Rapid Communication

Effect of Smoking on Arterial Stiffness and

Pulse Pressure Amplification
Azra Mahmud, John Feely

Abstract—The brachial artery pressure waveform is abnormal in smokers, but the effect of smoking on the aortic pressure
waveform in both smokers and nonsmokers, particularly in the younger population, is unknown. We compared the acute
and chronic effects of smoking on large-artery properties in 185 healthy young smokers and nonsmokers (mean⫾SD,
22⫾5 years). We matched 41 chronic smokers for age, height, weight, and gender with 116 nonsmokers. The
augmentation index, a measure of arterial wave reflection in the aorta, was measured by applanation tonometry
(Sphygmocor). We also compared augmentation index, aortic pulse wave velocity (Complior), and blood pressure in 28
subjects (11 chronic smokers) before and for 15 minutes after smoking 1 cigarette (nicotine content, 1.2 mg). Although
brachial blood pressure was not different, the aortic systolic blood pressure (101⫾8 versus 97⫾9 mm Hg) and
augmentation index (0.7⫾13 versus ⫺5.7⫾14) were higher (P⬍0.01) in chronic smokers than in nonsmokers, whereas
aortic-brachial pulse pressure amplification was reduced (13.7⫾8 versus 17.7⫾5 mm Hg, P⬍0.01). These effects were
seen in both male and female subjects. Acutely in both groups, smoking significantly increased (P⬍0.01) both brachial
and aortic blood pressure, augmentation index, and pulse wave velocity. No changes were seen after sham smoking. This
study shows an acute increase in arterial stiffness after smoking 1 cigarette in chronic smokers and nonsmokers. Higher
aortic systolic blood pressure and greater arterial stiffness, in part due to reduced pulse pressure amplification and
increased arterial wave reflection, suggest that the adverse hemodynamic effects have hitherto been underestimated in
young chronic smokers. (Hypertension. 2003;41:183-187.)
Key Words: smoking 䡲 arterial stiffness 䡲 pulse pressure amplification

S moking is a major risk factor in the development and chronic smoking on an elastic artery such as the ascending
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progression of cardiovascular disease.1 Despite extensive
research, the pathophysiological mechanisms that are respon-
sible for smoking-related vascular damage have not been
elucidated. In addition to alterations in hemostatic factors,
endothelial function, and blood lipids,2 the dynamic proper-
ties of the arterial wall may play an important role. There is
evidence that compliance of both large and medium-sized
arteries decreases immediately after smoking 1 cigarette.3–5
Arterial stiffness is increasingly being recognized as an
important cardiovascular risk factor and an independent
predictor of all-cause and cardiovascular death.6 – 8 Stiffness
may be assessed indirectly by measuring pulse wave velocity
(PWV); the stiffer the artery, the faster a pressure wave
travels through it and the extent to which the arterial wave is
reflected from the periphery. Another indirect measure of
arterial elasticity is aortic-brachial pulse pressure amplifica-
tion, which is reduced with ageing.9
McVeigh et al,10 using invasive methods, demonstrated
abnormalities in the brachial artery pressure waveforms of
chronic smokers. In older subjects, smoking is associated
with increased carotid artery stiffness,11 even in the absence
of atherosclerosis of the vessel. However, the effect of
aorta has not been fully characterized. We first studied the
acute effects of cigarette smoking on the aortic pressure
waveform by measuring the augmentation index (AIx) and
PWV in healthy smokers and nonsmokers. Young subjects
were chosen to minimize the compounding influence of age
and disease states. We then studied the effects of chronic
smoking on blood pressure (BP), the aortic pressure wave-
form, and pulse pressure amplification in healthy young
subjects compared with nonsmokers.
Methods
Subjects
The study group comprised 185 (91 female) healthy volunteers, 52
chronic smokers with a mean (⫾SD) age of 22⫾5 years. None of the
participants (university students) had systemic hypertension (BP
⬎140/90 mm Hg), diabetes mellitus (fasting glucose,
4.9⫾0.3 mmol/L or 88⫾5 mg%), hypercholesterolemia (fasting total
cholesterol, 5⫾0.2 mmol/L or 190⫾7 mg%), or cardiac disease or
were taking any medications. The smoking habits and fitness levels
were assessed from a questionnaire. The smokers smoked an average
of 15 cigarettes per day for 6 to 10 years. The subjects were studied
fasting, having abstained from caffeine, alcohol, or smoking in the
previous 12 hours. Subjects rested in a supine position for 15 minutes

Received August 1, 2002; first decision September 6, 2002; revision accepted November 5, 2002.
From the Department of Pharmacology and Therapeutics, Trinity College Dublin, and the Hypertension Clinic, St James’s Hospital, Dublin, Ireland.
Correspondence to Prof John Feely, Department of Pharmacology and Therapeutics, Trinity Centre for Health Sciences, St James’s Hospital, Dublin
8, Ireland. E-mail jfeely@tcd.ie
© 2003 American Heart Association, Inc.
Hypertension is available at http://www.hypertensionaha.org DOI: 10.1161/01.HYP.0000047464.66901.60

183
 184 Hypertension January 2003

Demographic and Hemodynamic Data and BP for Smokers and Nonsmokers

Acute Chronic
Demographic and Hemodynamic
Variables Smokers Nonsmokers Smokers Nonsmokers
No. (female) 11 (5) 17 (9) 41 (21) 116 (58)
Age, y 22⫾3 22⫾4 22.7⫾4 23⫾6
Height, cm 174⫾12 170⫾9 173⫾9 170⫾15
Weight, kg 66⫾11 67⫾12 69⫾12 68⫾16
Brachial systolic BP, mm Hg 114⫾7 114⫾12 115⫾12 118⫾13
Brachial diastolic BP, mm Hg 67⫾5 66⫾7 70⫾10 68.4⫾8
Aortic systolic BP, mm Hg 98.3⫾5 95⫾9 101⫾8* 97⫾9
Aortic diastolic BP, mm Hg 67.5⫾4 66⫾7 70.6⫾9 69⫾8
Pulse pressure amplification, mm Hg 16⫾6 19⫾5 13.7⫾8* 17.7⫾5
Heart rate, bpm 57⫾7 63⫾8 68⫾13 71⫾12
Augmentation index, % 6.45⫾18* ⫺11⫾15 0.7⫾13* ⫺5.7⫾14
Data are mean⫾SD.
*P⬍0.05.

in a quiet room at 22°C before the baseline hemodynamic measure-
ments were obtained. Brachial BP and heart rate (mean, 3 readings)
were measured in the left arm with an automated digital oscillometric
sphygmomanometer (Omron, model 705-CP, Omron Corp). The
subjects gave informed consent, and the study had institutional ethics
committee permission.
mean⫾SD. The acute changes in the hemodynamic parameters over
time in the acute study were analyzed by repeated-measures
ANOVA, testing for the effect of time and interaction between time
and treatment. Because the AIx is heart-rate dependent, we also
analyzed it over time corrected for the heart rate increase in the acute
study.15

Acute Effects of Smoking Results

Each subject (11 chronic smokers, 17 nonsmokers) smoked 1
cigarette (nicotine content, 1.2 mg) within 5 minutes, using a Acute Effects of Smoking in Smokers and Nonsmokers
standardized protocol, and measurements of brachial and aortic BP, At baseline, the AIx was significantly higher in smokers
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heart rate, AIx, and PWV were made at 5, 10, and 15 minutes after
baseline. In addition, 8 of these subjects had the measurements
performed after sham-smoking an unlit cigarette.
Chronic Effects of Smoking
Chronic smokers (n⫽41) were matched for age, height, weight, and
gender with nonsmokers (n⫽116). Brachial and aortic BP, pulse
pressure amplification, heart rate, and AIx were measured in both
groups. Aortic-brachial pulse pressure amplification was calculated
by subtracting aortic from brachial pulse pressure.
Derivation of the Aortic Pressure Waveform
The technique of pulse wave analysis was used. A high-fidelity
micromanometer (SPC-301, Millar Instruments) was used to flatten
the radial artery, and the radial pulse was continuously recorded. The
aortic pressure waveform was derived from radial tonometry by
using a previously validated transfer function relating radial to aortic
pressure waveform within the system software of the Sphygmocor
apparatus (Sphygmocor Atecor Medical, version 6.2), as previously
described.8,12 Ascending aortic pressures and the AIx were derived
from the aortic pressure waveform. The validity of the derived AIx
has been confirmed by simultaneously recorded direct aortic mea-
surements and is highly reproducible in both healthy and diseased
populations.8,13
PWV Measurements
Carotid-femoral PWV was determined according to the foot-to-foot
method, using the Complior device (Complior, Dupont Medical) as
previously validated.14
Statistical Analysis
Results were analyzed with JMP (JMP IN, version 3.2.1 SAS
Institute Inc), and a value of P⬍0.05 considered significant. The
differences between the smokers and nonsmokers in both acute and
chronic studies were analyzed by 1-way ANOVA and expressed as
compared with nonsmokers (Table). Although the PWV was
higher in smokers than nonsmokers (Figure), the difference
was not statistically significant. No acute changes were seen
in the hemodynamic parameters after sham smoking.
Short-term smoking caused a significant increase in bra-
chial systolic and diastolic BP and heart rate, which was
maximal at 5 minutes and returned to baseline 15 minutes
after smoking (Figure). The aortic systolic and diastolic BP
also increased significantly after smoking 1 cigarette both in
smokers and nonsmokers, with the greatest changes seen in
the first 5 minutes after smoking (Figure). Although AIx,
which is heart rate– dependent, decreased in both smokers and
nonsmokers after smoking, by applying a correction factor15
for changes in heart rate, the AIx increased significantly after
smoking in both smokers and nonsmokers. PWV increased
significantly both in smokers and nonsmokers from baseline
and remained higher for the entire duration of the study for 15
minutes (Figure).
Chronic Smoking, Aortic Pressure Waveform, and
Pulse Pressure Amplification
The demographic and hemodynamic profiles of the smokers
and nonsmokers are shown in the Table. The aortic systolic
BP was significantly higher in smokers than in nonsmokers,
and pulse pressure amplification was significantly reduced
compared with nonsmokers. The AIx was significantly higher
in smokers (0.7⫾13 versus ⫺5.7⫾14%, P⬍0.01) than in
nonsmokers.
Because gender is such an important determinant of arterial
stiffness, we analyzed the data for male and female subjects
 Mahmud and Feely Smoking, Arterial Stiffness, and Pressure Amplification
Changes in brachial and aortic BPs, corrected augmentation index, and pulse wave velocity at 5, 10, and 15 minutes after smoking 1
cigarette (nicotine content, 1.2 mg) in healthy smokers (n⫽11) and nonsmokers (n⫽17). Data are presented as mean⫾SEM, *P⬍0.05
between smokers and nonsmokers.
separately. The male subjects in our study had higher
(P⬍0.001) brachial systolic (120⫾11 versus 109 versus
⫾11), aortic systolic BP (101⫾9 versus 95⫾9), and pulse
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pressure amplification (19⫾6 versus 15⫾7, all in mm Hg)
than female subjects. The AIx was significantly higher in
female subjects (0.7⫾12 versus ⫺8.7⫾14%, P⬍0.001) than
in male subjects. There was no difference in brachial BP,
aortic diastolic BP, and heart rate between male smokers and
nonsmokers. However, as in the whole group, the aortic
systolic BP was higher (105⫾6 versus 100⫾9 mm Hg,
P⬍0.05) and pulse pressure amplification less (15⫾6 versus
20⫾5 mm Hg, P⬍0.01) in the male smokers than nonsmok-
ers. Also, the AIx was higher (⫺4.4⫾14 versus ⫺11⫾11%,
P⬍0.05) in male smokers than nonsmokers. Results were the
same for the female subjects with a higher aortic systolic BP
(98⫾8 versus 93⫾9 mm Hg, P⬍0.05) and lower pulse
pressure amplification (12⫾9 versus 16⫾5 mm Hg, P⬍0.05)
in female smokers compared with female nonsmokers. Also,
female smokers had stiffer arteries, as shown by a signifi-
cantly higher AIx (5.4⫾10 versus ⫺1.3⫾14%, P⬍0.05) than
nonsmokers.
As the level of fitness may influence the results, we graded
the smokers and nonsmokers into sedentary, moderately
active, and actively involved in sports and analyzed the
effects of smoking in each group separately. In the sedentary
subjects (n⫽41), AIx was higher (6.35⫾7 versus 2.7⫾9,
P⫽0.2) and pulse pressure amplification less (13⫾6 versus
17⫾6 mm Hg, P⫽0.09) in smokers than nonsmokers, but not
statistically significant. In the moderately active group
(n⫽77), the smokers had significantly higher aortic systolic
BP (104⫾8 versus 94⫾9 mm Hg, P⬍0.05) and lower pulse
pressure amplification (12⫾10 versus 17⫾5, P⬍0.01) than
nonsmokers. The AIx was higher in the smokers (4⫾11
185
versus ⫺3.3⫾11, P⬍0.05) than in nonsmokers. The subjects
who were actively engaged in sports (n⫽39) also differed,
depending on smoking habits, the smokers having higher AIx
(⫺9⫾14 versus -17⫾12, P⫽0.1) and aortic systolic BP
(104⫾9 versus 99⫾9, P⫽0.16) than nonsmokers, though it
was not statistically significant. The pulse pressure amplifi-
cation was, however, significantly reduced (14⫾6 versus
20⫾6 mm Hg, P⬍0.05) in smokers than in nonsmokers.
Discussion
We have shown a significant effect of smoking on large-
artery properties. Acutely, cigarette smoking increased the
AIx and PWV, suggesting an increase in arterial stiffness.
Perhaps the most interesting finding was that young, other-
wise healthy smokers have higher aortic systolic pressure and
AIx compared with nonsmokers as the result of increased
arterial wave reflection in the aorta, suggesting stiffer arter-
ies. Decreased elasticity of such arteries is also suggested by
the reduced pulse pressure amplification in chronic smokers.
The effect of acute cigarette smoking in healthy nonsmok-
ers on forearm arterial hemodynamics showed an increase in
BP, heart rate, and PWV.16 Acute cigarette smoking de-
creased arterial compliance in both large elastic and medium-
sized muscular arteries.3,17 More recently, Stefanadis et al,5
using invasive methods, showed decreased aortic compliance
acutely after smoking 1 cigarette in middle-aged men with
coronary artery disease.
In the current study, AIx was significantly higher at
baseline in smokers than in nonsmokers. PWV was also
higher, although not significantly, presumably because of the
relatively small number of subjects in this part of our study.
PWV increased immediately after smoking. Arterial wave
reflection depends on the timing of ventricular ejection.
 186 Hypertension January 2003
Because of the proportionality between ejection time and
cardiac cycle duration,18,19 the peak of the forward traveling
wave occurs earlier at faster heart rates. In such a setting,
even with a fixed reflection site and PWV, there is an altered
relation between forward and backward waves. AIx is there-
fore lower at higher heart rates and vice versa. Wilkinson et
al15 recently demonstrated a linear relation between AIx and
heart rate in a pacing study, showing that AIx decreased by
4% for every 10-beat/min increment in heart rate. By apply-
ing this correction factor, the AIx increased in parallel with
the PWV in our acute study (Figure). However, the correction
may need to be interpreted with caution because there may be
different mechanisms by which heart rate changes affect the
AIx in different maneuvers, for example, smoking versus
pacing. The mechanisms underlying the acute increase in BP
and arterial stiffness may be several, including an increase in
circulating and local catecholamines; nicotine stimulates
sympathetic ganglia and increases the central nervous system
sympathetic neural discharge–impaired nitric oxide produc-
tion and endothelial dysfunction.2,20
The chronic effects of smoking have been controversial.
Wollersheim et al21 described increased arterial stiffness of
the popliteal artery and a tendency toward stiffening of the
common femoral and carotid arteries in 13 habitual smokers
measured ultrasonographically by the pressure-strain elastic
modulus. Also, an invasive study showed abnormalities of the
brachial artery pressure waveform in smokers,10 but others2,3
found no difference in regional arterial compliance between
smokers and nonsmokers. In contrast, in the current study, we
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observed a much higher AIx in smokers compared with
nonsmokers (Table) in a young homogenous group of healthy
adults who were matched for age, height, weight, and
hemodynamic status. In such a group, the confounding effects
of age, hypertension, atherosclerosis, and so forth, are mini-
mized. The earlier studies were carried out in a heterogeneous
group of subjects; the age ranges were wide, and none of
these measured aortic BP or pulse pressure amplification.
Because pulse pressure amplification is age-dependent, de-
creasing markedly with age, the failure to measure it in the
earlier studies may have led to underestimation of the chronic
effects of smoking, particularly in the young. We were able to
measure aortic systolic BP and pulse pressure amplification
in our study and have clearly shown for the first time that the
deleterious effects of chronic smoking would be overlooked
if only peripheral BP and compliance measurements are
made, as in the earlier studies. Furthermore, we have shown
that the deleterious effects of smoking are seen in young
people regardless of their gender and their level of fitness,
although the extent of statistical significance here is less,
partly as a result of the relatively lower numbers.
This study extends the earlier observations by McVeigh et
al10 that older smokers have abnormal brachial artery pressure
waveforms compared with nonsmokers and the recent study
showing increased stiffness index in the carotid artery in
middle-aged and elderly smokers compared with nonsmok-
ers.11 The additional finding of a higher aortic systolic BP,
despite a similar or somewhat lower systolic BP in the
brachial artery, is important and may be attributed to reduced
pulse pressure amplification in the smokers. A number of
epidemiological studies have reported either a similar or
lower BP in smokers compared with nonsmokers,22 but this
may be related to gender, alcohol intake, and body mass
index. In a recent report on the Annual Health Survey for
England, systolic BP was lower in women who smoked but
higher in male smokers ⬎60 years of age.22 Similarly, in
12 417 French men, current and former smokers were at
greater risk of systolic hypertension, particularly over the age
of 60 years.23 Our data may provide an insight into the
mechanisms involved. In the ARIC study,24 lower arterial
elasticity was independently related to the development of
hypertension. With aging and reduced pulse pressure ampli-
fication, the brachial systolic BP equates more with the aortic
systolic BP,25 and the higher aortic systolic BP in smokers
may, with time, because of additional smoking-related re-
duced aortic brachial pulse pressure amplification, become
evident as a higher brachial systolic BP.
Perspectives
These results suggest that the hemodynamic consequences of
chronic smoking may have been underestimated. We believe
that smoking reduces pulse pressure amplification largely as
a consequence of increased arterial stiffness and increases
arterial wave reflection, which leads to increased aortic
systolic BP. The latter has not been suspected because
peripheral BP and is usually deceptively lower in chronic
smokers because of poor aortic brachial pressure amplifica-
tion. Arterial stiffness is increasingly recognized as a more
sensitive prognosticator of vascular events than either systolic
or diastolic BP alone in populations with hypertensive and
end-stage kidney disease.7,26 Smoking in the younger popu-
lation, particularly women, is on the increase in many
Western countries. We now provide evidence that smoking-
related hemodynamic changes and increased stiffness may be
evident in subjects as young as 22 years. Our ability to detect
these changes may also provide an opportunity for interven-
tion. Female gender and exercise are not protective from such
vascular effects.
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