134 Clinical methods and pathophysiology
Aortic systolic pressure derived with different calibration
methods: associations to brachial systolic pressure in the
general population
Siegfried Wassertheurera, Bernhard Hametnera, Christopher C. Mayera,
Ahmed Hafezb, Kazuaki Negishic, Theodore G. Papaioannoud,
Athanase D. Protogeroue, James E. Sharmanc and Thomas Weberb
Background There is increasing evidence that the method
of calibration directly influences the association between
brachial systolic blood pressure (bSBP) and estimated aortic
systolic blood pressure (aSBP) and subsequently affects
prognostic and diagnostic differentiation power of the latter.
Objective The aim of this study was to investigate
associations between different methods of systolic
pressure assessment in a large cohort and its comparison
with recently published evidence.
Participants and methods During a public health
campaign, cardiovascular hemodynamic data were assessed
using a validated oscillometric device in a pharmacy setting.
The device measures bSBP, mean arterial pressure, and
diastolic blood pressure (DBP), and records brachial
waveforms at the DBP level. aSBP1 was derived using bSBP
and DBP and aSBP2 using measured mean arterial pressure
and DBP for waveform calibration. In addition to pressures,
age, sex, and anthropometric data were recorded. Regression
analysis was carried out to investigate associations.
Results A total of 7409 (5133/2276, female/male) individuals
with a median age of 54 years were sampled. aSBPs differed
significantly from bSBP (126.0 mmHg) for aSBP1
(117.0 mmHg) and aSBP2 (127.5 mmHg, both P < 0.0001).
Regression analysis showed that aSBP2 (R2 = 0.853) is
significantly less associated with bSBP than aSBP1
Introduction
Noninvasive brachial systolic blood pressure (bSBP) proved
to be a powerful predictor in cardiovascular disease for over a
century on the basis of the method introduced by Riva-
Rocci. The concept of aortic systolic blood pressure (aSBP)
separate from bSBP evolved as a clinical concept within the
last two decades [1]. Recently, it has been argued that the
strong association between both parameters a-priori limits
the incremental clinical value of aSBP [2]. In contrast, actual
clinical evidence suggests that this association is modifiable
by the measurement procedure, in particular, by the cali-
bration method [3–6]. Noninvasive systolic aortic pressure
estimates are commonly derived by either systolic and
diastolic (aSBP1) pressure or mean and diastolic pressure
(aSBP2) calibration [7]. By using bSBP as a direct input
1359-5237 Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.
Copyright r 2018 Wolters Kluwer Health, Inc. All rights reserved.
(R2 = 0.937) (Williams’ test, P < 0.001 for comparison).
Subgroup analysis showed the major influence of sex and
heart rate. The association between bSBP, aSBP1 (R2 = 0.83),
and aSBP2 (R2 = 0.66), respectively, reduced significantly for
borderline hypertensives (P < 0.001 for comparison).
Conclusion In contrast to aSBP1, the association between
bSBP and aSBP2 is significantly less dominant and
therefore aSBP2 may have potential prognostic superiority
over bSBP. Blood Press Monit 23:134–140 Copyright ©
2018 Wolters Kluwer Health, Inc. All rights reserved.
Blood Pressure Monitoring 2018, 23:134–140
Keywords: aortic blood pressure, arterial stiffness, brachial blood pressure,
calibration
a
Department of Biomedical Systems, Center for Health & Bioresources, Austrian
Institute of Technology (AIT), Vienna, bDepartment of Cardiology, Klinikum Wels-
Grieskirchen, Wels, Austria, cMenzies Institute for Medical Research, University of
Tasmania, Hobart, Tasmania, Australia, dBiomedical Engineering Unit, First
Department of Cardiology, Medical School, Hippokration Hospital and
e
Cardiovascular Prevention and Research Unit, Department of Pathophysiology,
‘Laiko’ Hospital, Medical School, National and Kapodistrian University of Athens,
Athens, Greece
Correspondence to Siegfried Wassertheurer, MSc, PhD, Center for Health &
Bioresources, Austrian Institute of Technology (AIT), Donau-City Street 1,
1220 Vienna, Austria
Tel: + 43 505 504 830; fax: + 43 505 504 840;
e-mail: siegfried.wassertheurer@ait.ac.at
Received 9 October 2017 Revised 27 February 2018 Accepted 5 March 2018
variable for aSBP1 estimation, an inherent link is established
systematically and a strong association between variables is
predestined. Therefore, aSBP2 calibration waives the use of
bSBP and utilizes measured mean arterial pressure (MAP)
instead to attenuate the influence of bSBP. Among several
studies, aSBP2 consistently showed less association with
bSBP compared with traditional calibrated aSBP1, and fur-
thermore, aSBP2 estimates were closer to invasive measured
aortic pressures [3–6]. However, the investigated cohorts
were limited in size and it is still unclear whether the
observed associations between pressures are preserved in
the general population.
Therefore, the primary aim of this work is to investigate
associations between different methods of aSBP assessment
DOI: 10.1097/MBP.0000000000000319

in a large cohort. We aimed to investigate the mechanisms of
systemic differences introduced by different calibrations and
to determine the inherent clinical potential and outcomes.
Participants and methods
Study population
Participation in this study was voluntary and data
assessment was performed during a public health cam-
paign in Summer 2015 in the general population. Design
and procedures were adopted from dedicated preceding
studies [8]. Participants had to be older than 18 years and
were approached by healthcare personal in pharmacies
and public places, and were asked whether they would
be interested in having their blood pressure measured. In
addition to blood pressure, heart rate, sex, height, weight,
and age were recorded. Consent was provided for anon-
ymized processing of data and dissemination of results.
The study protocol adhered to the Declaration of
Helsinki and was approved by the local ethics committee.
Earlier published invasive validation data [9] were used
for additional retrospective analyses to confirm observed
trends in noninvasive data.
Brachial and aortic blood pressure measurement
Blood pressure readings were performed in a dedicated,
quiet area by healthcare professionals and trained para-
medics after at least a minute of rest [10]. The Mobil-O-
Graph PWA (IEM GmbH, Stolberg, Germany) device
used for the measurements is a validated oscillometric
sphygmomanometer with a brachial cuff [11,12] and
inbuilt ARCSolver (Austrian Institute of Technology,
Vienna, Austria) pulse wave analysis to provide aSBP
among other parameters [13]. For aSBP, this particular
configuration has been validated extensively against
invasive solid-state catheters and against tonometry with
respect to reproducibility, accuracy, and feasibility by
different groups [8,9,14]. Furthermore, it has been
cleared by the USA (Food and Drug Administration),
Europe (CE), and Japan (JPAL) regulatory authorities.
Calibration
In the absence of an invasive pressure, there is no alter-
native to the use of a noninvasive calibration mechanism,
although the method of calibration strongly influences the
desired magnitude of absolute values provided by a method
[3,7]. Actual methods for the noninvasive quantification of
aSBP often use a generalized transfer function [13,15,16] to
convert the shape of recorded peripheral pulse waves into
estimates of aortic pulse wave shapes. Various transfer
function such as methods from different research groups
have shown their ability to predict aortic pressure on the
basis of invasive pressure reading and the concept of per-
ipheral waveform transformation [17,18]. By definition, this
waveform transformation is based on relative numbers and
is invariant to absolute pressure levels. Typically, positive
aortic to peripheral pressure wave amplification is observed.
The noninvasive quantification of this dimensionless wave
Copyright r 2018 Wolters Kluwer Health, Inc. All rights reserved.
Aortic systolic pressure Wassertheurer et al. 135
shape amplification into a physical unit such as ‘Torr’
(mmHg) or ‘Pascal’ (Pa) requires an external (sphygmo)
manometer. As reported earlier [18], the Mobil-O-Graph
(IEM GmbH) device provides different methods of pulse
wave calibration. Method 1 (aSBP1) is based on brachial
systolic and diastolic pressure, which is the most commonly
used method in the literature independent of a specific
device [13,14]. Method 2 (aSBP2) uses measured brachial
MAP on the basis of the maximum magnitude of the
oscillogram and diastolic pressure. This feature of the
Mobil-O-Graph devices has been validated successfully
against invasive solid-state catheters [9]. Furthermore, it is
important to consider that unlike peripheral SBP and DBP,
various definitions for noninvasive MAP have been pro-
posed [19] that are not fully investigated here.
Statistics
All statistical analyses were carried out using MedCalc
Statistical Software, version 16.4.3 (MedCalc Software
bvba, Ostend, Belgium). For the continuous investiga-
tion of associations among variables, regression analysis
and Williams’ test were used. Furthermore, multiple
regression analysis was carried out to study determinants
of differences. For subgroup analysis, we categorized the
sample into age deciles (20–29, 30–39, 40–49, 50–59,
60–69, 70–79, 80 +) and brachial blood pressure cate-
gories (optimal, <120/80; normal, > 120/80 to <130/85;
high normal, > 130/85 to <140/90; grade I hypertension,
> 140/90 to <160/100; and grade II/III hypertension,
> 160/100 mmHg) [15]. Wilcoxon, Mann–Whitney, or
Kruskal–Wallis tests were used as appropriate. A
threshold value of 130 mmHg with respect to aSBP2 for
the presence of hypertension was defined [20].
Results
Overall 7409 individuals (2276 men and 5133 women)
with a median age of 54 years (age range: 20–100 years)
were included in the analysis. Baseline results are shown
in Table 1.
Associations between systolic pressures
Regression analysis showed that aSBP2 (R2 = 0.85) is
significantly (Williams’ test, all P < 0.001 for comparison)
less associated with bSBP than aSBP1 (R2 = 0.94) as
shown in Fig. 1. In the selective subgroup analysis with
respect to bSBP, aSBP2 always showed a significantly
lower R2 than aSBP1 for each pressure and age category.
Stratification for sex showed significant effects between
calibrations and groups as shown in Fig. 2. Furthermore,
it is notable that the categorization of blood pressure
categories ‘normal’, ‘high normal’, and ‘grade 1 hyper-
tension’, representing 4536 patients or about 61% of our
cohort, leads to associations between bSBP, aSBP1, and
aSBP2 of R2 = 0.83 and 0.66, respectively. Differences in
sex (male/female) are consistent and again more pro-
nounced for aSBP2 (R2 = 0.59 vs. 0.70) than for aSBP1
(R2 = 0.81 vs. 0.83).
136 Blood Pressure Monitoring 2018, Vol 23 No 3

Magnitudes of systolic pressure earlier catheter data [6]. As shown in Fig. 4a and b, the same
Table 1 shows that the mode of calibration obviously trends could be observed for invasive aortic data compared
influences the magnitude of aSBP estimation and even with traditional (brachial oscillometric) bSBP.
shows apparently higher aSBP2 compared with brachial
This difference in absolute pressure values may lead to
readings (Wilcoxon test, P < 0.001). misleading classifications of hypertension between methods
In contrast, aSBP1 typically shows a positive aortic to per- as exemplarily illustrated in the upper left rectangle of
ipheral systolic amplification. Figure 3a shows that the Fig. 1 showing 1721 individuals (∼23% of the total cohort)
apparent negative aortic to peripheral systolic amplification being normotensive according to bSBP (≤ 140 mmHg), but
for aSBP2 is not constant over the lifespan. The influence of being hypertensive as stratified by aSBP2 (≥130 mmHg).
pressure levels is presented by the Bland–Altman plot in
Fig. 3b, showing a slight inverse trend and a mean difference Analysis of differences
of about 1 mmHg with 95% limits of agreement between As reported in Table 2, the continuous analysis of the
bSBP and aSBP2 of about ± 13 mmHg. To invasively con- determinants of differences between aSBP1 and the
firm the trends depicted in Fig. 3a and b, we reanalyzed mean pressure-derived aSBP2 showed the differential
influence of tested confounders. Heart rate and sex
turned out to be clinically relevant determinants in this
Table 1 Baseline data particular relation, whereas the influence of age and
Male (N = 2276) Female (N = 5133) actual blood pressure levels did not differ significantly
between calibrations. Heart rate and age showed a weak,
2.5–97.5 2.5–97.5
Median percentiles Median percentiles but significant inverse relation in our data.
Age (years) 54 24–83 54 20–81
HR (1/min) 76 54–104 76 58–103 Discussion
MAP (oscillations) 106 85–133 99 79–129 The presented study evaluated the relation between bSBP
(mmHg)
DBP (mmHg) 84 63–109 77 58–102 and aSBP, with a focus on the influence of different calibration
bSBP (mmHg) 131 107–168 124 100–165 methods for aSBP estimation in a cohort of 7409 participants.
aSBP1 (mmHg) 121 98–153 115 92–153
aSBP2 (oscillations) 133 109–173 125 101–167
(mmHg) Associations between systolic pressures
aSBP, aortic systolic blood pressure; bSBP, brachial systolic blood pressure; The first finding was that the associations between bSBP
DBP, diastolic blood pressure; HR, heart rate; MAP, mean arterial pressure. and aSBP2 on a large cohort level did not change markedly

Fig. 1

Regression on the cohort level. Associations between bSBP, aSBP1, and aSBP2, respectively, show different offsets and slopes (right). The upper
left quarter represents those readings that are normotensive according to bSBP (dotted vertical line, ≤ 140 mmHg, x-axis), but hypertensive according
to aSBP1 (left) and aSBP2 (center) (dotted horizontal line, ≥ 30 mmHg, y-axis). aSBP, aortic systolic blood pressure; bSBP, brachial systolic blood
pressure; HTN, hypertension.

Copyright r 2018 Wolters Kluwer Health, Inc. All rights reserved.


Fig. 2
Associations between bSBP and aSBP1 (lighter gray bars) and bSBP and aSBP2 (darker gray bars) by sex and age groups (a, b) as well as
hypertension classes (c, d). The numbers on top of the bars represent the according regression coefficients (R2). aSBP, aortic systolic blood
pressure; bSBP, brachial systolic blood pressure.
(Fig. 1) compared with earlier reported data in small
populations and therefore is highly relevant as the con-
firmation of this disparity in large cohorts provides a formal
rationale for earlier published results with respect to
hypertensive end organ damage and all-cause mortality
[4–6,18,21]. According to these data, the most promising
application of aSBP2 is among people with borderline
hypertension (e.g. upper normal to grade 1 hypertension)
because of the observation that only 66% of aSBP2 are
explained by bSBP in this subgroup.
Magnitudes of systolic pressures
Mediated by heart rate and sex, the second key finding
was that different calibrations finally led to different
classifications in hypertension. The observed influence
of the calibration method on the magnitude of aSBPs
reported in Table 1 as well as its causes, including the
nonphysiological effects of apparent negative central on
peripheral pressure amplification, have already been
observed and particularly explained in the recent litera-
ture [18,22–24]. In contrast, brachial systolic and diastolic
pressures actually used in clinical routine relate to a dif-
ferent reference standard (Korotkoff) than measured
MAP (invasive pressure by catheter). Furthermore, only
Copyright r 2018 Wolters Kluwer Health, Inc. All rights reserved.
Aortic systolic pressure Wassertheurer et al. 137
the oscillometric method, but not the Korotkoff method,
can directly measure MAP noninvasively. This leads to
inherent methodological offsets. Given a pressure-
invariant transfer function, different pressure measure-
ment paradigms will lead to consistent results within each
particular paradigm (aSBP1 and bSBP Korotkoff-based),
but will be misleading if methods are mixed (aSBP2
MAP-based and bSBP Korotkoff-based). In contrast,
the results of the determinants of differences analysis
presented in Table 2 underpin that differences between
aSBP1 and aSBP2 in relation to bSBP are also because
of a different sensitivity to heart rate and sex, and
that aSBP2 obviously depends more on the actual wave
shape than aSBP1. Similar effects have been reported and
explained earlier for different calibrations with respect to
pulse pressure amplification [25]. The latter seems to be a
more direct successor of bSBP from a mathematical view-
point. This novel numerical exploration is therefore in line
with physiological evidence showing that female waveforms
differ significantly in shape compared with those from
males [1,26]. Furthermore, systolic pressure amplification
among bSBP and aSBP2 (as illustrated in Fig. 3a) shows a
nonlinear pattern over the investigated age decades. In the
younger individuals, the brachial cuff overestimates aSBP2
138 Blood Pressure Monitoring 2018, Vol 23 No 3

Fig. 3 Fig. 4

Differences between bSBP and aSBP2 over age groups (a) and
pressure range (b). Younger and individuals with lower pressures are Scatterplot (a) of differences between noninvasive oscillometric brachial
overestimated by bSBP compared with aSBP2 and vice versa. aSBP, systolic pressure and invasive aortic catheter pressure over age shows
aortic systolic blood pressure; bSBP, brachial systolic blood pressure. that younger individuals’ blood pressure is overestimated by brachial
cuff measurement compared with aortic catheter measurement and
vice versa. (b) Bland–Altman plot shows that brachial cuff measurement
overestimates lower systolic pressure compared with aortic catheter
readings. Trends in both plots are significant. aSBP, aortic systolic blood
significantly, but around the age of 40, this association is pressure; bSBP, brachial systolic blood pressure.
inverted. A similar effect can be observed in Fig. 4a for the
invasive data. Furthermore, Figs 3b and 4b show that tradi-
tional brachial cuff measurements seem to overestimate at
lower systolic pressures, but underestimate at higher systolic Table 2 Determinants of differences between aSBP1 and aSBP2
pressures compared with aSBP2. Similar observations with
aSBP1 − aSBP2 Coefficient SE Rpartial P
respect to brachial cuff and invasive pressures have been
reported by several invasive studies [27–29]. These results Constant − 36.0170
Age − 0.03394 0.004223 − 0.093 < 0.001
are remarkable with respect to pressure classification and the Sex 5.7493 0.9101 0.073 < 0.001
discussion on spurious hypertension in young individuals. Heart rate 0.4435 0.01997 0.249 < 0.001
Sex × heart rate − 0.05635 0.01168 −0.055 < 0.001

Analysis of differences aSBP, aortic systolic blood pressure.

The third key finding was that calibration influences the
differences between aSBP1 and aSBP2 for a given aortic
waveform (Table 2) and that heart rate and sex play a
predominant role in this association. With respect to the
contribution of heart rate, a change of 10 beats/min for a
given patient will affect the absolute difference between
aSBP1 and aSBP2 by 4.4 mmHg. This reflects a remarkable
relation between peripheral pressure, calibration mode, and
transfer function. In other words, not only the magnitude
and amplitude of the peripheral pressure but also the cho-
sen transfer function affect the resulting aortic pressure.
The calibration method itself contributes independently
toward the result.

Copyright r 2018 Wolters Kluwer Health, Inc. All rights reserved.


Potential clinical consequences
The clinical outcome on the basis of the analyses is
therefore the observed apparent inconclusive classi-
fication of 1721 patients with respect to hypertension.
This subsequently means that classification of risk rela-
ted to BP may be significantly different because these
individuals are labeled as normotensive on the basis of
cuff bSBP, but in fact may have hypertension accord-
ing to aSBP2 thresholds. This has potential clinical
impact, especially in the light of a recently published
meta-analysis on the accuracy of brachial blood pressure
measurement in comparison with invasive catheter
measurements [30]. The mentioned work reports that
the accuracy of traditionally brachial cuff techniques is
significantly lower in the range between 130 and
160 mmHg. Misleading classification of hypertension is
likely to be a clinical consequence also with respect
to proper therapy. Another important point is the con-
sideration of different classifications whenever patient
matching or aggregation to comparable groups before
prospective tests or studies is needed. Therefore, further
investigations and research addressing this issue seem
worthwhile and promising. As discussed, several recent
studies showed the incremental prognostic value of
aSBP2 over bSBP. The data of this study suggest that
this physiologically relevant superiority can be shown
because of the reduced correlation between bSBP and
aSBP2 compared with aSBP1. This highlights that aSBP2
has a higher degree of freedom (i.e. variability) from the
cuff-based bSBP than suggested initially by aSBP1 [31].
For these reasons, we strongly recommend that in future
research studies, aSBP should not be calculated mathe-
matically (by adding a systematic error), but measured
by the available methodology of DBP and mean blood
pressure (aSBP2) calibration.
Limitations
It needs to be considered that the study is cross sectional
in nature and patient selection was uncontrolled; thus, no
information for smoking, dietary habits, or activities
before measurement is known. Furthermore, the results
may be device dependent.
Conclusion
The presented findings potentially influence future
considerations on diagnostic thresholds, patient matching
in case–control settings, reference values as well as efforts
toward invasive validation procedures for MAP. To our
knowledge, this is the first study in which this behavior
has been analyzed and reported in this context, and the
findings warrant further investigations.
Acknowledgements
This work was supported by the program ‘Talente’ by the
Austrian Ministry for Transport, Innovation and Technology
BMVIT (FEMCOR Project, FFG no. 849808). S.W. and
Copyright r 2018 Wolters Kluwer Health, Inc. All rights reserved.
Aortic systolic pressure Wassertheurer et al. 139
C.M. are inventors (not holder) of a patent that is used in the
ARCSolver method.
Conflicts of interest
There are no conflicts of interest.
References
1 Nichols WW, O’Rourke MF. McDonald’s blood flow in arteries, 4th ed.
London, UK: Arnold; 1998.
2 Mitchell GF. Central pressure should not be used in clinical practice. Artery
Res 2015; 9:8–13.
3 Papaioannou TG, Karageorgopoulou TD, Sergentanis TN, Protogerou AD,
Psaltopoulou T, Sharman JE, et al. Accuracy of commercial devices and
methods for noninvasive estimation of aortic systolic blood pressure a
systematic review and meta-analysis of invasive validation studies.
J Hypertens 2016; 34:1237–1248.
4 Negishi K, Yang H, Wang Y, Nolan MT, Negishi T, Pathan F, et al. Importance
of calibration method in central blood pressure for cardiac structural
abnormalities. Am J Hypertens 2016; 29:1070–1076.
5 Protogerou AD, Argyris AA, Papaioannou TG, Kollias GE, Konstantonis GD,
Nasothimiou E, et al. Left-ventricular hypertrophy is associated better with
24-h aortic pressure than 24-h brachial pressure in hypertensive patients: the
SAFAR study. J Hypertens 2014; 32:1805–1814.
6 Nakagomi A, Okada S, Shoji T, Kobayashi Y. Crucial effect of calibration
methods on the association between central pulsatile indices and coronary
atherosclerosis. Am J Hypertens 2017; 30:24–27.
7 Mahieu D, Kips J, Rietzschel ER, de Buyzere ML, Verbeke F, Gillebert TC,
et al. Asklepios Investigators. Noninvasive assessment of central and
peripheral arterial pressure (waveforms): implications of calibration methods.
J Hypertens 2010; 28:300–305.
8 Nunan D, Wassertheurer S, Lasserson D, Hametner B, Fleming S, Ward A,
Heneghan C. Assessment of central haemomodynamics from a brachial cuff
in a community setting. BMC Cardiovasc Disord 2012; 12:48.
9 Weber T, Wassertheurer S, Rammer M, Maurer E, Hametner B, Mayer CC,
et al. Validation of a brachial cuff-based method for estimating central systolic
blood pressure. Hypertension 2011; 58:825–832.
10 Mancia G, Fagard R, Narkiewicz K, Redón J, Zanchetti A, Böhm M, et al. Task
Force Members. 2013 ESH/ESC guidelines for the management of arterial
hypertension: the Task Force for the management of arterial hypertension of
the European Society of Hypertension (ESH) and of the European Society of
Cardiology (ESC). J Hypertens 2013; 31:1281–1357.
11 Franssen PM, Imholz BP. Evaluation of the Mobil-O-Graph new generation
ABPM device using the ESH criteria. Blood Press Monit 2010;
15:229–231.
12 Weiss W, Tölle M, Zidek W, van der Giet M. Validation of the mobil-O-Graph:
24 h-blood pressure measurement device. Blood Press Monit 2010;
15:225–228.
13 Wassertheurer S, Kropf J, Weber T, van der Giet M, Baulmann J, Ammer M,
et al. A new oscillometric method for pulse wave analysis: comparison with a
common tonometric method. J Hum Hypertens 2010; 24:498–504.
14 Weiss W, Gohlisch C, Harsch-Gladisch C, Tölle M, Zidek W, van der Giet M.
Oscillometric estimation of central blood pressure: validation of the Mobil-O-
Graph in comparison with the SphygmoCor device. Blood Press Monit
2012; 17:128–131.
15 Karamanoglu M, O’Rourke MF, Avolio AP, Kelly RP. An analysis of the
relationship between central aortic and peripheral upper limp pressure
waves in man. Eur Heart J 1993; 14:160–167.
16 Chen C, Nevo E, Fetics B, Pak P, Yin F, Maughan L, et al. Estimation of
central aortic pressure waveform by mathematical transformation of radial
tonometry pressure: validation of generalised transfer function. Circulation
1997; 95:1827–1836.
17 Pauca AL, O’Rourke MF, Kon ND. Prospective evaluation of a method for
estimating ascending aortic pressure from the radial artery pressure
waveform. Hypertension 2001; 38:932–937.
18 Wassertheurer S, Baumann M. Assessment of systolic aortic pressure and
its association to all cause mortality critically depends on waveform
calibration. J Hypertens 2015; 33:1884–1888.
19 Papaioannou TG, Protogerou AD, Vrachatis D, Konstantonis G, Aissopou E,
Argyris A, et al. Mean arterial pressure values calculated using seven different
methods and their associations with target organ deterioration in a single-
center study of 1878 individuals. Hypertens Res 2016; 3:640–647.
20 Cheng HM, Chuang SY, Sung SH, Yu WC, Pearson A, Lakatta EG, et al.
Derivation and validation of diagnostic thresholds for central blood pressure
140 Blood Pressure Monitoring 2018, Vol 23 No 3
measurements based on long-term cardiovascular risks. J Am Coll Cardiol
2013; 62:1780–1787.
21 Weber T, Wassertheurer S, Schmidt-Trucksäss A, Rodilla E, Ablasser C,
Jankowski P, et al. Relationship between 24-hour ambulatory central systolic
blood pressure and left ventricular mass: a prospective multicenter study.
Hypertension 2017; 70:1157–1164.
22 Papaioannou TG, Vavuranakis M, Tousoulis D. Calibration of noninvasive
central blood pressure devices and negative aortic-to-brachial systolic
pressure amplification. Kidney Int 2017; 91:253–254.
23 Wassertheurer S, Hametner B, Sharman J, Weber T. Systolic blood pressure
amplification and waveform calibration. Hypertens Res 2017; 40:518.
24 Boutouyrie P, London GM, Sharman JE. Estimating central blood pressure in
the extreme vascular phenotype of advanced kidney disease. Kidney Int
2016; 90:736–739.
25 Agnoletti D, Zhang Y, Salvi P, Borghi C, Topouchian J, Safar ME. Pulse
pressure amplification, pressure waveform calibration and clinical
applications. Atherosclerosis 2012; 224:108–112.
26 Segers P, Mahieu D, Kips J, Rietzschel E, de Buyzere M, de Bacquer D,
et al. Asklepios Investigators. Amplification of the pressure pulse in the
upper limb in healthy, middle-aged men and women. Hypertension 2009;
54:414–420.
Copyright r 2018 Wolters Kluwer Health, Inc. All rights reserved.
27 Finnegan TP, Spence JD, Wong DG, Wells GA. Blood pressure
measurement in the elderly: correlation of arterial stiffness with
differences between intra-arterial and cuff pressures. J Hypertens
1985; 3:231–235.
28 Fagher B, Magnusson J, Thulin T. Direct and indirect blood pressure in
normotensive and hypertensive subjects. Intern Med 1994; 236:85–90.
29 Pickering TG, Hall JE, Appel LJ, Falkner BE, Graves J, Hill MN, et al.
Subcommittee of Professional and Public Education of the American Heart
Association Council on High Blood Pressure Research. Recommendations
for blood pressure measurement in humans and experimental animals: Part
1: blood pressure measurement in humans: a statement for professionals
from the Subcommittee of Professional and Public Education of the
American Heart Association Council on High Blood Pressure Research.
Hypertension 2005; 45:142–161.
30 Picone D, Schultz MG, Otahal P, Aakhus S, Al-Jumaily AM, Black JA, et al.
Accuracy of cuff-measured blood pressure: systematic reviews and meta-
analyses. J Am Coll Cardiol 2017; 70:572–586.
31 Chemla D, Hébert JL, Aptecar E, Mazoit JX, Zamani K, Frank R, et al.
Empirical estimates of mean aortic pressure: advantages, drawbacks and
implications for pressure redundancy. Clin Sci (Lond) 2002; 103:7–13.