Arterial Stiffness Assessed by Cardio-Ankle Vascular Index in Patients With Abdominal Aortic Aneurysm and Its Alterations After Treatment

Abstract

Purpose:

The aim of the present study was to investigate a potential difference on the arterial stiffness among aneurysm patients and non-aneurysm controls, as well as to explore potential changes between patients treated either with endovascular or open repair.

Materials and Methods:

A 110 patients with an infrarenal AAA were prospectively enrolled in this study. Fifty-six patients received an EVAR, whereas 54 patients received an open surgical repair. Moreover, 103 gender and age-matched subjects without AAA served as controls. The cardio-ankle vascular index (CAVI) was applied for measurement of the arterial stiffness.

Results:

CAVI values were statistically higher in the AAA patients when compared with control subjects. Although at 48 hours postoperatively the CAVI values were increased in both groups when compared to baseline values, the difference in CAVI had a tendency to be higher in the open group compared to the endovascular group. At 6 months of follow up the CAVI values returned to the baseline for the patients of the open repair group. However, in the endovascular group CAVI values remained higher when compared with the baseline values.

Conclusion:

Patients with AAAs demonstrated a higher value of CAVI compared to healthy controls. A significant increase of arterial stiffness in both groups during the immediate postoperative period was documented. The increase in arterial stiffness remained significant at 6 months in EVAR patients. Further studies are needed to elucidate the impact of a decreased aortic compliance after stentgraft implantation on the cardiac function of patients with AAA.

Keywords

abdominal aortic aneurysm EVAR open repair arterial stiffness mortality

Introduction

Despite the evolution of the treatment options and screening programs for abdominal aortic aneurysms (AAAs), the incidence, rupture risk and consequently the associated mortality rates remain considerable.¹ In the setting of an aneurysm, through complex pathways the normal vessel architecture is damaged, as the protease-antiprotease system of the arterial wall is unbalanced. The resultant elastin disturbances cause a stiffer, less compliant arterial wall. Enzymatic destruction of elastin is known to reduce elasticity, and in aneurysm formation.² The aneurysmal aorta is, therefore, significantly stiffer, than undilated age-matched aortas.³

To date several methods have been suggested to assess arterial stiffness. Among them, pulse wave velocity (PWV),^4-6 augmentation index,^7,8 stiffness parameter β⁹ and carotid-femoral pulse wave velocity (cfPWV)¹⁰ have been used to quantitatively express arterial stiffness. During the last decade another parameter, the brachial-ankle pulse wave velocity (baPWV)^11,12 has initiated as a further marker of cardiovascular disease. However, the blood pressure at the time of PWV measurement has considerable influence on final results and remains the main limitation of the aforementioned techniques of PWV assay.^13,14 The cardio-ankle vascular index (CAVI) based on the theory of stiffness parameter β, was developed with the objective of obtaining an arterial stiffness index that is not affected by the blood pressure at the time of measurement.^15,16 Moreover, several clinical studies have showed a great prognostic value of CAVI for cardiovascular events on patients with coronary artery disease, chronic renal insufficiency or diabetes mellitus.^13,16-18 However limited data are up today available on the use of CAVI in patients with an AAA.

The aim of the present study was to investigate a potential difference on the CAVI values among aneurysm patients and non-aneurysm controls, as well as to explore potential changes of CAVI between patients treated either with endovascular or open repair.

Materials and Methods

Study Population

Between January 2014 and March 2015 110 consecutive patients with AAA were prospectively enrolled before undergoing elective endovascular or open surgical repair of their AAA (AAA group) at a tertiary institute. Fifty-six patients received an EVAR with a bifurcated stent-graft: Anaconda (Vascutek, a Terumo company, Inchinnan, Scotland); Endurant and Talent (Medtronic Vascular, Santa Rosa, CA, USA); Excluder (W.L. Gore & Associates, Flagstaff, AZ, USA); and Zenith FB (Cook Inc., Bloomington, IN, USA), whereas 54 patients received an open surgical repair with polyester graft (Gelsoft, Vascutek, a Terumo company, Inchinnan, Scotland).

Patients with thoraco-abdominal, thoracic or juxtarenal aortic aneurysms, aortic para-anastomotic pseudoaneurysms and ruptured aneurysms were excluded from our analysis. Also, patients with previous aortic surgery, aortic dissection, Marfan syndrome or other collagen-related disorders, advanced renal failure (GFR<30ml/min), or peripheral arterial occlusive disease (Ankle-brachial index ≤ 0.9 were excluded from the study.

Moreover, a total of 103 gender and age-matched subjects without AAA (91.3% males, mean age 71.1 ± 6.8 years), who were referred to our Institution for varicose or inguinal hernia repair, served as controls (CO group). The absence of AAA (infrarenal aortic diameter ≤ 3 cm) was documented by ultrasound or computed tomography examination within the last 2 years. They were considered eligible if they had negative functional testing for myocardial ischemia within the last 6 months.

Endpoints of the Study

The primary endpoints of the study were: to investigate a potential difference on the CAVI values among aneurysm patients and non-aneurysm controls and to explore potential changes of CAVI between patients treated either with endovascular or open repair. An ad hoc analysis was performed in an effort to correlate the changes in CAVI values with morphologic parameters of the aneurysm anatomy. This study was approved by the Committee on Research Ethics of our Institution (IRB Nr 806/23.09.2013) and informed consent was taken from all patients.

Patient’s Characteristics—Variables of Interest

Demographic data (gender, age) and co-morbidities (diabetes mellitus (DM); hypertension; coronary artery disease (CAD); nicotine consumption; chronic obstructive pulmonary disease (COPD); chronic renal insufficiency (CRI)) were obtained by a single researcher using explicit medical history. Systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (HR) as well as ankle-brachial index (ABI) were obtained at the time of CAVI measurement.

Moreover, morphologic parameters of the aneurysm (left iliac calcification, luminal volume (cm³), neck length (mm), left iliac diameter (mm), calcification >50% of the circumference, thrombus volume (cm³), neck diameter (mm), left iliac length (mm), neck angle > 45, thrombus > 50% of the circumference, right iliac diameter (mm), left iliac length (mm), right iliac calcification, AP diameter (mm), max length (cm), LL diameter (mm), MAX diameter (mm), sac volume (cm³)) were defined based on analysis of CT-angiography (CTA) with the Osirix MD software (Pixmeo SARL, Bernex, Switzerland).

Measurement of PWV With CAVI

The CAVI was measured 1-3 days before the procedure, within 48 h postoperatively and at 6-month follow-up visit using a VaseraVS-1000 vascular screening system (Fukuda Denshi, Tokyo, Japan). The participants rested in a supine position for 10 min, ECG electrodes were placed on both wrists, a phonograph for detecting heart sounds was placed on the sternum, and cuffs were wrapped around both the arms and ankles. CAVI can be calculated from PWV at the origin of the aorta to the distal segment of tibial artery (ankle), and the systolic and diastolic blood pressures can be measured at the brachial artery. After automatic measurements, obtained data were analyzed by software automatically and the CAVI was estimated.^15,19 This index derives from the stiffness parameter β (β = In(P_s/P_d) x (2ρ/ΔP)xPWV²), as suggested by Hayashi⁹ by applying the Bramwell-Hill’s equation.^15,16,18,20 In particular, CAVI is calculated by using the following equation: CAVI = aβ + b, where a and b are scale conversion constants, and β stiffness parameter. Hence, the equation for CAVI is: CAVI = a[(2ρ/ΔP × In (P_s/P_d) × PWV²] + b, where ρ: blood density; ΔP: blood pressure change; Ps: systolic BP in mm Hg; Pd: diastolic BP in mm Hg; PWV: pulse wave velocity from aortic valve to ankle.

Statistical Analysis

Continuous data were presented as the mean ± standard deviation or median (range), after Shapiro-Wilk test of normality of the distribution. Categorical data were given as the counts (percentages). Parametric variables were analyzed using Student t tests. A chi-square test was used for categorical data. A regression analysis was performed to explore the association between potential covariates related to arterial stiffness and the CAVI values. Furthermore, a multivariate analysis on AAA patients was conducted, in order to identify morphologic parameters that influence CAVI values. A p value < 0.05 was considered statistically significant for all measurements. All analyzes were performed using SPSS® Statistics Software Version 23 (IBM, Armonk, New York, USA).

Results

Comparison of PWV Between AAA and Control Patients

During the study, 1 patient succumbed due to respiratory failure, 4 patients dropped out due to personal reasons, and 2 patient experienced acute myocardial infarction 1 and 4 months after hospital discharge respectively. Thus, the final analysis included 103 patients (91.3% males, median age 71 years, range 62-84 years). Of these 53 underwent EVAR, whereas 50 underwent OSR.

The Table 1 describes the baseline characteristics of all subjects. There was not a statistically significant difference in terms of gender (p = 0.99), median age (p = 0.94), SBP (p = 0.33), DBP (p = 0.23), HR (p = 0.99) between AAA patients and control subjects. However a statistically significant difference with regard to the frequency of history of CAD (P = 0.03), COPD, hypertension (p < 0.001), DM (p = 0.02), smoking (p < 0.001) and COPD (p < 0.001) was recorded.

Table 1.

Baseline Characteristics of All Subjects (AAA and Controls) Included in the Study.

Variable	AAA	Control	p value
Number of patients (n)	103	103
Age (years, median, range)	71 (62-84)	71 (64-78)	matched variable
SBP (mmHg, median, range)	137 (118-164)	133 (117-150)	0.33
DBP (mmHg, median, range)	83 (72-97)	80 (71-89)	0.23
HR (BPM, median, range)	65 (54-92)	64 (52-86)	0.99
Gender (male)	94 (91.3%)	94 (91.3%)	matched variable
CAD	35 (34.0%)	21 (20.4%)	0.03
Hypertension	87 (84.5%)	23 (22.3%)	< 0.001
DM	20 (19.4%)	8 (7.8%)	0.02
Smoking	76 (73.8%)	24 (23.3%)	< 0.001
COPD	51 (49.5%)	16 (15.5%)	< 0.001
CRF	3 (2.9%)	0 (0.0%)	0.67
rABI (mean ± SD)	1.08 ± 0.94	1.03 ± 0.91	0.60
lABI (mean ± SD)	1.03 ± 0.40	1.03 ± 0.10	0.91

The right CAVI (RCAVI) as well as left CAVI (LCAVI) were statistically higher in the AAA patients when compared with control subjects (9.86 ± 2.58 vs 8.80 ± 1.38, p < 0.001 and 9.54 ± 2.32 vs 8.79 ± 1.21, p = 0.003 respectively, Figure 1). The multivariate analysis revealed that only the presence of an AAA was a statistical significant confounder of the CAVI values (Table 2).

Figure 1.

Comparison of CAVI values between AAA and control patients.

Table 2.

Multivariate Analysis for Confounders of the CAVI.

	LCAVI		RCAVI
Variable	Beta	P value	Beta	P value
Age	−.013	.849	.111	.107
HR	−.015	.835	−.021	.766
SBP	.063	.435	−.011	.891
DBP	−.064	.421	.016	.841
CAD	−.012	.879	−.094	.209
HTN	−.007	.942	.111	.255
DM	−.023	.745	.025	.726
Smoking	−.111	.279	−.058	.558
COPD	−.133	.144	.011	.903
CRI	−.045	.537	.212	.346
Gender	−.034	.637	.009	.901
Aneurysm/control	−.383	.000	−.170	.004
ABI	−.163	.194	.079	.240

Abbreviations: HR, Heart Rate; SBP, Systolic Blood Pressure; DP, Diastolic Blood Pressure; CAD, Coronary Artery Disease; HTN, Hypertension; DM, Diabetes Mellitus; COPD, Chronic Obstructive Pulmonary Disease; CRI, Chronic Renal Insufficiency; ABI, Ankle-Brachial Index; RCAVI, Right Cardio-Ankle Vascular Index; LCAVI, Left Cardio-Ankle Vascular Index.

In an effort to identify potential morphological parameters, which could have an impact on the CAVI value, we conducted a regression analysis. None of the investigated variables was found to significant influence the CAVI values (Table 3).

Table 3.

Regression Analysis Correlating Changes in PWV With Morphologic Parameters of the Aneurysm Anatomy.

	RCAVI		LCAVI
	Beta	Sig.	Beta	Sig.
MAX diameter (mm)	.267	.112	−.076	.636
AP diameter (mm)	−.129	.235	.077	.489
LL diameter (mm)	−.177	.102	−.020	.843
max length (cm)	.097	.514	−.031	.783
luminal volume(cm³)	.014	.100	−.004	.623
thrombus volume(cm³)	.001	.875	.002	.599
neck length (mm)	−.025	.275	.021	.307
neck diameter (mm)	−.132	.151	−.070	.399
neck angle > 45	.629	.345	.407	.519
calcification > 50% of the circumference	−.401	.650	1.121	.151
thrombus > 50% of the circumference	−.546	.264	−.085	.897
iliac diameter (mm)	−.078	.318	.064	.016
iliac length (mm)	.020	.263	4.321E-5	.998
iliac calcification	.492	.282	.188	.712

Abbreviations: RCAVI, right Cardio-Ankle Vascular Index; LCAVI, left Cardio-Ankle Vascular Index.

Comparison of PWV in Patients Undergoing Endovascular and Open Repair

In Table 4 are listed the baseline characteristics of the AAA patients undergoing endovascular or open repair. The CAVI was found significantly higher 48 hours postoperatively in the open repair group compared to the preoperative values (1.16 mean difference for LCAVI, p = 0.04, and 1.57 mean difference for RCAVI p = 0.024,) (Table 5). The CAVI was found significantly higher also in the endovascular group 48 hours postoperatively compared to the baseline values (mean difference 0.8 for LCAVI p = 0.04 and 0.8 for RCAVI p = 0.04) (Table 5)

Table 4.

Baseline Characteristics of the AAA Patients Undergoing Endovascular or Open Repair.

Variable	OPEN	ENDO	Total	p value
Number of patients (n)	50	53	103
Age (years, median, range)	71 (62-81)	72 (68-84)	71 (62-84)	0.647
Weight (Kg, median, range)	82 (76-94)	84 (79-101)	84 (76-101)	0.612
Height (cm, median, range)	169 (157-194)	171 (172-178)	169 (157-194)	0.673
BMI (median, range)	27 (22-31)	28 (24-33)	28 (22-33)	0.346
SBP (mmHg, median, range)	137 (118-157)	139 (130-164)	139 (118-164)	0.264
DBP (mmHg, median, range)	80 (72-89)	83 (77-97)	83 (72-97)	0.113
HR (BPM, median, range)	65 (54-72)	63 (55-92)	65 (54-92)	0.846
Gender / Male (n)	43 (86.0%)	51 (96.2%)	94 (91.3%)	0.067
CAD (n)	14 (28.0%)	24 (45.3%)	38 (36.9%)	0.03
Hypertension (n)	43 (86.0%)	48 (90.6%)	91 (88.3%)	0.339
DM (n)	10 (20.0%)	10 (18.9%)	20 (19.4%)	0.541
Smoking (n)	16 (32.0%)	21 (39.6%)	37 (35.9%)	0.882
Ex-smokers	20 (40.0%)	20 (37.7%)	40 (38.8%)
COPD (n)	23 (46.0%)	26 (49.1%)	49 (47.6%)	0.455
CRF (n)	8 (16.0%)	2 (3.8%)	10 (9.7%)	0.037
AAA diam (mean ± SD)	59.2 ± 10.9	59.0 ± 11.8	58.9 ± 11.1	0.827
rABI (mean ± SD)	1.18 ± 0.35	0.98 ± 0.22	1.08 ± 0.94	0.304
lABI (mean ± SD)	0.99 ± 0.19	1.0 ± 0.52	1.03 ± 0.39	0.297

Abbreviations: RCAVI, right Cardio-Ankle Vascular Index; LCAVI, left Cardio-Ankle Vascular Index.

Table 5.

CAVI Values in the Endovascular and Open Repair Group Preoperatively, at 48 Hours Postoperatively and at FU. Dif.1: Difference Between Preoperative Values and Values 48h Postoperatively (Mean ± SD); Dif.2: Difference Between Preoperative Values and Values at Follow up Visit (Mean ± SD).

	Pre	Post 48 h	FU	Dif.1	Dif. 2	Sig.1	Sig.2
OPEN
LCAVI	9.9 ± 2.0	11.00 ± 3.10	9.65 ± 3.0	1.16 ± 3.56	−.25 ± 2.8	0.04	0.123
RCAVI	10.2 ± 2.8	11.70 ± 2.70	9.0 ± 1.8	1.57 ± 3.11	−1.2 ± 2.3	0.024	0.067
ENDO
LCAVI	9.1 ± 2.4	9.9 ± 2.4	10.3 ± 2.8	0.80 ± 2.48	1.2 ± 2.2	0.04	0.031
RCAVI	9.5 ± 2.4	10.4 ± 2.5	10.2 ± 1.6	0.80 ± 2.55	0.7 ± 1.8	0.04	0.047

Bold values are the statistically significant values.

Although at 48 hours postoperatively, the difference in CAVI had a tendency to be higher in the open group (Open: 1.16 for LCAVI and 1.57 for RCAVI vs Endo: 0.8 for LCAVI and 0.8 for RCAVI) compared to the endovascular, the difference between the 2 groups, did not reach a statistical significance (p = 0.59).

At 6 months of follow up the CAVI values returned to the baseline for the patients of the open repair group (9.65 ± 3.0 for LCAVI and 9.0 ± 1.8 for RCAVI). However, in the endovascular group CAVI values remained higher (10.3 ± 2.8 for LCAVI, p = 0.031 and 10.2 ± 1.6 for RCAVI, p = 0.047) when compared with the baseline values. (Table 5)

Discussion

It has been well documented from the literature that arterial stiffness is an independent predictor of increased cardiovascular morbidity and mortality as an indicator of extension of atherosclerosis through the arterial tree.^13,16-18,20 This could be attributed in several risk factors such as advanced age, smoking history hypercholesterolemia, hypertension, ect. Moreover, previous studies have shown that arterial stiffness appears to be significantly increased in patients with AAA.^5,21 This is due to the reasonable hypothesis that on molecular basis infrarenal abdominal aortic aneurysms are associated with elastin degradation on the aortic wall, overproduction of abnormal collagen and calcium deposition leading to a stiffer, less compliant aneurysmal aorta.^2,3 It is well known that these changes in aortic wall in case of aneurysm degeneration could have common risk factors with atherosclerosis.

We conducted this study applying a relatively novel marker of measuring the PWV, the cardio-ankle vascular index (CAVI), which has the considerable advantage of not being affected by the blood pressure at the time of measurement.^15,16 It can, also, predict the cardiovascular events on patients with coronary artery disease, chronic renal insufficiency or diabetes mellitus.^16,18 Although widely adopted, the reference values of CAVI are not worldwide standardized and several cut-off values have been proposed along age for PWV. In a large-scale study, which was conducted in Japan in healthy individuals free of cardiovascular disease, CAVI linearly increased with age, from 20 to 70 years. CAVI in men was higher than that in women for almost all age groups, but men and women showed a similar rate of increase in CAVI of approximately 0.5 per year. The clinical threshold appied was set at a value of 9.0.²⁰ The mean CAVI value in our control group of healthy patients was 8.80 ± 1.38. The multivariate analysis revealed that only the presence of an AAA was the statistical significant parameter that can influence the PWV, as expressed with CAVI values, in the study population (AAA patients and control subjects). This finding can highlight the prognostic significance of increased arterial stiffness and justify why the life expectancy of patients who undergo successful AAA repair is not as good as that of the age and sex-matched general population.²²

Aiming to further investigate the increased CAVI values of aneurysm patients compared to control subjects, we attempted to correlate the CAVI with morphologic parameters of the aneurysm. Several studies have suggested that the presence of intraluminal thrombus or the large diameter of the aorta can affect the haemodynamic properties of the aorta.²³ Thus, our initial hypothesis was that the quantity of wall thrombus, the maximum diameter of the aneurysm and parameters of the proximal and distal landing zone might affect arterial stiffness. However, none of the investigated variables was found to significant influence the CAVI values.

Another endpoint of our study was to explore comparatively changes of CAVI in patients treated either with endovascular or open repair. On this point it should be noticed that, on the contrary to aneurysmatectomy in open repair, the aneurysm sac in EVAR remains intact after aortic endovascular repair, and an intrasac pressure may often persist, due to endoleaks.²⁴ In EVAR patients a remodeling of the sac, which evolves over time, reflects the complex interactions between the intra-aneurysm sac pressure, the thrombus and the mechanical characteristics of the endograft.²⁵ We documented an increase of arterial stiffness in the early postoperative period with both techniques. There is an adaptation period for arterial elasticity after any arterial intervention, which might explain the temporal elevation of the CAVI values.

Although at 48 hours postoperatively, the difference in CAVI had a tendency to be higher in the open group compared to the endovascular, the difference between the 2 groups, did not reach the threshold of statistical significance. Our results are consistent with a study on 50 patients (39 with a graft-prosthesis and 11 with a stentgraft) by Lantelme et al, who suggested that stentgraft increases reflected waves, as recorded with carotid-femoral PWV, more than graft-prostheses.²⁶ Moreover, another study by Gray et al²⁷ reported a significantly higher postoperative PWV measurement than those undergoing open abdominal aortic aneurysm repair.

Six months after the procedure the CAVI values returned to the baseline levels for the patients of the open repair group, while in the endovascular group the CAVI values remained significantly higher when compared with the baseline levels. The hemodynamic impact and the clinical implication of altered arterial stiffness after EVAR remains obscure. A study by Takeda et al²⁵ investigating the echocardiographic changes of patients undergoing EVAR found that endografting leads to left ventricular (LV) hypertrophy and impaired LV diastolic function in the acute and chronic phase, which can severely affect cardiovascular reserve function. Increased arterial stiffness augments myocardial work and oxygen demands in systole and reduces myocardial oxygen supply in diastole, leading to subendocardial ischemia.²⁵ As a result, especially in high risk patients with preexisted cardiac disease who have LV diastolic dysfunction, EVAR may aggravate or even cause the clinical syndrome of heart failure in the mid or long term.^28,29 A meta-analysis of individual-patient data from the 4 multicentre randomized trials of EVAR versus open repair, showed a lower risk of perioperative mortality with EVAR compared with open repair.³⁰ However after 3 years the aneurysm-related mortality was significantly higher in the EVAR group. Moreover, the authors reported no early survival advantage under EVAR in patients with previous coronary artery.³⁰

Our study has several limitations, which should be taken into consideration when interpreting the results. Although we included more than 100 patients, the inability to achieve a longer follow up, due to patients incompliance, led to a lack on the mid- to long-term results regarding mortality and cardiac morbidity. Moreover, our results could have further been supported with echocardiographic findings, which would have confirmed an alteration of the cardiac function after the aneurysm treatment. Another parameter, which could have an impact on the arterial stiffness and not further analyzed is the perioperative medication of the recruited patients. However, the application of the CAVI technique on estimating the PWV of the aorta, which overcomes the impact of the blood pressure on the measurements, as well as the presence of a control group improve the robustsness of our findings.

In conclusion, our study documented an increased PWV, as expressed with CAVI values, for patients with an AAA. Moreover, a significant increase of arterial stiffness in both groups—EVAR and open repair—48 hours postoperatively and a significant increase of arterial stiffness at 6 months in EVAR patients compared to the baseline values were found. Further studies are needed to elucidate the impact of a decreased aortic compliance after stentgraft implantation on the cardiac function of patients with AAA.

Footnotes

Authors’ Note

EBD 806 /23.09.2013 Review Board “Attikon” University Hospital Athens, Greece. Concept and design: SNM, KGM, NK. Analysis and interpretation: SNM. Data collection: SNM. Writing the article: SNM, KGM, NK. Critical revision of the article: TEK, JK, KK, CL. Final approval of the article: all authors. Statistical analysis: SNM, CA. Overall responsibility: SNM.

Declaration of Conflicting Interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

ORCID iD

Spyridon N. Mylonas

Konstantinos G. Moulakakis

Constantinos Antonopoulos

References

Sidloff

Stather

Dattani

, et al. Aneurysm global epidemiology study: public health measures can further reduce abdominal aortic aneurysm mortality. Circulation. 2014;129(7):747–753.

Hinson

. Mechanical properties of the aneurysmal aorta. Br J Surg. 1993;80(12):1628.

Vorp

Vande Geest

. Biomechanical determinants of abdominal aortic aneurysm rupture. Arterioscler Thromb Vasc Biol. 2005;25(8):1558–1566.

Tanaka

Munakata

Kawano

, et al. Comparison between carotid-femoral and brachial-ankle pulse wave velocity as measures of arterial stiffness. J Hypertens. 2009;27(10):2022–2027.

Kadoglou

NPE

Moulakakis

Papadakis

, et al. Changes in aortic pulse wave velocity of patients undergoing endovascular repair of abdominal aortic aneurysms. J Endovasc Ther. 2012;19(5):661–666.

O’Rourke

Staessen

Vlachopoulos

Duprez

Plante

. Clinical applications of arterial stiffness; definitions and reference values. Am J Hypertens. 2002;15(5):426–444.

Lemogoum

Flores

Van den Abeele

, et al. Validity of pulse pressure and augmentation index as surrogate measures of arterial stiffness during beta-adrenergic stimulation. J Hypertens. 2004;22(3):511–517.

Ruegg

Mason

Hardinge

, et al. Augmentation index and central aortic blood pressure in patients with abdominal aortic aneurysms. J Hypertens. 2010;28(11):2252–2257.

Hayashi

Handa

Nagasawa

Okumura

Moritake

. Stiffness and elastic behavior of human intracranial and extracranial arteries. J Biomech. 1980;13(2):175–184.

10.

Kawasaki

Sasayama

Yagi

Asakawa

Hirai

. Non-invasive assessment of the age related changes in stiffness of major branches of the human arteries. Cardiovasc Res. 1987;21(9):678–687.

11.

Yamashina

Tomiyama

Takeda

, et al. Validity, reproducibility, and clinical significance of noninvasive brachial-ankle pulse wave velocity measurement. Hypertens Res. 2002;25(3):359–364.

12.

Kim

Nam

Park

, et al. Usefulness of brachial-ankle pulse wave velocity as a predictive marker of multiple coronary artery occlusive disease in Korean type 2 diabetes patients. Diabetes Res Clin Pract. 2009;85(1):30–34.

13.

Matsushita

Ding

Kim

, et al. Cardio-ankle vascular index and cardiovascular disease: systematic review and meta-analysis of prospective and cross-sectional studies. J Clin Hypertens (Greenwich). 2019;21(1):16–24.

14.

Nye

. The effect of blood pressure alteration on the pulse wave velocity. Br Heart J. 1964;26(2):261–265.

15.

Shirai

Hiruta

Song

, et al. Cardio-Ankle Vascular Index (CAVI) as a novel indicator of arterial stiffness: theory, evidence and perspectives. J Atheroscler Thromb. 2011;18(11):924–938.

16.

Saiki

Sato

Watanabe

, et al. The role of a novel arterial stiffness parameter, Cardio-Ankle Vascular Index (CAVI), as a surrogate marker for cardiovascular diseases. J Atheroscler Thromb. 2016;23(2):155–168.

17.

Namba

Masaki

Takase

Adachi

. Arterial stiffness assessed by cardio-ankle vascular index. Int J Mol Sci. 2019;20(15):3664.

18.

Hayashi

Yamamoto

Takahara

Shirai

. Clinical assessment of arterial stiffness with cardio-ankle vascular index: theory and applications. J Hypertens. 2015;33(9):1742–1757.

19.

Kato

Takita

Furuhashi

Maruyama

Miyajima

Kumagai

. Brachial-ankle pulse wave velocity and the cardio-ankle vascular index as a predictor of cardiovascular outcomes in patients on regular hemodialysis. Ther Apher Dial. 2012;16(3):232–241.

20.

Namekata

Suzuki

Ishizuka

Shirai

. Establishing baseline criteria of cardio-ankle vascular index as a new indicator of arteriosclerosis: a cross-sectional study. BMC Cardiovasc Disord. 2011;11:51.

21.

Van Disseldorp

EMJ

Van Dronkelaar

Pluim

JPW

Van De Vosse

Van Sambeek

MRHM

Lopata

RGP

. Ultrasound based wall stress analysis of abdominal aortic aneurysms using multiperspective imaging. Europ J Vasc Endovasc Surg. 2020;59(1):81–91.

22.

Bulder

RMA

Bastiaannet

Hamming

Lindeman

JHN

. Meta-analysis of long-term survival after elective endovascular or open repair of abdominal aortic aneurysm. Br J Surg. 2019;106(5):523–533.

23.

Lyck Hansen

Dahl Thomsen

Rasmussen

Lindholt

. Abdominal aortic aneurysm, arterial stiffening and the role of the intraluminal thrombus. Vasa. 2015;44(5):349–353.

24.

Morris

Stefanov

McGloughlin

. Stent graft performance in the treatment of abdominal aortic aneurysms: the influence of compliance and geometry. J Biomech. 2013;46(2):383–395.

25.

Takeda

Sakata

Ohtani

, et al. Endovascular aortic repair increases vascular stiffness and alters cardiac structure and function. Circ J. 2014;78(2):322–328.

26.

Lantelme

Dzudie

Milon

, et al. Effect of abdominal aortic grafts on aortic stiffness and central hemodynamics. J Hypertens. 2009;27(6):1268–1276.

27.

Gray

Goodman

Badger

O’Malley

O’Donohoe

McDonnell

. Endovascular aneurysm repair increases aortic arterial stiffness when compared to open repair of abdominal aortic aneurysms. Vasc Endovascular Surg. 2016;50(5):317–320.

28.

Kanzaki

Aortic compliance and left ventricular diastolic function: do endovascular repairs for aortic aneurysm alter aortic stiffness?

Circ J. 2014;78(2):307–308.

29.

Gregory

Kruger

Maher

Moore

Dobson

. Non-invasive determination of aortic mechanical properties and their effects on left ventricular function following endovascular abdominal aneurysm repair. J Med Biolog Eng. 2019;39(5):739–751.

30.

Powell

Sweeting

Ulug

, et al. Meta-analysis of individual-patient data from EVAR-1, DREAM, OVER and ACE trials comparing outcomes of endovascular or open repair for abdominal aortic aneurysm over 5 years. Br J Surg. 2017;104(3):166–178.