Title: Effects of Environmental Tobacco Smoke Exposure on Central Aortic Systolic Pressure in Chronic

Hypertensive

Introduction

1.0 Introduction

Passive smoking, or environmental tobacco smoke (ETS) exposure, is associated with the development of
atherosclerosis, coronary artery disease and stroke [1, 2]. Among possible mechanisms, the effect of passive
smoking on the mechanical properties of the arterial wall may play an important role in generating
cardiovascular dysfunction [3]. A recent study has shown that acute exposure to passive smoking generates
endothelial dysfunction in the coronary arteries in both smokers and nonsmokers [8].

The mechanisms by which passive smoking may increase cardiovascular risk are becoming increasingly
clear(,1,2) with added insights offered by an intriguing study appearing in this issue of Hypertension.3 Using an
elegant experimental design, Argacha et al(3) assessed the vascular effects of ETS exposure in humans. They
hypothesized, first, that vascular effects of ETS are in part secondary to increased plasma nicotine levels after
ETS exposure and, second, that the vascular effects of passive smoking are sustained even after stopping the
smoke exposure. Some experimental studies have also shown that blood pressure is elevated for a short time
period [16] or for 24 hours after brief ETS exposure [[15].

Environmental tobacco smoke exposure was defined as exposure to another persons tobacco smoke at home or
in the workplace for at least 2 years during the past 10 years. (Chinese reference)
Clinicians have long been aware that a patients brachial and central blood pressures differ significantly. Studies
show that measuring central pressure is vitally important in assessing the effects of anti-hypertension therapy
and detecting elevated risk for cardiovascular events such as heart attack and stroke.

According to a study by McEniery et al, they highlight the issue of relating a measurement of brachial pressure
given quite large range of overlap because of pulse amplification. The pressure wave generated by the left
ventricle travels down the arterial tree and then is reflected at multiple peripheral sites, mainly at resistance
arteries. Consequently, the pressure waveform recorded at any site of the arterial tree is the sum of the forward
traveling waveform generated by left ventricular ejection and the backward traveling wave, the echo of the
incident wave reflected at peripheral sites. When the large conduit arteries are healthy and compliant, the
reflected wave merges with the incident in the proximal aorta during diastole, thereby augmenting the diastolic
BP and aiding coronary perfusion.

Central Aortic Systolic Pressure (CASP) is the blood pressure at the root of the aorta or the largest artery in the
body, as the blood is being pumped out of the heart. This pressure is called Central Aortic Systolic Pressure or
CASP. CASP has been shown to be an important factor in the relation to strokes and cardiovascular events,
more so than the brachial pressure, or the pressure at the arm commonly. CASP is different and usually lower
than the brachial pressure in normal people. When we are young, below 40 years old, the difference between
CASP and the brachial pressure can be significant (up to 30 mmHg). However, as we age, the aorta gets stiffer
and the compliance reduces. As a result, the CASP increases and comes much closer to the brachial pressure. In
 patients with high blood pressure, the CASP can be abnormally high for his age, showing pre-mature
stiffening of the aorta.

Throughout most of the world today, high blood pressure is defined as chronic elevations in BP 140/90 mm
Hg. ( The journal of clinical hypertension, Volume 7, Issue 9, pages 505512, September 2005 by Thomas D.
Giles MD, Bradford C. Berk MD, PhD, Henry R. Black MD, Jay N. Cohn MD, John B. Kostis MD, Joseph L.
Izzo Jr. MD, Michael A. Weber MD on behalf of the Hypertension Writing Group)

Hypertension is defined as a laboratory-measured blood pressure of at least 140/90 mm Hg or the use of

antihypertensive medications. (Prospective Study of the Association between Sleep-Disordered Breathing and
Hypertension by Paul E. Peppard, Ph.D., Terry Young, Ph.D., Mari Palta, Ph.D., and James Skatrud, M.D. N
Engl J Med 2000; 342:1378-1384May 11, 2000

The categories were as follows: optimal: systolic blood pressure <120 and diastolic blood pressure <80 mm
Hg; normal, not optimal: systolic 120 to 129 mm Hg and diastolic <84 mm Hg or diastolic 80 to 84 mm Hg and
systolic <130 mm Hg; high normal: systolic 130 to 139 mm Hg and diastolic <90 mm Hg or diastolic 85 to 89
mm Hg and systolic <140 mm Hg; stage 1 hypertension: systolic 140 to 159 mm Hg and diastolic <100 mm Hg
or diastolic 90 to 99 mm Hg and systolic <160 mm Hg; stage 2 hypertension: systolic 160 to 179 mm Hg and
diastolic <110 mm Hg or diastolic 100 to 109 mm Hg and systolic <180 mm Hg; stage 3 hypertension: systolic
180 to 209 mm Hg and diastolic <120 mm Hg or diastolic 110 to 119 mm Hg and systolic <210 mm Hg; and
stage 4 hypertension: systolic >210 mm Hg or diastolic >120 mm Hg.( Blood Pressure and End-Stage Renal
Disease in Men by Michael J. Klag, M.D., M.P.H., Paul K. Whelton, M.D., Bryan L. Randall, M.S., James D.
Neaton, Ph.D., Frederick L. Brancati, M.D., M.H.S., Charles E. Ford, Ph.D., Neil B. Shulman, M.D., and
Jeremiah Stamler, M.D.N Engl J Med 1996; 334:13-18January 4, 1996)

Research Question

Does exposure to tobacco smoke increase the central aortic systolic pressure in chronic hypertensive?

2.0 Research Hypothesis

Null Hypothesis:

There is no relationship between exposure to environmental tobacco smoke and increase in baseline central
aortic systolic pressure in chronic hypertensive.

Alternative Hypothesis:

There is relationship between exposure to environmental tobacco smoke and increase in baseline central aortic
systolic pressure in chronic hypertensive.

3.0 Research Objectives

To determine the relationship between exposure of environmental tobacco smoke to central aortic systolic
pressure in chronic hypertensive.
4.0 Research Methodology

Study Population and Sample Size

All the participants involved in this study are diagnosed to have chronic hypertension by their physician. The
participants will randomly select at outpatient department in Klinik Kesihatan Dengkil during their follow up..
A set of questions regarding demographic data and exposure to environmental tobacco smoke will be given.
Based on the feedback forms, they will be classified into two groups, based on the exposure to environmental
tobacco smoke, exposure to ETS and non-exposure to ETS. The central aortic systolic pressure will be
measured by using CASPro device for all selected participants. Then, we will compare the mean of central
aortic systolic pressure for both groups.

Definition of Environmental Tobacco Smoke Exposure

Environmental tobacco smoke exposure was defined as exposure to another persons tobacco smoke at home or
in the workplace for at least 2 years during the past 10 years. Every participant will ask about personal lifetime
exposure to environmental tobacco smoke in the home and workplace. For environmental tobacco smoke
exposure at home, we will ask 3 questions: How many people living with you smoked cigarettes? How many
cigarettes per day were smoked by these smokers who live with you? And for how long per day were you
exposed to these smokers? An estimation of workplace environmental tobacco smoke exposure are based on 3
questions: Did you have coworkers who smoked cigarettes near you so that you frequently breathed in their
smoke? If yes, how many cigarettes per day were you exposed to by these smokers? For how long per day were
you exposed to these coworkers who smoked?

Central Aortic Systolic Pressure Measurement

The central aortic blood pressure measurement will be performing in a quiet room at room temperature (37C)
after resting for 15 minutes. The CASP will be measure at the right wrist of selected participants and the data
will be recorded.

Inclusion and Exclusion Criteria

Inclusion Criteria

1. Passive smoker who are exposed to another persons tobacco smoke at home or in the workplace for at least
2 years during the past 10 years.
2. 40-65 years old
3. Diagnosed with chronic hypertension

Exclusion Criteria

1. Active smokers
2. <40 years old and >65 years old

5.0 Statistical Methods

We use Statistical Package for the Social Sciences (SPSS) version 4.0 to determine the association between
exposures to environmental tobacco smoke with central aortic systolic pressure in chronic hypertension
participants.

6.0 Expected Outcome

Exposure to environmental tobacco smoke (passive smoker) will increase the central aortic systolic pressure in
chronic hypertensive.
7.0 References

1 Jiang HE, Vupputuri S, Allen K, Prerost MR, Hughes J, Whelton PK. Passive smoking and the risk of coronary
heart disease a meta analysis of epidemiological studies. N Engl J Med 1999; 340: 9206.

2 Bonita R, Duncan J, Teuelsen T, Jackson RT, Beaglehole R. Passive smoking as well as active smoking increases
the risk of acute stroke. Tobacco Control 1999; 8: 15660.

3 Calermajer DS, Sorensen KE, Georgakopoulos D, et al. Cigarette smoking is associated with dose-related and
potentially reversible impairment of endothelium-dependent dilation in healthy young adults. Circulation 1993; 88:
214955.

8 Otsuka R, Watanabe H, Hirata K, et al. Acute effects of passive smoking on the coronary circulation in healthy
young adults. JAMA
2001; 286: 43641.

Ref: McEniery CM, Yasmin, McDonnell B, Munnery M, Wallace SM, Rowe CV, Cockcroft JR, Wilkinson IB; on
behalf of the Anglo-Cardiff Collaboration Trial Investigators. Central pressure: variability and impact of
cardiovascular risk factors: the Anglo-Cardiff Collaborative Trial II. Hypertension. 2008; 51:14761482. (kecik
punyer)

1. Barnoya J, Glantz SA. Cardiovascular effects of secondhand smoke: nearly as large as smoking. Circulation.
2005;111:2684 2698.

2. Celermajer DS, Adams MR, Clarkson P, Robinson J, McCredie R, Donald A, Deanfield JE. Passive smoking and
impaired endotheliumdependent
arterial vasodilation in healthy young adults. N Engl J Med. 1996;334:150 154.

3. Argacha J-F, Adamopoulos D, Gujic M, Fontaine D, Amai N, Berkenboom G, van de Borne P. Acute effects of
passive smoking on peripheral vascular function. Hypertension. 2008;51:1506 1511.