Blood pressure (BP) is one of the most important contributing factors to pulse wave velocity (PWV), a classic measure of arterial stiffness. Although there have been many non-invasive studies to show the relation between arterial stiffness and BP, the results are controversial. The aim of this study is to evaluate the role of BP as an influencing factor on PWV using invasive method. We observed 174 normotensive and untreated hypertensive subjects using coronary angiography. Arterial stiffness was assessed through aorto-femoral PWV by foot-to-foot velocity method using fluid-filled system. And BP was measured by pressure wave at the right common femoral artery. From univariate analysis, age, diabetes mellitus (DM), hypertension, waist, waist-to-hip ratio, total cholesterol-to-high-density lipoprotein cholesterol ratio, systolic BP (SBP), pulse pressure (PP) and mean arterial pressure (MAP) showed significant association with PWV. To avoid multiple colinearity among SBP, PP and MAP, we performed multiple regression analysis predicting PWV thrice. Age, DM and each BP were significantly and consistently correlated to PWV. In the first and third modules, compared to age, SBP and MAP were less strong predictors, respectively. However, PP was the stronger predictor than age and DM in the second module. Lastly, we simultaneously forced MAP and PP with other variables in the fourth multivariate analysis. Age, DM and PP remained significantly correlated with PWV, but the significance of MAP was lost. This is the first invasive study to suggest that PP has the strongest correlation with PWV among a variety of BP parameters.
Arterial stiffening increases with age1 and is associated with generalized atherosclerotic vascular disease.2, 3, 4 In population-based studies, aortic stiffness is an independent predictor of cardiovascular outcomes after adjustment for traditional cardiovascular risk factors.4, 5, 6, 7 Arterial stiffness has been shown to predict coronary artery disease8, 9, 10, 11 and cardiovascular mortality in patients with essential hypertension,12 end-stage renal disease13, 14 and impaired glucose tolerance and diabetes mellitus (DM).15 Although there are many measures to quantify stiffness, none of them is a gold standard, but approximations.16, 17 It is believed that the most reliable (and still probably the best) measure of arterial stiffness is pulse wave velocity (PWV).16
PWV is known to be associated with age, gender, blood pressure (BP), heart rate, salt intake, genetic factors and others. Although BP is one of the strongest factors influencing PWV, varying correlation coefficients have been reported between the various PWV (aorta-leg-arm) and BP (systolic, diastolic, mean, pulse) using non-invasive methods.5, 18, 19, 20, 21, 22, 23, 24 This variation may be attributable, at least in part, to the inherent variability of both PWV and BP within and across individual subjects and also to the method of BP25 and PWV measurements.
The aim of this study is to elucidate the relationship between the various BP and aortic PWV through direct measurement of BP wave in the artery using invasive method.
Materials and methods
Investigations were carried out in the cardiology department at the Korea University Guro Hospital, Seoul, Korea, between March 2002 and July 2003. To obtain BP and aortic PWV through a direct pressure wave in the artery using invasive method, we selected the study population from those who underwent coronary angiography owing to chest symptoms or preoperative evaluation. Of the 435 subjects who gave written informed consents for PWV measurement, 227 were receiving antihypertensive drug therapy and 17 were not clear of their medical history and, therefore, were excluded from the study. Additional 17 patients were excluded owing to one or more of the exclusion criteria; acute myocardial infarction, cardiomyopathy, more than mild valvular disease, post-cardiac surgery, atrial fibrillation, aortic dissection and chronic renal failure. Thus, 174 normotensive and untreated hypertensive subjects (101 women; 73 men) were observed. Their median age was 59.0±12.03 years (±1s.d.). The study was approved by the local ethics committee.
Hypertension was characterized with repeated measurements of ⩾140?mm Hg systolic BP (SBP) or ⩾90?mm Hg diastolic BP (DBP). DM was defined as a fasting blood glucose concentration ⩾126?mg/dl or antihyperglycaemic drug treatment. Current smoking was defined as having smoked the last cigarette less than 1 month before coronary angiography.
Measurement of haemodynamic variables
Haemodynamic measurements were obtained from patients in supine position. PWV was measured along the descending thoraco-abdominal aorta using the foot-to-foot velocity method. Briefly, waveforms were obtained using a fluid-filled system (5Fr right Judkin’s catheter) at the descending aorta, just below the origin of left subclavian artery and the right common femoral artery (Figure 1). At each site, the pressure waves were simultaneously recorded with the electrocardiography using polygraph at the speed of 100?mm/s. We defined T1 as the time interval from the starting point of QRS complex to the foot of pressure wave in the descending aorta and T2 as the time interval from the starting point of QRS complex to the foot of pressure wave in the right common femoral artery. We measured T1 and T2 from three different QRS complexes and pressure waves, and computed the mean value to minimize the error. The time delay (T) was calculated as T2−T1 and the distance (D) was obtained by the length of the catheter between the two recording sites. PWV was calculated by PWV=D (m)/T (s). We measured SBP, DBP and pulse pressure (PP) by pressure tracing method in the right common femoral artery. Mean arterial pressure (MAP) was obtained by the formula MAP=DBP+PP/3.
Values were expressed as mean±one standard deviation (s.d.). Differences in the mean value of PWV between the two groups were compared using a Student’s t-test for a parametric statistical test and Mann–Whitney’s test for a non-parametric analysis. A P<0.05 was considered significant. Correlations between each of the measured variables and PWV were assessed by Pearson’s correlation coefficient. The effects of traditional cardiovascular risk factors and haemodynamic variables on PWV were analysed by multivariate regression analysis. With the variables selected from univariate analyses, we performed the analysis thrice to avoid multiple colinearity among SBP, PP and MAP. Variables included in the first module were common ones, such as age, DM, waist-to-hip ratio, total cholesterol-to-high-density lipoprotein cholesterol (HDL-C) ratio and SBP. The second and third modules included common variables along with PP and MAP. We also performed the fourth multiple regression analysis including the same non-haemodynamic variables, PP and MAP with a test of variance influence factor. Statistical analyses were performed using the SPSS 10.0 software package (SPSS Inc., Chicago, IL, USA).
The baseline clinical characteristics of the study population are presented in Table 1. Table 2 shows the results of the independent-samples t-test for comparison of the PWV mean value between the two groups according to gender, hypertension, DM and smoking status. Compared with subjects who did not have hypertension or DM, subjects who had hypertension or DM showed significantly higher PWV mean value (for hypertension, 13.2±6.2 vs 10.3±3.5?m/s, P<0.001; for DM, 15.6±8.6 vs 11.1±4.3?m/s, P=0.003). However, the differences of PWV between men and women, or smoker and non-smoker were not prominent. In bivariate analysis (Table 3), age, waist-to-hip ratio, total cholesterol-to-HDL-C ratio, SBP, PP and MAP were positively correlated with PWV. The relations of PWV to age, SBP, PP and MAP were displayed in Figures 2, 3, 4 and 5, respectively. To avoid multiple colinearity among SBP, PP and MAP, we performed multiple regression analysis predicting PWV three times with variables selected from univariate analyses (Table 4). In every multiple regression analysis, age, waist-to-hip ratio, DM and total cholesterol-to-HDL-C ratio were used as common independent variables and each of the three modules also included SBP, PP and MAP, separately. The results indicated that age and DM were significantly and consistently correlated to PWV. And within each analysis, SBP, PP and MAP also showed significant association with PWV. The first and third module showed that age was the strongest predictor among 3 significant correlating factors (age, DM, SBP or MAP). In the second module, on the other hand, PP was the stronger predictor than age or DM (for age, β=0.233, P=0.001; for DM, β=0.201, P=0.005; for PP, β=0.255, P<0.001). When we used age as an index variable for comparison, this result indirectly demonstrated that PP was the only stronger predictor for PWV compared to age among BP parameters. That is, PP showed the most potent correlation with PWV over a variety of BP parameters.
Lastly, we included both MAP and PP with other common independent variables in the fourth multiple regression model (Table 4). Considering continuous characteristic of MAP and pulsatile characteristic of PP, we tried to determine whether PP remained significantly correlated with PWV after other factors including MAP were forced in the model. In the analysis, age (β=0.356, P<0.001), DM (β=0.161, P=0.028) and PP (β=0.221, P=0.023) remained significantly correlated with PWV, but MAP lost the significance of correlation with PWV (β=0.129, P=0.154). The variance influence factors for all independent variables were less than 2, thereby the multiple colinearity was not prominent. The analysis was also performed adding SBP as an independent variable (data not shown). However, the result was the same as the fourth module except automatic exclusion of SBP from the analysis because its multi colinearity was over the limit. In our cross-sectional study, it is suggested that the pulsatile BP had more effect on PWV than the continuous part of BP.
The key finding of our study was that in normotensive and untreated hypertensive middle-aged and elderly subjects (median age of 59.0±12.03 years) PP showed the strongest correlation with aortic PWV over other haemodynamic BP parameters.
PWV measured along the aortic and aorto-femoral pathways has been known to be the most clinically relevant because the aorta and its first branches are responsible for most of the pathophysiological effects of arterial stiffness. Although non-invasive technique showed acceptable reproducibility, the length of arterial segment was usually estimated by direct superficial measurement of the distance between two transducers. Therefore aortic PWV by non-invasive method would be underestimated because arteries become longer and more tortuous with age. In vivo measurement of the travel distance was calculated by subtracting (i) the known sheath length and (ii) the external catheter length behind the sheath, from the known length of the total catheter and obtained more accurate PWV. Also, we minimized the error of BP measurement by using intra-arterial pressure wave.
Arterial stiffness has been known to be related to BP; however, there are controversial results in the literature regarding the relation between PWV and each BP (SBP, DBP, PP and MAP). Ngim et al.19 reported that carotid-femoral PWV was correlated with SBP and also MAP, but not with DBP in untreated hypertensive and normotensive middle-aged Malay men. Stompor et al.24 also found out that aortic PWV was correlated significantly with SBP, MAP and PP, but not with DBP in peritoneal dialysis patients. Those findings are consistent with our results. In some studies, PWV was only correlated with SBP,20, 21 but in others with both SBP and DBP.22 Sa Cunha et al.23 suggested gender difference; SBP showed correlation with PWV in both genders, whereas DBP was correlated with PWV only in women. In contrast to the previous studies, Nurnberger et al.18 reported that DBP was an only important haemodynamic determinant of PWV in young healthy males.
The causes of controversial results may be different demographic characteristics such as age range, gender distribution and body size. Whether the subjects were on antihypertensive agents and the kinds of drugs, if used, might also affect the results.26 Also, the different methods of BP measurement (e.g. 24-h ambulatory BP monitoring, casual BP measurement, automatic BP monitoring for 30?min) could attribute to the results.27 In particular, as indirect measurement of DBP by cuff-mercury sphygmomanometer tends to be overestimated, the true intra-arterial PP might be underestimated, which could also affect the results.28 In terms of PWV measurement, different methods and locations were used in the studies, and most non-invasive methods basically had a limitation mentioned above, therefore, showed controversial results.
Because this study used invasive method for the measurement of BP and aortic PWV excluding subjects on antihypertensive agents, our findings reflect the effect of BP on aortic PWV more clearly.
In population-based studies, aortic PWV has been known to be a superior independent predictor of cardiovascular outcome even after adjusting the traditional cardiovascular risk factors5, 7 and elevated PP also has been known to be an independent risk factor of cardiovascular disease.29, 30, 31
Haemodynamic patterns of age-related changes in BP was shown in the Framingham heart study.32 After age 50–60 years, DBP declined, PP rose steeply and MAP reached a plateau. The changes were mainly attributed to the age-related large artery stiffness. The effect of ageing on the prognostic significance of BP was reported in hypertensive subjects33 and Framingham population.34 By ambulatory intra-arterial BP monitoring, DBP parameters provided the best prognostic value for cardiovascular outcomes in the middle aged (<60 years), whereas PP parameters were the most predictive in the elderly (⩾60 years) individuals.33 With increasing age, the relative prognostic value of BP for coronary heart disease was gradually shifted from DBP to SBP and then to PP in the Framingham heart study.34 In subjects aged <50 years, DBP was the strongest predictor. Age 50–59 years was a transition period when SBP, DBP and PP were similar predictors, whereas from age 60 years and over, DBP was negatively related to the risk of coronary events so that PP became a better predictor than SBP. We suggest that as the median age of our subjects is 59 years, these age-related trends of the Framingham heart study could be similarly applied to our research, which demonstrates PP as the strongest determinant of aortic PWV. Because our results also showed prognostic significance of SBP and MAP for aortic PWV and no correlation of DBP with PWV, the findings were in agreement with the previous data.32, 33, 34
Interestingly, Nurnberger et al.18 reported a contrary result. They showed DBP was the only important determinant of PWV among all BP parameters. But, the study population included only young (23–35 years old) healthy males, in whom DBP has been known to be the strongest predictor of coronary heart disease in the Framingham heart study. Although the results of the present study and Nurnberger’s report are different, together they might reflect the age-related different relation between BP parameters and PWV. It is suggested that aortic PWV and BP are strongly influenced by age, and the role of BP parameters as a predictor of PWV could be different according to the age range of the population studied.
Elastic properties of the arterial wall are highly pressure dependent. At low levels of arterial pressure, wall stress is supported by compliant elastin fibres, whereas at higher levels of pressure, wall stress is supported by much stiffer collagen fibres. An increase in elastic artery stiffness is related to arterial wall composition and occurs over a long period, for example, with advancing age, hypertension and arteriosclerosis. Acute changes can occur in elastic arteries with changes in distending MAP, but these are passive. For example, during vasodilation, both pressure and diameter decrease in elastic arteries, causing a passive decrease in wall stiffness and a decrease in PWV.35 As it was cross-sectional and because there was no BP manipulation, our study reveals chronic changes of elastic arteries well. It was further supported by the fourth module of multiple regression analysis (Table 4). MAP, which is more related to acute BP influence on PWV, lost the significance of correlation with PWV when it was adjusted for other factors. However, age, DM and PP remained significantly correlated with PWV in the analysis. In terms of the relationship between PWV and two important BP characteristics, continuous and pulsatile, the result also suggested that the pulsatile BP had more impact on aortic PWV than the continuous part of BP.
We found no significant relationship of PWV with total cholesterol, triglycerides, low-density lipoprotein cholesterol or HDL-C. Although positive and negative associations of aortic stiffness with cholesterol have been reported using different methods, most studies using PWV have shown no correlation with total cholesterol.5, 25 The present findings are in agreement with a recent large population-based study by Amar et al.5 These investigators found no significant relationship between PWV and total cholesterol and the various components of the metabolic syndrome, including body mass index, fasting glucose, insulin, triglycerides and HDL-C. The lack of correlation of PWV with smoking in the present study is also consistent with previous reports.5, 36, 37, 38
The effect of heart rate on arterial stiffness is somewhat a controversial issue. In a recent observational study, Sa Cunha et al.23 showed that high heart rate was strongly associated with elevated PWV even after adjustment for age and BP. The increase in heart rate by isoproterenol and pacing was associated with an increase in PWV.39 Our result, however, demonstrated no significant correlation and is in agreement with other previous studies.40, 41, 42 There was also a contradictory study showing reduced aortic stiffness and increased distensibility during incremental pacing.43 Therefore, in order to clarify the relationship between arterial distensibility and heart rate, and its pathophysiology, further specific studies are necessary.
Several aspects of validity need to be discussed. There was a potential limitation in PWV measurement method, as we could not obtain pressure wave at two recording sites at the same time. However, we think that there were no significant haemodynamic variations between the two assessments obtained from two different sites because it took less than 3?s to disconnect the catheter from the manifolder, remove it and connect the side arm of the introducer sheath to the manifolder. That is, there was a time interval of less than 3?s between the aortic pressure wave and the right common femoral arterial pressure wave. Nevertheless, we could not affirm whether there was a variation of BP between the two assessments, because the patient’s real-time BP was being monitored and was obtained through the catheter at each recording site in the arterial system. However, in terms of heart rate, no significant variation between the two assessments was affirmed by paired t-test (heart rate in femoral artery, 74.5± 13.8?b.p.m. vs heart rate in aorta, 74.4±13.6?b.p.m., P=0.49). In addition, we measured T1 and T2 by electrocardiography gating and averaged the values from three measurements at each site (mean T1=108.0?ms, mean s.d.=4.9?ms (0.6–13.2?ms); mean T2=149.3?ms, mean s.d.= 4.4?ms (1.2–13.0?ms)). One other potential problem of our study is the confinement to symptomatic patients referred for coronary angiography. Thus, our findings might not be applicable to the general population. In terms of the relation between BP parameters and aortic PWV, we think, however, the subjects studied matter little to the results. Moreover, it is unlikely that confounding explains our results because we were able to adjust for many important potential confounders.
In conclusion, PP showed the strongest correlation with aortic PWV among a variety of BP parameters in the normotensive and untreated hypertensive middle aged and elderly subjects, and it was first confirmed by an invasive method. In combination with the previous studies,18, 32, 33, 34 the present study also suggests that the role of BP parameters as a predictor of PWV could be different according to the age range of the population studied. Further large population-based studies are needed to characterize the age-related changes in the impact of BP on large artery stiffness.
Ohmori K, Emura S, Takashima T . Risk factors of atherosclerosis and aortic pulse wave velocity. Angiology 2000; 51: 53–60.
Farrar DJ, Bond MG, Riley WA, Sawyer JK . Anatomic correlates of aortic pulse wave velocity and carotid artery elasticity during atherosclerosis progression and regression in monkeys. Circulation 1991; 83: 1754–1763.
O’Neal DN, Dragicevic G, Rowley KG, Ansari MZ, Balazs N, Jenkins A et al. A cross-sectional study of the effects of type 2 diabetes and other cardiovascular risk factors on structure and function of nonstenotic arteries of the lower limb. Diabetes Care 2003; 26: 199–205.
van Popele NM, Grobbee DE, Bots ML, Asmar R, Topouchian J, Reneman RS et al. Association between arterial stiffness and atherosclerosis: the Rotterdam Study. Stroke 2001; 32: 454–460.
Amar J, Ruidavets JB, Chamontin B, Drouet L, Ferrieres J . Arterial stiffness and cardiovascular risk factors in a population-based study. J Hypertens 2001; 19: 381–387.
Meaume S, Rudnichi A, Lynch A, Bussy C, Sebban C, Benetos A et al. Aortic pulse wave velocity as a marker of cardiovascular disease in subjects over 70 years old. J Hypertens 2001; 19: 871–877.
Willum-Hansen T, Staessen JA, Torp-Pedersen C, Rasmussen S, Thijs L, Ibsen H et al. Prognostic value of aortic pulse wave velocity as index of arterial stiffness in the general population. Circulation 2006; 113: 664–670.
Boutouyrie P, Tropeano AI, Asmar R, Gautier I, Benetos A, Lacolley P et al. Aortic stiffness is an independent predictor of primary coronary events in hypertensive patients: a longitudinal study. Hypertension 2002; 39: 10–15.
Mattace-Raso FU, van der Cammen TJ, Hofman A, van Popele NM, Bos ML, Schalekamp MA et al. Arterial stiffness and risk of coronary heart disease and stroke: the Rotterdam Study. Circulation 2006; 113: 657–663.
Weber T, Auer J, O’Rourke MF, Kvas E, Lassnig E, Berent R et al. Arterial stiffness, wave reflections, and the risk of coronary artery disease. Circulation 2004; 109: 184–189.
Lim HE, Park CG, Shin SH, Ahn JC, Seo HS, Oh DJ . Aortic pulse wave velocity as an independent marker of coronary artery disease. Blood Press 2004; 13: 369–375.
Laurent S, Boutouyrie P, Asmar R, Gautier I, Laloux B, Guize L et al. Aortic stiffness is an independent predictor of all-cause and cardiovascular mortality in hypertensive patients. Hypertension 2001; 37: 1236–1241.
Blacher J, Guerin AP, Pannier B, Marchais SJ, Safar ME, London GM . Impact of aortic stiffness on survival in end-stage renal disease. Circulation 1999; 99: 2434–2439.
Blacher J, Safar ME, Guerin AP, Pannier B, Marchais SJ, London GM . Aortic pulse wave velocity index and mortality in end-stage renal disease. Kidney Int 2003; 63: 1852–1860.
Cruickshank K, Riste L, Anderson SG, Wright JS, Dunn G, Gosling RG . Aortic pulse-wave velocity and its relationship to mortality in diabetes and glucose intolerance: an integrated index of vascular function? Circulation 2002; 106: 2085–2090.
O’Rourke MF, Staessen JA, Vlachopoulos C, Duprez D, Plante GE . Clinical applications of arterial stiffness; definitions and reference values. Am J Hypertens 2002; 15: 426–444.
Lemogoum D, Van Bortel L, Van den Abeele W, Ciarka A, Degaute JP, van de Borne P et al. Effect of beta-adrenergic stimulation on pulse wave velocity in black and white subjects. J Hypertens 2004; 22: 2349–2353.
Nurnberger J, Dammer S, Opazo Saez A, Philipp T, Schafers RF . Diastolic blood pressure is an important determinant of augmentation index and pulse wave velocity in young, healthy males. J Hum Hypertens 2003; 17: 153–158.
Ngim CA, Abdul Rahman AR, Ibrahim A . Pulse wave velocity as an index of arterial stiffness: a comparison between newly diagnosed (untreated) hypertensive and normotensive middle-aged Malay men and its relationship with fasting insulin. Acta Cardiol 1999; 54: 277–282.
Tanaka H, DeSouza CA, Seals DR . Absence of age-related increase in central arterial stiffness in physically active women. Arterioscler Thromb Vasc Biol 1998; 18: 127–132.
Blacher J, Asmar R, Djane S, London GM, Safar ME . Aortic pulse wave velocity as a marker of cardiovascular risk in hypertensive patients. Hypertension 1999; 33: 1111–1117.
Yasmin MB . Similarities and differences between augmentation index and pulse wave velocity in the assessment of arterial stiffness. Q J Med 1999; 92: 595–600.
Sa Cunha R, Pannier B, Benetos A, Siche JP, London GM, Mallion JM et al. Association between high heart rate and high arterial rigidity in normotensive and hypertensive subjects. J Hypertens 1997; 15: 1423–1430.
Stompor T, Rajzer M, Sulowicz W, Dembinska-Kiec A, Janda K, Kawecka-Jaszcz K et al. An association between aortic pulse wave velocity, blood pressure and chronic inflammation in ESRD patients on peritoneal dialysis. Int J Artif Organs 2003; 26: 188–195.
Asmar R . Arterial Stiffness and Pulse Wave Velocity Clinical Applications. Elsevier: Paris, 1999, pp 67, 101–102.
Blacher J, Protogerou AD, Safar ME . Large artery stiffness and antihypertensive agents. Curr Pharm Des 2005; 11: 3317–3326.
Asmar RG, Brunel PC, Pannier BM, Lacolley PJ, Safar ME . Arterial distensibility and ambulatory blood pressure monitoring in essential hypertension. Am J Cardiol 1988; 61: 1066–1070.
Vardan S, Mookherjee S, Warner R, Smulyan H . Systolic hypertension. Direct and indirect BP measurements. Arch Intern Med 1983; 143: 935–938.
de Simone G, Roman MJ, Koren MJ, Mensah GA, Ganau A, Devereux RB . Stroke volume/pulse pressure ratio and cardiovascular risk in arterial hypertension. Hypertension 1999; 33: 800–805.
Benetos A, Safar M, Rudnichi A, Smulyan H, Richard JL, Ducimetieere P et al. Pulse pressure: a predictor of long-term cardiovascular mortality in a French male population. Hypertension 1997; 30: 1410–1415.
Verdecchia P, Schillaci G, Borgioni C, Ciucci A, Pede S, Porcellati C . Ambulatory pulse pressure: a potent predictor of total cardiovascular risk in hypertension. Hypertension 1998; 32: 983–988.
Franklin SS, Gustin WT, Wong ND, Larson MG, Weber MA, Kannel WB et al. Hemodynamic patterns of age-related changes in blood pressure. The Framingham heart study. Circulation 1997; 96: 308–315.
Khattar RS, Swales JD, Dore C, Senior R, Lahiri A . Effect of aging on the prognostic significance of ambulatory systolic, diastolic, and pulse pressure in essential hypertension. Circulation 2001; 104: 783–789.
Franklin SS, Larson MG, Khan SA, Wong ND, Leip EP, Kannel WB et al. Does the relation of blood pressure to coronary heart disease risk change with aging? The Framingham heart study. Circulation 2001; 103: 1245–1249.
Nichols WW . Clinical measurement of arterial stiffness obtained from noninvasive pressure waveforms. Am J Hypertens 2005; 18: 3S–10S.
Mahmud A, Feely J . Effect of smoking on arterial stiffness and pulse pressure amplification. Hypertension 2003; 41: 183–187.
Rehill N, Beck CR, Yeo KR, Yeo WW . The effect of chronic tobacco smoking on arterial stiffness. Br J Clin Pharmacol 2006; 61: 767–773.
Kim JW, Park CG, Hong SJ, Park SM, Rha SW, Seo HS et al. Acute and chronic effects of cigarette smoking on arterial stiffness. Blood Press 2005; 14: 80–85.
Millasseau SC, Stewart AD, Patel SJ, Redwood SR, Chowienczyk PJ . Evaluation of carotid-femoral pulse wave velocity: influence of timing algorithm and heart rate. Hypertension 2005; 45: 222–226.
Wilkinson IB, Mohammad NH, Tyrrell S, Hall IR, Webb DJ, Paul VE et al. Heart rate dependency of pulse pressure amplification and arterial stiffness. Am J Hypertens 2002; 15: 24–30.
Nichols WW, Conti CR, Walker WE, Milnor WR . Input impedance of the systemic circulation in man. Circ Res 1977; 40: 451–458.
Noble MI, Gabe IT, Trenchard D, Guz A . Blood pressure and flow in the ascending aorta of conscious dogs. Cardiovasc Res 1967; 1: 9–20.
Stefanadis C, Dernellis J, Vavuranakis M, Tsiamis E, Vlachopoulos C, Toutouzas K et al. Effects of ventricular pacing-induced tachycardia on aortic mechanics in man. Cardiovasc Res 1998; 39: 506–514.
This work was partially supported by a grant from the Seoul R LBD program, Republic of Korea (10528).
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Kim, E., Park, C., Park, J. et al. Relationship between blood pressure parameters and pulse wave velocity in normotensive and hypertensive subjects: invasive study. J Hum Hypertens 21, 141–148 (2007). https://doi.org/10.1038/sj.jhh.1002120
- pulse wave velocity
- pulse pressure
- large artery stiffness
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