Am J Physiol Heart Circ Physiol 289: H2497–H2502, 2005.
First published July 15, 2005; doi:10.1152/ajpheart.00411.2005.
Waveform dispersion, not reflection, may be the major determinant of aortic
pressure wave morphology
Sarah A. Hope,1,2 David B. Tay,3 Ian T. Meredith,1,2 and James D. Cameron1,2
1
Cardiovascular Research Centre, Monash Medical Centre, 2Monash
University, and 3La Trobe University, Melbourne, Victoria, Australia
Submitted 25 April 2005; accepted in final form 13 July 2005
augmentation index; pressure wave reflection; Fourier analysis; aorta
central systolic blood pressure
determines cardiac afterload and is thus a determinant of
cardiac work and energy requirement. In both physiological
and pathological states central blood pressure is considered to
result from the interaction of the heart and systemic vasculature
through peripheral resistance and large-artery impedance. Central (as opposed to brachial) blood pressure has been proposed
to be important in causing or accelerating cardiovascular pathology and in determining risk (21, 25), and techniques
involving aortic pressure “pulse wave analysis” have been
proposed to predict cardiovascular risk. If central blood pressure is indeed a more relevant determinant of cardiovascular
function than conventional brachial blood pressure or if, as has
also been suggested, the difference in central and brachial
systolic blood pressure is a risk indicator, knowledge of what
determines the central blood pressure waveform is essential to
target appropriate intervention.
The augmentation of central systolic pressure, associated
with cardiovascular mortality, is often described by the aug-
IN NORMAL PHYSIOLOGICAL STATES
Address for reprint requests and other correspondence: J. D. Cameron,
Cardiovascular Research Centre, Monash Medical Centre, 246 Clayton Rd.,
Clayton, Victoria 3168, Australia (e-mail: [email protected].
edu.au).
http://www.ajpheart.org
mentation index (16). Although not universally accepted, the
augmentation of central pressure is widely believed to result
from the superimposition upon the forward traveling wave,
resulting from cardiac contraction, of a pressure wave returning from a peripheral reflection site (11, 19). The site of the
putative reflection point has been debated, with some authors
suggesting the predominant reflection point to be either at the
renal arteries or at the aortic bifurcation and others suggesting
that the reflection point has no physical reality but represents
the combined effects of reflection from many peripheral sites
(8, 9, 14). Consistent with the hypothesis of wave reflection are
the findings that increased central augmentation index is associated with increased pulse wave velocity, when the reflected
wave would be expected to return earlier in systole because of
the decreased transit time, and independently associated with
small height (22), when the reflected wave would be expected
to return earlier in systole because of the shorter distance to the
putative reflection point (15, 16, 22).
According to the hypothesis that central pressure augmentation is caused by the reflection of pressure waves from the
periphery, the time to the inflection point on the pressure
waveform, marking the putative onset of influence of a reflected wave, would be expected to decrease, and the augmentation index to increase, with distal progression from the aortic
root toward the putative reflection point. This hypothesis has
been previously tested, and supported, in only two small
groups of subjects (14, 18).
METHODS
The study was performed in the cardiac catheterization laboratory
of Monash Medical Centre. The study was approved by the institutional Human Research and Ethics Committee and performed in
accordance with institutional guidelines. Participants gave written
informed consent. Forty subjects, twenty-six men and fourteen
women, were studied at the time of clinically indicated coronary
angiography (32 subjects) or percutaneous coronary intervention (8
subjects). Mean age was 65 ⫾ 12 yr, mean height 170 ⫾ 8 cm, mean
weight 79 ⫾ 14 kg, and mean body mass index 28 ⫾ 5 kg/m2. Four
subjects were current smokers, and twenty-two had hypertension, nine
diabetes mellitus, thirty-four hypercholesterolemia, and nine family
history of cardiovascular disease. All subjects were in sinus rhythm at
the time of the study.
Data acquisition. Data were acquired under baseline conditions
after completion of the clinically indicated procedure. Aortic waveforms were acquired with a 2-Fr Millar Mikro-tip catheter transducer
introduced via a 6-Fr multipurpose or right coronary guiding catheter
positioned at the aortic root under fluoroscopic control. The Millar
transducer was positioned just distal to the tip of the guiding catheter.
The costs of publication of this article were defrayed in part by the payment
of page charges. The article must therefore be hereby marked “advertisement”
in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
0363-6135/05 $8.00 Copyright © 2005 the American Physiological Society
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Hope, Sarah A., David B. Tay, Ian T. Meredith, and James D.
Cameron. Waveform dispersion, not reflection, may be the major
determinant of aortic pressure wave morphology. Am J Physiol Heart
Circ Physiol 289: H2497–H2502, 2005. First published July 15, 2005;
doi:10.1152/ajpheart.00411.2005.—The objective of this study was to
investigate the determinants of aortic pressure waveform morphology
in the thoracoabdominal aorta with specific reference to features of
potential prognostic value for cardiovascular disease. In particular, we
aimed to determine the location of major pressure wave reflection
sites within the aorta. Aortic pressure waveforms were acquired with
2-Fr Millar Mikro-tip catheter transducers in 40 subjects (26 men, 14
women), and repeated in 10 subjects, at five predetermined points
within the aorta: aortic root, transverse arch, and at the levels of the
diaphragm, renal arteries, and aortic bifurcation. Waveforms were
analyzed for augmentation index (AI), time to inflection point (Ti),
and pressure parameters. AI decreased progressively between the
aortic root and bifurcation (P ⬍ 0.001), and Ti increased (P ⬍ 0.01).
There was the expected progressive peripheral amplification of systolic and pulse pressures and fall in time to peak pressure (all P ⬍
0.001). There was no difference on repeat pullback or between sexes.
These data are at variance with the concept that central AI results
solely from pressure wave reflection, when Ti would be expected to
decrease and AI increase with distal progression. Pressure wave
propagation phenomena may contribute, and the potential role of
frequency dispersion merits investigation.
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PRESSURE WAVE MORPHOLOGY AND FREQUENCY DISPERSION
Frequency-domain waveform analysis. Ten representative waveforms defined by the R-R interval of the electrocardiogram were
identified for each aortic site for each subject. These were averaged
and subjected to a 256-point fast Fourier transformation spectral
analysis, yielding a fundamental frequency of 0.78 Hz for transfer
function derivation. Although there was a short time interval between
the acquisition of data from the different sites, the average waveforms
were assumed to be acquired simultaneously for the purposes of the
derivation of transfer functions between the aortic sites using the R
wave as the constant reference point (the waveform at the proximal
site was defined as the input and that at the distal site as the output of
the system). For each subject apparent phase velocities were calculated from the local gradient of the phase of the transfer function
between the aortic root and distal sites and the measured distance
between the two sites.
Statistical analysis. All continuous variables are presented as
means (SD) or graphically as means ⫾ SE. The change in waveform
parameters with distal progression along the aorta was assessed by
repeated-measures analysis of variance. Within subjects simple contrasts were explored to identify where significant differences lay.
Significance was taken as P ⬍ 0.05, and statistical analysis was
performed with SPSS 11.0 for Windows (SPSS).
Fig. 1. Top: schematic representation of the
describing parameters used for waveform
analysis. Abbreviations are given in Table 1.
Bottom: example of recorded pressure waveforms at given points in the aorta. Decreasing augmentation index with distal progression along the aorta is highlighted. From
inferior to superior the traces represent the
electrocardiogram and pressure waveforms
at the aortic root (augmentation index 52.3%),
transverse arch (augmentation index 45.0%),
level of the diaphragm (augmentation index
20.8%), level of the renal arteries (augmentation index 14.7%) and aortic bifurcation
(augmentation index 14.6%) in a single subject, synchronized to the peak of the R wave
of the electrocardiogram.
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Waveforms were recorded to a personal computer with Chart for
PowerLab (ADInstruments) at 2,000 Hz. After the acquisition of 30 s
of data from the aortic root, the guiding catheter and Millar transducer
were pulled back together and similar data were recorded from the
transverse aortic arch, the level of the diaphragm, the level of the renal
arteries, and at the aortic bifurcation. All positions were confirmed by
fluoroscopy, and the levels of the renal arteries and aortic bifurcation
were also confirmed by angiography. The physical distance between
recording sites was measured by the use of a marker catheter. The
electrocardiogram was recorded simultaneously with all pressure
measurements.
In 10 subjects the catheter and transducer were repositioned at the
same point at the aortic root guided by fluoroscopy and the marker
catheter. Repeat data were then acquired from the same five aortic
points. Data were resampled at 200 Hz for waveform analysis.
Time-domain waveform analysis. Ten representative waveforms
identified by the onset of the systolic pressure upstroke were analyzed
for each subject for each of the five aortic sites. In those subjects
experiencing ectopic beats, preectopic, ectopic, and postectopic beats
were excluded from analysis. Waveforms were analyzed for waveform characteristics of potential clinical interest with purpose-written
software, as previously described (Fig. 1, top; Ref. 10).
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PRESSURE WAVE MORPHOLOGY AND FREQUENCY DISPERSION
Table 1. Waveform characteristics at five aortic sites
Arch
Diaphragm
Renal
Bifurcation
0.059 (0.015)
63 (10)
135 (22)
68 (10)
92 (13)
67 (21)
53.26 (12.50)
38.27 (8.80)
1.43 (0.35)
31.3 (19.6)
0.127 (0.028)
0.336 (0.037)
0.242 (0.037)
112 (17)
23 (17)
0.066 (0.017)
63 (10)
136 (23)
68 (10)
90 (18)
68 (20)
54.16 (12.88)
38.18 (8.25)
1.45 (0.34)
20.3 (14.9)
0.140 (0.029)
0.329 (0.035)
0.230 (0.033)
120 (20)
15 (12)
0.089 (0.020)
62 (11)
142 (23)
72 (10)
96 (12)
70 (20)
57.30 (13.83)
38.43 (9.68)
1.64 (0.99)
16.4 (9.9)
0.138 (0.026)
0.321 (0.033)
0.215 (0.028)
130 (18)
12 (8)
0.103 (0.023)
63 (11)
141 (23)
69 (10)
93 (13)
72 (19)
54.33 (13.04)
38.40 (8.25)
1.44 (0.33)
11.2 (11.1)
0.146 (0.035)
0.316 (0.032)
0.199 (0.029)
134 (20)
9.3 (9)
0.111 (0.024)
64 (11)
143 (24)
69 (10)
93 (14)
75 (19)
53.48 (12.99)
38.73 (9.09)
1.41 (0.35)
7.9 (9.1)
0.156 (0.044)
0.316 (0.035)
0.193 (0.030)
138 (24)
7 (7)
Brachial
140 (22)
73 (10)
95 (12)
67 (18)
Variables are presented as means (SD). Delay, time between electrocardiogram and foot of pressure wave; SBP, systolic blood pressure, DBP, diastolic blood
pressure; MAP, mean arterial pressure; PP, pulse pressure; Ad, diastolic pressure time integral (area under diastolic portion of pressure waveform); As, systolic
pressure time integral (area under systolic portion of pressure waveform); SVI, subendocardial viability index; AP, augmentation pressure; AI, augmentation
index [(AP/PP) ⫻ 100]; Ti, time to the inflection; Ts, time to the end of systole; Tp, time to peak pressure; Pi, pressure at the inflection. All times (except Delay)
are relative to the start of systole. *P ⬍ 0.05, †P ⬍ 0.01, ‡P ⬍ 0.001 for difference between aortic sites.
RESULTS
Waveform characteristics at the five aortic sites, together
with noninvasively measured brachial pressures, are detailed in
Table 1. An example of waveforms from the five sites in an
individual subject is presented in Fig. 1, bottom. Terminology
and abbreviations used to describe waveform morphology are
given in Fig. 1, top, and Table 1. Mean augmentation index
was found to decrease progressively between the aortic root
and bifurcation (P ⬍ 0.001) and time to inflection point was
found to increase (P ⬍ 0.01) (Fig. 2). Despite this, as expected
there was progressive peripheral amplification of systolic and
pulse pressures and a fall in the time to peak pressure (all P ⬍
0.001; Fig. 3). The time to the end of systole also decreased
progressively (Fig. 3). Augmentation index was associated
with both time to inflection point and heart rate (P ⬍ 0.001) but
was not associated with measured pulse wave velocity over any
aortic segment. On multiple regression analysis aortic pulse
wave velocity was associated with proximal pulse pressure and
systolic pressure time integral only (P ⬍ 0.001). Heart rate did
not differ by more than 2 beats/min between individual recordings, and the difference cannot explain the progressive differences observed in the waveform parameters between aortic
sites. There was no difference with sex or between those who
had undergone percutaneous coronary intervention rather than
simple angiography. There was also no difference between the
first and second pullback in the 10 patients who had the
procedure repeated.
Mean arterial blood pressure differed significantly among
the five aortic sites (P ⬍0.05; Fig. 4), with post hoc analysis
revealing the mean arterial pressure to be significantly higher at
the diaphragm than at all other sites (P ⬍ 0.05). However, the
difference between the mean arterial pressure at the aortic root
and the diaphragm was small [3.6 (SD 4.6) mmHg]. The
pattern of diastolic pressure was similar to that of mean arterial
pressure (Fig. 4), with a significant difference between sites
(P ⬍ 0.001) and diastolic pressure being higher at the diaphragm than at all other sites (P ⬍ 0.001). Again, mean
differences between the aortic root and diaphragm were small
[3.7 (3.4) mmHg]. The differences between noninvasively
measured brachial and aortic root mean arterial pressure and
diastolic pressure were also small [3.5 (6) and 5 (6) mmHg,
respectively].
Magnitude and phase diagrams for the average transfer
functions between the aortic root and the four distal aortic sites
are depicted in Fig. 5. There is variability in the slope of the
phase of the transfer functions, and looking particularly at the
transfer functions between the aortic root and diaphragm and
more distal sites, the slope appears flatter for the lower than the
Fig. 2. Mean augmentation index and times
to inflection point at 5 aortic sites. Bars
indicate SE.
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Delay, s‡
Heart rate, min⫺1*
SBP, mmHg‡
DBP, mmHg‡
MAP, mmHg*
PP, mmHg‡
Ad, mmHg䡠s‡
As, mmHg䡠s
SVI
AI, %‡
Ti, s†
Ts, s‡
Tp, s‡
Pi, mmHg‡
AP, mmHg‡
Root
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PRESSURE WAVE MORPHOLOGY AND FREQUENCY DISPERSION
higher harmonics, in keeping with higher phase velocities for
the lower frequencies. The pattern of the calculated phase
velocities for most subjects was consistent with this, with the
measured foot-to-foot pulse wave velocity of the arterial pressure waveform being similar to the average apparent phase
velocity of the higher frequencies (⬎3 Hz) (Fig. 5). However,
in some individuals there were peaks of apparent phase velocity at differing specific harmonics, suggestive of significant
wave reflection at these particular frequencies (Fig. 5).
DISCUSSION
The progressive decrease in augmentation index and corresponding increase in time to the inflection point with distal
progression along the aorta was contrary to the expected
findings according to the hypothesis that the inflection point
marks the onset of influence of a reflected pressure wave.
Although our findings for the time to inflection differ from
those of two previous small studies, there are previously
published waveforms that appear consistent with our observa-
tions (14, 18, 20). Our findings for other waveform characteristics are in accordance with previously published data, with
the expected peripheral amplification of systolic pressure and
pulse pressure and increase in delay in the foot of the pressure
wave and decrease in time to peak pressure (9, 12, 20). It might
be argued that, because our pressure recordings were not
acquired simultaneously from the different aortic sites, there
may have been some systematic change in the physiological
condition of the subjects between recordings that might account for our findings for time to the inflection point. However,
the finding that there was no difference when the measurements were repeated in a group of 10 subjects suggests that this
was not the case. It is interesting to speculate that the differences in mean and diastolic pressures at the diaphragm, and
apparent nonlinear changes in systolic pressure and time to
inflection point, may be due to external constraints on the aorta
as it traverses the diaphragmatic hiatus, leading to apparent
increase in local aortic stiffness. However, the differences
between mean arterial pressure and diastolic pressure at the
Fig. 4. Mean and diastolic pressures at 5
aortic sites. Mean difference between aortic
root and diaphragm in mean arterial pressure
is 3.6 (SD 4.6) mmHg and in diastolic pressure is 3.7 (3.4) mmHg. Bars indicate SE.
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Fig. 3. Peripheral amplification of pressures
and fall in times to peak pressure and end of
systole with distal progression in the aorta.
Bars indicate SE.
PRESSURE WAVE MORPHOLOGY AND FREQUENCY DISPERSION
different aortic sites were small, as were the differences between noninvasively measured brachial and aortic root measurements of both mean and diastolic pressures. Indeed, the
latter lie within the criteria set by the Association for the
Advancement of Medical Instrumentation for equivalence for
blood pressure measuring devices (26). Thus the assumption
that mean and diastolic pressures are equivalent throughout the
arterial system (9), which is often adopted, remains reasonable
on the basis of this data.
Because the findings for augmentation index and time to the
inflection point appear inconsistent with the theory of pressure
wave reflection, the question arises as to what else might be
responsible for this phenomenon. Because it has long been
known that the apparent phase velocities of different frequencies within the arterial pressure waveform differ, with higher
velocities for the lower frequencies (14, 17, 23), consistent
with our data, it is conceivable that the phenomenon of central
pressure augmentation may arise because of frequency dispersion. The foot of the arterial waveform and the augmentation
AJP-Heart Circ Physiol • VOL
point are dependent on high-frequency components of the
waveform (5, 17) and would therefore be predicted to become
relatively delayed compared with the lower-frequency components with distal waveform progression. This concept was first
described by Bramwell and Hill (3) in 1923, in relation to
relative delay in wave front progression, and would be expected to result in the types of progressive changes along the
aorta that have been demonstrated in this study, with relative
delay of both the foot of the pulse wave and inflection point
relative to the peak. The concept is not inconsistent with the
previously described association between a short time to inflection and small stature, although this association was not
evident in our data, because height might simply represent a
surrogate measure of aortic diameter and pulse wave and phase
velocities are determined not only by properties of the arterial
wall but also by the physical dimensions of the vessel, with
pulse wave velocity being inversely proportional to the square
root of the radius (Moens-Korteweg equation) (4). The previously described association between a short time to inflection
and pulse wave velocity might also be explained because the
latter is largely equivalent to the phase velocity of the higher
frequencies in the pulse pressure waveform (17). Alternatively,
if the systemic arterial system is modeled as an asymmetric T
tube, reflections from the shorter (cephalic) branch would be
progressively delayed and attenuated with distal progression in
the longer branch as reported. We feel, however, that there is
unlikely to be sufficient energy reflection from this mechanism
to account fully for our observed waveform morphologies.
Changes in the phase velocities of the higher frequencies,
with or without changes in the lower frequencies, would be
expected to result in a change in the degree of frequency
dispersion, which would be reflected by changes in time to the
inflection point and augmentation index. This phenomenon
also provides a possible explanation for the previously described dissociations between pulse wave velocity and augmentation index observed, for example, after caffeine ingestion, when pulse wave velocity has been described to remain
elevated while the augmentation index has returned toward
baseline levels, and with oral vasoactive drugs (7, 13, 24). It
may be that differential effects on the phase velocities of high
and low frequencies are responsible for observations that
appear inconsistent with wave reflection phenomena.
We do not suggest that the influence of wave reflection
should be completely dismissed. In any wave guiding system
reflection, dispersion and attenuation will be operative and will
be dependent on both guide dimensions and wave frequency.
The findings for the increasing amplitude, particularly of the
sixth harmonic, of the average transfer functions between the
aortic root and progressively more distal sites presented in Fig.
5 suggest that significant reflection of this harmonic may be
occurring either at, or distal to, the aortic bifurcation but that
there is substantial attenuation of the reflected wave at more
proximal sites with much reduced contribution of the reflected
wave at the aortic root. The interpretation of apparent phase
velocities is also complicated by any wave reflection. We have
demonstrated variation in the transfer function phase, which
was significantly more marked in the individual than average
transfer functions and has previously been accepted to indicate
the presence of wave reflection (23). In addition to this, the
peaks in apparent phase velocity seen at individual frequencies
in some subjects are highly suggestive of significant wave
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Fig. 5. Magnitude (top) and phase (middle) diagrams for transfer functions
between pressure waveforms at the 5 aortic sites for all subjects. TF1–2,
between aortic root and arch; TF1–3, between aortic root and diaphragm;
TF1– 4, between aortic root and renal arteries; TF1–5, between aortic root and
bifurcation. Harmonic 1 represents the mean (or 0-Hz frequency) of the
waveform; Examples of phase velocities in 2 individuals (bottom). }, typical
example of pattern of phase velocities; ‚, example with peak of apparent phase
velocity suggestive of reflection at this frequency.
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GRANTS
This study was supported by a Grant in Aid from the National Heart
Foundation of Australia (G 01M 0343). S. A. Hope is supported by Medicine
International and Faculty Postgraduate Research Scholarships from Monash
University and a Cardiovascular Research Centre PhD Scholarship from
Monash Medical Centre.
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reflection at these frequencies. This may explain the finding
that, although there was progressive reduction in augmentation
index with distal progression along the aorta as analyzed by
repeated-measures analysis of variance, there was variation at
different sites in individuals with a locally increased augmentation index, consistent with only a very localized impact of
reflected waves on the augmentation index.
Although pressure wave reflection may play a role in the
manifestation of the augmentation of central systolic pressure,
it does not appear to be solely, or perhaps even primarily,
responsible for the phenomenon, and indeed the term itself
may be a misnomer. The possible contribution of frequency
dispersion to this phenomenon merits further investigation.
In terms of the practical application of our findings, it is
often proposed that central augmentation index is a measure of
pressure reflection and of aortic stiffness that might predict risk
and response to treatment. This is based on assumptions
regarding reflection phenomena— our results raise questions
regarding this interpretation and may therefore impact directly
on diagnosis and treatment of cardiovascular risk. Pulse wave
velocity is associated with cardiovascular outcome (1, 2, 6).
Because dispersion depends on differences in pulse wave
velocity of different frequency components and as such may
provide further indication of risk than group velocity measurement, it may also be a potential surrogate end point to clinical
trials of agents aimed at directly modulating arterial stiffness.