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Pulmonary hypertension in Young

Smokers by Doppler Echo Study

A Thesis Submitted to the Scientific Council of Medicine in Partial
Fulfillment of the Requirement for the Degree of Fellowship of the arab
Council for Medical Specialization in Medicine
Ali Asaad Mohammed Ali

Supervised by
Assistant professor
Dr. Hussain .A. Naser
M.B.Ch.B, D.M, C.A.B.M.(Med.)
Al-Kufa training centre
April 2016


‫بسم هللا الرحمن الرحيم‬
‫ان أَنَّا َخلَ ْقنَاهُ ِم ْن قَ ْب ُل َولَ ْم يَ ُ‬
‫اْل ْن َس ُ‬
‫ك َش ْيئًا‬
‫أَ َو ََل يَ ْذ ُك ُر ْ ِ‬
‫صدق هللا العلي العظيم‬
‫سورة مريم‬


A thesis submitted to The Scientific Council of internal Medicine in
partial fulfillment for the requirement for the fellowship of the Arabic
Council for Medical Specialization in Medicine.

Aliasaad Mohammed Ali


I certify that this thesis (pulmonary hypertension in young smokers
by doppler echo study) was prepared by Ali Asaad Mohammed Ali under
our supervision at The Scientific Council of Medicine in partial fulfillment
for the requirement for the fellowship of the Arab Council for Medical
Specialization in Medicine.

Assistant Professor
Dr. Hussain.Aziz.Naser
M.B.Ch.B, D.M, C.A.B.M.(Med.)
Al-Kufa training centre


We, the examining committee, after reading this thesis (pulmonary
hypertension in young smokers by Doppler echo study ) and examining
the candidate, Ali Asaad Mohammed Ali, in it is content, found that it
meets the standards and requirement as a thesis in partial fulfillment for the
requirement for the fellowship of the Iraqi Council for Medical
Specialization in Medicine

Dr.Sameer Abdul-Majeed Alkhawaja
M.B.Ch.B, D.M, C.A.B.M
Consultant of Diabetes and Endocrinology

Assistant Professor

Dr. Falah.A.dali
M.B.Ch.B, F.I.C.M.S




I, the chairman of the scientific council of Internal Medicine, certify
that this thesis (pulmonary hypertension in young smokers by Doppler
echo study) was prepared by the candidate, Ali Asaad Mohammed Ali and
submitted to our council.


Dr. Faleh Al Biaty
Chairman of the scientific council of Internal Medicine



To my family ….


I would like to thank my almighty Allah for helping me to complete
this study.I would like to express my deepest thanks to my supervisor, Dr.
Hussain .A.Naser for his valuable support and guidance at all stages of this
study. I would like to express my thanks to the doctors and paramedical
staff in the Al-Sadr hospital in Najaf.


List of abbreviations :

AMI …………….. Acute myocardial infarction .
BMI ……………. Body mass index
PAH …………… pulmonary arterial hypertension
CPEF……….. combined pulmonary emphysema AND fibrosis
COPD …………….. chronic obstructive pulmonary disease
ECG …………… Electrocardiography
CTEPH……… chronic thromboembolism pulmonary

PVR ……………. Pulmonary vascular resistant
VIP ………......... vasoactive intestinal polypeptide

BNp ……………..brain natriuretic peptide


Subject :
Introduction ………………………………………… 2
Material and methods ………………………….


Results …………………………………………


Discussion ……………………………………..16
Conclusion add recommendations ……………. 21
References ……………………………………




Background :
Smoking is risk factor for developing chronic obstructive air way disease
and lung emphysematous changes it can affect pulmonary vasculature in
current study interest to evaluate the effect of smoking habits in pulmonary
artery pressure in young adults population and before development of
sever pathological and clinical lung disease. .
Method : pulmonary artery pressure compared between 93 young smokers
without any medical disease with 93 nonsmokers by Doppler echo study
between in ALSADER .teaching . hospital between January 2015 and
December 2015
Results : The mean age of smokers was 25.2 ± 4.1for non-smokers the
mean age was 24.9 ± 3.1 , no statistically significant differences between
both groups had been found neither in age (P=0.60), nor in BMI (P=0.51)
it had been significantly found that all clinical parameters including
maximum tricuspid valve velocity, mean pressure gradient, JVP and
pulmonary artery pressure were significantly higher in smokers group than
non-smokers, in all comparison P. value was highly significant (<0.001).
pulmonary hypertension was not reported among the participants. a direct
(positive) significant correlation of the pulmonary artery pressure had
been found with amount of smoking (r = 0.27, P = 0.002) duration of
smoking index (r = 0.42, P = 0.001

Conclusion :
There is strong relation between smoking and pulmonary
hypertension before emphysematous changes .


Pulmonary hypertension (PAH) refers to elevated pulmonary arterial
pressure. PAH can be due to a primary elevation of pressure in the
pulmonary arterial system alone (pulmonary arterial hypertension), or
secondary to elevations of pressure in the pulmonary venous and
pulmonary capillary systems (pulmonary venous hypertension). PH can be
a progressive, fatal disease if untreated, although the rate of progression is
highly variable. Most patients with PH should be evaluated in a center with
expertise in the diagnosis and management of this population(1)
Pulmonary arterial hypertension (PAH) is either

idiopathic or

associated with different conditions, such as a genetic background,
collagen vascular diseases surgically corrected congenital heart diseases,
andothers.(2) PAH is characterized by histomorphologicchanges in small
and middle-sized pulmonary arteries with onionskin-like thickened vessel
walls and pathognomonic plexiform lesions. 3Normal pulmonary arterial
systolic pressure ranges from 15 to 30 mmHg, diastolic pressure from 4 to
12 mmHg and normal PAP is ≤20 mmHg. Many clinicians consider PAP
of 21 to 24 mmHg as borderline elevated and of uncertain clinical
significance (2)


World Health Organization (WHO) has re-classified PAH based
upon etiology and mechanism into the five groups listed below [4,5].
Pulmonary arterial hypertension (PAH) refers to group (1) PAH.
Pulmonary hypertension (PH) refers to any of group 2 through group 5 PH,
and is also used when referring to all five groups collectively.
● Group 1 – PAH
● Group 2 – PH due to left heart disease
● Group 3 – PH due to chronic lung disease and/or hypoxemia
● Group 4 – Chronic thromboembolic pulmonary hypertension (CTEPH)
●Group 5 – PH due to unclear multifactorial mechanisms
Hereditary IPAH may be underdiagnosed. In one study, among five
apparently unrelated families, 18 (out of 400) individuals had hereditary
BMPR2 mutations, 12 of whom were initially classified as sporadic IPAH

In contrast to group 1 PH, where the pulmonary vascular resistance
(PVR) is by definition greater than 3.0 Wood units, group 2 PH is
associated with a near normal PVR and a normal trans pulmonary gradient
(less than 12 mmHg.(22)


Smoking is one of risk factors of pulmonary hypertension .
Smoking cessation is critical to attenuating the ongoing endothelial







remodeling and PH development from tobacco exposure. Recent studies
show that cigarette smoke can induce PH though iNOS activation, even
before the parenchymal changes of emphysema develop

[14 ].


smoking cessation also prevents further parenchymal damage as a
contributor to PH development
Nitric oxide (NO) is a vasodilator that inhibits platelet activation and
vascular smooth muscle cell proliferation. Synthesis of NO is by
nitricoxide synthase (NOS) and there is evidence that enzymatic activity of
NOS is reduced in PAH The vasodilatory effects of NO are mediated
through the secondary messenger cyclic guanosine monophosphate, which
is rapidly metabolized by phosphodiesterase (PDE), with PDE-5 being the
predominant pulmonary isoform. PDE-5 activity has been shown to be
upregulated in PAH

Prevalence of smoking in Iraq as
Male 26 %
Female 2.9%


Prognostic factors — Data from prospective trials suggest that the
following factors may portend a poor prognosis in patients with pulmonary
arterial hypertension (PAH)
● Age >45 years
● Male gender
● World Health Organization (WHO) functional class III or IV
●Failure to improve to a lower WHO functional class during treatment
● Echocardiographic findings of a pericardial effusion, large right atrial
size, elevated right atrial pressure, or septal shift during diastole
● Decreased pulmonary arterial capacitance (ie, the stroke volume divided
by the pulmonary arterial pulse pressure)
● Poor right ventricular contractile reserve determined by an increase in
pulmonary artery systolic of <30 mmHg with exercise (stress
● Low right ventricular ejection fraction (<25 percent) as determined by
planar radionuclide angiography
● Increased N-terminal pro-brain natriuretic peptide level (NT-pro-BNP)
● Prolonged QRS duration
● Hypocapnia
● Comorbid conditions (eg, COPD, diabetes)
● Selective serotonin reuptake inhibitor

Material and method :
Design of study :
One hundred and eighty six young people selected 93 smokers and
93 nonsmokers with age group between 18 and 35 years old with smoking
history between 2years and 10 years and measure pulmonary artery
pressure by Doppler echo in relation to duration and amount of smoking.
One hundred and eighty six young age group enrolled in current
study after take permission of them and agreement and explanation the
aim of study to them and benefit in future
Inclusion criteria:
Young age group
BMI <30
Normal spirometery
Negative past medical history
Smoking history between 2-10 years
Exclusion criteria:
Old age group
Benzene workers
Tricuspid valve regurgitation which
Mitral valve regurgitation
Left aterial enlargement
Thyroid dysfunction

Pulmonary artery pressure estimation:
One hundred and eighty six young persons with age 18 to 35years
were enrolled in this study At at Al-Sadr Medical City in Najaf from
January 2015 to September 2015 93 of them were smoking more than 2
years duration. Current study used pulsed Doppler echocardiography to
measure the flow velocity in the right ventricular outflow tract or
pulmonary artery and have found that Doppler measurements of right
ventricular systolic time intervals and flow velocity pattern correlate well
with pulmonary artery pressures by Doppler mode Each patient was
asked to rest in a left lateral decubitus position and to breath in a relaxed
way during Doppler examination The Doppler estimate of diastolic
pressure gradient between the pulmonary artery and right ventricle during
diastole was calculated by applying the
transthoracic echo

use Doppler wave

Bernoulli equation

by 2D

parasternal long and shor axis

,apical four chambers .
By examination normal JVP, NORMAL 2nd heart sound no (p2) no right
parasternal heave , no arrhythmia and no splenectomy .
By Doppler echo and measurement of pulmonary artery pressure across
tricuspid valve by using BERNOLI EQUATION


In current study spirometery done and exclude obstructive and restrictive
pattern , measure weight and height and exclude high BMI >30 ECG was
done to exclude any abnormality , also examination was done and exclude
JVP distension ,prominent right ventricle impulse ,third heart sound
,hepatomegaly and peripheral edema .basilar crackle excluded from study
Right ventricle thickness is about 2 – 2.5 mm with in normal range to


exclude right ventricle thickness which is the cause of pulmonary
hypertension. By using general health care VIVID S5
Study design
Data of the 186 participants were transformed into computerized
data form and analyzed using the statistical package for social sciences
(SPSS) version 22, IBM, Chicago, US, 2013. Descriptive statistics were
expressed as mean, standard deviation, frequencies (No.) and proportions
Student’s t test (independent) was used to compare two means of
continuous variables, such as age, BMI, Maximum tricuspid valve
velocity, Mean pressure gradient, JVP and Pulmonary artery pressure,
between smokers vs. non-smokers. Chi square test was used to compare
BMI categories between the studied groups.
Pearson’s correlation and Regression curve estimation tests was
used to assess the correlation between pulmonary artery pressure and other
variables; Amount and Duration of smoking among smokers. Correlation
coefficient ( r ) was calculated, value of (r ) , statistically, ranged between
(0) indicated complete no correlation and (1) for perfect correlation,
however, values < 0.4 indicated weak correlation, (0.4 – 0.7) moderate
and > (0.7) for strong correlation.

Level of significance, of ≤ 0.05,

considered as significant difference or association. Finally, results
presented in tables and figures with an explanatory paragraph for each.



There were 186 participants enrolled in this cross sectonal study, 93
participants were smokers (study group) and 93 participants were nonsmoker as control group.
The mean age of smokers was 25.2 ± 4.1 (range: 18 – 35) years and
for non-smokers the mean age was 24.9 ± 3.1 (range: 19 – 32) years. The
mean body mass index (BMI) in smokers group was 23.7 ± 1.8 (range:
20.1 – 29.2) kg/m2 and it was 23.6 ± 1.2 (range: 20.9 – 26.3) kg/m2 in nonsmokers, furthermore, most of participants in both groups had normal
range of BMI, and only 20.4% and 15.1% were overweight in smokers and
non-smokers group, respectively. Additionally, no statistically significant
differences between both groups had been found neither in age (P=0.60),
nor in BMI (P=0.51), (Table 3.1).
Table 1. Age and BMI distribution of the studied groups


Non-smoker P

(n = 93) (n = 93)
Mean ± SD*

25.2 ± 4.1 24.9 ± 3.1


Normal n (%) 74 (79.6) 79 (84.9)

BMI (kg/m )

Overweight n
719 (20.4) 14 (15.1)


Mean ± SD


23.7 ± 1.8 23.6 ± 1.2


As it shown in table 3.2, it had been found that all clinical
parameters including maximum tricuspid valve velocity, mean pressure
gradient, JVP and pulmonary artery pressure were significantly higher in
smokers group than non-smokers, in all comparison P. value was highly
significant (<0.001). From other point of view, pulmonary hypertension
was not reported among the participants where none of the participants had
the value of pulmonary artery pressure corresponding to pulmonary
hypertension leading to an incidence of (0%).

Table 3.2. Comparison of clinical parameters of the studied groups.

t test


df = 184

(n = 93)
Maximum tricuspid
valve velocity

Mean ± SD* 0.9 ± 0.1

(n = 93)
0.60 ± 0.20


0.6 – 1.5

0.3 – 1.0

Mean ± SD

3.4 ± 1.0

1.5 ± 0.8


1.7 – 8.0

0.4 – 3.6

Mean ± SD

8.90 ± 1.1

7.15 ± 0.82


5.0 – 10.0

5.0 – 9.0

Mean ± SD

12.3 ± 1.35

8.53 ± 0.48


8.31 – 15.5

8 – 10.4


< 0.001


< 0.001


< 0.001


< 0.001

Mean pressure gradient


Pulmonary artery


Table 3.3 demonstrates the relationship between the pulmonary
artery pressure with the duration and amount of smoking, as it shown in
this table a direct (positive) significant correlation of the pulmonary artery
pressure had been found with amount of smoking (r = 0.27, P = 0.002)
when the amount measured in cigarettes/ day and (r = 0.35, P=0.003) when
measured in pack-year. Similarly, a direct (positive) significant correlation
was also found with the duration of smoking (r = 0.42, P = 0.001). It is
worth mentioning that these significant correlations were obtained after
adjustment for age and BMI to exclude any confounding effect of these
two variables on the results. Further demonstration for these direct
correlations are shown in figures (3.1 and 3.2)
Table 3.3. Relationship of pulmonary artery pressure with the duration and
amount of smoking after adjustment for the age and BMI
Amount of smoking

Correlation coefficient (r)


(cigarette /day)



Amount of smoking

Correlation coefficient (r)





Duration of smoking

Correlation coefficient (r)





Figure 3.1. The direct correlation between pulmonary artery pressure and
amount of smoking after adjustment for age and BMI

Figure 3.2. The direct correlation between pulmonary artery pressure and
duration of smoking after adjustment for age and BMI


Mean Maximum tricuspid valve







Figure 3.3 Comparison of mean maximum tricuspid velocity in smoker
and non-smoker.

Mean pressure gradient








Figure 3.4 . Comparison of mean pressure gradient in smoker and nonsmoker.



Mean JVP








Figure 3.5 direct relation between smoking and JVP


Mean Pulmonary artery pressure








Figure 3,6 direct relation between smoking and pulmonary artery pressure


This current study demonstrated that there is an increase in the arterial
pulmonary pressure in the young age smokers population even before
the development of the clinical COAD or the abnormal Pulmonary
Function Test . Wright J L 1991 described an increase in the pulmonary
vascular structure mainly an increase in the masculinization of the
arterioles in the guinea pig exposed to the smoke after one month and
when there was no evidence of emphysema(28). Animal model of smoke
induced emphysema and pulmonary hypertension suggested that
Pulmonary hypertension

associated COPD is due in some part to

hyperinflation and gas trapping that compress the pulmonary vessels


however Pulmonary hypertension has not shown to improve after lung
volume reduction surgery( LVRS) and this showed that Pulmonary
hypertension occurs in the smokers by added mechanisms to that caused
by COAD(29)

.Jugular venous pressure was looked after in this study as raised jugular
venous pressure is usually found in patients with pulmonary hypertension
and should be looked early for proper evaluation of the patients(31).
Again, similar regulation profiles were found in smokers without COPD.
leads to and alterations in vascular and alveolar structure and function
(26)Goss k,Lahmt found also smoking lead to development of pulmonary
hypertension without emphysema by expression of (INOS) ( 14)


Peaked Tricuspid Velocity was studied in this current study with the
Bernoulli equation to detect and to measure the pulmonary pressure and
found to have significant difference between smoker group and those
nonsmoker .To make more valuable results, the Right Ventricular
hypertrophy was studied according to the European Guideline
Echocardiography detecting of pulmonary hypertension 2015 and the
mean right ventricular wall thickness in this study was (2-5mm) which
excluded the right ventricular hypertrophy .The pulmonary pressure in
smoker group and in nonsmoker group in the current study was not
reaching the elevated level of high pulmonary pressure but the difference
between the pulmonary pressure level in the smoker group is more and
still significant when it was compared with the nonsmoker group. Reports
from Barberà and associates (2003) from Spain indicated that vascular
remodeling process is also associated with and possibly preceded by an
inflammatory process in which the vessels become infiltrated with a
population of cells similar to those found around the small airways
Normal level of the pulmonary arterial pressure which is detected by Echo
Doppler study is estimated to be 8- 20mmHg and pulmonary hypertension
is considered when the pulmonary pressure >25mmHg.The mean
pulmonary pressure in the smoker group in the current study was(12.3)
and that of non smoker was(8.5) and both in the normal range and still we
found a significant difference between both groups. The age of the
smoker group and that of the non smoker relatively the same and in both
groups(smokers25.2-4.1)and (nonsmoker24.9-3.1) . The age showed no
statistical difference. In this study we tried to avoid old population for
possible association with emphysematous lung changes. (American Lung
Association 2013 Epidemiology and Stastic). Pulmonary hypertension can

develop at any age according to underlining cause .It was found that the
mean age at diagnosis of pulmonary hypertension is 45
years in USA(.32) BMI of the smoker group and non smoker group in this
study was <25 ( normal BMI level) and the pulmonary pressure was not
showed statistically difference between two groups. Obesity was found in
several studies to be associated with hypoventilation and elevation in the
pulmonary pressure(30). In our study there was a positive correlation
between the amount and the duration of the smoking with the increase in
the pulmonary pressure .
. The least duration of the smoking in this study was 2 years with a mean
of (2pack per day ) and the mean smoking index was(24)which reflects the
exposure and the smoking severity .In experimental model of smoking in

smoking was induced pulmonary hypertension within four

weeks of exposure and remodeling was achieved within 6 months from
cessation of the smoking . Barbara et al had found that changes in the
many changes occur in the pulmonary vessels occur in the early stages
before the airway obstruction. The pathological changes include intimal
hyperplasia proliferation that resulted from proliferating mesenchymal
cells with elastic and collagen deposition as well as endothelial
The endothelial dysfunction associated with the vessel remodeling and an
increase in the inflammatory cells that invade the vascular adventitia. The
most constituting cells include activated T lymphocytes with a
predominance of CD8 T cells subset(7,8)
.P value was significant for both CD8 Lymphocytes and for the ratio of
CD4/CD8 .Salud Santos and Victor I Pained found an increase in the
expression of vascular endothelial growth factor( VEGF)

in smoker

population when was compared with non smoker without the
development of COAD with significant increase in both the intimal and the
medial vascular layers in the smokers when was compared without
smoking population and in the absence of the emphysematous lung
Goss K Lahmt found that smoking leads to the development of pulmonary
hypertension without the emphysematous changes by expression of
Nitrous Oxide Synthase( NOS) .The Nitrous Oxide helps to modulate
vascular tone ,insulin secretion ,airway tone and is involved in the
. Pulmonary function test was done in all cases in the current study so to
exclude serious pulmonary diseases .Chest CT was not done as the
European guidelines stated that Chest CT approved for patients with
COAD for age 55-80 years
Nearly all form of World Health Organization WHO demonstrated a
skewed gender ratio with more females affected with pulmonary
hypertension than males

and the last facts explained by the possible

effect of estrogen hormone .A group of researcher in Glasgow and
Novartis Institute tested the effect of estrogen on the pulmonary pressure
and they confirmed the effect of estrogen to increase the pulmonary

This revealed that apoptosis markers were consistently upregulated in the
vascular compartment by 3 months of smoke exposure.(


V.I. Peinado,

and S. Santos, found that both endothelial dysfunction and structural
derangement of pulmonary arteries were already present in patients with

mild COPD who were not hypoxaemic, and even in smokers with normal
lung function then development of vascular remodeling and increase
pulmonary arterial pressure (19) also V.I. Peinado, and S. Santos found that
The findings demonstrated smooth muscle cell proliferation, as well as
elastin and collagen deposition, in the thickened intimas of pulmonary
arteries in moderate chronic obstructive pulmonary disease patients and
smokers without COPD, suggesting that these abnormalities may originate
at an early stage in cigarette smoke-induced pulmonary hypertension also
abundant proliferation of SMC (smooth muscle action ) and intense
deposition of both elastin and collagen fibres in the intimal layer of
pulmonary muscular arteries in patients with mild COPD and in smokers
with normal lung Furthermore, the presence of desmin- and vimentinpositive muscle cells in the intima, in a ratio different from that shown in
the media, suggests an ongoing process of pulmonary vascular
remodelling. In this process, the deposition of collagen into the intima may
denote an advanced stage, leading to greater vessel narrowing that might
contribute to the development of pulmonary hypertension. References (20)

Joan Albert Barberà found that changes in pulmonary vessels are already
apparent at early disease stages, and in smokers without airflow
obstruction. Changes in pulmonary vessels include intimal hyperplasia,
resulting from proliferating mesenchymal cells, and elastic and collagen
deposition as well as endothelial dysfunction. Dysregulation of
endothelium‑derived mediators and growth factors and inflammatory
mechanisms underlie the endothelial dysfunction and vessel remodeling
increased number of inflammatory cells infiltrating the adventitia of
pulmonary muscular arteries, largely constituted by activated T
lymphocytes with a predominance of the CD8 T cell subset.[7,8]


The number of neutrophils, macrophages, and B lymphocytes are minimal
and do not differ from control nonsmokers (23)

J. L. Wright

found that

Simvastatin returned the pulmonary artery

pressure to control levels within 4 weeks of starting treatment, and
ameliorated smoke-induced small arterial remodeling as well as
emphysema measured both physiologically and morphometrically at 6
months, but did not prevent smoke induced small airway remodeling either
physiologically or morphologically. Simvastatin reversed small arterial
endothelial dysfunction and partially reversed smoke-induced loss of
vascular NO generation.(24)

There is direct relation and significant relation between smoking and
early elevation in pulmonary artery pressure

before any clinical and

histological changes I lung

1 advise to stop smoking
2serial monitoring of pulmonary pressure


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‫‪32. Adanni E.Frost,,MD,FCCP.american chest journal 2011‬‬

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‫من قبل‬
‫علي اسعد محمد علي النجار‬
‫بكالوريوس طب وجراحه عامه‬

‫بأشراف األستاذ المساعد‬

‫د‪.‬حسين عزيز ناصر‬
‫مركز الكوفه التدريبي نيسان‬


‫الخالصة ‪:‬‬
‫خلفية الدراسة ‪:‬‬
‫التدخين من العادات السيئة المنتشرة عند الشباب وعدة دراسات ناقشت العالقة بين التدخين‬
‫وارتفاع ضغط الشريان الرئوي وقد اوضحت تلك الدراسات وجود عالقة وثيقة بين التدخين‬
‫وارتفاع ضغط الشريان الرئوي ‪.‬‬
‫ألهدف من الدراسة ‪ :‬تقييم العالقة بين التدخين وضغط الشريان الرئوي قبل حدوث التغييرات‬
‫النسيجية غير قابلة للر جوع في رئة المدخن ‪.‬‬
‫ألمرضى والطرق ‪ :‬ثالثة وتسعون مدخنا شابا وثالثة وتسعون غير مدخن من نفس العمر ومعدل‬
‫تدخين عشرين سيكارة في اليوم او اكثر وبمعدل سنتين تدخين او اكثر مع وزن طبيعي وتخطيط‬
‫قلب طبيعي وفحص وظائف الرئة طبيعية مع قياس ضغط الشريان الرئوي بوساطة الدوبلر ايكو‬
‫بين شهري كانون الثاني وسبتمبر من سنة ‪2015‬‬
‫ألنتائج ‪:‬‬
‫لقد وجدت عالقة ملحوظة بين كمية التدخين وفترة التدخين مع ارتفاع في معدل ضغط الشريان‬
‫الرئوي مقارنة مع غير المدخنين من نفس الجنس والعمر ولم توجد عالقة ملحوظة بين العمر‬
‫والجنس مع ارتفاع ضغط الشريان الرئوي ‪.‬‬
‫أألستنتاج ‪:‬‬
‫ان ارتفاع ضغط الشريان الرئوي مرتبط مع التدخين قبل حدوث التغيرات النسيجية وقبل ظهور‬
‫االعراض السريرية للمدحنين ‪.‬‬