Effects of smoking cessation on central blood pressure and arterial stiffness
Vascular Health and Risk Management
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Effects of smoking cessation on central blood
pressure and arterial stiffness
This article was published in the following Dove Press journal:
Vascular Health and Risk Management
19 October 2011
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Takeshi Takami 1
Yoshihiko Saito 2
Department of Internal Medicine,
Clinic Jingumae, Kashihara, Nara,
Japan; 2First Department of Internal
Medicine, Nara Medical University,
Kashihara, Nara, Japan
1
Purpose: Smoking affects arterial stiffness, thus causing an elevation in central blood pressure
(CBP). The present study was designed to examine whether smoking cessation treatment
improved CBP and arterial stiffness.
Patients and methods: We conducted an observational study of 70 patients receiving smoking
cessation treatment. Before and 60 weeks after the start of a 12-week varenicline treatment,
we measured brachial blood pressure, CBP, brachial-ankle pulse wave velocity (baPWV),
normalized radial augmentation index (rAIx@75), left ventricular weight, and left ventricular
diastolic function of each patient. The data were compared between the patients who succeeded
in quitting smoking (smoking cessation group; n = 37) and those who failed to quit smoking
(smoking group; n = 33).
Results: Baseline characteristics were similar in both groups. Brachial blood pressure remained
unchanged in both groups. CBP, baPWV, and rAIx@75 decreased significantly in the smoking
cessation group, while these parameters showed no significant change in the smoking group. Thus,
CBP, baPWV, and rAIx@75 showed greater decrease in the smoking cessation group than in the
smoking group (CBP, −7.1 ± 1.4 mmHg vs 1.2 ± 2.7 mmHg; P , 0.01; baPWV, −204 ± 64 cm/s
vs −43 ± 72 cm/s; P , 0.01; rAIx@75, −6.4 ± 2.8% vs −1.0 ± 3.9%; P , 0.01). Left ventricular
weight and left ventricular diastolic function remained unchanged in both groups.
Conclusion: Patients in the smoking cessation group showed significant improvement in CBP,
baPWV, and rAIx@75. These results indicate that smoking cessation can improve arterial stiffness and CBP.
Keywords: central blood pressure, augmentation index, brachial-ankle pulse wave velocity,
smoking cessation, varenicline
Introduction
Correspondence: Takeshi Takami
Department of Internal Medicine,
Clinic Jingumae, 5-4-41 Naizencho,
Kashihara, Nara 634-0804, Japan
Tel +81 744 23 8568
Fax +81 744 23 6818
Email
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http://dx.doi.org/10.2147/VHRM.S25798
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Smoking induces a temporary elevation in blood pressure. The elevation in blood
pressure induced by smoking one cigarette lasts for a period of 15 minutes or more.1
Blood pressure may remain elevated in heavy smokers. Habitual smokers show
elevation in blood pressure during daytime activities,2 or they show an elevation in
central blood pressure (CBP).3 CBP induces a more direct mechanical stress on the
left ventricle, large arteries, and vital organ vasculature than does brachial blood
pressure. The impact of CBP has been reported in large-scale intervention trials and
population-based studies, such as the CAFÉ–ASCOT study4 and the SHS study.5 In
addition, smoking might cause masked hypertension.6 However, a detailed evaluation of the influence of chronic smoking on blood pressure has not been performed
thus far.7 The relationship between smoking cessation and arterial wall thickness and
Vascular Health and Risk Management 2011:7 633–638
633
© 2011 Takami and Saito, publisher and licensee Dove Medical Press Ltd. This is an Open Access article
which permits unrestricted noncommercial use, provided the original work is properly cited.
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Takami and Saito
stiffness has been reported by van den Berkmortel et al.8 CBP
can now be measured noninvasively, and CBP measurement
using such methods has yielded many new findings. It is
well known that elevation in CBP, rather than elevation in
brachial blood pressure, is more closely associated with the
onset of cardiovascular events.9 The impact of smoking cessation with nicotine replacement on arterial stiffness remains
unknown. In recent years, drug therapy with varenicline, an
α4β2 nicotinic acetylcholine receptor partial agonist, has
been actively used in helping smokers to quit smoking.10,11
The present study was undertaken to evaluate the influence
of smoking cessation with varenicline on CBP.
Methods
Patients and study design
We conducted an observational study for 1 year on 70 patients
receiving smoking cessation treatment at our clinic. Brachial
blood pressure, CBP, radial augmentation index (AI),
brachial-ankle pulse wave velocity (baPWV), left ventricular
weight, and left ventricular diastolic function were measured
before and 60 weeks after the start of the smoking cessation
treatment. Varenicline, which was administered for 12 weeks
(0.5 mg once daily for 3 days, 0.5 mg twice daily for 4 days,
and then 1.0 mg twice daily for a total of 12 weeks), was used
for smoking cessation. The carbon monoxide (CO) level in
expired gas was measured at 2-week intervals using a piCO
Smokerlyzer (Bedfont, Kent, UK) to check whether the
patients had quit smoking. Of the 70 patients, 56 completed
the 12-week treatment. Of these 56 patients, 19 resumed
smoking during the treatment period. During the 1-year
observational study after the end of smoking cessation,
data were analyzed by dividing the patients into a smoking
cessation group (37 patients who quit smoking until 1 year
after the end of treatment) and a smoking group (33 patients
who resumed smoking).
All patients were informed about the study procedure.
Written informed consent was obtained from all patients
participating in the study. The study protocol was approved
by the Institutional Ethics Committee.
Brachial blood pressure, CBP, and radial AI were measured
by radial tonometry by using HEM9000-AI (Omron Healthcare, Kyoto, Japan). Because the radial AI is affected by meals,
it was measured on an empty stomach. To account for the influence of heart rate (HR), radial AI was corrected for HR (75/m)
and expressed as rAIx@75. The baPWV was determined from
the pulse waveforms recorded from both forearms and both
ankles using the formula PWV (Omron Healthcare, Kyoto,
Japan). Left ventricular weight and left ventricular diastolic
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f unction were measured by echocardiography (VIVID™ S6;
GE Healthcare, Milwaukee, WI). Left ventricular weight was
determined from the M-mode ultrasound image by using the
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