(Hypertension. 2001;38:434.)
© 2001 American Heart Association, Inc.
Scientific Contributions |
Arterial Wave Reflections and Survival in End-Stage Renal Failure
Service d’Hémodialyse, Hôpital F.H. Manhès, Fleury-Mérogis (G.M.L., B.P., A.P.G., S.J.M.), Ste-Geneviève-des-Bois, and Service de Médecine Interne, Hôpital Broussais (J.B., M.E.S.), Paris, France.
Correspondence to Dr G.M. London, Hôpital F.H. Manhès, 8, Grande Rue, Fleury-Mérogis, 91712, Ste-Geneviève-des-Bois Cedex, France. E-mail glondon{at}club-internet.fr
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Abstract |
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Abstract—— The increased effect of arterial wave reflections on central arteries like the common carotid artery seen in end-stage renal failure (ESRF) patients favors myocardial hypertrophy and oxygen consumption and alters coronary blood flow distribution. Nevertheless, the impact of wave reflection on the outcome and end points such as mortality remains to be demonstrated. One hundred eighty ESRF patients (age, 54±16 years) were monitored for 52±36 months (mean±SD). Seventy deaths, including 40 cardiovascular (CV) and 30 non-CV events, occurred. At entry, patients, in addition to standard clinical and biochemical analyses, underwent aortic pulse wave velocity measurement and determination of arterial wave reflexion by applanation tonometry on the common carotid artery that was expressed as augmentation index. Cox analyses demonstrated that predictors of all-cause and CV mortality were age, aortic pulse wave velocity, low diastolic blood pressure, preexisting CV disease, and increased augmentation index, whereas the prescription of an ACE inhibitor had a favorable effect on survival. After adjustment for all confounding factors, the risk ratio for each 10% increase in augmentation index was 1.51 (95% confidence interval, 1.23 to 1.86; P<0.0001) for all-cause mortality and 1.48 (95% confidence interval, 1.16 to 1.90; P<0.0001) for CV mortality. These results provide the first direct evidence that in ESRF patients increased effect of arterial wave reflections is an independent predictor of all-cause and CV mortality.
Key Words: end-stage renal failure • aortic stiffness • mortality • arterial wave reflection
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Introduction |
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The results of several studies support the evidence that pulse pressure (PP) is an independent predictor of cardiovascular (CV) risk in general population.1–4 PP is determined by the interaction of cardiac factors (stroke volume and ejection time) and vascular factors (arterial stiffness and arterial wave reflections).5–7 Epidemiological studies have shown that PP is increased in end-stage renal failure (ESRF) patients in association with increased arterial stiffness of large elastic-type arteries and pronounced effect of arterial wave reflections.7–9 A recent study demonstrated that aortic stiffening, determined by measurement of aortic pulse wave velocity (PWV), was an independent predictor of all-cause and CV mortality of ESRF patients.10 The impact of wave reflections on the outcome and decisive end points like mortality remains to be demonstrated. The purpose of this prospective study was to analyze the impact of early wave reflection on the outcome of this high-risk population. The results indicate that independent of arterial stiffness, blood pressure (BP), and the usual CV risk factors, a marked effect of wave reflections on central arteries is a significant predictor of ESRF patient mortality.
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Methods |
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Patients
The recruitment period extended from January 1990 to September 1999, and follow-up ended May 31, 2000. Patients were eligible when they had been on hemodialysis (HD) for
3 months and they agreed to participate in the study, which was approved by our institutional board. One hundred eighty patients were included. Patients who underwent renal transplantation and patients who moved were censored on the day of transplantation or departure. All but 17 patients were white, 60% were men, 10% had diabetes mellitus, and 34% had a prior history of CV disease (CVD). During follow-up, all patients were hemodialyzed with the same technique.7 One hundred thirty-five patients received erythropoietin. At inclusion, 52% of the patients were receiving antihypertensive therapy, which was continued during follow-up. Patients were assigned to receive an ACE inhibitor, calcium antagonists, or a beta-blocker alone or in combination.
Data Collection
Data on mortality were obtained for the entire cohort. Information included personal and family histories, smoking habits, and history of CVD. Blood chemistry analyses were repeated monthly. Heart rate was determined from the ECG. BP was measured with a mercury sphygmomanometer and a cuff of appropriate size. Phases I and V of the Korotkoff sounds were taken as the systolic BP (SBP) and diastolic BP (DBP), respectively. Mean BP (MBP) was calculated as follows: MBP=DBP+[(SBP-DBP)/3]. PP was defined as follows: PP=SBP-DBP. Echocardiography (Hewlett-Packard Sonos 100 with a 2.25-MHz probe) was analyzed according to American Society of Echocardiography criteria.11
Aortic PWV (foot-to-foot method) was determined from simultaneous Doppler flow tracings taken from the common carotid artery (CCA) and the femoral artery in the groin.7,8,12 The CCA pressure waveform was recorded noninvasively with a high-fidelity strain-gauge transducer (SPT-301, Millar Instruments)6,13,14 and analyzed according to the method of Murgo et al15 (Figure 1). The augmented pressure, 
P, was determined as the height of the late systolic peak (ppk) above the inflection pi (P=ppk-pi), and the ratio of P to PP defines the augmentation index (AIX, in percent; the effect of arterial wave reflections on BP in CCA). tp represents the travel time (milliseconds) of the pulse wave to peripheral reflecting sites and back. Left ventricular ejection time (LVET) was determined from the foot of the pressure wave to the diastolic incisura. AIX was averaged from 10 to 12 successive waves; its spontaneous variability was 3.1±1%.
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Statistical Analyses
The outcome studied was all-cause and CV mortality. Factors prognostic of survival were identified with the Cox model. The proportional-hazards assumptions were satisfied. Adjusted hazards risk ratios (RRs) were calculated with all the potential prognostic variables. Ninety-five percent confidence intervals (95% CIs) for the RR were obtained as antilogarithm (ß±1.96SE). Survival was assessed by the Kaplan-Meier method and the log-rank test. The sensitivities, specificities, and optimal cutoff values for AIX were analyzed through the use of receiver-operating characteristic (ROC) curves.16 Data are expressed as mean±SD. ANOVA was used to compare normally distributed variables. Frequency differences were tested by the 
2 test. Gender (0=male; 1=female), history of CVD, ACE inhibitor use, ß-blocker use, and calcium blocker use were used as dummy variables (0=no; 1=yes). Reproducibility of the methods was defined by the British Standards Institution.17
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Results |
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Patient Characteristics
The characteristics of the entire cohort at the time of inclusion are shown in Table 1. The age at inclusion was 54±16 years (range, 14 to 88 years), and patients were on HD for 59±64 months (range, 3 to 260 months). PP was positively correlated with stroke volume, LVET, aortic PWV, and AIX (Table 2). In a multiple regression analysis, AIX was correlated with body height (P=0.016), LVET (P<0.0001), aortic PWV (P=0.038), age (P<0.01), gender (P=0.013), and MBP (P<0.001) (adjusted r2=0.488 for the multiple regression).
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Outcome and Prognostic Impact of AIX
The duration of the follow-up was 52±36 months (range, 3 to 122 months). During the follow-up period, 40 CV and 30 non-CV deaths were recorded. According to the Cox analysis using a model including PP, the only independent covariates retained for all-cause mortality were age (P<0.001) (positive influence) and ACE inhibitor prescription (P<0.001) (negative influence), whereas PP was not significantly associated (P=0.0932). According to the Cox analysis using a model including PP, the only independent covariates retained for CV mortality were age (P<0.001) and PP (P=0.012) (positive influence) and ACE inhibitor prescription (P<0.01) (negative influence) (2 for the model 61.9; P<0.00001; pseudo-r2=0.3716).
Cox analyses in which PP was replaced by its determinants, aortic PWV and AIX, are shown in Table 3. The significant covariates retained by the model for all-cause mortality were age, aortic PWV, and AIX (positive association) and DBP and ACE inhibitor prescription alone or in combination (negative association) (Table 3). The significant covariates retained by the model for CV mortality were AIX, aortic PWV, and history of CVD (positive association) and ACE inhibitor prescription alone or in combination (negative association) (Table 3). The adjusted RR for AIX (10% increase) was 1.51 (95% CI, 1.23 to 1.86) for all-cause mortality and 1.48 (95% CI, 1.16 to 1.90) for CV mortality. Stroke volume was not prognostically associated with outcomes (z value, 0.67; P=0.504).
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Other factors such as gender, heart rate, smoking, duration of HD, and blood chemistry analyses were not significant. Figure 2 shows the probabilities of all-cause and CV survival as a function of the AIX quartiles. Comparisons between survival curves were highly significant. According to the ROC curve analyses for AIX, the best cutoff value of AIX for all-cause mortality was 24.5%; its sensitivity was 83%, its specificity 67%, and ROC area under the curve (AUC) 0.76±0.04. The best cutoff value of AIX for CV mortality was 25%; its sensitivity was 80%, its specificity 70%, and AUC 0.74±0.05. The best cutoff value of PWV was 11.5 m/s for all-cause mortality (specificity, 80%; sensitivity, 74%; AUC, 0.82±0.03) and 11.3 m/s for CV mortality (specificity, 79%; sensitivity, 64%; AUC, 0.76±0.04). The ROC AUCs were not statistically different between AIX and PWV.
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The data (Table 3) indicate that AIX is an independent determinant of mortality; however, regression analysis showed this factor to be correlated with PWV. Thus, one could wonder what the determination of arterial wave reflection adds to the predictive role of aortic PWV. For this reason, we performed a complementary analysis including only ESRF patients with normal aortic PWV <11.0 m/s. (A previous study has shown that the significant RR for all-cause and CV mortality was associated with aortic PWV >12 m/s.10) Of 180 patients, 83 fulfilled this criterion (Table 4). They had been on HD for 56±63 months (range, 3 to 252 months), and the mean follow-up was 56±37 months. Forty-three were men; 40 were women. Twelve patients (14%) had a history of CVD. During follow-up, 10 deaths were recorded, 7 CV and 3 non-CV. According to the Cox analyses, the only significant covariates retained for CV (and all-cause) mortality were age and AIX, with borderline significance for ACE inhibitor prescription (Table 5).
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Discussion |
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Arterial disease develops rapidly in ESRF patients and is responsible for the high incidence of CV complications.18 Large arteries in ESRF patients are characterized by dilation, wall thickening, and a high frequency of calcified atherosclerotic plaques.7,19 The principal functional alterations are increased arterial stiffness, incremental elastic modulus, and a marked effect of arterial wave reflections on central arteries such as the CCA.6–9 Results of earlier studies showed that increased aortic stiffness and incremental elastic modulus were independent predictors of mortality in ESRF patients undergoing HD.10,20 In this study, arterial wave reflections were a major predictor of mortality in ESRF patients on HD. The impact was independent of other factors known to affect the outcome of uremic patients, namely age, prior CVD, anemia, albuminemia, and aortic PWV. The increased effect of wave reflections on the aorta and central arteries causes increased pressure during systole and decreased DBP and/or diastolic tension-time index.5,21 These alterations increase LV oxygen requirements and predispose to LV hypertrophy. The reduced DBP contributes to modifications of coronary perfusion with relative subendocardial ischemia.5,7,21–24 An important result of the present study concerns the fact that the association of mortality with wave reflections was independent of arterial stiffening estimated as aortic PWV.
PP has previously been shown to be an independent CV risk factor.5 In this study, PP was associated with CV mortality. As shown in Table 2, PP is a surrogate marker that is dependent on cardiac and vascular factors, including stroke volume, LVET, aortic stiffness, and intensity of wave reflections. When the major determinants of PP, mainly aortic PWV and AIX, were included in the Cox models, these factors were predictive of outcome, with a predictive power superior to that of PP alone.
AIX is frequently and simplistically considered to be an index of arterial stiffness. AIX depends on many factors, including age, PWV, traveling distance of pressure waves (body height), LVET, and reflective properties of the arterial system. Arterial stiffening increases PWV and influences the transit time of pressure waves (tp in Figure 1).6 By increasing PWV, arterial stiffening reduces the tp from the peripheral reflection sites toward central arteries, thereby altering the timing of incident and reflected waves. Although arterial stiffening is responsible for the acceleration of the pressure wave transmission, the intensity of wave reflection is dependent on the reflective properties of the vascular tree that could be altered independently of arterial stiffening.25 This independence is shown by the persistent association of wave reflections as a predictor of mortality of patients with normal PWV (Tables 4 and 5). Arterial stiffening, in addition to its own role in CV alterations, enhances the expression of abnormal reflective properties of the vasculature in the aorta and central arteries by favoring an early return of reflected waves.
The peripheral "reflectance" is influenced by physical properties, vasomotor tone, and the number of smaller resistive arteries and branch points.24,25 In this study, we did not evaluate the intensity of wave reflections at their reflective site, but several abnormalities in the microcirculation of ESRF patients have been reported in the literature, including rarefaction of vessels, increased ratios of wall to lumen of small arteries, calcifications of small arterioles, and decreased endothelium-mediated vasodilation.26–28 In ESRF patients, the pathological alterations of these smaller arteries may therefore contribute to increased "reflectance." Whether the prognosis and outcome associated with the pronounced effect of wave reflection are related to augmentation of late SBP in the central arteries or primarily to alteration of microcirculation remains to be determined.
The results presented here show that prolonged survival was associated with an ACE inhibitor used as an antihypertensive agent. Prescription of ß-blocker and/or dihydropyridine calcium blocker had no direct relationship with outcome. The association between survival and ACE inhibitor prescription (Table 3) must be interpreted cautiously, because the study was not designed to compare the effect of different antihypertensive drugs on survival as such and the regimen was influenced by drug tolerance and the optimal effect on BP. Studies on high-risk populations have shown that ACE inhibitors have a favorable prognostic effect, reducing death rates and CV complications.29 The present findings suggest that ACE inhibitors can have a similar favorable effect on ESRF patients, but a specifically designed, prospective, therapeutic trial is needed to confirm this idea.
The ability to generalize the results of this study may be limited because of the characteristics of ESRF patients. Indeed, the CV morbidity and mortality in these patients are much higher than in nonuremic and general populations. The second limitation is that the relationship between mortality and AIX does not imply direct causation. To clarify the causality of the association between wave reflections and mortality or morbidity, the effect of "interventions" aimed at reducing the amplitude of wave reflections will have to be examined.
In conclusion, the results presented herein indicate that an increased effect of wave reflections on central arteries is a strong and independent predictor of mortality of ESRF patients on HD. The effect of wave reflections is dissociated from the changes of aortic stiffness as expressed by PWV, and the significance of wave reflections cannot be confused with that of stiffness. Elucidating the mechanisms at work between arterial wave reflections and mortality in this population necessitates further studies, including direct evaluation of reflective properties30 of the arterial tree and the alterations responsible for this abnormality.
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Acknowledgments |
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This study was supported by Groupe d’ Etude de la Physiopathologie de l’Insuffisance Renale.
Received January 18, 2001; first decision February 19, 2001; accepted March 1, 2001.
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References |
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S. Munir, A. Guilcher, T. Kamalesh, B. Clapp, S. Redwood, M. Marber, and P. Chowienczyk Peripheral Augmentation Index Defines the Relationship Between Central and Peripheral Pulse Pressure Hypertension, January 1, 2008; 51(1): 112 - 118. [Abstract] [Full Text] [PDF]
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 M. F. O'Rourke Arterial aging: pathophysiological principles Vascular Medicine, November 1, 2007; 12(4): 329 - 341. [Abstract] [PDF]
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 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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 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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F. Verbeke, W. Van Biesen, P. Peeters, L. M. Van Bortel, and R. C. Vanholder Arterial stiffness and wave reflections in renal transplant recipients Nephrol. Dial. Transplant., October 1, 2007; 22(10): 3021 - 3027. [Abstract] [Full Text] [PDF]
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M. Crilly, C. Coch, M. Bruce, H. Clark, and D. Williams Indices of cardiovascular function derived from peripheral pulse wave analysis using radial applanation tonometry: a measurement repeatability study Vascular Medicine, August 1, 2007; 12(3): 189 - 197. [Abstract] [PDF]
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 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. [Abstract] [Full Text] [PDF]
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E. Agabiti-Rosei, G. Mancia, M. F. O'Rourke, M. J. Roman, M. E. Safar, H. Smulyan, J.-G. Wang, I. B. Wilkinson, B. Williams, and C. Vlachopoulos Central Blood Pressure Measurements and Antihypertensive Therapy: A Consensus Document Hypertension, July 1, 2007; 50(1): 154 - 160. [Full Text] [PDF]
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N. A. Jatoi, P. Jerrard-Dunne, J. Feely, and A. Mahmud Impact of Smoking and Smoking Cessation on Arterial Stiffness and Aortic Wave Reflection in Hypertension Hypertension, May 1, 2007; 49(5): 981 - 985. [Abstract] [Full Text] [PDF]
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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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 S. Laurent, J. Cockcroft, L. Van Bortel, P. Boutouyrie, C. Giannattasio, D. Hayoz, B. Pannier, C. Vlachopoulos, I. Wilkinson, H. Struijker-Boudier, et al. Expert consensus document on arterial stiffness: methodological issues and clinical applications Eur. Heart J., November 1, 2006; 27(21): 2588 - 2605. [Abstract] [Full Text] [PDF]
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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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 S. Oren, I. Isakov, B. Golzman, J. Kogan, S. Turkot, R. Peled, and C. Yosefy The Influence of Smoking Cessation on Hemodynamics and Arterial Compliance Angiology, October 1, 2006; 57(5): 564 - 568. [Abstract] [PDF]
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A. Covic, N. Mardare, P. Gusbeth-Tatomir, O. Prisada, R. Sascau, and D. J. A. Goldsmith Arterial wave reflections and mortality in haemodialysis patients--only relevant in elderly, cardiovascularly compromised? Nephrol. Dial. Transplant., October 1, 2006; 21(10): 2859 - 2866. [Abstract] [Full Text] [PDF]
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P. Verdecchia, F. Angeli, and S. Taddei At the Beginning of Stiffening: Endothelial Dysfunction Meets "Pulsology" Hypertension, October 1, 2006; 48(4): 541 - 542. [Full Text] [PDF]
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 M. F. O'Rourke and J. B. Seward Central Arterial Pressure and Arterial Pressure Pulse: New Views Entering the Second Century After Korotkov Mayo Clin. Proc., August 1, 2006; 81(8): 1057 - 1068. [Abstract] [Full Text] [PDF]
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 C. Vlachopoulos, N. Alexopoulos, I. Dima, K. Aznaouridis, I. Andreadou, and C. Stefanadis Acute Effect of Black and Green Tea on Aortic Stiffness and Wave Reflections J. Am. Coll. Nutr., June 1, 2006; 25(3): 216 - 223. [Abstract] [Full Text] [PDF]
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J. E. Sharman, R. Lim, A. M. Qasem, J. S. Coombes, M. I. Burgess, J. Franco, P. Garrahy, I. B. Wilkinson, and T. H. Marwick Validation of a Generalized Transfer Function to Noninvasively Derive Central Blood Pressure During Exercise Hypertension, June 1, 2006; 47(6): 1203 - 1208. [Abstract] [Full Text] [PDF]
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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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M. M. H. Hermans, V. Brandenburg, M. Ketteler, J. P. Kooman, F. M. van der Sande, U. Gladziwa, P. L. Rensma, K. Bartelet, C. J. A. M. Konings, A. P. G. Hoeks, et al. Study on the relationship of serum fetuin-A concentration with aortic stiffness in patients on dialysis Nephrol. Dial. Transplant., May 1, 2006; 21(5): 1293 - 1299. [Abstract] [Full Text] [PDF]
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A. M. Dart, C. D. Gatzka, B. A. Kingwell, K. Willson, J. D. Cameron, Y.-L. Liang, K. L. Berry, L. M.H. Wing, C. M. Reid, P. Ryan, et al. Brachial Blood Pressure But Not Carotid Arterial Waveforms Predict Cardiovascular Events in Elderly Female Hypertensives Hypertension, April 1, 2006; 47(4): 785 - 790. [Abstract] [Full Text] [PDF]
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The CAFE Investigators, for the Anglo-Scandinavian Cardiac Outcomes Trial, CAFE Steering Committee and Writing Committee, B. Williams, P. S. Lacy, S. M. Thom, K. Cruickshank, A. Stanton, D. Collier, A. D. Hughes, et al. Differential Impact of Blood Pressure-Lowering Drugs on Central Aortic Pressure and Clinical Outcomes: Principal Results of the Conduit Artery Function Evaluation (CAFE) Study Circulation, March 7, 2006; 113(9): 1213 - 1225. [Abstract] [Full Text] [PDF]
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A. Covic, N. Mardare, P. Gusbeth-Tatomir, O. Brumaru, C. Gavrilovici, M. Munteanu, O. Prisada, and D. J. A. Goldsmith Increased arterial stiffness in children on haemodialysis Nephrol. Dial. Transplant., March 1, 2006; 21(3): 729 - 735. [Abstract] [Full Text] [PDF]
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 C. Vlachopoulos, F. Kosmopoulou, N. Alexopoulos, N. Ioakeimidis, G. Siasos, and C. Stefanadis Acute mental stress has a prolonged unfavorable effect on arterial stiffness and wave reflections. Psychosom Med, March 1, 2006; 68(2): 231 - 237. [Abstract] [Full Text] [PDF]
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T. Weber, J. Auer, M. F. O'Rourke, E. Kvas, E. Lassnig, G. Lamm, N. Stark, M. Rammer, and B. Eber Increased arterial wave reflections predict severe cardiovascular events in patients undergoing percutaneous coronary interventions Eur. Heart J., December 2, 2005; 26(24): 2657 - 2663. [Abstract] [Full Text] [PDF]
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S. A. Hope, D. B. Tay, I. T. Meredith, and J. D. Cameron Waveform dispersion, not reflection, may be the major determinant of aortic pressure wave morphology Am J Physiol Heart Circ Physiol, December 1, 2005; 289(6): H2497 - H2502. [Abstract] [Full Text] [PDF]
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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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S. Van Doornum, G. McColl, and I. P. Wicks Tumour necrosis factor antagonists improve disease activity but not arterial stiffness in rheumatoid arthritis Rheumatology, November 1, 2005; 44(11): 1428 - 1432. [Abstract] [Full Text] [PDF]
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A. Mahmud and J. Feely Arterial Stiffness Is Related to Systemic Inflammation in Essential Hypertension Hypertension, November 1, 2005; 46(5): 1118 - 1122. [Abstract] [Full Text] [PDF]
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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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S. S. Najjar, A. Scuteri, and E. G. Lakatta Arterial Aging: Is It an Immutable Cardiovascular Risk Factor? Hypertension, September 1, 2005; 46(3): 454 - 462. [Abstract] [Full Text] [PDF]
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F. Verbeke, P. Segers, S. Heireman, R. Vanholder, P. Verdonck, and L. M. Van Bortel Noninvasive Assessment of Local Pulse Pressure: Importance of Brachial-to-Radial Pressure Amplification Hypertension, July 1, 2005; 46(1): 244 - 248. [Abstract] [Full Text] [PDF]
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 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. A. Chirinos, J. P. Zambrano, S. Chakko, A. Veerani, A. Schob, H. J. Willens, G. Perez, and A. J. Mendez Aortic Pressure Augmentation Predicts Adverse Cardiovascular Events in Patients With Established Coronary Artery Disease Hypertension, May 1, 2005; 45(5): 980 - 985. [Abstract] [Full Text] [PDF]
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 J. Swampillai, S. Doshi, A. G Fraser, J. Goodfellow, and C. J. Jones Review: Clinical assessment of endothelial function -- an update The British Journal of Diabetes & Vascular Disease, March 1, 2005; 5(2): 72 - 76. [Abstract] [PDF]
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 J. R. Greenfield, K. Samaras, C. S. Hayward, D. J. Chisholm, and L. V. Campbell Beneficial Postprandial Effect of a Small Amount of Alcohol on Diabetes and Cardiovascular Risk Factors: Modification by Insulin Resistance J. Clin. Endocrinol. Metab., February 1, 2005; 90(2): 661 - 672. [Abstract] [Full Text] [PDF]
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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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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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A. Scuteri, S. S. Najjar, D. C. Muller, R. Andres, H. Hougaku, E. J. Metter, and E. G. Lakatta Metabolic syndrome amplifies the age-associated increases in vascular thickness and stiffness J. Am. Coll. Cardiol., April 21, 2004; 43(8): 1388 - 1395. [Abstract] [Full Text] [PDF]
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A. Covic, D. J. A. Goldsmith, P. Gusbeth-Tatomir, and M. Covic Haemodialysis acutely improves endothelium-independent vasomotor function without significantly influencing the endothelium-mediated abnormal response to a {beta}2-agonist Nephrol. Dial. Transplant., March 1, 2004; 19(3): 637 - 643. [Abstract] [Full Text] [PDF]
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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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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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 C. M. Giachelli Vascular Calcification: In Vitro Evidence for the Role of Inorganic Phosphate J. Am. Soc. Nephrol., September 1, 2003; 14(90004): S300 - 304. [Abstract] [Full Text]
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J. R. Greenfield, K. Samaras, L. V. Campbell, A. B. Jenkins, P. J. Kelly, T. D. Spector, and C. S. Hayward Physical activity reduces genetic susceptibility to increased central systolic pressure augmentation: a study of female twins J. Am. Coll. Cardiol., July 16, 2003; 42(2): 264 - 270. [Abstract] [Full Text] [PDF]
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M. E. Safar, B. I. Levy, and H. Struijker-Boudier Current Perspectives on Arterial Stiffness and Pulse Pressure in Hypertension and Cardiovascular Diseases Circulation, June 10, 2003; 107(22): 2864 - 2869. [Full Text] [PDF]
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 C. Meune, I. Mahe, J.-J. Mourad, A. Cohen-Solal, B. Levy, J.-P. Kevorkian, G. Jondeau, A. Habib, M. Lebret, A.-L. Knellwolf, et al. Aspirin alters arterial function in patients with chronic heart failure treated with ACE inhibitors: a dose-mediated deleterious effect Eur J Heart Fail, June 1, 2003; 5(3): 271 - 279. [Abstract] [Full Text] [PDF]
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S. C. Millasseau, S. J. Patel, S. R. Redwood, J. M. Ritter, and P. J. Chowienczyk Pressure Wave Reflection Assessed From the Peripheral Pulse: Is a Transfer Function Necessary? Hypertension, May 1, 2003; 41(5): 1016 - 1020. [Abstract] [Full Text] [PDF]
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 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. [Abstract] [Full Text] [PDF]
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A. Mahmud and J. Feely Effect of Smoking on Arterial Stiffness and Pulse Pressure Amplification Hypertension, January 1, 2003; 41(1): 183 - 187. [Abstract] [Full Text] [PDF]
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 M. Tamminen, J. Westerbacka, S. Vehkavaara, and H. Yki-Jarvinen Insulin-Induced Decreases in Aortic Wave Reflection and Central Systolic Pressure Are Impaired in Type 2 Diabetes Diabetes Care, December 1, 2002; 25(12): 2314 - 2319. [Abstract] [Full Text] [PDF]
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G. M. London, S. J. Marchais, A. P. Guerin, F. Metivier, and H. Adda Arterial structure and function in end-stage renal disease Nephrol. Dial. Transplant., October 1, 2002; 17(10): 1713 - 1724. [Full Text] [PDF]
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M. O'Rourke Target organ damage: use of pulse wave analysis as a manifestation of aortic degeneration in the assessment of hypertension Vascular Medicine, May 1, 2002; 7(2): 83 - 85. [PDF]
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J. Blacher and M. Safar Specific aspects of high blood pressure in the elderly Journal of Renin-Angiotensin-Aldosterone System, March 1, 2002; 3(1_suppl): S10 - S15. [PDF]
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