Letters to the Editor
Letters to the Editor will be published, if suitable, as space permits. They should not exceed 1000 words
(typed double-spaced) in length and may be subject to editing or abridgment.
Arterial Pulse Wave Velocity and Heart Rate
To the Editor:
The concerns raised by Lantelme et al1 about the relationship
between heart rate and pulse wave velocity (PWV) properly
apply to the method they employed, not to the conventional
method, nor to the long-established relationship between PWV
and arterial stiffness. Lantelme et al used Complior, as did the 3
other studies (Lantelme references 8, 15, 17), which appeared to
show increasing PWV with increasing heart rate. In Complior,
the sensor used to detect the pulse produces a signal, which is
related to the derivative of the pressure pulse. A proprietary
algorithm is then used to identify the waveform in a proximal and
in a peripheral artery, to measure the time difference between the
2 sites, and thereby to calculate pulse wave velocity from the
distance between the sites. In the conventional method, PWV is
measured from the time delay between the foot (sharp initial
systolic upstroke) of the wave at the 2 sites.
The theoretical and experimental basis for using PWV as a
measure of arterial stiffness was established in the nineteenth
century, and the earliest clinical studies were conducted in 1922.2
We are unaware of data similar to those presented by Lantelme,
showing any significant relationship between heart rate and
PWV using the conventional method, nor can we conceive any
theoretic basis for such.3,4 Because increasing heart rate is
associated with an in increase in the rate of systolic rise and
abbreviated diastolic duration, the most likely explanation for
Lantelme and coworkers’ finding is that the algorithm used to
obtain transit time from the whole waveform is affected by these
changes in waveform shape. The foot of the waveform is
determined by the high frequency components in the pulse wave
(greater than 10 Hz), and their contribution to the wave foot does
not change with heart rate.3 The foot-to-foot velocity is related to
the phase velocity of the high frequency components, and
because the dynamic elastic properties of the arterial wall do not
alter appreciably at high frequencies, it is inconceivable that
there should be a passive effect on arterial stiffness simply by
altering the input frequency. The alternate explanation the
authors offer in terms of tachycardia resulting in vessel stiffening
as a passive effect by shortening the time available for recoil then
becomes difficult to understand.
Complior is a convenient method for measuring PWV. Its
initial evaluation5 did not include studies as comprehensive as
those described by Lantelme et al. Unless these concerns can be
addressed, the conventional method for measuring PWV from
the wave foot is preferred when any change in heart rate is
possible.
The authors of this paper described carotid-femoral pulse
wave velocity as a marker of atherosclerosis. This is simplistic
and incorrect.3 Our earliest studies showed no difference in PWV
between comparable groups of subjects in populations with high
and low prevalence of atherosclerosis, but similar changes in
each with aging.6 Megnien et al7 from Paris showed that aortic
stiffening does not predict atherosclerotic disease in asymptom-
atic men at risk. Elevated arterial PWV is a measure of sclerosis,
and this results most commonly from aging and hypertensive
medial degeneration, not from intimal atherosclerosis.3
Michael O’Rourke is a Director of Atcor Medical Pty. Limited,
Sydney, Australia, maker of instruments for analyzing the arterial pulse.
1 at SWETS #63870916 on May 5, 2015
Downloaded from http://hyper.ahajournals.org/
Christopher S. Hayward
St Vincent’s Hospital
Sydney, Australia
E-mail cshayward@stvincents.com.au
Alberto P. Avolio
Graduate School of Biomedical Engineering
University of New South Wales
Sydney, Australia
Michael F. O’Rourke
St Vincent’s Hospital
Sydney, Australia
1. Lantelme P, Mestre C, Lievre M, Gressard A, Milon H. Heart rate: an
important confounder of pulse wave velocity assessment. Hypertension.
2002;39:1083–1087.
2. Bramwell JC, Hill AV. Velocity of transmission of the pulse wave and
elasticity of arteries. Lancet. 1922;1:891– 892.
3. Nichols WW, O’Rourke MF. McDonald’s Blood Flow in Arteries. 4th ed.
London: Arnold; 1998:65– 68.
4. Bergel DH. The dynamic elastic properties of the arterial wall. J Physiol.
1961;156:458 – 469.
5. Asmar R, Benetos A, Topouchian J, Laurent P, Pannier B, Brisac A-M,
Target R, Levy BI. Assessment of arterial distensibility by automatic
pulse wave velocity measurement: validation and clinical application
studies. Hypertension. 1995;26:485– 490.
6. Avolio AP, Chen S, Wang R, Zhang C-L, Li M-F, ORourke MF. Effects
of aging on changing arterial compliance and left ventricular load in a
northern Chinese urban community. Circulation. 1983;68:50 –58.
7. Megnien JL, Simon A, Denarie N, Del-Pino M, Gariepy J, Segound P,
Levenson J. Aortic stiffening does not predict coronary and intracoronary
atherosclerosis in asymptomatic men at risk for cardiovascular disease.
Am J Hypertens. 1998;11:293–301.
Response: Heart Rate and Pulse Wave Velocity
In our recent report,1 we used an automatic device for pulse wave
velocity (PWV) measurement that is commercially available
(Complior, Colson). This decision was based on the fact that, for
a clinical application, an automatic method rather than a manual
one (which remains the gold standard) would be preferentially
chosen. Indeed, the conventional (ie, the manual) method is
tedious and time consuming, which probably precludes its
application on a routine basis. The Complior device has been
validated in comparison with the manual method in more than 50
men and women of various age, blood pressure, and heart rate
levels.2 We are unaware of any report of an effect of heart rate on
the algorithm used to calculate the delay between the 2 pulse
waves. In the validation study,2 the range of heart rate levels
within the group was probably wide. If our finding of an effect
of heart rate on PWV measurement were due to the Complior
device, it would have been difficult to observe such a high
agreement between the 2 methods (r⫽0.99, P⬍0.001). More-
over, the relationship between PWV and heart rate found in our
study1 was continuous among the pacing frequencies tested, each
additional 10 bpm leading to a PWV increase. It is very unlikely
that such a minor heart rate variation would influence the
algorithm of the Complior device.
A relationship between heart rate and PWV assessed by the
conventional method has indeed been reported in an epidemio-
logical study.3 Other major determinants were age and blood
pressure. Using the Complior device, the very same determinants
(including heart rate) were able to significantly influence PWV,
further emphasizing the similarity of PWV determined by the 2
methods.4 When considering the effect of heart rate on PWV
2 Letters to the Editor
within individuals, we found at least one report using the
conventional method showing a relationship between heart rate
and PWV during exercise.5 More recently, using the Complior in
paced patients, Albaladejo et al6 also showed a trend for PWV to
increase with heart rate.
Also, the effect of heart rate on PWV is in accordance with
animal studies. Using atrial pacing, it has been shown that heart rate
changes were able to influence arterial distensibility.7 Because the
viscous component of the elastic wall is highly frequency depen-
dent, it can be expected that higher heart rate values are associated
with reduced distensibility. The shortening of the time available for
recoil may be a plausible, although not an exclusive, explanation.
It is very likely that automatic methods of PWV measurement
will be preferred for large studies or routine clinical application.
In addition, the Complior has been shown to provide with an
estimate of PWV that is of high clinical value because it is a
strong marker of cardiovascular risk in hypertension,8 in line
with previous reports obtained with the conventional method.9,10
We believe that it is critical to determine the potential confound-
ers of the automatic methods of PWV determination.
Pierre Lantelme
Christine Mestre
Service de Cardiologie
Hôpital de la Croix-Rousse
Hospices Civils de Lyon
Faculté de Médecine Lyon-Nord
E-mail pierrelantelme@hotmail.com
Michel Lievre
Service de Pharmacologie clinique
Lyon, France
Alain Gressard
Hugues Milon
Service de Cardiologie
Hôpital de la Croix-Rousse
Downloaded from http://hyper.ahajournals.org/ at SWETS #63870916 on May 5, 2015
Hospices Civils de Lyon
Faculté de Médecine Lyon-Nord
Lyon, France
1. Lantelme P, Mestre C, Gressard A, Milon H. Heart rate: an important
confounder of pulse wave velocity assessment. Hypertension. 2002;39:
1083–1087.
2. Asmar R, Benetos A, Topouchian J, Laurent P, Pannier B, Brisac AM,
Target R, Levy BI. Assessment of arterial distensibility by automatic
pulse wave velocity measurement. Validation and clinical application
studies. Hypertension. 1995;26:485– 490.
3. Sa Cunha R, Pannier B, Benetos A, Siche JP, London GM, Mallion JM,
Safar ME. Association between high heart rate and high arterial rigidity
in normotensive and hypertensive subjects. J Hypertens. 1997;15:
1423–1430.
4. Lantelme P, Khettab F, Custaud MA, Rial MO, Joanny C, Gharib C,
Milon H. Spontaneous baroreflex sensitivity: toward an ideal index of
cardiovascular risk in hypertension? J Hypertens. 2002;20:935–944.
5. Siche JP, de Gaudemaris R, Mallion JM. Value of the measurement of
pulse wave velocity during exertion. Arch Mal Coeur Vaiss. 1989;
82(suppl 2):23–27.
6. Albaladejo P, Copie X, Boutouyrie P, Laloux B, Descorps Déclère A,
Smulyan H, Bénétos A. Heart rate, arterial stiffness, and wave reflections
in paced patients. Hypertension. 2001;38:949 –952.
7. Mangoni AA, Mircoli L, Giannattasio C, Ferrari AU, Mancia G. Heart
rate-dependence of arterial distensibility in vivo. J Hypertens. 1996;14:
897–901.
8. 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.
9. Blacher J, Guerin AP, Pannier B, Marchais SJ, Safar ME, London GM.
Impact of aortic stiffness on survival in end-stage renal disease. Circu-
lation. 1999;99:2434 –2439.
10. Guerin AP, Blacher J, Pannier B, Marchais SJ, Safar ME, London GM.
Impact of aortic stiffness attenuation on survival of patients in end-stage
renal failure. Circulation. 2001;103:987–992.
 Arterial Pulse Wave Velocity and Heart Rate
Christopher S. Hayward, Alberto P. Avolio and Michael F. O'Rourke

Hypertension. 2002;40:e8-e9; originally published online October 21, 2002;

doi: 10.1161/01.HYP.0000038734.25997.A9
Hypertension is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 2002 American Heart Association, Inc. All rights reserved.
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