. This is in line with the increased risk of
cardiovascular complications in COPD patients with exacerbations [23, 24].
In a study that evaluated aortic AIx as a measure of arterial stiffness, only
a week correlation was found between this parameter of arterial stiffness and
COPD, and only in men older than 60 years [25].
Increased markers of arterial stiffness, evaluated at the level of the carotid
artery by an echo-taking system, were found in COPD patients, compared to
healthy controls matched for age and sex. Arterial stiffness increased in the
most severe stages of pulmonary disease [26].
https://t.me/med1917
Соседние файлы в папке Библиотека им академика М.И. Перельмана