Surrogate Measure Of Arterial Stiffness Research Articles

Abstract 19485: Migrant South Asian Women Have Increased Arterial Stiffness Compared to Black and White Women Residing in the United States

Introduction: Death from cardiovascular disease (CVD) is proportionally higher in Black and South Asians (SA) residing in the United States (U.S.) compared to their White counterparts. While all other sex- ethnic groups demonstrated a decline in all cause and CVD mortality, it has recently been shown that Asian Indian women residing in the U.S. experienced an increase. Arterial Stiffness indices, such as Augmentation Index, have been associated with CVD in western populations. We hypothesized that, in a community setting, migrant SA Women in the U.S. have a greater degree of arterial stiffness than do their Black (BW) and White Women (WW) counterparts. Methods: We studied 697 volunteers residing in the metro Atlanta area from 2006-2010 that include 263 SA women (age 49±12 years), 140 BW (age 46±10 years), and 294 WW (age 48±10 years). Using radial artery tonometry (Sphygmocor©, Atcor) we calculated Augmentation Index Adjusted for heart rate (AIX) as a surrogate measure of arterial stiffness. Anthropometric, clinical and lipid levels were assessed. Women were studied as a whole and a subset of women free of traditional CVD risk factors were analyzed separately. Univariate and multivariate regression models adjusted for age, race, BMI, hypertension, diabetes, dyslipidemia, smoking status, and lipid levels were performed. Results: SA women had a greater AIX compared to their BW and WW counterparts respectively (32 vs 25 vs 23, p<0.001). BMI was lowest in SA Women followed by WW and BW respectively (26.7 vs 26.8 vs 31.7, p<0.001). There was a similar amount of hypertension (18%) and dyslipidemia (6%) in SA women but more diabetes (23%) compared to WW (17%, 22%, 5%) and BW (29%, 16%, 6%) (p<0.001 for all). In the subset of women free of CVD risk factors, SA women still had a greater degree of arterial stiffness compared to their BW and WW counterparts (31 vs 24 vs 22, p<0.001). In the entire cohort and in the subset of women free of traditional CVD risk factors, LDL, age and race (p<0.001 for both groups) were significant independent predictors of AIX. Conclusions: Community dwelling migrant SA women have a significantly greater degree of arterial stiffness compared to their WW and BW counterparts despite having similar traditional CVD risk factors.

Serum phosphate and calcium concentrations are associated with reduced patient survival following kidney transplantation

The impact of disordered mineral and bone metabolism following kidney transplantation is not well defined. We studied the association of serum phosphate and calcium concentrations, and surrogate measures of arterial stiffness (augmentation index: AIx and Timing of the reflected wave: Tr), with long-term kidney transplant recipient and allograft survival. Prevalent adult renal transplant patients (n = 270) were prospectively studied over a median 88-month follow-up. Detailed demographic, clinical and laboratory data, in addition to both peripheral and central non-invasive blood pressure measurements, were recorded. Higher serum phosphate and calcium levels were associated with increased all-cause mortality (HR: 1.21; 95% CI 1.09,1.35, p < 0.001 and HR: 1.22; 95% CI 1.01,1.48; p < 0.04, respectively; adjusted Cox model) and death-uncensored graft loss (p < 0.001 and p = 0.03, respectively). In addition, serum calcium and phosphate were associated with death-censored graft loss on univariable analysis (p < 0.001 and p = 0.02, respectively), but did not retain significance on multivariable analysis. AIx and Tr were not associated with mortality or graft loss on multivariable analysis. This is the first report to demonstrate that both higher serum phosphate and calcium levels are associated with increased mortality in kidney transplant recipients. It highlights the need for randomized trials assessing current interventions available for improving disordered mineral-bone metabolism post transplantation.

Evaluating the effects of sevelamer carbonate on cardiovascular structure and function in chronic renal impairment in Birmingham: the CRIB-PHOS randomised controlled trial

BackgroundSerum phosphate is an independent predictor of cardiovascular morbidity and mortality in patients with chronic kidney disease and the general population. There is accumulating evidence that phosphate promotes arterial stiffening through structural vascular alterations such as medial calcification, which are already apparent in the early stages of chronic kidney disease.AimTo determine the effects of phosphate binding with sevelamer carbonate on left ventricular mass and function together with arterial stiffness in patients with stage 3 chronic kidney disease.Methods/DesignA single-centre, prospective, randomised, double-blind, placebo-controlled trial of 120 subjects with stage 3 chronic kidney disease recruited from University Hospitals Birmingham NHS Foundation Trust. Baseline investigations include transthoracic echocardiography and cardiac magnetic resonance imaging to assess ventricular mass, volumes and function, applanation tonometry to determine pulse wave velocity and pulse wave analysis as surrogate measures of arterial stiffness and dual energy x-ray absorptiometry scanning to determine bone density. During an open-label run in phase, subjects will receive 1600 mg sevelamer carbonate with meals for four weeks. They will then be randomised to either continue sevelamer carbonate or receive an identical placebo (60 subjects per arm) for the remaining 36 weeks. Four-weekly monitoring of serum electrolytes and bone biochemistry will be performed. All baseline investigations will be repeated at the end of the treatment period. The primary endpoint of the study is a reduction in left ventricular mass after 40 weeks of treatment. Secondary endpoints are: i) change in aortic compliance; ii) change in arterial stiffness; iii) change in arterial elastance; iv) change in left ventricular systolic and diastolic elastance; v) change in left ventricular function; and vi) change in bone density.Trial RegistrationThis trial is registered at ClinicalTrials.gov: NCT00806481 and Current Controlled Trials: ISRCTN35254279.

45: Effects of magnesium on central arterial compliance in preeclampsia

To investigate the effect of MgSO4 infusion on central arterial compliance, using noninvasive radial artery pulse wave forms by applanation tonometry in women diagnosed with preeclampsia (PRE). This is a prospective observational study. Women diagnosed with PRE were recruited prior to receiving MgSO4. Measurements of the radial pulse waveform were obtained longitudinally. Using a validated internal transfer function, the aortic waveform was derived and the indices Augmentation Pressure (AP) and Augmentation Index corrected @75bpm ([email protected]) were calculated. The AP and [email protected] are surrogate measures of arterial stiffness. We compared the time periods: prior to MgSO4 (t1), 1hr after MgSO4 bolus (t2), 4hrs after MgSO4 maintenance infusion (t3), 24hrs after delivery and MgSO4 completion (t4). An 80% power assuming an increase in compliance of 25%, =0.05, required 70 subjects. Statistical analysis was performed using differences of least squared means with Tukey Kramer adjustment. Institutional IRB approval was obtained. Data was analyzed from seventy women. AP and [email protected] at t2-t4 were significantly lower compared with t1, (pvalue =.008, <.001, and .002) and (pvalue =.039, <.001, and .005) respectively, with greatest decrease in arterial stiffness at t3- 4hrs after MgSO4 maintenance. AP and [email protected] at t3 was significantly lower when compared with t2 (p-value<.001 and .001). AP at t3 was significantly lower compared with t4 (p=.018). No significant difference in [email protected] was noted between t3 and t4. In women with PRE, MgSO4 improved central arterial compliance. This effect was most exaggerated after 4hrs of infusion and remained 24hrs following MgSO4 completion following delivery. This suggests either a sustained vascular compliance effect from MgSO4 or resolution of the vasoconstrictive effect of preeclampsia. Further, MgSO4 may improve perfusion to end organs by decreasing arterial stiffness, this information could be used to direct future management, suggesting a benefit of its use beyond seizure prophylaxis.

Pulse pressure: a surrogate measure of arterial stiffness in a diabetic Cuban American (CA) population

The study examined the difference in pulse pressure (PP) among CA with (N=183) and without (N=184) type 2 diabetes (T2D). Subjects were randomly recruited from Miami‐Dade and Broward Counties, FL. An average of two blood pressure readings was used for the calculation of PP, as the difference between the systolic blood pressure (SBP) and diastolic blood pressure (DBP); (SBP ‐ DBP). Analyses used SPSS and included descriptive statistics, ANCOVA, correlations, multiple linear and logistic regressions. Results revealed T2D subjects had higher PP (52.35) than non diabetics (49.35), p=.033. This association was still significant; F (1,331) = 4.77, p= .030; after controlling for all co‐variates: age, waist circumference, BMI, saturated fatty acid, calcium, HDL cholesterol, C‐ reactive protein, potassium, sodium, diabetes status, gender, smoking and hypertension medications. A predictive model was developed which controlled for covariates. The association was still significant (p=.025); with diabetes status, age and hypertension medication being the strongest predictors for PP. The model explained 18.8% variability in PP between diabetics and non diabetics (R square = 0.188). Diabetics had twice the odds for higher PP than non diabetics; (OR=2.040, p=.012). We conclude that CA with T2D have a higher PP than non‐diabetics and this may explain the higher risk of heart disease among diabetics.

Self–measured (blood pressure) arterial stiffness index: A promising new measure of arterial stiffness

Increased arterial stiffness is predictive of increased cardiovascular risk. The ambulatory arterial stiffness index is a new measure derived from 24–hour ambulatory blood pressure (BP) monitoring. We retrospectively studied 59 consecutive patients, (36 females; age 62 ± 12 years), evaluated for hypertension in an academic cardiology practice. All had eight or more self–measured BP recorded over a period of 2 through 8 weeks while stable. The self–measured arterial stiffness index (SMASI) was calculated according to the same formula as the ambulatory arterial stiffness index, 1 minus the regression slope of the regression line of diastolic plotted against systolic BP. Mean SMASI was 62 ± 0.20. SMASI correlated directly with age ( r = 0.27; P = .03), BP load ( r = 0.40; P = .002), home pulse pressure ( r = 0.47; P < .001), and office pulse pressure ( r = 0.44; P = .001). SMASI was higher in patients with multiple cardiovascular risk factors and correlated with pulse wave velocity ( r = 0.45; P = .04) among 21 patients who underwent arterial tonometry. SMASI correlated with left ventricle (LV) mass/body surface area (BSA) ( r = 0.30; P = .035) in 50 patients. SMASI increases with age, is associated with weaker BP control, hypertensive organ damage and correlates with pulse wave velocity. SMASI obtained by self–measured BP may serve as a useful surrogate measure of arterial stiffness.

Increased Arterial Augmentation and Augmentation Index as Surrogate Parameters for Arteriosclerosis in Subjects with Diabetes Mellitus and Nondiabetic Subjects with Cardiovascular Disease

Arterial augmentation (AP) and the augmentation index (Aix) are surrogate parameters of arterial stiffness and are commonly used as predictors for cardiovascular risk. The aim of this study is to compare these parameters in diabetic subjects and nondiabetic cardiovascular risk subjects with healthy control subjects. One hundred sixty-six nonsmoking subjects aged between 35 and 70 years were included in the study, which included 100 subjects with cardiovascular disease but not diabetes (mean age 62.73+/-8.75 years), 33 subjects with type 2 diabetes (66.58+/-2.69 years), and 33 healthy controls (51.89+/-8.91 years). In these subjects, arterial stiffness was measured by the difference between the second and the first systolic peak of the central pressure waveform, and the Aix was calculated as the percentage of Aix from pulse pressure. Arterial augmentation was increased in subjects with diabetes (DM) with 10.21+/-6.97 mm Hg and in subjects with cardiovascular disease but not diabetes (CV) with 10.74+/-5.29 mm Hg in comparison to healthy controls (C) with 6.59+/-3.97 mm Hg (p < 0.0005 DM vs C; p < 0.00005 CV vs C). Moreover, Aix was increased with 26.00+/-9.91% in CV subjects compared to healthy controls with 19.84+/-9.37% (p < 0.02 CV vs C). The augmentation index was increased with 21.12+/-11.21% in subjects with type 2 diabetes mellitus compared to controls, but failed to be statistically significant. There was no statistical significance in arterial augmentation or the augmentation index between CV and diabetic subjects. The results of our study revealed a comparable increased augmentation index as a surrogate measure of arterial stiffness and arteriosclerosis in subjects with diabetes mellitus and in nondiabetic subjects with cardiovascular disease.

Letter to the Editor

To the Editor: Recent hypertension research has shown that large artery compliance is an important determinant of systolic pressure, pulse pressure, and cardiovascular disease. Many methods exist to determine compliance or its inverse, arterial stiffness; the time constant of the aortic pressure decay in diastole, the ratio of stroke volume over pulse pressure, and pulse wave velocity are among the most used. These methods require either invasive measurements or 2 simultaneous measurements and are not practical to use in epidemiological studies or in night–day variations. Dolan et al1 recently suggested the use of the Ambulatory Arterial Stiffness Index (AASI), defined as 1 minus the slope of the (linear) relation between diastolic and systolic pressure, as a measure of arterial stiffness. The AASI is easy to …

Ambulatory Blood Pressure Measurement

One of the consequences of hypertension is increasing stiffness of the arteries, which leads to cardiovascular events and increased mortality.1 Clearly this process is a continuous one and, contrary to acceptance that such change is inevitable, it is not now unreasonable to assume that if stiffening in the arterial system could be detected at an early rather than at a late stage, therapeutic interventions might be initiated to delay or even prevent its occurrence. However, measuring arterial stiffness requires special equipment and trained staff, facilities that are not generally available and that are, moreover, costly. It has been proposed recently that a measure of arterial stiffness could be obtained from the routine use of ambulatory blood pressure measurement (ABPM) by using the dynamic relationship between diastolic and systolic blood pressure over 24 hours, calculated as 1 minus the regression slope of diastolic on systolic blood pressure. The rationale underlying the ambulatory arterial stiffness index (AASI) is that average distending pressure varies during the day and that the relation between diastolic and systolic blood pressure, with this changing distending pressure, depends largely on the structural and functional characteristics of the large arteries. In the Dublin Outcome Study, AASI predicted cardiovascular mortality in a large cohort of hypertensive individuals. Moreover, this prediction withstood additional adjustment for other risk factors, including pulse pressure. Interestingly, AASI was a stronger predictor of fatal …

Ambulatory arterial stiffness index: rationale and methodology

Increased arterial stiffness is associated with the development of cardiovascular disease and may even predict its development at an early stage. Increased pulse pressure is seen as a marker of increased arterial stiffness and can be readily measured by ambulatory blood pressure monitoring. We propose another surrogate measure of arterial stiffness derived from ambulatory blood pressure monitoring that may predict cardiovascular mortality over and above pulse pressure, namely, the dynamic relationship between diastolic and systolic blood pressure over 24 h--the ambulatory arterial stiffness index. Using all blood pressure readings over the 24-h period from 11 291 (5965 women; mean age 54.6 years) patients referred for ambulatory blood pressure monitoring to a blood pressure clinic, diastolic blood pressure was plotted against systolic blood pressure, and the regression slope was calculated; ambulatory arterial stiffness index was defined as one minus this regression slope. Both ambulatory arterial stiffness index and pulse pressure were higher in women (0.42 vs. 0.40 and 57.0 vs. 55.3 mmHg, respectively). For the entire group, the correlation between ambulatory arterial stiffness index and pulse pressure was 0.5. Ambulatory arterial stiffness index is a new measure that is readily available from ambulatory blood pressure monitoring and may provide added prognostic information for cardiovascular outcome.

Surrogate Measures of Arterial Stiffness

Recent epidemiological studies have shown that arterial stiffness, measured through carotid-femoral pulse wave velocity (PWV), has an independent predictive value for cardiovascular (CV) events in several populations, including patients with uncomplicated essential hypertension1,2 and type 2 diabetes.3 Arterial stiffness is thus an intermediate end point for CV events, predicting CV events independently of and beyond peripheral pulse pressure (PP). Peripheral PP, central PP, and augmentation index, which provide additional information on wave reflection, are considered “surrogates” of arterial stiffness, because their pathophysiological meaning is clearly different.4–6 Central PP and augmentation index are dependent on the speed of wave travel, the amplitude of reflected wave, the reflectance point, and the duration and pattern of ventricular ejection, especially with respect to change in heart rate and ventricular contractility. Aortic PWV, which is the speed of wave travel, represents intrinsically arterial stiffness, according to the Bramwell-Hill formula.4–6 Two articles7,8 in the present issue of Hypertension raise the issue of the predictive value of “surrogates of arterial stiffness” for CV events. Li et al7 studied the dynamic relationship between diastolic blood pressure (DBP0 and systolic blood pressure (SBP) in ambulatory blood pressure monitoring (ABPM) data throughout the day and calculated a novel index as 1− the regression slope of DBP on SBP. This index was named ambulatory arterial stiffness index (AASI) on the basis that “average distending BP …

Gender-ethnic differences in increased arterial pulse pressure among young adults

Arterial stiffness (AS) can be measured in a variety of invasive and noninvasive techniques. AS is most frequently seen among older adults as it is considered a sign of aging. Hence, AS studies are sparse among young adults of different ethnic backgrounds. A common, noninvasive, surrogate measure of AS is arterial pulse pressure (APP). The objective of this study was to assess if ethnic differences in APP exist among young adults. College students attending an urban university in Florida were examined cross-sectionally in 2002. Data were initially collected to assess the Coronary Heart Disease Risk Factors among tri-ethnic population. Students of both genders belonging to one of the three ethnic groups (Hispanic, Black not of Hispanic origin, or White not of Hispanic origin) were included in the study. Data collection was performed via several self-administered questionnaires (e.g. Food Frequency, Cardiac Risk Evaluation), measurements of blood pressure (BP), body composition via Bioelectrical Impedance Analysis (BIA), and blood lipid and homocysteine (Hcy) levels. APP is derived mathematically as the difference between systolic and diastolic blood pressure. There were a total of 300 subjects in the current analyses. Mean age (years) and standard deviation (SD) of the subjects was 20.89 ± 3.75. Gender and ethnic breakdown of the study sample were as follows: 150 subjects in each gender group and 100 subjects in each ethnic group. The mean (mmHg) difference between males (43.11 ± 6.13) and females (40.80±8.01) was statistically significant ( p < 0.05). However, ethnic differences were not significant with 41.75±7.65, 41.00±7.69 and 43.12±7.27 for Hispanic, Black not of Hispanic origin, and White not of Hispanic origin respectively. The public health implication derived from a better understanding of the etiologic role of arterial stiffness in cardiovascular disease would be considerable and would play an important role in the prevention of hypertension in later life.

Prevalence of increased arterial pulse pressure among children and adolescents

Purpose Arterial pulse pressure (APP) is used as a noninvasive measurement of arterial stiffness (AS). Most AS studies were conducted in adult populations as it is often considered a phenomenon of aging. The objective of this study is to assess the longitudinal change in prevalence of AS among children and adolescents. Methods The Minneapolis Children's Blood Pressure Study (MCBPS) is a prospective cohort study and the initial (1978) and multiple timed measurements of systolic blood pressure (SBP) and fourth phase diastolic blood pressure (DBP4) were made semiannually or annually. Visit 16 was completed in 1987. Black and white subjects who participated in all 16 visits were included in the analysis (n = 487). APP, a surrogate measure of AS, is derived mathematically as the difference between SBP and DBP4. The level of 60 mmHg or higher of APP was defined as presence of AS. Results There were 218 females, 269 males, 114 blacks and 373 whites. The mean ages of children in visits 1 and 16 were 7.7 (SD = 0.7) and 16.6 (SD = 0.7) years, respectively. Similarly, the mean APP levels at these two visits were 36.3 (SD = 12.0), and 43.6 (SD = 11.5) mmHg, respectively. Prevalence of increased APP varied at each timed point. At the beginning of the study (1978), prevalence was 3.9%. In 1987, prevalence increased to 10.1%. Proportions of those with increased APP ranged from 3.3% to 21.4% during 8 years of follow-up. Conclusion Our results indicate that AS, as defined by APP, exists even during childhood and adolescence. These results should be confirmed by using a more accurate measure of AS that can be used in population studies.

Augmentation index is associated with cardiovascular risk.

Augmentation index is a parameter measured by pulse wave analysis (PWA) and is used as a surrogate measure of arterial stiffness. The aim of this study was to assess whether augmentation index is associated with cardiovascular risk, as well as to evaluate whether the determinants of augmentation index are different in patients with cardiovascular disease compared to healthy subjects. We related augmentation index to risk scores in 216 subjects with or without a cardiovascular disease. Subjects without cardiovascular disease were classified according to the 'coronary risk chart' of the European Society of Cardiology (ESC), and those with cardiovascular disease were classified using the SMART (Second Manifestations of ARTerial disease) score and the EPOZ (Epidemiological Prevention study Of Zoetermeer) function. Augmentation index was derived by PWA using carotid applanation tonometry. Augmentation index was also correlated to age, blood pressure, heart rate, smoking history, cholesterol, height, body mass index and gender in subjects categorized as healthy or with cardiovascular disease. Augmentation index significantly increased with increasing risk scores (P < 0.0001) and was significantly correlated to cardiovascular risk (ESC: P < 0.0001; SMART: P < 0.0001; EPOZ: P < 0.0001). In subjects with and without cardiovascular disease, augmentation index was correlated with diastolic blood pressure, heart rate, height and gender. Age was found to be significantly correlated with augmentation index only in healthy subjects but not in those with atherosclerotic disease. Our findings suggest that augmentation index may be a useful marker of cardiovascular risk. Further studies are required to investigate the relationship between age and augmentation index in subjects with atherosclerotic disease.

Assessment of arterial stiffness in clinical practice.

There has been much recent interest in the relationship between arterial stiffness and cardiovascular disease. Pulse pressure and pulse wave velocity, surrogate measures of arterial stiffness, indicate that arterial stiffness increases both with age and in certain disease states that are themselves associated with increased cardiovascular risk, including hypertension, diabetes mellitus, hypercholesterolaemia and end‐stage renal failure.1 As changes can be detected before the appearance of clinically apparent vascular disease, arterial stiffness may act either as a marker for the development of future atherosclerotic disease, or may be more directly involved in the process of atherosclerosis. Arterial stiffening has been particularly implicated in the development of isolated systolic hypertension, a disease mainly affecting the elderly population and associated with considerable excess morbidity and mortality. Arterial stiffness may be measured using a variety of different techniques, although at present the majority of measurements are made for experimental and physiological studies rather than in clinical practice. However, it is likely that over the next few years measurement of arterial stiffness will become an increasingly important part of the process of risk assessment, and may possibly also improve the monitoring of therapy in patients with conditions such as isolated systolic hypertension. Therefore, it will become necessary for physicians both in primary care and hospital practice to understand the importance of arterial stiffness and the techniques available for its clinical assessment, which will be the focus of this review. Assessment of the arterial pulse has always been an important part of clinical examination, and the ancients recognized that changes in the character of the pulse indicated the presence of disease. However, the ‘golden era’ of the pulse was the 19th century. With the development of the sphygmograph by Marey2 and its refinement over the next few years by Mahomed,3 Broadbent4 and …

Correction of carotid augmentation index for heart rate in elderly essential hypertensives

Carotid augmentation index (AI) is used as a surrogate measure of arterial stiffness. Although arterial stiffness has been shown to either remain unchanged or increase with an increase in heart rate, AI decreases as heart rate increases. This study aimed to quantify this confounding effect of heart rate on AI. We investigated 873 hypertensives, mean age 72 ± 5 years, 44% men, mean brachial blood pressure 161 ± 21/82 ± 11 mm Hg. Carotid artery tonometry with simultaneous continuous wave Doppler measurement of ascending aortic blood flow was performed. AI was calculated from the carotid pressure waveform. Waveforms were decomposed into their forward and backward components and the time to reflection between the maxima of the forward and backward pressure waves was measured. AI showed a stronger ( P < .001) association with ejection time (r = 0.48, P < .001) than with heart rate (r = −0.28, P < .001). Although AI is strongly related to the time to reflection (r = −0.51, P < .001), only a weak association was seen between time to reflection and heart rate (r = 0.16, P < .001) or ejection time (r = −0.12, P < .001). Our analysis in an elderly cohort of patients with essential hypertension demonstrates that AI is related to the time to reflection. It also reiterates that AI is confounded by heart rate without any underlying heart rate-dependent change in wave reflection. In population-based studies the confounding effect of heart rate can potentially be corrected. AI remains strongly (r = −0.52) related to time to reflection after correction for the effects of ejection time on AI.

Changes in the derived central pressure waveform and pulse pressure in response to angiotensin II and noradrenaline in man.

Peripheral pulse pressure provides a surrogate measure of arterial stiffness. Analysis of the central pressure waveform allows assessment of central pulse pressure and arterial stiffness. The aim of the present study was to assess the effect of vasoconstrictor drugs on pulse pressure amplification and arterial stiffness in vivo. Eight healthy male subjects (mean age 30 years) received an infusion of angiotensin II (1, 3, 6 and 10 ng kg(-1) min(-1)), noradrenaline (10, 30, 60 and 100 ng kg(-1) min(-1)) and matching placebo, in random order, on separate occasions. Peripheral blood pressure and cardiac index were recorded non-invasively. Pulse wave analysis was used to determine augmentation index (AIx), which provides a measure of systemic arterial stiffness, aortic stiffness and central arterial pressure. Infusion of both active drugs resulted in a significant increase in peripheral mean arterial pressure (PMAP), peripheral vascular resistance, AIx, aortic stiffness and central pulse pressure, but only angiotensin II reduced cardiac index. Peripheral pulse pressure was unaffected by infusion of angiotensin II but increased with noradrenaline, which also produced a greater reduction in pulse pressure amplification than angiotensin II. However, the linear relationship of PMAP with both AIx and aortic stiffness did not differ significantly between drugs. These results demonstrate that intravenous infusion of angiotensin II and noradrenaline increase aortic and systemic arterial stiffness. Despite a similar effect on both parameters, for a given change in PMAP, the two drugs had divergent effects on peripheral pulse pressure and pulse pressure amplification. These data reveal that assessment of peripheral pulse pressure does not always reliably predict changes in central pulse pressure or arterial stiffness.