Impact of smoking and smoking cessation on arterial stiffness and aortic wave reflection in hypertension.

Abstract

Cigarette smoking is an important modifiable cardiovascular risk factor and pathophysiological mechanisms may include a stiff vascular tree. Although smokers have stiffer arteries, whether smoking cessation is associated with reduced arterial stiffness is not known. We compared never-treated patients with essential hypertension (n=554) aged 18 to 80 years (56% females) classified as current smokers (n=150), ex-smokers (n=136), and nonsmokers (n=268). Ex-smokers were categorized into <1 year, >1 and <10 years, and >10 years of smoking cessation. Measurements included aortic stiffness, assessed as pulse wave velocity (Complior), wave reflection (augmentation index [AIx]), and transit time (T(R)) (Sphygmocor). Current and ex-smokers had significantly higher pulse wave velocity and AIx compared with nonsmokers (pulse wave velocity for current smokers: 10.7+/-0.2; ex-smokers: 10.6+/-0.2; nonsmokers: 9.9+/-0.1 m/s; P<0.001; AIx for current smokers: 31+/-1; ex-smokers: 30+/-1; nonsmokers: 27+/-0.8%; P<0.05), whereas T(R) was lower in current and ex-smokers compared with nonsmokers (T(R) for current smokers: 131+/-1.0; ex-smokers: 135+/-1; nonsmokers: 137+/-0.8 m/s; P<0.0001). There was a significant linear relationship between smoking status and pulse wave velocity (P<0.001), AIx (P<0.001), and T(R) (P<0.001), even after adjusting for age, sex, mean arterial pressure, heart rate, and body mass index. In ex-smokers, duration of smoking cessation had a significant linear relationship with improvement in pulse wave velocity (P<0.001), AIx (P<0.001), and T(R) (P<0.001), with arterial stiffness parameters returning to nonsignificant levels after a decade of smoking cessation.

Full text

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Noor A. Jatoi, Paula Jerrard-Dunne, John Feely and Azra Mahmud
Reflection in Hypertension
Impact of Smoking and Smoking Cessation on Arterial Stiffness and Aortic Wave
Print ISSN: 0194-911X. Online ISSN: 1524-4563
Copyright © 2007 American Heart Association, Inc. All rights reserved.
is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Hypertension
doi: 10.1161/HYPERTENSIONAHA.107.087338
2007;49:981-985; originally published online March 19, 2007;
Hypertension.

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Impact of Smoking and Smoking Cessation on Arterial
Stiffness and Aortic Wave Reflection in Hypertension
Noor A. Jatoi, Paula Jerrard-Dunne, John Feely, Azra Mahmud
Abstract—Cigarette smoking is an important modifiable cardiovascular risk factor and pathophysiological mechanisms
may include a stiff vascular tree. Although smokers have stiffer arteries, whether smoking cessation is associated with
reduced arterial stiffness is not known. We compared never-treated patients with essential hypertension (n?554) aged
18 to 80 years (56% females) classified as current smokers (n?150), ex-smokers (n?136), and nonsmokers (n?268).
Ex-smokers were categorized into ?1 year, ?1 and ?10 years, and ?10 years of smoking cessation. Measurements
included aortic stiffness, assessed as pulse wave velocity (Complior), wave reflection (augmentation index [AIx]), and
transit time (TR) (Sphygmocor). Current and ex-smokers had significantly higher pulse wave velocity and AIx compared
with nonsmokers (pulse wave velocity for current smokers: 10.7?0.2; ex-smokers: 10.6?0.2; nonsmokers: 9.9?0.1
m/s; P?0.001; AIx for current smokers: 31?1; ex-smokers: 30?1; nonsmokers: 27?0.8%; P?0.05), whereas TRwas
lower in current and ex-smokers compared with nonsmokers (TRfor current smokers: 131?1.0; ex-smokers: 135?1;
nonsmokers: 137?0.8 m/s; P?0.0001). There was a significant linear relationship between smoking status and pulse
wave velocity (P?0.001), AIx (P?0.001), and TR(P?0.001), even after adjusting for age, sex, mean arterial pressure,
heart rate, and body mass index. In ex-smokers, duration of smoking cessation had a significant linear relationship with
improvement in pulse wave velocity (P?0.001), AIx (P?0.001), and TR(P?0.001), with arterial stiffness parameters
returning to nonsignificant levels after a decade of smoking cessation. (Hypertension. 2007;49:981-985.)
Key Words: smoking ? arterial stiffness ? pulse wave velocity ? augmentation index ? hypertension
?smoking cessation
C
rial stiffness may be one of the underlying pathophysiological
mechanisms. Chronic cigarette smoking has been shown to be
associated with increased arterial stiffness2,3and increases
immediately after smoking 1 cigarette.3The standard mea-
surement of arterial stiffness, aortic pulse wave velocity
(PWV) in conjunction with augmentation index (AIx), an
estimate of aortic wave reflection, provide a comprehensive
assessment of arterial stiffness.4There is evidence that both
PWV5,6and AIx7are independent predictors of cardiovascu-
lar events.
Smoking cessation is an important lifestyle measure for the
prevention of cardiovascular disease, and patients with myo-
cardial infarction may experience as much as a 50% reduction
in risk of reinfarction, sudden cardiac death, and total
mortality if they quit smoking.8However, the speed and
magnitude of risk reduction when a smoker quits is debatable,
with studies quoting 3 to 20 years of smoking cessation
associated with significant risk reductions in coronary artery
disease.8
Whether long-term smoking cessation is associated with a
reduction in arterial stiffness compared with chronic smokers
igarette smoking is one of the most important avoidable
causes of cardiovascular diseases worldwide,1and arte-
is not known. Therefore, we compared differences in arterial
stiffness among nonsmokers, ex-smokers, and current smokers
in a cross-sectional study.
Methods
Subjects
A total of 554 untreated subjects aged 18 to 80 years (47.8?0.6
years, mean?SEM), 56% female, undergoing assessment for hyper-
tension, were studied. None of the patients had secondary hyperten-
sion, coronary artery disease, valvular heart disorders, dysrhythmias,
diabetes, heart failure, or renal impairment, and none were taking
any vasoactive drugs. Current smokers were defined as those who
had smoked ?1 cigarette per day for ?1 year, nonsmokers as those
who had never smoked, and former or ex-smokers as those who had
stopped smoking ?1 month before examination. Ex-smokers were
categorized into 3 subgroups according to smoking cessation dura-
tion: those who quit cigarette smoking for ?1 year, between 1 and 10
years, and ?10 years.
Body weight, height, waist, and hip measurements were recorded
in each patient. Body mass index (BMI) was calculated as body
weight (kilograms) divided by height (meters squared), and the
waist:hip ratio was calculated. Fasting venous blood samples were
drawn, and total cholesterol, high-density lipoprotein cholesterol,
triglycerides, plasma glucose, and serum creatinine were measured
by standard methods. The subjects gave informed consent, and the
study had institutional ethics committee permission.
Received January 11, 2007; first decision January 28, 2007; revision accepted February 23, 2007.
From the Department of Pharmacology and Therapeutics, Trinity College Dublin, Trinity Centre, St James’s Hospital, Dublin, Ireland.
Correspondence to Noor Ahmed Jatoi, Department of Pharmacology and Therapeutics, Trinity Centre for Health Sciences, St James’s Hospital, Dublin
8, Ireland. E-mail jatoina@tcd.ie
© 2007 American Heart Association, Inc.
Hypertension is available at http://www.hypertensionaha.orgDOI: 10.1161/HYPERTENSIONAHA.107.087338
981
Arterial Stiffness
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Blood Pressure Measurements
Subjects rested in a supine position for 5 minutes in a quiet room at
22°C before the baseline hemodynamic measurements were ob-
tained. Brachial blood pressure (BP) and heart rate were measured in
the left arm with an automated digital oscillometric sphygmoma-
nometer (Omron, Model HEM 705-CP, Omron Corporation). Three
readings separated by 1-minute intervals were taken, and the mean
was used for analysis. Peripheral pulse pressure was calculated as the
difference between brachial systolic and diastolic BP.
Measures of Arterial Stiffness and
Wave Reflection
The aortic pressure waveform was derived using radial applanation
tonometry by using a previously validated transfer function relating
radial to aortic pressure waveform within the system software of the
Sphygmocor (SphygmoCor, AtCor Medical, Version 8.0) by a single
operator, and 2 measurements were performed in each subject.
Ascending aortic pressures and the AIx were derived from the aortic
pressure waveform, as described previously.3Transit time (TR) was
measured from the foot of the wave to the inflection point on the
aortic pressure waveform. Carotid–femoral PWV was measured with
an automated system (Artech Medical) using the foot-to-foot
method. The carotid and femoral waveforms were acquired simul-
taneously with 2 pressure-sensitive transducers, and the TRof the
pulse was calculated by the system software. The distance between
the 2 arterial sites was measured on the body using a tape measure,
and PWV was calculated as the distance divided by time (meters per
second). At least 12 successive readings were used for analysis to
cover a complete respiratory cycle. The interclass correlation coef-
ficients between the first and second measurements on the 544
subjects were 0.94 for AIx, 0.89 for TR, and 0.84 for PWV. The
coefficients of variation for AIx, TR, and PWV were ?5%. The
reproducibility of the measured variables was comparable to previ-
ous studies.9,10
Statistical Analysis
Data were analyzed using SPSS (version 12.0). PWV, AIx, and TR
approximated normal distributions. Data are expressed as
mean?SEM or 95% confidence intervals, with P?0.05 considered
significant. Mean differences in PWV, AIx, and TRbetween never
smokers, ex-smokers, and current smokers and the effects of duration
of smoking cessation were assessed using ANOVA with posthoc
Bonferroni corrections. To determine whether ex-smokers had arte-
rial stiffness levels intermediate between never and current smokers,
linear regression analysis was used to establish the presence of a
linear trend. Three models were used: (1) adjusted for age and sex;
(2) adjusted for age, sex, and mean arterial pressure; and (3)
additional multivariate adjustment for the other major determinants
of arterial stiffness, that is, heart rate and BMI.
Results
Patient Characteristics
The clinical characteristics of the study population are shown in
Table 1. The ex-smokers were 5 years older than nonsmokers
(P?0.01) and 3 years older than current smokers, although
this did not reach statistical significance (P?0.09). Although
there was no difference in sex distribution for smokers,
significantly more males quit smoking than females
TABLE 1.
Smoking Status (n?554, Mean?SEM)
Clinical Characteristics of the Hypertensive Patients Population Categorized According to
Variables
Smoking Status
Current (n?150)Former (n?136)Never (n?268)P
Age, y
Sex, male:female
Height, cm
Weight, kg
BMI, kg/m2
Waist, cm
Hip, cm
Waist:hip ratio
Heart rate, bpm
Brachial systolic BP, mm Hg
Brachial diastolic BP, mm Hg
Brachial pulse pressure, mm Hg
Mean arterial pressure, mm Hg
Aortic systolic BP, mm Hg
Aortic diastolic BP, mm Hg
Aortic pulse pressure, mm Hg
AIx, %
PWV, m/s
TR, ms
Total cholesterol, mmol/L
High-density lipoprotein cholesterol, mmol/L
Triglycerides, mmol/L
Fasting glucose, mmol/L
Serum creatinine, ?mol/L
48.39?1
78:72
169.13?0.84
81.34?1.45
28.16?0.4
95.85?1.45
105?1.2
0.91?0.01
71.5?1.0
158?1.83
92.78?0.93
65.4?1.4
112.03?1.28
146.27?1.82
94.26?0.95
52.13?1.41
30.60?0.1
10.72?1.93
130.96?1.05
5.36?0.08
1.34?0.03
1.92?0.11
5.3?0.06
86.12?1.09
50.66?1
89:47
170.62?0.88
84.29?1.52
28.98?0.42
96.95?1.36
105?1.1
0.92?0.01
70.2?1.0
160?1.93
94.53?0.98
65.5?1.5
113.48?1.15
148.87?1.91
95.79?0.99
53.08?1.41
30.07?1.02
10.6?0.2
134.63?1.03
5.19?0.08
1.33?0.03
1.97?0.11
5.31?0.06
89.57?1.13
45.99?0.8
126:142
168.52?0.63
81.79?1.08
28.73?0.3
92.92?1.04
106?0.8
0.89?0.01
70.4?0.7
154?1.38
92.69?0.70
61.7?1.1
110.34?0.8
142.86?1.37
94.08?0.71
48.78?0.97
27.33?0.84
9.95?0.12
136.83?0.82
5.07?0.06
1.34?0.02
1.43?0.08
5.23?0.04
86.86?0.83
0.003
0.001
0.32
0.3
0.34
0.04
0.83
0.01
0.55
0.05
0.27
0.05
0.09
0.02
0.35
0.02
0.03
0.001
0.0001
0.02
0.92
0.001
0.44
0.02
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(P?0.001). There was no significant difference in BMI
among the 3 groups, although there was a trend for higher
waist circumference and waist:hip ratio in ex-smokers. Total
cholesterol was raised in smokers (P?0.05), and plasma
creatinine (P?0.05) was higher in ex-smokers.
Smoking Status and Arterial Stiffness
Brachial and aortic systolic BP and pulse pressure were
significantly lower in nonsmokers compared with both
smokers and ex-smokers (P?0.05). For PWV, AIx, and TR
there was a direct linear relationship between smoking status
and arterial stiffness, with ex-smokers having levels interme-
diate between current smokers and nonsmokers (Table 1). To
study whether there was an independent relationship between
arterial stiffness and smoking status, we constructed linear
regression models for PWV, AIx, and TR. We took PWV as
the dependent variable and the independent variables in-
cluded in the first model were age and sex; age, sex, and mean
arterial pressure in the second model; and age, sex, mean
arterial pressure, heart rate, and BMI in the third model.
There was a significant linear relationship between PWV and
smoking status (Table 2). Similar models with AIx and TRas
the dependent variables showed significant linear relation-
ships with smoking status (Table 2).
Smoking Cessation Status and Arterial Stiffness
Data on duration of smoking cessation were available for 122
ex-smokers, and the demographics categorized according to
smoking cessation status are given in Table 3. Ex-smokers of
?1-year duration had arterial stiffness similar to current
smokers, ex-smokers of 1 to 10 years in duration had
intermediate levels, and arterial stiffness in ex-smokers of
?10 years duration was not significantly different to that of
never smokers (Figure). Linear regression models showed a
significant direct relationship between the duration of smok-
ing cessation and PWV (P?0.001), AIx (P?0.001), and TR
(P? 0.001) in ex-smokers, after adjusting for age, sex, BMI,
and mean arterial pressure.
Discussion
This study confirms in a large, untreated homogenous popu-
lation that there is a significant linear relationship between
smoking status and PWV, AIx, and TR, even when adjusted
for covariates including age, sex, mean arterial pressure, and
BMI (Table 2). Further analysis that included duration of
smoking cessation showed that reversal of the deleterious
effects of smoking on arterial stiffness is likely to take ?10
years to achieve levels of stiffness similar to that of never
smokers (Figure).
Because arterial stiffness is an independent predictor of
events in hypertensive patients,5–7it may be one of the
mechanisms for smoking-related vascular disease in such
patients. Although chronic smoking has been shown to be
associated with increased stiffness in healthy subjects,2,3data
on the effects of smoking on arterial stiffness are lacking in an
untreated hypertensive population. To the best of our knowl-
edge, this is the first study to show that, in untreated
hypertensive patients, a population characterized by already
stiff vessels, chronic smoking further increases arterial stiff-
TABLE 2.PWV, AIx, and TRin Never, Ex-, and Current Smokers (Mean, 95% CI)
Model
Never Smoker
(n?150)
Ex-Smoker
(n?136)
Current Smoker
(n?268)
P
ANOVA
P
Linear Trend
PWV, m/s
Model 1*
Model 2†
Model 3‡
AIx, %
Model 1*
Model 2†
Model 3‡
TR, ms
Model 1*
Model 2†
Model 3‡
10.3 (10.0 to 10.5)
10.3 (10.1 to 10.5)
10.3 (10.1 to 10.6)
10.5 (10.1 to 10.8)
10.4 (10.1 to 10.7)
10.4 (10.0 to 10.7)
10.9 (10.5 to 11.2)
10.9 (10.5 to 11.2)
10.9 (10.5 to 11.2)
0.02
0.02
0.03
0.006
0.008
0.017
28 (26 to 29)
28 (27 to 29)
28 (27 to 29)
30 (28 to 32)
30 (28 to 31)
29 (28 to 31)
30 (29 to 32)
30 (29 to 32)
31 (29 to 32)
0.04
0.05
0.01
0.015
0.016
0.001
137 (135 to 138)
137 (135 to 138)
137 (135 to 138)
135 (133 to 137)
135 (133 to 137)
135 (133 to 137)
131 (129 to 133)
131 (129 to 133)
132 (130 to 133)
0.001
0.001
0.001
0.001
0.001
0.001
The 3 models were used *(1) adjusting for age and sex; †(2) adjusting for age, sex, and mean arterial pressure;
and ‡(3) with additional multivariate adjustment for mean heart rate and BMI.
TABLE 3.
According to Smoking Cessation Status (Mean?SEM, n?122)
Clinical Characteristics of Ex-Smokers Categorized
Parameters
?1 y
(n?22)
?1 and ?10 y
(n?40)
?10 y
(n?60)P
Age, y
Sex, male/female
BMI, kg/m2
Waist:hip ratio
Systolic BP, mm Hg
Diastolic BP, mm Hg
Total cholesterol,
mmol/L
Triglycerides, mmol/L
High-density lipoprotein
cholesterol, mmol/L
Glucose, mmol/L
47?3
9/13
28?0.8
0.90?0.02
156?5
92?2
5?0.2
49?2
16/24
28?0.6
0.90?0.02
157?3
94?2
5.2?0.2
55?1
15/45
30?0.5
0.94?0.01
164?3
96?1
5.3?0.1
0.01
0.19
0.12
0.14
0.15
0.23
0.84
2?0.4
1.40?0.07
1.9?0.2
1.3?0.05
2?0.2
1.3?0.04
0.96
0.50
5.3?0.09 5.2?0.07 5.4?0.07 0.16
Jatoi et alSmoking and Arterial Stiffness in Hypertension
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ness. We also think that, as the increased aortic stiffness is
independent of BP, the effects of hypertension and smoking
on the vascular wall may be cumulative.
Although effects of smoking cessation on BP are well
documented,11those on arterial stiffness parameters are
variable. A comparative longitudinal study over 2 years12did
not show any effect of smoking cessation on carotid param-
eters, including intimal thickness, stiffness, or distensibility in
people who stopped smoking compared with smokers and
nonsmokers. This was a relatively small (n?33) study, and
the nonsmoking group included ex-smokers. In a recently
published longitudinal study of 4 weeks of smoking cessa-
tion, AIx was reduced but not to the level of the nonsmokers,13
whereas PWV was unchanged in this short-term study.
However, our findings are in agreement with the recent study
by Li et al,2where, in healthy younger normotensive subjects,
again in a somewhat older group, smoking cessation was
associated with a significant reduction in arterial stiffness and
systemic vascular resistance. Also, in agreement, they
showed a reduction in arterial stiffness in former smokers to
the level of nonsmokers after 10 years of smoking cessation.
However, using radial pressure waveform analysis, they did
not find any difference in large artery stiffness. It is possible
that the measure, PWV, used in our study is more specific for
a large artery (aorta), or perhaps the presence of hypertension
in an older population amplified the effects of smoking on
large artery stiffness.2The mechanisms involved in amelio-
ration in arterial stiffness with smoking cessation may include
lipid-soluble smoke particles,14endothelial dysfunction,15or
vascular inflammation,16because smoking cessation leads to
reduction in levels of inflammatory markers.17BP does not
appear to be involved, because ex-smokers have higher BP
levels than current smokers in our study, as seen previously,11
and when adjusted for both age and BP, the association with
arterial stiffness remained significant in our study (Table 2).
Although it may take more than a decade to reverse these
vascular changes, and the effect is relatively small, smoking
cessation may help reduce cardiovascular events through
amelioration in arterial stiffening even in long-term hyper-
tensive smokers. Our results are in agreement with published
data reporting cardiovascular risk reduction with smoking
cessation for periods ranging from 3 to 20 years.8
There are certain caveats in our study. Using a cross-
sectional design, we can only observe an association between
vascular parameters and smoking status and cannot establish
a causal relationship. Although we have adjusted for all of the
major confounders in the analysis, the presence of unknown
confounders cannot be ignored. For example, people who
successfully quit smoking may be different from those who
continue in different ways, including age, sex, psychosocial
characteristics, and other factors. We have adjusted for age
and sex in our analysis, because ex-smokers were older and
predominantly male. A further limitation may be the misclas-
sification of smoking status, because patients who continued
to smoke may claim to have quit smoking, as we do not have
data on biochemical markers of smoking in this study.
However, self-reporting has been shown to be quite accurate
when compared with biochemical evidence of tobacco inha-
lation.18Despite these caveats, we believe that our study
shows not only that smoking-induced arterial stiffness is in-
creased in hypertensive smokers compared with nonsmokers
but suggests also that these vascular changes are reversible,
although it may take more than a decade for values to revert
to that of never smokers. This highlights the importance of
avoidance of smoking and the great need to promote smoking
cessation in hypertensive patients who continue to smoke, as
reduction in arterial stiffness may still be possible. However,
these results need to be confirmed in a prospective longitu-
dinal study.
Aortic stiffness (PWV), wave reflection (AIx), and TRagainst dura-
tion of smoking cessation (estimated marginal means after
adjustment for age, sex, mean arterial pressure, mean heart
rate, and BMI). Values for current and never smokers included
for comparison.
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Perspectives
We have shown in a large, untreated hypertensive population
that chronic cigarette smoking is associated with increased
aortic stiffness and wave reflection, which are reversible with
smoking cessation, although it may take more than a decade
to see levels of nonsmokers. The high aortic stiffness and
wave reflection seen with chronic smoking may be 1 of the
underlying mechanisms for the increased cardiovascular
events observed in hypertensive patients. Therefore, consid-
ering the independent prognostic usefulness of arterial stiff-
ness in the hypertensive population,5–7,19its assessment may
not only identify hypertensive patients at higher cardiovas-
cular risk but may also be used to monitor arterial health in
those who quit smoking.
Source of Funding
This study was funded in part by the Royal City of Dublin Hospital
Research Trust.
Disclosures
None.
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In the Hypertension article by Jatoi et al (Jatoi NA, Jerrard-Dunne P, Feely J, Mahmud A. Impact
of smoking and smoking cessation on arterial stiffness and aortic wave reflection in hypertension.
Hypertension. 2007;49:981–985), the corresponding author should be Azra Mahmud, Department
of Pharmacology and Therapeutics, Trinity Centre for Health Sciences, St James’s Hospital,
Dublin 8, Ireland. E-mail mahmuda@tcd.ie The authors regret the error.
(Hypertension. 2007;50:e11.)
© 2007 American Heart Association, Inc.
Hypertension is available at http://www.hypertensionaha.org DOI: 10.1161/HYPERTENSIONAHA.107.009418
e11
Correction
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