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Hypertension. 1999;33:1111-1117

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(Hypertension. 1999;33:1111-1117.)
© 1999 American Heart Association, Inc.


Scientific Contributions

Aortic Pulse Wave Velocity as a Marker of Cardiovascular Risk in Hypertensive Patients

Jacques Blacher; Roland Asmar; Saliha Djane; Gérard M. London; Michel E. Safar

From the Department of Internal Medicine and Inserm U 337, Broussais Hospital, Paris, France.

Correspondence to Pr M. Safar, Service de Médecine Interne, 96, rue Didot, Hôpital Broussais, 75014 Paris, France. E-mail michel.safar{at}brs.ap-hop-paris.fr


*    Abstract
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Abstract—Large artery damage is a major contributory factor to cardiovascular morbidity and mortality of patients with hypertension. Pulse wave velocity (PWV), a classic evaluation of arterial distensibility, has never been ascertained as a cardiovascular risk marker. To determine the factors influencing aortic PWV and the potential predictor role of this measurement, we studied a cohort of 710 patients with essential hypertension. Atherosclerosis alterations (AA) were defined on the basis of clinical events. Calculation of cardiovascular risks, by use of Framingham equations, was performed in subjects without AA. PWV was higher in the presence of AA (14.9±4.0 versus 12.4±2.6 m/s, P<0.0001), even after adjustments on confounding factors and was the first determinant (P<0.0001) of the extent of atherosclerosis assessed as the sum of the atherosclerotic sites. In patients without AA, all cardiovascular risks increased constantly with PWV. Furthermore, at a given age, aortic PWV was the best predictor of cardiovascular mortality. The odds ratio of being in a high cardiovascular mortality risk group (>5% for 10 years) for patients in the upper quartile of PWV was 7.1 (95% confidence intervals 4.5 to 11.3). The presence of a PWV >13 m/s, taken alone, appeared as a strong predictor of cardiovascular mortality with high performance values. This study shows that aortic PWV is strongly associated with the presence and extent of atherosclerosis and constitutes a forceful marker and predictor of cardiovascular risk in hypertensive patients.


Key Words: atherosclerosis • hypertension, essential • aortic stiffness • cardiovascular risk


*    Introduction
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Hypertension is a well-recognized cardiovascular risk factor.1 Interventional studies in hypertensive populations have demonstrated the significant decrease in cardiovascular events obtained by antihypertensive drug treatment.2 Nevertheless, in these studies, the number of patients needed to be treated in order to avoid 1 cardiovascular event remains high, particularly in the younger population. Clearly, the consideration of the other cardiovascular risk factors associated with hypertension would enable a more accurate evaluation of individual risk, risk stratification, and cost-effective preventive therapy.3 From the Framingham population, evaluations have been proposed, taking into account simultaneously the contribution of blood pressure (BP), tobacco consumption, gender, lipid profile, diabetes mellitus, and ECG left ventricular hypertrophy.4 However, an appropriate and simple evaluation of individual risk, based on a single measurement, is still lacking.

Arterial stiffness increases with age5 and hypertension6 and is also enhanced in subjects with diabetes mellitus,7 atherosclerosis,8 and end-stage renal disease.9 The most obvious consequences of arterial stiffening are increased pulsatile BP caused by higher systolic BP (SBP) and lower diastolic BP (DBP), thereby causing increased left ventricular afterload and altering coronary perfusion.6 9 High SBP and pulse pressure, low DBP, and left ventricular hypertrophy have been identified as independent factors of cardiovascular morbidity and mortality in the general population.1 10 11 12 Arterial stiffness can be assessed noninvasively with the use of pulse wave velocity (PWV) measurement, that is, the velocity of the pulse wave to travel a given distance between 2 sites of the arterial system. Nevertheless, whether aortic stiffening is predictive of clinical outcome and/or mortality needs to be established.

The goal of the present study was (1) to test the ability for aortic PWV to act as a marker of individual cardiovascular risk, integrating the atherosclerotic vascular damages caused by the most common cardiovascular risk factors, and (2) to identify high-risk patients from a hypertensive population never treated or even treated medically by antihypertensive agents. To determine (1) the factors influencing aortic stiffness (estimated by measuring the carotid-femoral PWV), and (2) the potential predictor role of this measurement on cardiovascular risk assessed by a scale, we conducted this cross-sectional study on a cohort of 710 patients with essential hypertension. The results indicate (1) that aortic PWV determined from a single measurement is strongly associated with the presence and extent of atherosclerosis, (2) and that this measurement is highly related to cardiovascular risk as assessed by the standard Framingham equations.4


*    Methods
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Study Cohort
From January 1996 to June 1997, {approx}1500 patients entered the Department of Internal Medicine of Broussais Hospital for a cardiovascular check-up ordered by their general practitioner or their cardiologist because of the presence of 1 or several cardiovascular risk factors involving high BP, smoking, dyslipidemia, diabetes mellitus, and/or family history of premature cardiovascular disease (CVD), with or without previously identified atherosclerotic alterations (AA). From those 1500 patients, only subjects with essential hypertension were selected. In never-treated hypertensive subjects (n=105), high BP was defined as an SBP >140 mm Hg and/or a DBP >90 mm Hg, measured by sphygmomanometry, in the supine position with a minimum of 3 casual measurements during the last month. In treated hypertensive subjects (n=605), patients were included regardless of whether BP was well controlled (SBP <140 mm Hg and DBP <90 mm Hg). Patients with all forms of secondary hypertension, on the basis of classic laboratory and radiology tests, were not included. Patients with cancer (other than basal cell carcinoma), with insulin-dependent diabetes, or with severe renal insufficiency (creatinine >300 µmol/L) were not included in the study. The study cohort was then composed of 710 hypertensive consecutive patients (412 men, 298 women) with mean age (±SD) of 60±13 years. From the 710 patients, 605 (85%) were treated with antihypertensive therapy at inclusion; the mean number of antihypertensive drugs was 1.48±1.01 per patient. The antihypertensive drugs included calcium antagonists (323 patients), ß-blockers (225 patients), diuretics (212 patients), angiotensin-converting enzyme inhibitors (195 patients), central-acting agents (68 patients), angiotensin II antagonists (17 patients), and {alpha}-blockers (11 patients), either alone or in combination. One hundred eight (15%) patients were medically treated for dyslipidemia (drugs including statins or fibrates). Sixty-six (9%) patients were medically treated for diabetes mellitus (drugs including sulfamids and/or biguanids). Each subject provided informed consent for the study, which was approved by our institutional review board.

Information compiled from the questionnaire filled out at inclusion included gender, age, weight and height, body mass index, family (first-degree relatives) history of premature cardiovascular events (<55 years old in men and <60 in women), personal history of diabetes mellitus, personal history of dyslipidemia, smoking habits, previous diseases, and use of medications including antihypertensive drugs. From the clinical questionnaire and the findings of the check-up during hospitalization, AA was present in 180 patients and absent in 530 patients. For a description of AA in hypertensive patients, the usual criteria were used according to the International Classification of Diseases (9th revision) for coronary heart disease (CHD), cerebrovascular disease, peripheral vascular disease, and abdominal aortic aneurysm. Dyslipidemia was defined as a total/high-density (HDL) cholesterol ratio >5 or the presence of a hypocholesterolemic drug (statins or fibrates). Diabetes mellitus was defined as a fast glycemia >7.8 mmol/L or the presence of hypoglycemic agents (sulfamids and/or biguanids).

One hundred eighty patients had AA involving >=1 vascular site, including CHD (106 patients), peripheral vascular disease (58 patients), cerebrovascular disease (56 patients), and abdominal aorta aneurysm (37 patients). The mean number of vascular sites involved by AA in the population of the 180 patients was 1.43±0.65 per patient. Extent of atherosclerosis was assessed as the number of vascular sites involved by AA: 0 (530 patients), 1 (119 patients), 2 (45 patients), or 3 (16 patients).


*    Methods
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The measurements were performed in the morning after an overnight fast, each patient being in supine position. Brachial BP was measured with a mercury sphygmomanometer after 15 minutes of rest. Phases I and V of the Korotkoff sounds were considered respectively as SBP and DBP. The mean BP (MBP) was calculated as MBP=DBP+(SBP-DBP/3). Five measurements 2 minutes apart were averaged.

After BP determination, the PWV measurement was performed before the 3-lead orthogonal ECG and blood sample in a controlled environment at 22±2°C. PWV was determined with the use of an automatic device: the Complior (Colson), which allowed an online pulse wave recording and automatic calculation of PWV with 2 transducers, 1 positioned at the base of the neck for the common carotid artery and the other over the femoral artery, as previously described.13 The validation of this automatic method and its reproducibility have been previously described, with an intraobserver repeatability coefficient of 0.935 and an interobserver reproducibility coefficient of 0.890.13

Heart period was determined from the 3-lead orthogonal ECG. On the basis of the 8-second recording, the average heart rate was calculated (in beats per minute) during that period. ECG left ventricular hypertrophy was defined as a Sokolow index superior to 35 mm. Waist circumference midway between the lowest rib and the iliac crest and hip circumference at the level of the great trochanters were measured with flexible tape. Venous blood samples were obtained in subjects after an overnight fast. Plasma was separated without delay at 4°C in a refrigerated centrifuge and stored at 4°C (for the determination of routine chemistry profile by standard methods) until analysis. Total cholesterol and triglycerides were determined with the use of a Technicon Chem assay (Technicon Instruments), and HDL cholesterol was measured in the supernatant after precipitation of apolipoprotein B–containing lipoproteins with heparin-manganese chloride. Low-density lipoprotein cholesterol was calculated by the formula of Friedewald et al14 for patients with serum triglyceride concentrations <4.0 mmol/L.

Statistical Analysis
Overall Population (n=710)
Data are expressed as mean±SD. Student's t test was used for comparison of normally distributed continuous variables. Differences in frequency were tested by {chi}2 analysis. Gender was used as a dummy variable (1, male; 2, female). Statistical analysis was performed on NCSS 6.0.21 software.15 A value of P<0.05 was considered significant. All testing was double-sided. Multiple regression analysis was performed to assess linear associations between aortic pulse wave velocity, extent of atherosclerosis, and determinants of clinical, biochemical, and cardiovascular parameters. Logistic regression analysis was used to assess the correlations between the presence of AA (1=yes, 0=no) and determinants of clinical, biochemical, and cardiovascular parameters. Prognostic variables for the presence of AA, determined from the logistic regression analysis, were divided into 2, 3, or 4 clinically pertinent subgroups. The relative risk of AA in each group of any prognostic variable compared with the reference group was estimated as the crude odds ratio. Confidence limits of crude odds ratios were calculated according to Woolf's method.16 The adjusted relative risk of AA in each group compared with the reference group was estimated as the adjusted odds ratio. Adjusted odds ratios were calculated as the antilogarithm of the ß-coefficient of the logistic regression of AA with all the prognostic variables divided into 2, 3, or 4 groups (plasma creatinine, tobacco life-long dose, age, PWV, DBP, and diabetes mellitus). Ninety-five percent confidence intervals (CI) around the adjusted odds ratios estimated were obtained from the formula antilogarithm (ß±1.96xSEß), where SEß is the standard error of ß.

Population Without AA
Of the 530 patients without AA, age range was from 30 to 74 years in 462 patients. In this group corresponding to the age range of the Framingham cohorts, before the 12 years of follow-up, 10-year different cardiovascular risks were calculated on the basis of the equations derived from the Framingham Heart Study and from the Framingham Offspring Study.4 Calculations were made for the following outcomes: myocardial infarction (MI) (including silent and unrecognized MI); death from CHD (sudden or nonsudden); CHD (consisting of MI, angina pectoris, coronary insufficiency and CHD death); stroke, including transient ischemia; CVD (including all the above plus congestive heart failure and peripheral vascular disease); and death from CVD.

In this population of 462 patients, PWV was divided into 4 quartiles of 115 or 116 patients. A 10-year absolute MI risk >5%, a 10-year absolute CHD risk >15%, a 10-year absolute CHD mortality risk >5%, a 10-year absolute stroke risk >5%, a 10-year absolute CVD risk >20%, and a 10-year cardiovascular mortality risk >5% were defined as high risks. The relative risk of being in the high-risk group according to the presence versus absence of cardiovascular risk factors was calculated as the crude odds ratio.

PWV as a Diagnostic Test
To assess the performance of PWV considered as a diagnostic test, with the use of receiver operating characteristic (ROC) curves, we calculated sensitivities, specificities, positive predictive values, and negative predictive values of PWV at different cutoff values, first to detect the presence of AA in the overall population and second to detect patients with high 10-year cardiovascular mortality risk in the subgroup of 462 patients without AA with age range from 30 to 74 years. Optimal cutoff values of PWV were defined as the maximization of the sum of sensitivity and specificity.


*    Results
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Overall Population
Table 1 shows the characteristics of the patients according to the presence or absence of AA. Mean (±SD) PWV was 14.9±4.0 m/s in the group of patients with AA and 12.4±2.6 m/s for the patients without AA (P<0.0001).


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Table 1. Characteristics of Patients According to Presence or Absence of Atherosclerotic Alterations

Age (P<0.0001), SBP (P<0.0001), plasma glucose (P<0.0001), the presence of AA (P<0.0001), plasma creatinine (P=0.0001), and gender (P=0.03) were the only independent factors modulating PWV. Lipids, smoking, duration of antihypertensive therapy, and the presence of any antihypertensive drug did not significantly enter the multiple regression analysis.

The only independent factors modulating the presence of AA were plasma creatinine (P<0.0001), tobacco life-long dose (P<0.0001), age (P=0.0001), PWV (P=0.0004), DBP (P=0.03), and the presence of diabetes mellitus (P=0.06). When the extent of atherosclerosis was considered as the independent variable, only PWV (P<0.0001), tobacco life-long dose (P<0.0001), plasma creatinine (P<0.0001), body mass index (P=0.002), DBP (P=0.003), the presence of dyslipidemia (P=0.007), and age (P=0.008) entered the multiple regression analysis. Considering the presence of AA or extent of atherosclerosis as the dependent variable in multivariate analysis, SBP did not significantly persist in the model, probably because of the strong colinearity between SBP and PWV (r=0.354, P<0.0001) and, to a lesser extent, between SBP and age (r=0.155, P<0.0001).

Table 2 shows the odds ratios of AA according to prognostic variables (defined by the logistic regression). Adjustments were made on all the prognostic variables in this table. Patients with PWV >15 m/s, with creatinine >110 µmol/L, >70 years old or those who smoked >20 pack-years had an increased adjusted risk of AA, whereas those whose DBP was >110 mm Hg had a decreased adjusted risk of AA.


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Table 2. Odds Ratios of Atherosclerotic Alterations According to Prognostic Variables

Population Without AA: PWV as a Predictor of Cardiovascular Risks According to the Framingham Equations
We observed a constant increase for all the risks (MI, CHD, death from CHD, stroke, CVD, and death from CVD) with the increase of PWV. Figure 1 shows the relation between PWV and 10-year CVD risk (r=0.495; P<0.0001). The relations between PWV and the other risks (MI, CHD, death from CHD, stroke and death from CVD) had the same levels of statistical significance, with correlation coefficients ranging between 0.44 and 0.50 (data not shown).



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Figure 1. Relation between 10-year CVD risk and aortic pulse wave velocity.

Table 3 shows the odds ratios of being in a high-risk group according to the presence versus absence of a cardiovascular risk factor. Aortic PWV appeared (1) as a stronger predictor than plasma creatinine, left ventricular hypertrophy, and total/HDL cholesterol for any type of cardiovascular risks, (2) as a stronger predictor than smoking for all risks but MI, and (3) as a stronger predictor than hypertension for all risks but stroke. Furthermore, at a given age, PWV appeared as the strongest predictor of cardiovascular mortality. The odds ratio of being in the high-risk cardiovascular mortality group for patients with PWV >13.5 m/s was 7.1 (95% CI 4.5 to 11.3).


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Table 3. Odds Ratio of Being in High-Risk Group According to Presence Versus Absence of Cardiovascular Risk Factor

PWV as a Diagnostic Test
In the overall population, optimal cutoff value of PWV to detect the presence of AA was 13 m/s with the following performance: 62% sensitivity, 67% specificity, 39% positive predictive value, and 84% negative predictive value (area under ROC curve=0.69±0.07, data not shown)

In the subgroup of 462 patients without AA with age range from 30 to 74 years, optimal cutoff value of PWV to detect patients with high 10-year cardiovascular mortality risk was 13 m/s with the following performance: 60% sensitivity, 84% specificity, 67% positive predictive value, and 80% negative predictive value (area under ROC curve=0.78±0.07, Figure 2).



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Figure 2. ROC curve: Aortic pulse wave velocity in detection of patients with high 10-year cardiovascular mortality (area under curve=0.78±0.07).


*    Discussion
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*Discussion
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The salient findings of this study were that in a population of treated or untreated subjects with essential hypertension, aortic PWV was strongly related to the presence and extent of AA, including CHD, peripheral vascular disease, cerebrovascular disease, and abdominal aorta aneurysm and that PWV was a strong predictor of cardiovascular risks as determined by the Framingham equations. Furthermore, the presence of a PWV >13 m/s, taken alone, appeared as a strong predictor of cardiovascular mortality with high performance values.

In the present study, we used PWV, which is as a marker of aortic stiffness, since it is related to the square root of the elasticity modulus and to the thickness/radius ratio.6 The PWV determined from foot-to-foot transit time in the aorta offers a simple, reproducible, and noninvasive evaluation of regional aortic stiffness.17 18 This noninvasive superficial measurement allows only an estimate of the distance traveled by the pulse, and accurate measurements of this distance are obtained only with invasive procedures. In this regard, some authors suggested a possible correction based on anatomic dimensions of the body,19 whereas others recommended subtracting the distance between the suprasternal notch to the carotid location from the total distance when the carotid pulse is recorded instead of the aortic arch pulse, because the pulse traveling is in the opposite direction.6 In fact, because arteries become longer and tortuous with age, the path lengths determined from superficial linear measurements are underestimated. Repeatability studies, checks made with Bland and Altman diagrams,20 and modern computer technology13 now made it quite feasible to simply investigate aortic stiffness in cardiovascular epidemiologic studies. Since the principal factors modulating the level of PWV are age and BP,5 6 epidemiologic studies involving PWV should be adjusted to these 2 parameters. The studied population was composed of patients entering the Department of Internal Medicine of Broussais Hospital for a cardiovascular check-up, thus very close to clinical practice, and including young and old hypertensive subjects, with and without hypertensive drug treatment. Moreover, it should be noted that although a significant proportion of patients (25%) had confirmed AA, this proportion was probably underestimated, including unrecognized silent myocardial ischemia or cerebrovascular disease, since invasive explorations were not systematically performed.

In the totality of the present population, the presence of AA influenced the level of PWV independent of age and BP. Most of the studies relating PWV to cholesterol and/or dyslipidemia found minimal or inconsistent correlations.9 21 As suggested by others,22 23 24 the present correlation between PWV and AA points to the presence of diffuse and calcified atherosclerotic plaques in association with the development of extracellular matrix, mainly collagen tissue. Our finding that PWV was strongly related to the number of atherosclerotic sites confirms this interpretation. The presence of a negative correlation between DBP and the presence and extent of atherosclerosis has been previously reported.6 11 Indeed, the consequences of arterial stiffening on BP are not only increased SBP and pulse pressure but also decreased DBP at any given mean BP value. In fact increased pulse pressure, decreased DBP, and increased PWV are related to the same common denominator, namely increased aortic stiffness, a parameter that is associated with increased cardiovascular risk.25 Finally, we found that PWV was strongly associated with diabetes and renal insufficiency, 2 conditions in which AA and hypertension are commonly present, and increased arterial stiffness has been previously noted.7 9 26

An important result of the present study was that in the population of hypertensive subjects without AA, increased aortic PWV might be a significant predictor of cardiovascular events. The presence of a PWV >13 m/s, taken alone, appeared as a strong predictor of cardiovascular mortality with high performance values. In recent longitudinal studies, we and others have shown that increased pulse pressure, the major hemodynamic consequence of increased aortic PWV, was a strong independent predictor of cardiac mortality, mainly MI, in populations of normotensive and hypertensive subjects.10 11 12 The present study is somewhat different in nature because only cross-sectional data are presented. However, the use of the Framingham equation–based cardiovascular scale as comparator is important to consider because the evaluation of cardiovascular risks with this scale results from large (>5000 persons) and long-term (>=12 years) longitudinal studies with the use of a multifactorial approach, with none lost to follow-up. Using this scale, we showed that aortic PWV is, for a given age, the strongest predictor of cardiovascular mortality and mostly that this single measurement gives an individual evaluation of all cardiovascular risks very close to the level calculated by the multiple risk factors involved in the equations. Because cardiovascular risks according to Framingham equations are calculated on the basis of instant levels of major cardiovascular risk factors, PWV depends on the level of present and past exposure to vascular damage factors and therefore is more closely related to individual cardiovascular risk than any risk scale giving more of a population risk level than an individual risk level. Furthermore, because our population included both treated and untreated hypertensive subjects, the predictive value of PWV was adequate even in the presence of antihypertensive drug treatment. The same observation has been made for pulse pressure measurements that are predictive of MI even in treated hypertensive subjects.12

There are several methodological limitations involved with the cardiovascular risk scales. First, cardiovascular risk is lower in France than in the United States and has also shown a decline over the past few decades. Second, cardiovascular risk may differ significantly from one individual to the next, which has an impact on calculations based on part of the cardiovascular risk factors only. Third, the Framingham equations have been modeled on the basis of an asymptomatic population, consisting in a majority of normotensive subjects. These equations should probably be corrected for their application to hypertensive populations such as our study population. Finally, we have furthermore hypothesized for the risk calculation that regardless of whether drugs were involved, for the same blood pressure there was the same risk. Of course, given that our study is cross-sectional, we cannot project any hypothesis regarding the extent of antihypertensive drug–related benefit on cardiovascular risk assessment for the future. From a methodological point of view, therefore, the relation between PWV, atherosclerosis, and cardiovascular risk cannot be directly extended to include normotensive populations.

In conclusion, the present study has shown, in a cohort of untreated and treated hypertensive subjects, that increased aortic PWV was strongly associated with the presence of AA and was even a strong predictor of cardiovascular risk. These results could have important clinical implications in risk assessment strategies. Whether increased aortic PWV constitutes a trigger mechanism or rather a marker of morbid events cannot be evaluated from the present study. The longitudinal investigation of a large unselected population is required to evaluate the independent contribution of PWV to the individual cardiovascular risk.


*    Acknowledgments
 
The authors thank Wendy Kay Johnson for linguistic assistance, Pr Gilles Chatellier for methodological advice, Société Française d'Hypertension Artérielle, Groupe de Pharmacologie et d'Hémodynamique Cardio-vasculaire, and Daniel Brun and the Organica association for generous financial contributions.

Received August 4, 1998; first decision August 27, 1998; accepted December 29, 1998.


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up arrowAbstract
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*References
 
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K. Yamamoto, H. Kawano, Y. Gando, M. Iemitsu, H. Murakami, K. Sanada, M. Tanimoto, Y. Ohmori, M. Higuchi, I. Tabata, et al.
Poor trunk flexibility is associated with arterial stiffening
Am J Physiol Heart Circ Physiol, October 1, 2009; 297(4): H1314 - H1318.
[Abstract] [Full Text] [PDF]


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ChestHome page
T. Kumagai, T. Kasai, M. Kato, R. Naito, K.-i. Maeno, S. Kasagi, F. Kawana, S. Ishiwata, and K. Narui
Establishment of the Cardio-Ankle Vascular Index in Patients With Obstructive Sleep Apnea
Chest, September 1, 2009; 136(3): 779 - 786.
[Abstract] [Full Text] [PDF]


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J Am Coll CardiolHome page
N. C. Edwards, R. P. Steeds, P. M. Stewart, C. J. Ferro, and J. N. Townend
Effect of spironolactone on left ventricular mass and aortic stiffness in early-stage chronic kidney disease: a randomized controlled trial.
J. Am. Coll. Cardiol., August 4, 2009; 54(6): 505 - 512.
[Abstract] [Full Text] [PDF]


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Nephrol Dial TransplantHome page
I. Dursun, H. M Poyrazoglu, Z. Gunduz, H. Ulger, A. Yykylmaz, R. Dusunsel, T. Patyroglu, and M. Gurgoze
The relationship between circulating endothelial microparticles and arterial stiffness and atherosclerosis in children with chronic kidney disease
Nephrol. Dial. Transplant., August 1, 2009; 24(8): 2511 - 2518.
[Abstract] [Full Text] [PDF]


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J. Appl. Physiol.Home page
E. C. Tuday, D. Nyhan, A. A. Shoukas, and D. E. Berkowitz
Simulated microgravity-induced aortic remodeling
J Appl Physiol, June 1, 2009; 106(6): 2002 - 2008.
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ESC Textbook of Cardiovascular MedicineHome page
S. E. Kjeldsen, T. A. Aksnes, R. H. Fagard, and G. Mancia
CHAPTER 13 Hypertension
ESC Textbook of Cardiovascular Medicine, January 1, 2009; 2(1): med-9780199566990-chapter - med-9780199566990-chapter.
[Abstract] [Full Text] [PDF]


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J Am Coll Cardiol ImgHome page
J. Sugawara, K. Hayashi, T. Yokoi, and H. Tanaka
Age-associated elongation of the ascending aorta in adults.
J. Am. Coll. Cardiol. Img., November 1, 2008; 1(6): 739 - 748.
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Ther Adv Cardiovasc DisHome page
R. D. Smith and P. J. Levy
Review: New techniques for assessment of vascular function
Therapeutic Advances in Cardiovascular Disease, October 1, 2008; 2(5): 373 - 385.
[Abstract] [PDF]


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ANGIOLOGYHome page
S.-H. Lee, S. Choi, J.-H. Jung, and N. Lee
Effects of Atrial Fibrillation on Arterial Stiffness in Patients With Hypertension
Angiology, August 1, 2008; 59(4): 459 - 463.
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Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
T. Otsuki, S. Maeda, M. Iemitsu, Y. Saito, Y. Tanimura, R. Ajisaka, and T. Miyauchi
Systemic arterial compliance, systemic vascular resistance, and effective arterial elastance during exercise in endurance-trained men
Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2008; 295(1): R228 - R235.
[Abstract] [Full Text] [PDF]


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Ther Adv Cardiovasc DisHome page
M. E. Safar
Review: Pulse pressure, arterial stiffness and wave reflections (augmentation index) as cardiovascular risk factors in hypertension
Therapeutic Advances in Cardiovascular Disease, February 1, 2008; 2(1): 13 - 24.
[Abstract] [PDF]


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HypertensionHome page
A. Qasem and A. Avolio
Determination of Aortic Pulse Wave Velocity From Waveform Decomposition of the Central Aortic Pressure Pulse
Hypertension, February 1, 2008; 51(2): 188 - 195.
[Abstract] [Full Text] [PDF]


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Br J AnaesthHome page
R. A. Payne, D. Isnardi, P. J. D. Andrews, S. R. J. Maxwell, and D. J. Webb
Similarity between the suprasystolic wideband external pulse wave and the first derivative of the intra-arterial pulse wave
Br. J. Anaesth., November 1, 2007; 99(5): 653 - 661.
[Abstract] [Full Text] [PDF]


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Am. J. Physiol. Endocrinol. Metab.Home page
A. J. Sommerfield, I. B. Wilkinson, D. J. Webb, and B. M. Frier
Vessel wall stiffness in type 1 diabetes and the central hemodynamic effects of acute hypoglycemia
Am J Physiol Endocrinol Metab, November 1, 2007; 293(5): E1274 - E1279.
[Abstract] [Full Text] [PDF]


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Exp. Biol. Med.Home page
D. P. Casey, D. T. Beck, and R. W. Braith
Progressive Resistance Training Without Volume Increases Does Not Alter Arterial Stiffness and Aortic Wave Reflection
Experimental Biology and Medicine, October 1, 2007; 232(9): 1228 - 1235.
[Abstract] [Full Text] [PDF]


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HypertensionHome page
N. Cheung, A. R. Sharrett, R. Klein, M. H. Criqui, F.M. A. Islam, K. J. Macura, M. F. Cotch, B. E.K. Klein, and T. Y. Wong
Aortic Distensibility and Retinal Arteriolar Narrowing: The Multi-Ethnic Study of Atherosclerosis
Hypertension, October 1, 2007; 50(4): 617 - 622.
[Abstract] [Full Text] [PDF]


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J Am Coll CardiolHome page
M. F. O'Rourke and J. Hashimoto
Mechanical Factors in Arterial Aging: A Clinical Perspective
J. Am. Coll. Cardiol., July 3, 2007; 50(1): 1 - 13.
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Arch OphthalmolHome page
C. A. A. Hulsman, J. R. Vingerling, A. Hofman, J. C. M. Witteman, and P. T. V.M. de Jong
Blood Pressure, Arterial Stiffness, and Open-angle Glaucoma: The Rotterdam Study
Arch Ophthalmol, June 1, 2007; 125(6): 805 - 812.
[Abstract] [Full Text] [PDF]


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J Am Coll CardiolHome page
I. J. Kullo and A. R. Malik
Arterial Ultrasonography and Tonometry as Adjuncts to Cardiovascular Risk Stratification
J. Am. Coll. Cardiol., April 3, 2007; 49(13): 1413 - 1426.
[Abstract] [Full Text] [PDF]


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Diabetes CareHome page
C. Meyer, B. P. McGrath, and H. J. Teede
Effects of Medical Therapy on Insulin Resistance and the Cardiovascular System in Polycystic Ovary Syndrome
Diabetes Care, March 1, 2007; 30(3): 471 - 478.
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J. Appl. Physiol.Home page
E. C. Tuday, J. V. Meck, D. Nyhan, A. A. Shoukas, and D. E. Berkowitz
Microgravity-induced changes in aortic stiffness and their role in orthostatic intolerance
J Appl Physiol, March 1, 2007; 102(3): 853 - 858.
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Clin Med ResHome page
A. R. Khoshdel, S. L. Carney, B. R. Nair, and A. Gillies
Better Management of Cardiovascular Diseases by Pulse Wave Velocity: Combining Clinical Practice with Clinical Research using Evidence-Based Medicine
Clin. Med. Res., March 1, 2007; 5(1): 45 - 52.
[Abstract] [Full Text] [PDF]


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ANGIOLOGYHome page
A. S. Fjeldstad, C. Fjeldstad, L. S. Acree, K. J. Nickel, P. S. Montgomery, P. C. Comp, T. L. Whitsett, and A. W. Gardner
The Relationship Between Arterial Elasticity and Metabolic Syndrome Features
Angiology, February 1, 2007; 58(1): 5 - 10.
[Abstract] [PDF]


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ANGIOLOGYHome page
A. D. Achimastos, S. P. Efstathiou, T. Christoforatos, T. N. Panagiotou, G. S. Stergiou, and T. D. Mountokalakis
Arterial Stiffness: Determinants and Relationship to the Metabolic Syndrome
Angiology, February 1, 2007; 58(1): 11 - 20.
[Abstract] [PDF]


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QJMHome page
N.C. Edwards, R.P. Steeds, C.J. Ferro, and J.N. Townend
The treatment of coronary artery disease in patients with chronic kidney disease
QJM, November 1, 2006; 99(11): 723 - 736.
[Abstract] [Full Text] [PDF]


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HeartHome page
C Vlachopoulos, K Aznaouridis, and C Stefanadis
Clinical appraisal of arterial stiffness: the Argonauts in front of the Golden Fleece
Heart, November 1, 2006; 92(11): 1544 - 1550.
[Abstract] [Full Text] [PDF]


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HypertensionHome page
R. A. Payne and D. J. Webb
Arterial Blood Pressure and Stiffness in Hypertension: Is Arterial Structure Important?
Hypertension, September 1, 2006; 48(3): 366 - 367.
[Full Text] [PDF]


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CirculationHome page
R. S. Vasan
Biomarkers of Cardiovascular Disease: Molecular Basis and Practical Considerations
Circulation, May 16, 2006; 113(19): 2335 - 2362.
[Full Text] [PDF]


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HypertensionHome page
M. Iemitsu, S. Maeda, T. Otsuki, J. Sugawara, T. Tanabe, S. Jesmin, S. Kuno, R. Ajisaka, T. Miyauchi, and M. Matsuda
Polymorphism in Endothelin-Related Genes Limits Exercise-Induced Decreases in Arterial Stiffness in Older Subjects
Hypertension, May 1, 2006; 47(5): 928 - 936.
[Abstract] [Full Text] [PDF]


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Eur J EndocrinolHome page
S. G. Kim, O. H. Ryu, H. Y. Kim, K. W. Lee, J. A Seo, N. H. Kim, K. M. Choi, J. Lee, S. H. Baik, and D. S. Choi
Effect of rosiglitazone on plasma adiponectin levels and arterial stiffness in subjects with prediabetes or non-diabetic metabolic syndrome.
Eur. J. Endocrinol., March 1, 2006; 154(3): 433 - 440.
[Abstract] [Full Text] [PDF]


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Exp PhysiolHome page
K. Hayashi, M. Miyachi, N. Seno, K. Takahashi, K. Yamazaki, J. Sugawara, T. Yokoi, S. Onodera, and N. Mesaki
Variations in carotid arterial compliance during the menstrual cycle in young women
Exp Physiol, March 1, 2006; 91(2): 465 - 472.
[Abstract] [Full Text] [PDF]


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Am. J. Physiol. Heart Circ. Physiol.Home page
R. M. Fitch, J. C. Rutledge, Y.-X. Wang, A. F. Powers, J.-L. Tseng, T. Clary, and G. M. Rubanyi
Synergistic effect of angiotensin II and nitric oxide synthase inhibitor in increasing aortic stiffness in mice
Am J Physiol Heart Circ Physiol, March 1, 2006; 290(3): H1190 - H1198.
[Abstract] [Full Text] [PDF]


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HypertensionHome page
E. Dolan, L. Thijs, Y. Li, N. Atkins, P. McCormack, S. McClory, E. O'Brien, J. A. Staessen, and A. V. Stanton
Ambulatory Arterial Stiffness Index as a Predictor of Cardiovascular Mortality in the Dublin Outcome Study
Hypertension, March 1, 2006; 47(3): 365 - 370.
[Abstract] [Full Text] [PDF]


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Eur Heart JHome page
K. K. Naka, A. C. Tweddel, S. N. Doshi, J. Goodfellow, and A. H. Henderson
Flow-mediated changes in pulse wave velocity: a new clinical measure of endothelial function
Eur. Heart J., February 1, 2006; 27(3): 302 - 309.
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Am. J. Physiol. Heart Circ. Physiol.Home page
J. E. Davies, Z. I. Whinnett, D. P. Francis, K. Willson, R. A. Foale, I. S. Malik, A. D. Hughes, K. H. Parker, and J. Mayet
Use of simultaneous pressure and velocity measurements to estimate arterial wave speed at a single site in humans
Am J Physiol Heart Circ Physiol, February 1, 2006; 290(2): H878 - H885.
[Abstract] [Full Text] [PDF]


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HypertensionHome page
S. A. Bahous, A. Stephan, J. Blacher, and M. E. Safar
Aortic Stiffness, Living Donors, and Renal Transplantation
Hypertension, February 1, 2006; 47(2): 216 - 221.
[Abstract] [Full Text] [PDF]


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J. Clin. Endocrinol. Metab.Home page
T. Nagasaki, M. Inaba, Y. Kumeda, Y. Hiura, K. Shirakawa, S. Yamada, Y. Henmi, E. Ishimura, and Y. Nishizawa
Increased Pulse Wave Velocity in Subclinical Hypothyroidism
J. Clin. Endocrinol. Metab., January 1, 2006; 91(1): 154 - 158.
[Abstract] [Full Text] [PDF]


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LupusHome page
T K Tso, W-N Huang, H-Y Huang, and C-K Chang
Association of brachial-ankle pulse wave velocity with cardiovascular risk factors in systemic lupus erythematosus
Lupus, November 1, 2005; 14(11): 878 - 883.
[Abstract] [PDF]


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J Am Coll CardiolHome page
C. M. McEniery, Yasmin, I. R. Hall, A. Qasem, I. B. Wilkinson, J. R. Cockcroft, and on behalf of the ACCT Investigators
Normal Vascular Aging: Differential Effects on Wave Reflection and Aortic Pulse Wave Velocity: The Anglo-Cardiff Collaborative Trial (ACCT)
J. Am. Coll. Cardiol., November 1, 2005; 46(9): 1753 - 1760.
[Abstract] [Full Text] [PDF]


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CirculationHome page
C. Vlachopoulos, I. Dima, K. Aznaouridis, C. Vasiliadou, N. Ioakeimidis, C. Aggeli, M. Toutouza, and C. Stefanadis
Acute Systemic Inflammation Increases Arterial Stiffness and Decreases Wave Reflections in Healthy Individuals
Circulation, October 4, 2005; 112(14): 2193 - 2200.
[Abstract] [Full Text] [PDF]


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J. Clin. Endocrinol. Metab.Home page
C. Meyer, B. P. McGrath, and H. J. Teede
Overweight Women with Polycystic Ovary Syndrome Have Evidence of Subclinical Cardiovascular Disease
J. Clin. Endocrinol. Metab., October 1, 2005; 90(10): 5711 - 5716.
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Am. J. Respir. Crit. Care Med.Home page
L. F. Drager, L. A. Bortolotto, M. C. Lorenzi, A. C. Figueiredo, E. M. Krieger, and G. Lorenzi-Filho
Early Signs of Atherosclerosis in Obstructive Sleep Apnea
Am. J. Respir. Crit. Care Med., September 1, 2005; 172(5): 613 - 618.
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J. Clin. Endocrinol. Metab.Home page
C. Meyer, B. P. McGrath, J. Cameron, D. Kotsopoulos, and H. J. Teede
Vascular Dysfunction and Metabolic Parameters in Polycystic Ovary Syndrome
J. Clin. Endocrinol. Metab., August 1, 2005; 90(8): 4630 - 4635.
[Abstract] [Full Text] [PDF]


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HypertensionHome page
V. Gaillard, D. Casellas, C. Seguin-Devaux, H. Schohn, M. Dauca, J. Atkinson, and I. Lartaud
Pioglitazone Improves Aortic Wall Elasticity in a Rat Model of Elastocalcinotic Arteriosclerosis
Hypertension, August 1, 2005; 46(2): 372 - 379.
[Abstract] [Full Text] [PDF]


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Am. J. Clin. Nutr.Home page
C. Vlachopoulos, D. Panagiotakos, N. Ioakeimidis, I. Dima, and C. Stefanadis
Chronic coffee consumption has a detrimental effect on aortic stiffness and wave reflections
Am. J. Clinical Nutrition, June 1, 2005; 81(6): 1307 - 1312.
[Abstract] [Full Text] [PDF]


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J. Med. Genet.Home page
N Gaukrodger, B M Mayosi, H Imrie, P Avery, M Baker, J M C Connell, H Watkins, M Farrall, and B Keavney
A rare variant of the leptin gene has large effects on blood pressure and carotid intima-medial thickness: a study of 1428 individuals in 248 families
J. Med. Genet., June 1, 2005; 42(6): 474 - 478.
[Abstract] [Full Text] [PDF]


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Eur Heart JHome page
R. S. Reneman, J. M. Meinders, and A. P.G. Hoeks
Non-invasive ultrasound in arterial wall dynamics in humans: what have we learned and what remains to be solved
Eur. Heart J., May 2, 2005; 26(10): 960 - 966.
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J. Clin. Endocrinol. Metab.Home page
D. M. Sengstock, P. V. Vaitkevicius, and M. A. Supiano
Arterial Stiffness Is Related to Insulin Resistance in Nondiabetic Hypertensive Older Adults
J. Clin. Endocrinol. Metab., May 1, 2005; 90(5): 2823 - 2827.
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Cardiovasc ResHome page
H. H. Dao, R. Essalihi, C. Bouvet, and P. Moreau
Evolution and modulation of age-related medial elastocalcinosis: Impact on large artery stiffness and isolated systolic hypertension
Cardiovasc Res, May 1, 2005; 66(2): 307 - 317.
[Abstract] [Full Text] [PDF]


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J Am Coll CardiolHome page
P. Milliez, X. Girerd, P.-F. Plouin, J. Blacher, M. E. Safar, and J.-J. Mourad
Evidence for an increased rate of cardiovascular events in patients with primary aldosteronism
J. Am. Coll. Cardiol., April 19, 2005; 45(8): 1243 - 1248.
[Abstract] [Full Text] [PDF]


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Nephrol Dial TransplantHome page
A. Yildiz, E. Memisoglu, H. Oflaz, H. Yazici, H. Pusuroglu, V. Akkaya, F. Erzengin, and S. Tepe
Atherosclerosis and vascular calcification are independent predictors of left ventricular hypertrophy in chronic haemodialysis patients
Nephrol. Dial. Transplant., April 1, 2005; 20(4): 760 - 767.
[Abstract] [Full Text] [PDF]


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Physiol. Rev.Home page
P. Meneton, X. Jeunemaitre, H. E. de Wardener, and G. A. Macgregor
Links Between Dietary Salt Intake, Renal Salt Handling, Blood Pressure, and Cardiovascular Diseases
Physiol Rev, April 1, 2005; 85(2): 679 - 715.
[Abstract] [Full Text] [PDF]


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Eur J EndocrinolHome page
S G Kim, H Y Kim, J A Seo, K W Lee, J H Oh, N H Kim, K M Choi, S H Baik, and D S Choi
Relationship between serum adiponectin concentration, pulse wave velocity and nonalcoholic fatty liver disease
Eur. J. Endocrinol., February 1, 2005; 152(2): 225 - 231.
[Abstract] [Full Text] [PDF]


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HypertensionHome page
R. P. Wildman, G. N. Farhat, A. S. Patel, R. H. Mackey, S. Brockwell, T. Thompson, and K. Sutton-Tyrrell
Weight Change Is Associated With Change in Arterial Stiffness Among Healthy Young Adults
Hypertension, February 1, 2005; 45(2): 187 - 192.
[Abstract] [Full Text] [PDF]


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HypertensionHome page
D. Lemogoum, L. Van Bortel, B. Najem, A. Dzudie, C. Teutcha, E. Madu, M. Leeman, J.-P. Degaute, and P. van de Borne
Arterial Stiffness and Wave Reflections in Patients With Sickle Cell Disease
Hypertension, December 1, 2004; 44(6): 924 - 929.
[Abstract] [Full Text] [PDF]


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J Am Coll CardiolHome page
C. Vlachopoulos, F. Kosmopoulou, D. Panagiotakos, N. Ioakeimidis, N. Alexopoulos, C. Pitsavos, and C. Stefanadis
Smoking and caffeine have a synergistic detrimental effect on aortic stiffness and wave reflections
J. Am. Coll. Cardiol., November 2, 2004; 44(9): 1911 - 1917.
[Abstract] [Full Text] [PDF]


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CirculationHome page
M. Miyachi, H. Kawano, J. Sugawara, K. Takahashi, K. Hayashi, K. Yamazaki, I. Tabata, and H. Tanaka
Unfavorable Effects of Resistance Training on Central Arterial Compliance: A Randomized Intervention Study
Circulation, November 2, 2004; 110(18): 2858 - 2863.
[Abstract] [Full Text] [PDF]


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VASC ENDOVASCULAR SURGHome page
G. Saliashvili, W. W. Davis, M. T. Harris, N.-A. Le, and W. V. Brown
Simvastatin Improved Arterial Compliance in High-Risk Patients
Vascular and Endovascular Surgery, November 1, 2004; 38(6): 519 - 523.
[Abstract] [PDF]


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Journal of Renin-Angiotensin-Aldosterone SystemHome page
A. Mahmud and J. Feely
Review: Arterial stiffness and the renin-angiotensin-aldosterone system
Journal of Renin-Angiotensin-Aldosterone System, September 1, 2004; 5(3): 102 - 108.
[Abstract] [PDF]


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Am. J. Physiol. Heart Circ. Physiol.Home page
M. Schmitt, A. Qasem, C. McEniery, I. B. Wilkinson, V. Tatarinoff, K. Noble, J. Klemes, N. Payne, M. P. Frenneaux, J. Cockcroft, et al.
Role of natriuretic peptides in regulation of conduit artery distensibility
Am J Physiol Heart Circ Physiol, September 1, 2004; 287(3): H1167 - H1171.
[Abstract] [Full Text] [PDF]


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HypertensionHome page
C. M. McEniery, M. Schmitt, A. Qasem, D. J. Webb, A. P. Avolio, I. B. Wilkinson, and J. R. Cockcroft
Nebivolol Increases Arterial Distensibility In Vivo
Hypertension, September 1, 2004; 44(3): 305 - 310.
[Abstract] [Full Text] [PDF]


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Am. J. Respir. Crit. Care Med.Home page
D. K. Ng, K.-L. Kwok, D. Herrington, E. Benjamin, F. J. Nieto, S. Redline, J. Robbins, M. Ip, H.-F. Tse, B. Lam, et al.
Endothelial Dysfunction and Sleep Apnea
Am. J. Respir. Crit. Care Med., July 15, 2004; 170(2): 197 - 198.
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CirculationHome page
J. N. Cohn, A. A. Quyyumi, N. K. Hollenberg, and K. A. Jamerson
Surrogate Markers for Cardiovascular Disease: Functional Markers
Circulation, June 29, 2004; 109(25_suppl_1): IV-31 - IV-46.
[Full Text] [PDF]


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Arterioscler. Thromb. Vasc. Bio.Home page
Yasmin, C. M. McEniery, S. Wallace, I. S. Mackenzie, J. R. Cockcroft, and I. B. Wilkinson
C-Reactive Protein Is Associated With Arterial Stiffness in Apparently Healthy Individuals
Arterioscler Thromb Vasc Biol, May 1, 2004; 24(5): 969 - 974.
[Abstract] [Full Text]


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HypertensionHome page
M. E. Safar, G. M London, and G. E. Plante
Arterial Stiffness and Kidney Function
Hypertension, February 1, 2004; 43(2): 163 - 168.
[Abstract] [Full Text] [PDF]


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CirculationHome page
T. Weber, J. Auer, M. F. O'Rourke, E. Kvas, E. Lassnig, R. Berent, and B. Eber
Arterial Stiffness, Wave Reflections, and the Risk of Coronary Artery Disease
Circulation, January 20, 2004; 109(2): 184 - 189.
[Abstract] [Full Text] [PDF]


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J Am Coll CardiolHome page
Y.-f. Cheung, T.-c. Yung, S. C. F. Tam, M. H. K. Ho, and A. K. T. Chau
Novel and traditional cardiovascular risk factors in children after Kawasaki disease: Implications for premature atherosclerosis
J. Am. Coll. Cardiol., January 7, 2004; 43(1): 120 - 124.
[Abstract] [Full Text] [PDF]


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HeartHome page
M Eren, S Gorgulu, N Uslu, S Celik, B Dagdeviren, and T Tezel
Relation between aortic stiffness and left ventricular diastolic function in patients with hypertension, diabetes, or both
Heart, January 1, 2004; 90(1): 37 - 43.
[Abstract] [Full Text] [PDF]


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J Am Coll CardiolHome page
C. M. McEniery, A. Qasem, M. Schmitt, A. P. Avolio, J. R. Cockcroft, and I. B. Wilkinson
Endothelin-1 regulates arterial pulse wave velocity in vivo
J. Am. Coll. Cardiol., December 3, 2003; 42(11): 1975 - 1981.
[Abstract] [Full Text] [PDF]


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Vasc MedHome page
C. Vlachopoulos, K. Hirata, and M. F O'Rourke
Effect of sildenafil on arterial stiffness and wave reflection
Vascular Medicine, November 1, 2003; 8(4): 243 - 248.
[Abstract] [PDF]


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HypertensionHome page
A. D. Stewart, S. C. Millasseau, M. T. Kearney, J. M. Ritter, and P. J. Chowienczyk
Effects of Inhibition of Basal Nitric Oxide Synthesis on Carotid-Femoral Pulse Wave Velocity and Augmentation Index in Humans
Hypertension, November 1, 2003; 42(5): 915 - 918.
[Abstract] [Full Text] [PDF]


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CirculationHome page
S. Durier, C. Fassot, S. Laurent, P. Boutouyrie, J.-P. Couetil, E. Fine, P. Lacolley, V. J. Dzau, and R. E. Pratt
Physiological Genomics of Human Arteries: Quantitative Relationship Between Gene Expression and Arterial Stiffness
Circulation, October 14, 2003; 108(15): 1845 - 1851.
[Abstract] [Full Text] [PDF]


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ANGIOLOGYHome page
N. Nakanishi, K. Suzuki, and K. Tatara
Clustered Features of the Metabolic Syndrome and the Risk for Increased Aortic Pulse Wave Velocity in Middle-aged Japanese Men
Angiology, September 1, 2003; 54(5): 551 - 559.
[Abstract] [PDF]


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HypertensionHome page
C. O'Sullivan, J. Duggan, S. Lyons, J. Thornton, M. Lee, and E. O'Brien
Hypertensive Target-Organ Damage in the Very Elderly
Hypertension, August 1, 2003; 42(2): 130 - 135.
[Abstract] [Full Text] [PDF]


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Diabetes CareHome page
J. D. Cameron, C. J. Bulpitt, E. S. Pinto, and C. Rajkumar
The Aging of Elastic and Muscular Arteries: A comparison of diabetic and nondiabetic subjects
Diabetes Care, July 1, 2003; 26(7): 2133 - 2138.
[Abstract] [Full Text] [PDF]


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StrokeHome page
A.F.C. Schut, J.A.M.J.L. Janssen, J. Deinum, J.M. Vergeer, A. Hofman, S.W.J. Lamberts, B.A. Oostra, H.A.P. Pols, J.C.M. Witteman, and C.M. van Duijn
Polymorphism in the Promoter Region of the Insulin-like Growth Factor I Gene Is Related to Carotid Intima-Media Thickness and Aortic Pulse Wave Velocity in Subjects With Hypertension
Stroke, July 1, 2003; 34(7): 1623 - 1627.
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J. Clin. Endocrinol. Metab.Home page
K.-i. Hirose, H. Tomiyama, R. Okazaki, T. Arai, Y. Koji, G. Zaydun, S. Hori, and A. Yamashina
Increased Pulse Wave Velocity Associated with Reduced Calcaneal Quantitative Osteo-sono Index: Possible Relationship Between Atherosclerosis and Osteopenia
J. Clin. Endocrinol. Metab., June 1, 2003; 88(6): 2573 - 2578.
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ChestHome page
K. L. Kwok, D. K. K. Ng, and Y. F. Cheung
BP and Arterial Distensibility in Children With Primary Snoring
Chest, May 1, 2003; 123(5): 1561 - 1566.
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HeartHome page
M Kidawa, M Krzeminska-Pakula, J Z Peruga, and J D Kasprzak
Arterial dysfunction in syndrome X: results of arterial reactivity and pulse wave propagation tests
Heart, April 1, 2003; 89(4): 422 - 426.
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Arterioscler. Thromb. Vasc. Bio.Home page
J. J. Oliver and D. J. Webb
Noninvasive Assessment of Arterial Stiffness and Risk of Atherosclerotic Events
Arterioscler Thromb Vasc Biol, April 1, 2003; 23(4): 554 - 566.
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Diabetes CareHome page
H. Ohnishi, S. Saitoh, S. Takagi, J.-i. Ohata, T. Isobe, Y. Kikuchi, H. Takeuchi, and K. Shimamoto
Pulse Wave Velocity as an Indicator of Atherosclerosis in Impaired Fasting Glucose: The Tanno and Sobetsu Study
Diabetes Care, February 1, 2003; 26(2): 437 - 440.
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CirculationHome page
E. G. Lakatta and D. Levy
Arterial and Cardiac Aging: Major Shareholders in Cardiovascular Disease Enterprises: Part I: Aging Arteries: A "Set Up" for Vascular Disease
Circulation, January 7, 2003; 107(1): 139 - 146.
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HypertensionHome page
A. Mahmud and J. Feely
Effect of Smoking on Arterial Stiffness and Pulse Pressure Amplification
Hypertension, January 1, 2003; 41(1): 183 - 187.
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HeartHome page
J Amar, B Chamontin, J Ferrieres, N Danchin, O Grenier, C Cantet, and J-P Cambou
Hypertension control at hospital discharge after acute coronary event: influence on cardiovascular prognosis--the PREVENIR study
Heart, December 1, 2002; 88(6): 587 - 591.
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Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
D. M. Tham, B. Martin-McNulty, Y.-X. Wang, V. Da Cunha, D. W. Wilson, C. N. Athanassious, A. F. Powers, M. E. Sullivan, and J. C. Rutledge
Angiotensin II injures the arterial wall causing increased aortic stiffening in apolipoprotein E-deficient mice
Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2002; 283(6): R1442 - R1449.
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HypertensionHome page
C. S. Hayward, A. P. Avolio, M. F. O'Rourke, P. Lantelme, C. Mestre, M. Lievre, A. Gressard, and H. Milon
Arterial Pulse Wave Velocity and Heart Rate * Response: Heart Rate and Pulse Wave Velocity
Hypertension, December 1, 2002; e9(6): .
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CirculationHome page
Y.F. Cheung, G. C.F. Chan, and S.Y. Ha
Arterial Stiffness and Endothelial Function in Patients With {beta}-Thalassemia Major
Circulation, November 12, 2002; 106(20): 2561 - 2566.
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CirculationHome page
A. Singhal, I. S. Farooqi, T. J. Cole, S. O'Rahilly, M. Fewtrell, M. Kattenhorn, A. Lucas, and J. Deanfield
Influence of Leptin on Arterial Distensibility: A Novel Link Between Obesity and Cardiovascular Disease?
Circulation, October 8, 2002; 106(15): 1919 - 1924.
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J. Clin. Endocrinol. Metab.Home page
K. Obuobie, J. Smith, L. M. Evans, R. John, J. S. Davies, and J. H. Lazarus
Increased Central Arterial Stiffness in Hypothyroidism
J. Clin. Endocrinol. Metab., October 1, 2002; 87(10): 4662 - 4666.
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Arch. Dis. Child.Home page
Y F Cheung, P A Brogan, C B Pilla, M J Dillon, and A N Redington
Arterial distensibility in children and teenagers: normal evolution and the effect of childhood vasculitis
Arch. Dis. Child., October 1, 2002; 87(4): 348 - 351.
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