Public Institution NicolaeTestemițanu [601162]

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Public Institution “NicolaeTestemițanu”
State University of Medicine and Pharmacy
Republic of Moldova

Faculty of Medicine II
Department of Internal M edicine
" Cardiology "
Head Of Department : Professor LIVIU GRIB

DIPLOMA THESIS

„Smoking And Its Association With Coronary Heart
Disease ”

Author : Abu El Hija Muhammad
Scientific advisor : Vetrila Snejana assistant professor PhD MD

2015

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Contents
Introduction
Chapter 1 – General concepts on coronary artery disease and smoking
1.0 Definition of smoking ………………………………………………………….. 6
1.1 Epidemiology of tobacco use …………………………… ………………………8
1.2 Prevalence of cardiovascular disease worldwide ………………………………11
1.3 Coro nary heart disease risk factors…………………………………………….14
1.4 Pathophysiology of cigarette smoking and its influence on heart ……… ……18
1.5 Cardiovascular Disease Mortality ……………………………………………….30
Chapter 2 –Material And Methods………………………………………………34
Chapter 3 – Own Study And Results
3.1 Study Description ………… ………………… ……………………………… 35
3.2 Recommendation for general population about chronic complications of smoking
and its associated mechanisms of diseases development ……….. …………………………44
3.3 Effective approaches for to bacco control ……………………………………..46

Conclusion …… …………………………………………………………………… 54

References …………………………………………………………………… 55

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Abbreviations
 CAD , coronary artery disease ;
 CO, carbon monoxide ;
 CS, cigarette smoking ;
 CSE, cigarette smoke extract ;
 EDV , endothelium -dependent vasodilation ;
 HUVECs , human umbilical vein endothelial cells;
 LDL , low-density lipoprotein ;
 MI, myocardial infarction ;
 NO, nitric oxide;
 TF, tissue factor ;
 TFPI -1, tissue factor pathway inhibitor -1

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Introduction
Tobacco smoking is the largest preventable cause o f disease and death
worldwide , accounting for 15 ,511 deaths in 2003. Approximately 3,656
(24%) occurred in people aged 25 to 64, and 11,795 in people aged over
64.2 ages. Smoking is a major risk factor for cardiovascular disease, as
well as a range of cancers, stroke and other disabling conditions. Their
smoking will eventually kill approximately half of all people who smoke
regularly .
The risk of tobacco use extends beyon d actual smokers. There is clear
evidence of the harm to adults and children from exposure to second -hand
smoke in homes, workplaces and enclosed public places. In Australia,
more than a third (37%) of children aged 0 to 14 years live in households
with on e or more regular smokers, while 10% of children aged 0 to 14
years live in households where there is at least one reg ular smoker who
smokes indoors. In addition to causing morbidity and premature
mortality, smoking signifi cantly reduces quality of life and places a huge
financial drain on the health sector, as well as the broader community.
Throughout the world, leading governments and health agencies have
instigated tobacco -control policies to prevent tobacco use by young
people, reduce tobacco use by adu lts, and reduce the exposure of non –
smokers to second -hand smoke. Evidence shows that a comprehensive
approach to tobacco control is required to affect the prevalence of
smoking and reduce the terrible consequences and costs of tobacco use to
individuals, families, communities and the health system.
The literature data from overseas studies may not accurately reflect the
strength of the smok ing-mortality association and hypothesized that the
relative strength of this association in population as a whole, and for

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populations within it and over time, varies . Based on these conditions we
propose:
The aim of this study : To measure the strength of the association of
cigarette smoking with mortality from cardiovascular events, including
ischemic heart disease and s troke amon g adults in the world population .
The objectives :
1- To analyze the literature date regarding association of smoking
with cardiovascular morbidity and mortality in population .
2- To analyze the incidence of smoking and other risk factors in
patient with acute coronary syndrome .
3- To develop recommendations for the population about the dangers
of smoking and the prevention of cardiovascular disease .

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Chapter 1 General concepts on coron ary artery disease and smoking
1.0 Definition of smoking :
One of the difficulties encountered in identifying smokers by self
report is that there are many different ideas of what constitutes
smoking behavior. For example, when asked about th eir smoking
status, light or intermittent smokers will often classify themselves
as nonsmokers. In order to maintain consistency in the use of
various terms while gathering data on smoking behavior, the US
Centers for Disease Control and Prevention have de veloped and
updated the following definitions: (19)
 Never Smokers – Adults who have never smoked a cigarette
or who smoked fewer than 100 cigarettes in their entire
lifetime.
 Former Smokers – Adults who have smoked at least 100
cigarettes in their lifetime, but say they currently do not
smoke.
 Nonsmokers – Adults who currently do not smoke
cigarettes, including both former smokers and never
smokers.
 Current Smokers – Adults who have smoked 100 cigarettes
in their lifetime and currently smoke cigaret tes every day
(daily) or some days (nondaily).
Other terms not defined by the CDC are also frequently used:
 Light Smoker – There is no consensus on a definition for
light smoking. Various criteria used have included < 1 pack
per day, < 15 cigarettes per da y, < 10 cigarettes per day, and

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1-39 cigarettes per week. Light smokers include low -rate
daily smokers (< 5 cigarettes per day) and “chippers” who
consistently smoke = 5 cigarettes per day on the days when
they do smoke. (20)
 Intermittent Smoker – A broad term that covers a variety of
patterns of tobacco use but is generally defined as smoking
on a nondaily basis. Social smokers, who limit smoking to
contexts such as parties, bars, or nightclubs, often fit into
this category. Intermittent smoking is also co mmon among
younger smokers and minority populations. (20)

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1.1 Epidemiology of tobacco use
The world health organization (WHO) reported i n 2009 that
smoking among men was highest in the Western Pacific Region , with
51% of men aged 15 . Smoking am ong women was highest in the
European Region attested in 22% persons. In all
WHO regions except Europe , girls aged 13–15 years old are using
tobacco at higher rates than women aged 15 and older. This could be a
reflection of aggressive tobacco industry marketing to girls,
particularly in lower – and middle -income countries. The high rates
among girls is very concerning as these data suggest potential
substantial increases for women in the near future. The rates at which
adolescent boys use tobacco average ar ound 18% globally (1).
Cigarette smoking is a major cause of coronary heart disease, stroke,
aortic aneurysm, and peripheral vascular disease. The risk is manifest
both as an increased risk for thrombosis of narrowed vessels and as an
increased degree of atherosclerosis in those vessels. The
cardiovascular risks owing to cigarette smoking increase with the
amount smoked and with the duration of smoking. Smoking cigarettes
with lower machine -measured yields of tar and nicotine does not
reduce risks, but tho se who have only smoked pipes or cigars seem to
have a lower risk for cardiovascular diseases. Cessation of cigarette
smoking reduces disease risks, although risks may remain elevated for
a decade or more after cessation (7).
Since the first published Surg eon General s report on smoking and
health in 1964 more than 12 million premature deaths globally have
been attributed to smoking. Worldwide, tobacco smoking is a major
identifiable factor contributing to the gap in life expectancy between
those most in ne ed, and those most advantaged. Tobacco smoking is

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the leading preventable cause of death and accounts for 14 times more
deaths per year than alcohol and nine times the number of deaths
attributed to illicit drugs. Around 13% of deaths from cardiovascular
disease (the leading cause of death) are a ttributable to tobacco
smoking: in 1998, this represented over 6,600 deaths from
cardiovascular disease (8).
There has been a decline in the prevalence of smoking Worldwide
since the early 1980s, although this decli ne has not been continuous.
Large gains were made in the early 1980s; however, in the mid 1990s
the decline stalled before a significant drop was again achieved
between 1997 and 2001.121 In the 2004 National Drug Survey, 17.4%
of people aged 14 and over re ported daily smoking, declining from
21.8% in 1998, and since 1985 there has been a decline of 40% in
smoking rates ( 9).

Fig 1 : Prevalence of ciggarate smoking in EOCD countries

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Fig 2 : Smoking prevalence in israel , with compartion jewish and arab
smokers
Smoking in my country continues to decline as seen in the fig , The
survey was conducted in 2011 –2012 among 2,964 Israelis aged 21 and
up. It found that 17.7 percent of the adult po pulation in Israel smokes
cigarettes: Among Jewish men, 20.9 percent smoke, as do 12 percent
of Jewish women, 41.4 percent of Arab men and 8.1 percent of Arab
women.

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1.2Prevalence of cardiovascular disease worldwide
Cardiovascular disease (CVD) currently accounts for nearly half of no
communicable diseases (NCDs). NCDs have overtaken communicable
diseases as the world's major disease burden, with CVD remaining the
leading global cause of death, accounting for 17.3 million deaths per
year, a numbe r that is expected to grow to >23.6 million by 2030.
Increasingly, the populations affected are those in low – and middle –
income countries (LIMC) , where 80% of these deaths occur, usually at
younger ages than in higher income countries, and where the human and
financial resources to address them are most limited. (3)

Fig 3 : Incidence of diseases according countries development and
economic status
It is clear that low and medium income countries , have the higher
incidence of cardiovascular diseases than high income countries , that it is

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directly contributed to the high prevalence of tobacco use in low and
middle income countries as shown in the fi g below :
Country Males
% Females
%
Albania 41 4
Bangladesh 47 4
Cambodia 41 7
Chile 42 34
China 59 4
Cook
Islands 36 20
Ethiopia 8 <1
Fiji 24 5
Gambia 29 3
India 33 4
Indonesia 66 5
Islamic
Republic of
Iran 30 6
Fig 4 : Prevalence of tobacco use among adults in low and middile
income countries

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Fig 5 : The proportions of cardi ovascular deaths caused by isch emic heart
disease, cerebrovascular disease, inflammatory heart disease, rheumatic heart
disease, hypertensive heart disease, and other cardiovascular diseases in
2011.
A= in males B= in females
It is clear that the ischemic heart disease is the predominant cause for
death compared with the other types of cardiovascular disease causes ,
followed by cerebro vascular disease

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1.3 Cor onary heart disease risk factors
A- Obesity:
Globally, the prevalence of obesity (body mass index [BMI] ≥30 kg/m2)
doubled between 1980 and 2008, and it is estimated that 2.8 million
deaths annually are caused by being overweight (BMI ≥25 kg/m2) or
obese. In 2008, 10% of men and 14% of women globally were obese
compared with 5% of men and 8% of women in 1980. The Americas had
the highest prevalence of overweight (62%) and obese (2 6%) p ersons
(1,11). Figure display the mean BMI change by WHO region and
globally(4).

Fig 6 : The mean BMI change by WHO in different countries in the globe
B- Hypertension :
Globally, some 40% of people over the age of 25 years have high blood
pressure, and the number of people with elevated blood pressure (systolic
blood pressure ≥140 mm Hg or diastolic blood pressure ≥90 mm Hg) has
increased from 600 million in 1980 to a bil lion in 2008. The global
hypertensive percentage has improved over this period; however, some
regions have worsened in this respect. A decrease in the proportion of

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populations with high blood pressure was seen in the Western Pacific,
Europe, and th e Ameri cas, as shown in Figure . Systolic blood pressure is
highest in LMIC. Globally, elevated blood pressure is reported to cause
51% of stroke deaths and 45% of coronary heart disease deaths (4).

Fig 7 : Proportion of populations with high blood pressure
C- Dyslipidemia :
Mean total cholesterol levels around the world are highest in high -income
countries and have been dropping since 1980 throughout the world. The
most drastic decreases have been in high -income countries (5.62 to 5.19
mmol/l), but modest de creases in low -income countries (4.46 to 4.20
mmol/l) and middle -income countries (4.91 to 4.7 mmol/l) have also been
seen. Nevertheless, some 39% of the global population still has elevated
cholesterol, as do more than one -half of those in h igher income c ountries
(Figure ) . (4)

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Fig 8: Dyslipidemia in the global population

D- Smoking :
Smoking rates among adults in the United States have declined by
more than one -half over the past 25 years, from 33.5% in 1980 to
15.1% in 2010 —thought to be the fourth lowest rate among OECD
countries (countries that signed the convention on Organization for
Economic Cooperation and Development) after Iceland, Sweden, and
Mexico. In contrast, at least 25% of residents living in Greece, Chile,
Ireland, Hungary, Estonia, Spain, and Turkey smoke cigarettes,
according to the most recent data ( 4)

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Fig 9 : the smoking rate among adults within different countries
Smoking rates among adults in the United States have declined by
more than one -half over the past 25 years

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1.4 Pathophysiology of cigarette smoking and its influenc e on
coronary heart disease

Cigarette smoking (CS) continues to be a major health hazard, and it
contributes significantly to cardiovascular morbidity and mortality.
Cigarette smoking impacts all phases of atherosclerosis from endothelial
dysfunction to acute clinical events, the latter being largely thrombotic.
Both active and passive (environmental) cigarette smoke exposure
predispose to cardiovascular events. Whether there is a distinct direct
dose-dependent correlation between cigarette smoke exposure and risk is
debatable, as some recent experimental clinical studies have shown a non –
linear relation to cigarette smoke exposure. The exact toxic components
of cigarette smoke and the mechanisms involved in CS -related
cardiovascular dysfunction are largel y unknown, but CS increases
inflammation, thrombosis, and oxidation of low -density lipoprotein
cholesterol. Recent experimental and clinical data support the hypothesis
that cigarette smoke exposure increases oxidative stress as a potential
mechanism for i nitiating cardiovascular dysfunction.
Epidemiologic studies strongly support the assertion that cigarette
smoking (CS) in both men and women increases the incidence of
myocardial infarction (MI) and fatal coronary artery disease (CAD). Even
low-tar cigaret tes and smokeless tobacco have been shown to increase the
risk of cardiovascular events in comparison to non -smokers and
Furthermore, passive smoking (environmental tobacco exposure) with a
smoke exposure about one -hundredth that of active CS is associated with
approximately a 30% increase in risk of CAD, compared with an 80%
increase in active smokers . Thus, the evidence linking cigarette smoke
exposure with cardiovascular disease is clearly present, yet the exact

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components of cigarette smoke and the mechanisms responsible for this
association have not been clearly elucidated. The literature updates the
present clinical and experimental observations on the potential
patho physiology and mechanisms involved in smokin g-related
cardiovascular disease .
Conventionally, cigarette smoke is divided into two phases: a tar phase
and a gas phase. The tar or particulate phase is defined as the material that
is trapped when the smoke stream is passed through the Cambridge glass –
fiber filter that retains 99.9% of all particulate material with a size >0.1
μm . The gas phase is the material that passes through the filter. The
particulate (tar) phase of cigarette smoke contains >1017 free radicals/g,
and the gas phase contains >1015 free radicals/puff . The radicals
associated with the tar phase are long -lived (hours to months), whereas
the radicals associated with the gas phase have a shorter life span
(seconds)
Cigarette smoke that is drawn through the tobacco into an active smoke r's
mouth is known as mainstream smoke. Side stream cigarette smoke is the
smoke emitted from the burning ends of a cigarette. Mainstream cigarette
smoke comprises 8% of tar and 92% of gaseous components.
Environmental tobacco smoke results from the combin ation of side
stream smoke (85%) and a small fraction of exhaled mainstream smoke
(15%) from smokers. Side stream cigarette smoke contains a relatively
higher concentration of the toxic gaseous component than mainstream
cigarette smoke . Of all the known c onstituents, nicotine, a component of
the tar phase, is the addictive substance of cigarette smoke.

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Fig 10 : Physical and biochemical properties of cigarette smoke

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Cigarette smoking and atherosclerosis: clinical and experimental
observations
Cigarette smoking predisposes the individual to several different clinical
atherosclerotic syndromes, including stable angina, acute coronary
syndromes, sudden death, and stroke. Aortic and peripheral
atherosclerosis are also increased, leading to intermittent clau dication and
abdominal aortic aneurysms
Various clinical imaging techniques have been utilized to directly
ascertain the relationship between CS and atherosclerosis. Early studies
associated pack years of smoking with the severity of angiographically
determined atherosclerosis and Cigarette smok ing was also found to be an
independent predictor of new coronary lesion formation in the Canadian
Coronary Atherosclerosis Intervention trial . As angiography is an
insensitive indicator of the amount or progression of atherosclerosis,
other techniques ha ve been utilized to assess atherosclerotic changes
associated with cigarette smoke exposure. Thoracic aortic atherosclerosis
as assessed by transesophageal echocardiography was increased in
cigarette smokers. It has also been reported that both active and passive
smoking are associated with a consistent increase in intimal -medial
thickness of the carotid artery as assessed by carotid ultrasound.
Vasomotor dysfunction, inflammation, and modification of lipids are
integral components for the initiation and pr ogression of atherosclerosis.
These components precede the apparent structural and clinicopathologic
manifestations of atherosclerosis. The following sections address the
present knowledge regarding the effects of CS on these components of
atherogenesis.

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Vasomotor dysfunction
Impairment of vasodilatory function is one of the earliest manifestations
of atherosclerotic changes in a vessel. In both animal and human models,
several studies have demonstrated that both active and passive cigarette
smoke exposure were associated with a decrease in vasodilatory function.
In humans, cigarette smoke exposure impaired endothelium -dependent
vasodilation (EDV) in macrovascular beds such as coronary and brachial
arteries and in microvascular beds.
Nitric oxide (NO), a free radical, is primarily responsible for the
vasodilatory function of the endothelium. Using cigarette smoke extract
(CSE) or isolated components such as nicotine, multiple in vitro studies
have found that CS was associated with decreased NO availability.
Because there are numerous known and unknown components of
cigarette smoke whose metabolic fate in the human body is unknown, an
appropriate in vitro model of CS exposure remains to be established. In
an attempt to produce a more physiologic in vitro model, our group has
incubated endothelial cells with sera from smokers. Utilizing this model,
demonstrated that exposure to smokers' sera decreased NO availability
from both human umbilical vein endothelial cells (HUVECs) and human
coronary artery endothelial ce lls by altering the expression and activity of
the endothelial NO synthase enzyme. A significant correlation existed
between flow -mediated brachial artery EDV and NO availability from
cultured HUVECs exposed to serum from the same individuals.
Similarly, o ther studies utilizing an in vivo infusion of L -NMMA have
indirectly demonstrated that the reduced EDV associated with smoking
was attributable to a decreased NO availability.
Not only is NO a vasoregulatory molecule, it helps regulate
inflammation, leukoc yte adhesion, platelet activation, and thrombosis.
Therefore, an alteration in NO biosynthesis could have both primary and

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secondary effects on the initiation and progression of atherosclerosis and
on thrombotic events.
Inflammation
The inflammatory respon se is an essential component in the initiation and
evolution of atherosclerosis. Several studies have indicated that CS
causes about a 20% to 25% increase in the peripheral blood leukocyte
count . In vivo, CS is associated with an increased level of multip le
inflammatory markers including C -reactive protein, interleukin -6, and
tumor necrosis factor alpha in both male and female smokers .
Local recruitment of leukocytes on the surface of endothelial cells is an
early event in atherosclerosis. Elevations of v arious proinflammatory
cytokines increase leukocyte -endothelial cell interaction leading to
leukocyte recruitment. Indeed, soluble VCAM -1, ICAM -1, E -selectin
levels are higher in smokers.. Cigarette smoking also causes activation of
proatherogenic molecule s leading to alteration in cell -cell interactions.
Cigarette smoking extract exposure was associated with a 70% to 90%
increase in adherence between human monocytes and HUVECs in culture
attributable to the increased expression of adhesion molecules on the
surface of both monocytes and HUVECs. Exposure to CSE increased by
200% the rate of transendothelial migration of monocyte -like cells across
a HUVEC monolayer. Monocytes isolated from smokers increased
expression of the integrin CD 11b/CD 18, which augmen ted the
adhesiveness of the monocytes to HUVECs in culture . Similarly,
exposing human monocytes and HUVECs to smokers' serum, found a
significant increase in adhesion between these cells, which was associated
with increased expression of ICAM -1 on HUVECs. Thus, CS fuels the
fire of inflammation in the blood and at the vessel wall.

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Fig 11 : inflammatory response in cigarette smoking
Modification of lipid profile
Cigarette smoking could promote atherosclerosis, in part, by its effects on
lipid profile. Smokers have significantly higher serum cholesterol,
triglyceride, and low -density lipoprotein (LDL) levels, but high -density
lipoprotein is lower in smokers than in non -smokers . The mechanisms
responsible are not clearly elucidated, and the role of dieta ry differences
between smokers and non -smokers is unknown. The triglyceride/high –
density lipoprotein abnormalities have recently been suggested to be
related to insulin resistance. In fact, it has been proposed that insulin
resistance is a potential key li nk between CS and cardiovascular disease .
Cigarette smoking also increases oxidative modification of LDL.
Circulating products of lipid peroxidation and autoantibody titers to
oxidized LDL are significantly increased in smokers . In 1988, reported
that ex posure to CSE caused a modification of LDL, which was actively
taken up by the macrophages to form foam -cells in culture. observed that
exposure of human plasma to the gas phase of cigarette smoke caused
oxidative modification of plasma LDL. Furthermore, H UVECs isolated

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from smokers significantly increased oxidative modification of LDL
compared with HUVECs isolated from non -smokers. Cigarette smoke
extract exposure may also decrease the plasma activity of paraoxonase, an
enzyme that protects against LDL oxi dation (57). More recently, in a
hyperlipidemic rabbit model, injection of CSE accelerated atherosclerosis
through oxidative modification of LDL.
Genetic predisposition
Recently, genetic predisposition was found to influence the development
of atherogenesis in individuals exposed to cigarette smoke. The
intersubject variability in the atherosclerotic process in smokers may be
partially mediated by genetic v ariants. Either
CYP1A1 MSP polymorphism or certain endothelial NO synthase intron 4
polymorphisms increased the susceptibility to cigarette smoke exposure –
related atherosclerotic diseases including multi -vessel CAD and MI .
However, at present, the importa nce of these genetic variants is unknown,
as their prevalence in the entire population of cigarette smokers has not
been determined.
CS and thrombosis —clinical and experimental observations
Cigarette smoking is associated with an increased incidence of acu te MI.
Cessation of smoking significantly reduces this risk over a one – to three –
year period with an exponential decline approaching the risk in ex –
smokers within five years of cessation . Recent data indicate an
immediate reduction in thrombotic events wi th smoking cessation. A
preliminary, oral presentation study (presented by Sargent, Shepard, and
Glantz at the 52nd Annual American College of Cardiology Conference
in March 2003) reported that a citywide smoking ban in public places
over a six -month perio d in Helena, Montana, reduced the incidence of

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acute MI by 60% during that time period. Furthermore, pathologic studies
of sudden coronary death indicate that CS increased the risk of plaque
rupture and acute thrombosis of a lipid -rich, thin -capped atherom a in
men; in female smokers, the prevailing mechanism was plaque erosion
with superimposed thrombosis . Acute cigarette smoke exposure may also
increase coronary artery vascular resistance reducing coronary blood
flow . Smoking may also be a risk factor fo r coronary vasospasm .
The prothrombotic effects of exposure to cigarette smoke have been
repeatedly demonstrated to cause alterations in platelet function,
antithrombotic/prothrombotic factors, and fibrinolytic factors. The
following sections address the present knowledge regarding these effects.
Platelet dysfunction
Platelets isolated from smokers exhibited an increased stimulated as well
as spontaneous aggregation . After exposure to smokers' serum, platelets
isolated from non -smokers demonstrated hyperaggregability .Cigarette
smoking may decrease availability of platelet -derived NO and decrease
platelet sensitivity to exogenous NO, leading to increased activation and
adhesion .
Alteration of antithrombotic and prothrombotic factors
Current smokers have higher fibrinogen levels that correlate with the
number of cigarettes smoked. Ex -smokers have fibrinogen levels similar
to non -smokers . Alterations of tissue factor (TF) and TF pathway
inhibitor -1 (TFPI -1) and a consequent increase in thrombotic pot ential
have also been documented. Human umbilical vein endothelial cells
exposed to serum from chronic smokers showed a significantly decreased
TFPI -1 level and relatively higher but nonsignificant increase in TF level
in culture. An increased TF immunorea ctivity and an increase in TF

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activity were observed in atherosclerotic plaques isolated from apoE−/−
mice exposed to half of a non -filtered research cigarette five days a week,
for eight weeks . In smokers 2 h after smoking two cigarettes, an increase
in circulating TF activity has also been reported in human plasma .
Furthermore, higher red blood cell counts, hematocrits, blood viscosity,
and an ongoing inflammatory process potentiate the prothrombotic
process associated with smoke exposure .
Alteration i n fibrinolysis
Human umbilical vein endothelial cells exposed to chronic smoker's
serum have significant decreases in both basal and substance -P-
stimulated t -PA release in culture with a significant alteration in t –
PA/PAI -1 molar ratio. Similarly, decrease d plasma t -PA antigen and
activity were observed in smokers in samples isolated from brachial and
coronary arteries after pharmacologic stimulation .
Therefore, CS is associated with dysfunctional thrombo -hemostatic
mechanism(s) that promote the initiation and/or propagation of thrombus
formation and limit its effective dissolution.
Factors and mechanisms responsible for smoking -mediated vascular
dysfunction
Cigarette smoke contains over 4,000 known components, of which only a
few components have been examined in isolation. Carbon monoxide
(CO) is one such component, but its effects on athero -thrombotic disease
have been equivocal. An earlier study suggested t hat CO could be
responsible for smoking -related cardiovascular alterations . However,
more recent data suggest that CO from cigarette smoke was an unlikely
cause for atherosclerosis or thrombus . Polycyclic aromatic hydrocarbons
found in the tar fraction o f cigarette smoke have also been studied, and

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these components, at least in experimental models, accelerate
atherosclerosis .
Nicotine in cigarette smoke is probably the most studied component.
Although nicotine plays a major role in smoking -related increa ses in
cardiac output, heart rate, and blood pressure, its role in CS -related
athero -thrombotic disease remains controversial . Nicotine exposure
alone had been reported to cause no change, a decrease, or an increase in
EDV or NO availability . In various models, although high doses of
nicotine favor atherogenic changes, the majority of current evidence
suggests that nicotine, at concentrations similar to a smoker's blood level,
has a minor effect on the initiation or propagation of atherosclerosis .
Simila rly, the effect of nicotine on thrombo -hemostatic factors such as
platelets, fibrinogen, or t -PA, PAI -1 appears to be insignificant in the
setting of smoking . As mentioned earlier, nicotine is the known addictive
substance in cigarette smoke, and its addi ctive qualities likely perpetuate
exposure to the other more detrimental components.
Currently, free radical -mediated oxidative stress is emerging as the
pivotal step for the development of atherosclerosis . In a setting of CS,
free radicals could arise fr om: 1) the gas or tar phase of cigarette smoke;
2) circulating or in situ -activated macrophages and neutrophils; and 3)
endogenous sources of reactive oxygen species such as uncoupled eNOS,
xanthine oxidase, and the mitochondrial electron transport chain . A
reaction between free radicals such as superoxide and NO not only
decreases NO availability but also generates peroxynitrite, which further
enhances the cellular oxidative stress. Increased oxidative stress with the
loss of the protective effect of NO t ips the cellular balance towards a
proatherogenic and prothrombotic milieu. Many of the abnormalities
described above, including endothelial dysfunction, proinflammatory
effects on the vessel wall, prothrombotic effects such as increased platelet

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reactivity , reduced endogenous fibrinolysis, and lipid peroxidation, can
largely be explained by the effects of increased oxidative
stress. Furthermore , antioxidants or agents that reduced the oxidative
stress or increased NO availability have been shown to either i mprove or
reverse the proatherogenic, proinflammatory, and prothrombotic
attributes associated with CS.
Nonlinear dose effect of smoking on cardiovascular function
Although the association between CS and cardiovascular risk has clearly
been demonstrated, a n unanswered question is whether or not there is a
linear dose effect. Several recent large epidemiologic studies showing a
trend for more cardiovascular events in heavier active smokers have
failed to find a significant dose -dependent correlation between
cardiovascular risk and the number of cigarettes smoked or the pack –
years of exposure. More recently, heavy and light active smokers had a
similar decrease in brachial artery EDV and similar abnormalities of NO
biosynthesis. Similarly, even with passive smoking, certain athero –
thrombotic markers such as a reduced EDV and increased platelet
activation were similar to that of active smoking. The data presented
above suggest that the underlying biochemical and cellular processes may
become saturated with small doses of toxic components from cigarette
smoke causing a nonlinear dose -response on cardiovascular function. The
exact mechanisms involved require further study.

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1.5 Cardiovascular disease mortality
 Each year cardiovascu lar disease (CVD) causes over 4 million
deaths in Europe and over 1.9 million deaths in the European
Union (EU).
 CVD causes 47% of all deaths in Europe and 40% in the EU.
 CVD is the main cause of death in women in all countries of
Europe and is the main cause of death in men in all but 6 countries.
 Death rates from CHD are generally higher in Central and Eastern
Europe than in Northern, Southern and Western Europe.
 Death rates from stroke are many times higher in Central and
Eastern Europe than in Norther n, Southern and Western Europe.
 CVD mortality is now falling in most European countries,
including Central and Eastern European countries which saw large
increases until the beginning of the 21st century.
 Smoking remains a major public health issue in Euro pe. Although
smoking has declined in many European countries the rate of
decline is now slow, and rates remain stable or are increasing in
some countries, particularly among women.
 Women are now smoking nearly as much as men in many
European countries and girls often smoke more than boys.
 Fruit and vegetable consumption has increased overall across
Europe in recent decades, while overall fat consumption has
remained stable.
 Few adults in European countries participate in adequate levels of
physical activity , with inactivity more common among women than
men.
 Levels of obesity are high across Europe in both adults and
children, although rates vary substantially between countries.

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 The prevalence of diabetes in Europe is high and has increased
rapidly over the l ast ten years, increasing by more than 50% in
many countries.
 Overall CVD is estimated to cost the EU economy almost €196
billion a year.
 Of the total cost of CVD in the EU, around 54% is due to health
care costs, 24% due to productivity losses and 22% due to the
informal care of people with CVD (6).

Fig12 : Causes of death by gender in the European countries. WHO
indicates World Health Organization; CVD, cardiovascular
diseases; CHD, coronary heart disease.
Cardiovascular diseases are the leading cause of death in European
countries.

32

Fig 13 : the leading causes of death in usa
In the united states of America , the leading cause of death is cancer ,
while the cardiovascular diseases is in the 2nd place.
People with mental illness
Higher smoking prevalence has been reported for people with
depression and anxiety disorders, with people with schizophrenia
being three times more likely to smoke than those in the general
population. Around 35% of smokers between 18 and 39 years of age
reported some sort of mental health problem in an Australian survey.
Tobacco cessation is complex for this population group, where
smoking is sometimes used as a form of self -medication or a way of
coping with difficult life circumstances and where there i s a high level
of addiction. Smokers with mental health conditions may also
experience difficult withdrawal symptoms(9).

33
Smoking In Pregnancy
The prevalence of smoking is relatively high among pregnant women,
with an estimated 30% of Australian women being smokers when they
fall pregnant and 23% smoking during pregnancy. Smoking in
pregnancy among Aboriginal and Torres Strait Islander women is
even higher: in peri -natal data collected from five Australian states
and territories, 52.2% of Aboriginal and Torres Strait Islander mothers
giving birth in 2003 reported smoking during pregnancy, compared
with 15.8% of nonindigenous mothers. Smoking cessa tion programs
designed for pregnant women have been shown to increase the rates of
smoking cessation, which benefits maternal and infant health and is
cost effective (9).

Conclusion Of Chapter 1 :

1. Although the precise mechanisms responsible remain und etermined,
free radical -mediated oxidative stress appears to play a central role in CS –
mediated athero -thrombotic diseases. Furthermore, potentiated by
multiple prothrombotic and antifibrinolytic effects, intravascular
thrombosis is the predominant cause o f acute cardiovascular events.
2.An increasing body of epidemiologic, clinical, and experimental data
also suggests that the pathophysiologic effects of cigarette smoke
exposure on cardiovascular function may be nonlinear.
3.The broad aim of tobacco control is to reduce smoking and its health
consequences by: reducing uptake of smoking reducing consumption of
tobacco promoting cessation of smoking protecting non -smokers from
second -hand smoke.

34
Chapter 2 : Material And Methods :
The present study was conducted on a sample of 5 patients, all
hospitalized in cardiology no.3 Sfinta Treime Hospital , between October
2014 – April 2015.The patients in our study were examined by a special
sheet, which included: smoking, age, gender, previous medical history of
ischemic heart disease, high blood pressure (hypertension), diabetes
mellitus (DM) type 2, obesity, lipid profile (total cholesterol ,
triglycerides, HDL -cholesterol and LDL -cholesterol), the patient's
socioeconomic status, origin and presence of cardi ovascular disease in the
family.

35
Chapter 3 : Own Study And Results :
3.1 The study included three men and two women, all with acute
coronary syndrome ( ACS ), data is shown in Fig .

Fig14 . Distribution of patients with ACS after sex, n = 5.
The data obtained in our study results in a superior incidence in smokers
with ACS men than women, the ratio was 1.5: 1. Depending on the age
smokers with ACS patients were divided into 2 groups: 45 -64; > 65, t he
data is presented in Figure .
3

60% 2

40% patient gender ,ACS n=5
barbați
femei

36

Fig.15 . Distribution ACS patients according to age, n = 5
The data illustrated in Fig. 2 shows a higher incidence in patients who
developed ACS smokers aged 45 -64 years – 4 (80%). In the group aged
over 65 were recorded in one patient (20%) indicate that differs from the
results of studies conducted in developed countries, where life expectancy
increased population and morbidity in this category of people by 15 -30%
. We analyzed patients by area of origin smokers and noticed that most of
the SCA developed from urban areas (60%) than rural (40%).
Fig 16 . backgrounds of patients with ACS, n = 5.
0 1 2 3 4
45-64
>65 4

80%
1

20% Age Of Patients,ACS n=5
45-64
>65
0
1
2
3 urban rural
3

60% 2

40% Mediul de provenienta a pacienților cu
SCA, n=5
urban
rural

37
In terms of occupations found in the group studied, almost half of those
surveyed are retired (40%), the rest being farmers (10%), employees
(10%) or having other conditions, such as households, unemployed (40
%). There are significant differences between men and women
occupation: men are a higher percentage of farmers and workers, and
women have a higher percentage of occupations (mainly are housewives),
the data b eing reported in Fig. :

Fig 17 . socioeconomic status of patients with ACS, n = 5.
The habit of smoking is the main risk factor for cardiovascular diseases,
and they are the leading cause of mortality worldwide. About 30% of
cases of coronary atherosclerosis and thrombosis occur because of
smoking. Atherosclerosis describes fat clogging the arteries that narrows
and blocks, and thrombosis located describes a blood clot in the arteries
that supply the heart.To emphasize the major risk to which we submit
when we smoke, specialists announce that 9 out of 10 people who
underwent open -heart by pass surgery, smoke or have smoked in the past!
Crossing the brain blood vessels may also affected by smoking, they can
block and can reach collapse or paralysis. Renal arteries affected by
0 0,5 1 1,5 2
pensionari agricultori salariati casnici 2- 40%
1
10% 1
10% 2 -40 % %

38
smoking habit can cause hypertension or renal failure. For that sm oking
directly affects the entire circulatory system, femoral arteries have also
suffered in this case can lead to the appearance of gangrene or amputation
legs.Nicotine, the addictive, carbon monoxide, tar and hydrogen cyanide
are poisonous substances tha t smokers unconsciously they put in their
body. They are best known harmful substances in cigarettes, but you
should know that in reality we are dealing with more than 4,000
chemicals with different degrees of toxicity, of which only 43 are
recognized worl dwide as carcinogen.
1. Besides smoking, there are other major risk factors, such as
essential hypertension, diabetes, dyslipidemia, obesity, stress,
seden tary lifestyle, etc. In fig are often highlight the factors that
lead to acute coronary syndromes:

Fig 18 : Risk factors in patients with ACS, n = 5
Hypertension and cig.smoking remain the major 2 causes for
coronary heart disease development .

39
Coronary artery disease prevention and management
Cessation of smoking significantly reduces the risk of death from
CAD. Numerous studies concur that there is a ra pid decline in the risk
of CA D within one year of cessation. Thereafter, the risk more
gradually declines to the levels of a never -smoker,but there are
conflicting reports on how long this takes. A recent US Surgeon
General s report concluded that the excess risk of CAD caused by
smoking is reduced by about half after one year of smoking cessation
and then declines gradually, and that 15 years after abstaining from
smoking, the risk of CAD is simila r to that in those who have never
smoked. Other recent studies have found a more rapid reduction in
risk, concurring that the risk of heart attack or major coronary events
declines rapidly after quitting smoking, and returns to the level of risk
for never -smokers within two to six years. A large population -based
case-control study undertaken in Australia and New Zealand found that
the risk of having a major coronary event begins to fall within 12
months of cessation, is substantial one to three years follow ing
cessation, and returns to that of a never -smoker within four to six years
of quitting. However, more recent research has indicated that within
three years of quitting, risk of a myocardial infarction (heart attack)
reduced to 1.9 compared to never smok ing, but a residual excess risk
of 1.2 remained for 20 or more years after quitting. The reduction in
risk after cessation of smoking appears to be similar for men and
women. The risk of suffering a stroke begins to fall soon after the
cessation of smoking , with most of the benefit of quitting occurring
within two to five years.Similar reductions in risk of stroke have been
observed for men and women. There is conflicting evidence on
whether the benefits of smoking cessation for reduction in the risk of

40
stroke are influenced by the number of cigarettes smoked per day. Data
from the Nurses Health Study indicate that the patterns of reduction in
risk of stroke are the same regardless of number of cigarettes smoked,
the age of initiation of smoking, or the pres ence of other risk factors
for stroke, but another study found a longer legacy of elevated risk
among heavier smokers. There is a lower risk of peripheral arterial
disease among ex -smokers compared with current smokers, and
cessation improves the prognosis of patients with established
peripheral arterial disease. Complications from peripheral arterial
disease are reduced among patients who have quit smoking. Smoking
cessation in these patients also increases exercise tolerance, reduces the
risk of amputatio n after surgery, and increases overall survival. Unlike
other forms of cardiovascular disease for which there is a more rapid
reduction of risk following cessation, an excess risk for abdominal
aortic aneurysm can remain even 20 years after the cessation o f
smoking. However, the risk of abdominal aortic aneurysm does
decrease slowly after the cessation of smoking, with the reduction in
risk mainly attributed to the reduced duration of smoking. (5)
Diagnostic Studies of coronary artery disease
Coronary arte ry disease may be diagnosed based on medical and family
histories, your risk factors for CA D, a physical exam, and the results from
tests and procedures.No single test can diagnose CA D. If your doctor
thinks you have CA D, he or she may recommend one or more of the
following tests.

41
EKG (Electrocardiogram)
An EKG is a simple, painless test that detects and records the heart's
electrical activity. The test shows how fast the heart is beating and its
rhythm (steady or irregular). An EKG also records the strength and
timing of electrical signals as they pass through the heart. An EKG can
show signs of heart damage due to CA D and signs of a previous or
current heart attack .
Stress Testing
During stress testing , you exercise to make your heart work hard and beat
fast while heart tests are done. If you can't exercise, you may be given
medicine to raise your heart rate. When your heart is working hard and
beating fast, it needs more blood and oxygen. Plaque -narrowed arteries
can't supply enough oxygen -rich blood to meet your heart's needs.
A stress test can show p ossible signs and symptoms of CA D, such as:
 Abnormal changes in your heart rate or blood pressure
 Shortness of breath or chest pain
 Abnormal chang es in your heart rhythm or your heart's electrical activity
If you can't exercise for as long as what is considered normal for someone
your age, your heart may not be getting enough oxygen -rich blood.
However, other factors also can prevent you from exercising long enough
(for example, lung diseases, anemia , or poor general fitness).
As part of some stress tests, pictures are taken of your heart while you
exercise and while you rest. These imaging stress tests can show how
well blood is flowing in your heart and how well your heart pumps blood
when it beats.

42
Echocardiography
Echocardiography (echo) uses so und waves to create a moving picture of
your heart. The picture shows the size and shape of your heart and how
well your heart chambers and valves are working.
Echo also can show areas of poor blood flow to the heart, areas of heart
muscle that aren't cont racting normally, and previous injury to the heart
muscle caused by poor blood flow.
Chest X Ray
A chest x ray takes pictures of the organs and structures inside your chest,
such as your heart, lungs, and blood vessels. A chest x ray can reveal
signs of heart failure , as well as lung disorders and other caus es of
symptoms not related to CA D.
Blood Tests
Blood tests check the levels of certain fats, cholesterol, sugar, and
proteins in your blood. Abnormal levels might be a sign that you're at risk
for CA D.
Coronary Angiography and Cardiac Catheterization
Your doctor may recommend coronary angiography (an-jee-OG-rah-fee)
if other tests or factors show that you're likely to have CHD. This test
uses dye and special x rays to show the insides of your coronary
arteries.To get the dye into your coronary arteries, your doctor will use a
procedure called cardiac catheterizat ion (KATH -eh-ter-ih-ZA-shun).A
thin, flexible tube called a catheter is put into a blood vessel in your arm,
groin (upper thigh), or neck. The tube is threaded into your coronary

43
arteries, and the dye is released into your bloodstream. Special X -rays are
taken while the dye is flowing through your coronary arteries. The dye
lets your doctor study the flow of blood through your heart and blood
vessels.
Cardiac catheterization usually is done in a hospital. You're awake during
the procedure. It usually causes little or no pain, although you may feel
some soreness in the blood vessel where your doctor inserts the catheter
(12) .

44
3.2 Recommendation for general population about c hronic
complications of smoking and its associ ated mechanisms of
diseases development
It is demonstrated that smoking increase health risks in general
population. Smokers are more likely than nonsmokers to develop heart
disease, stroke, and lung cancer . According published date s moking i s
estimated to increase the risk:
o For coro nary heart disease by 2 to 4 times
o For stroke by 2 to 4 times
o Of men developing lung cancer by 25 times
o Of women developing lung cancer by 25.7 times
In addition s moking causes diminished overall heath, such as self-
reported poor health, increased absenteeism from work, and
increased health care utilization and cost. (2). Smokers are at greater risk
for diseases that affect the heart and blood v essels (cardiovascular
disease) .
 Smoking causes stroke and coronary heart disease —the leading causes
of death Worldwide.
 Even people who smoke fewer than five cigarettes a day can have
early signs of cardiovascular disease.
 Smoking’s damages blood vessels and contribute to development of
artery atherosclerosis. This increase heart beat and level of blood
pressures your blood pres sure.
 A heart attack occurs when a clot blocks the blood flow to your heart.
When this happens, your heart cannot get enough oxygen. This
damages the heart muscle, and part of the heart muscle can die.
 A stroke occurs when a clot blocks the blood flow to part of your
brain or when a blood vessel in or around your brain bursts.
 Blockages caused by smoking can also reduce blood flow to your legs
and skin (2).

45
Smoking can cause lung disease by damaging your airways and the small
air sacs (alveoli) found in your lungs.
 Lung disease s caused by smoking include chronic obstructive
pulmonary diseases, which includes emphysema and chronic
bronchitis.
 Cigarette smoking causes most cases of lung cancer.
 If you have asthma, tobacco smoke can trigger an attack or make an
attack worse.
 Smokers are 12 to 13 times more likely t o die from COPD than
nonsmokers (2)
Smoking can cause cancer almost anywhere in your body:
 Bladder
 Blood (ac ute myeloid leukemia)
 Cervix
 Colon and rectum (colorectal)
 Esophagus
 Kidney and ureter
 Larynx
 Liver
 Oropharynx (includes parts of the throat, tongue, soft palate, and the
tonsils)
 Pancreas
 Stomach
 Trachea, bronchus, and lung
If nobody smoked, one of every three -cancer deaths in the Worldwide
would not happen. Smoking increases the risk of dying from cancer and
other diseases in cancer patients and survivors. (2)

46
3.3 Effective Approaches for tobacco control
The broad aim of tobacco control is to reduce smoking and its health
consequences by: reducing uptake of smoking reducing consumption of
tobacco promoting cessation of smoking protecting non -smokers from
second -hand s moke. Tobacco -control advocates have long recognized the
need for a comprehensive app roach. International reviews consistently
demonstrate that the most effective approaches to tobacco control are
multifaceted and include a range of measures that complemen t and
reinforce each other. From such evidence -based reviews, 10 core
components of a n effective approach to reducing the use of tobacco and
its effects on health and society emerge The impact of each strategy when
it is used in isolation is likely to lead to an underestimate of their
combined impact b ecause of synergistic effects. Tobacco -control activity
in Australia has occurred in all of these areas, and the cur rent National
Tobacco Strategy is essentially based on such a comprehensive approach
: 10 core components of a comprehensive approach to tobacco control
1. Taxation and pricing of tobacco products.
2. Regulation of tobacco advertising and promotion.
3. Regulation of product availability and sale of tobacco to minors.
4. Product regulation.
5. Hard -hitting mass -media campaigns (including paid and unpaid).
6. Education about t he effects of smoking on health.
7. Support for cessation and prevention of relapse.
8. Health professional and healthcare system interventions.
9. Smoke -free policies and regulations.
10. Strategies to postpone or prevent the onset of smoking. (11)

47
How coronary artery disease could be prevented or managed
Treatments for coronary heart disease include lifestyle changes,
medicines, and medical procedures. Treatment goals may include:
 Relieving symptoms.
 Reducing risk factors in an effort to slow, stop, or reverse the buildup of
plaque.
 Lowering the risk of blood clots forming. (Blood clots can cause a heart
attack .)
 Widening or bypassing clogged arteries.
 Preventing complications of CHD.
Lifestyle Changes
Making lifestyle changes often can help prevent or treat CHD. Lifestyle
changes might be the only treatment that some people need.
Follow a Healthy Diet
A healthy diet is an important part of a healthy lifestyle. Fol lowing a
healthy diet can prevent or reduce high blood pressure and high blood
cholesterol and help you maintain a healthy weight.
Therapeutic Lifestyle Changes (TLC). Your doctor may recommend
TLC if you have high blood cholesterol. TLC is a three -part program that
includes a healthy diet, physical activity, and weight management.
With the TLC diet, less than 7 per cent of your daily calories should come
from saturated fat. This kind of fat is found in some meats, dairy
products, chocolate, baked goods, and deep -fried and processed foods.

48
No more than 25 to 35 percent of your daily calories should come from
all fats, including saturated, trans, monounsaturated, and polyunsaturated
fats.
You also should have less than 200 mg a day of cholesterol. The amounts
of cholesterol and the types of fat in prepared foods can be found on the
foods' Nutrition Facts labels.
Foods high in soluble fiber also are part of a healthy diet. They help
prevent the digestive tract from absorbing cholesterol. These foods
include:
 Whole -grain cereals such as oatmeal and oat bran
 Fruits such as apples, bananas , oranges, pears, and prunes
 Legumes such as kidney beans, lentils, chick peas, black -eyed peas, and
lima beans
A diet rich in fruits and vegetables can increase important cholesterol –
lowering compounds in your diet. These compounds, called plant stanols
or sterols, work like soluble fiber.
A healthy diet also includes some types of fish, such as salmon, tuna
(canned or fresh), and mackerel. These fish are a good source of omega -3
fatty acids. These acids may help protect the heart from blood clots and
inflammation and reduce the risk of heart attack . Try to have about two
fish meals every week.
You also should try to limit the amount of sodium (salt) that you eat. This
means choosing low -salt and "no added salt" foods and seasonings at the
table or while cooking. The Nutrition Facts label on food packaging
shows the amount of sodium in the item.

49
Try to limit drinks that contain alcohol. Too much alcohol will raise your
blood pressure and triglyceride level. (Triglycerides are a type of fat
found in the blood.) Alcohol also adds extra calories, which will cause
weight gain.
Men should have no more than two drinks containing alcohol a day.
Women should have no more than one drink containing alcohol a day.
One d rink is a glass of wine, beer, or a small amount of hard liquor.
Dietary Approaches to Stop Hypertension (DASH). Your doctor may
recommend the DASH eating plan if you have high blood pressure. The
DASH eating plan focuses on fruits, vegetables, whole grain s, and other
foods that are heart healthy and low in fat, cholesterol, and sodium.
DASH also focuses on fat -free or low -fat milk and dairy products, fish,
poultry, and nuts. The DASH eating plan is reduced in red meats
(including lean red meats), sweets, a dded sugars, and sugar -containing
beverages. It's rich in nutrients, protein, and fiber.
The DASH eating plan is a good healthy eating plan, even for those who
don’t have high blood pressure. For more information, go to the
NHLBI’s "Your Guide to Lowering Your Blood Pressure With DASH."
Be Physically Active
Routine physical activity can lower many CHD risk factors, including
LDL ("bad") cholesterol, high blood pressure, and excess weight.
Physical activity also can lower your risk for diabetes and raise your HDL
cholesterol level. HDL is the "good" cholesterol that helps prevent CHD.

50
Talk with your doctor before you start a new exercise plan. Ask him or
her how much and what kinds of physical activity are safe for you.
People gain health benefits from as little as 60 minutes of moderate –
intensity aerobic activity per week. The mo re active you are, the more
you will benefit.
Maintain a Healthy Weight
Maintaining a healthy weight can lower your risk for CHD. A general
goal to aim for is a body mass index (BMI) of less than 25.
BMI measures your weight in relation to your height and gives an
estimate of your total body fat . You can use the NHLBI's online BMI
calculator to figure out your BMI, or your doctor can help you.
A BMI between 25 and 29.9 is considered overweight. A BMI of 30 or
more is considered obese. A BMI of less than 25 is the goal for
preventing and treating CHD. Your doctor or other health care provider
can help you set an appropriate BMI goal.
Quit Smoking
If you smoke, quit. Sm oking can raise your risk for CA D and heart
attack and worsen other CA D risk factors. Talk with your doctor about
programs and products that can help you quit smoking . Also, try to avoid
secondhand smoke.
If you have trouble quitting smokin g on your own, consider joining a
support group. Many hospitals, workplaces, and community groups offer
classes to help people quit smoking.

51
For more information about how to quit smoking, go to the Health
Topics Smoking and Your Heart article and the NHLBI's "Your Guide to
a Healthy Heart."
Manage Stress
Research shows that the most commonly reported "trigger" for a heart
attack is an emotionally upsetting event —particularly one involving
anger. Also, some of the ways people cope with stress —such as drinking,
smoking, or overeating —aren't healthy.
Learning how to manage stress , relax, and cope with problems can
improve your emotional and physical health. Having supportive people in
your life with whom you can share your feelings or concerns can help
relieve stress.
Physical activity, medicine, and relaxation therapy also can help relieve
stress. You may want to consider taking part in a stress management
program.
Medicines
You may need medicines to treat CHD if lifestyle changes aren't enough.
Medicines ca n:
 Reduce your heart’s workload and relieve CHD symptoms
 Decrease your chance of having a heart attack or dying suddenly
 Lower your cholesterol and blood pressure
 Prevent blood clots
 Prevent or delay the need for a procedure or surgery (for
example, angioplasty corcoronary artery bypass grafting (CABG).

52
Medicines used to treat CHD include anticoagulants (AN-te-ko-AG-u-
lants), also called blood thinners; aspirin and other anticlotting medicines;
ACE inhibitors; beta blockers; calcium channel blockers; nitroglycerin;
glycoprotein IIb -IIIa; statins; and fish oil and other supplements high in
omega -3 fatty ac ids.
Procedures and Surgery
You may need a procedure or surgery to treat CHD. Both angioplasty and
CABG are used to treat blocked coronary arteries. You and your doctor
can discuss which treatment is right for you.
Percutaneous Coronary Intervention
Percutaneous coronary intervention (PCI), commonly known as
angioplasty, is a nonsurgical procedure that opens blocked or narrowed
coronary arteries.
A thin, flexible tube with a balloon or other device on the end is threaded
through a blood vessel to the narrowed or blocked coronary artery.
Once in place, the balloon is inflated to compress the plaque against the
wall of the artery. This restores blood flow through the artery.
During the procedure, the doctor may put a small mesh tube called
a stent in the artery. The stent helps prevent blockages in the artery in the
months or years after angioplasty.

53
Coronary Artery Bypass Grafting
CABG is a type of surgery. In CABG, arteries or veins from other areas
in your body are used to bypass (that is, go around) your narrowed
coronary arteries. CABG can improve blood flow to your heart, relieve
chest pain, and possibly prevent a heart attack.
Cardiac Rehabilitation
Your doctor may prescribe cardiac rehabilitation (rehab) for angina or
after CABG, angioplasty, or a heart attack. Almost everyone who has
CHD can benefit from cardiac rehab.Cardiac rehab is a medically
supervised program that may help improve the health and well being of
people who have heart problems.The cardiac rehab team may include
doctors, nurses, exercise specialists, physical and occupational therapists,
dietitians or nutritionists, and psychologists or other mental health
specialists.
Rehab ilation has two parts:
 Exercise training. This part helps you learn how to exercise safely,
strengthen your muscles, and improve your stamina. Your exercise plan
will be based on your personal abilities, needs, and interests.
 Education, counseling, and training. This part of rehab helps you
understand your heart condition and find ways to reduce your risk for
future heart problems. The rehab team will help you learn how to cope
with the stress of adjusting to a new lifestyle and deal w ith your fears
about the future (13) .

54
 Conclusion
1. Epidem iologic studies worldwide show that cigarette smoke
exposure is an important cause of cardiova scular morbidity and
mortality either active or passive exposure promotes all the smoking
complications mentioned in the thesis .
2. Coronary artery disease more likely to develop in people smoke
more often male (60%) compared t o those at female smokers
(40%) . Patients from urban areas (60% ) frequently develop
coronary heart disease more than those in rural areas (40%).
3. Smokers have a much higher risk of developing acute coro nary
syndromes because Tobacco use contribute to other complications
as: hypertension (100%), type II diabetes (60%), dyslipidemia
(60%), obesity (40 %).
4. International reviews consistently demonstrate that the most
effective approaches to tobacco control are multifaceted and
include a range of measures that complement and reinforce each other
includi ng education about the effects of smoking on health.

55
References
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6. http://www.ehnheart.org/cvd -statistics.html .
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