i

Prevalence and determinants of

hypercholesterolemia with hypertension
among known cases, Allied Hospital
Faisalabad, Pakistan
 ii

TABLE OF CONTENTS

SR. # CONTENTS PAGE #

1. Title Page i

2. Supervisor Certificate ii

3. Dedication iii

4. Acknowledgements iv

5. Table of Contents v

6. List of Tables vi

7. List of Graphs viii

8. List of Abbreviations x

9 Abstract 1

10. Introduction 3

11. Literature Review 8

12. Objectives 14

13. Methodology 15

14. Operational Definitions 18

15. Results 19

16. Tabular and Graphical Representation of Results 21

17. Discussion 67
 iii

18. Conclusion 71

19. Recommendations 72

20. Questionnaire 74

21. References 78

LIST OF TABLES

SR. # TABLE NAME PAGE #

1. Gender 21

2. Age 21

3. Monthly income 22

4. Educational Status 22

5. Childhood Vaccination Status 23

6. Cholesterol 23

7. Occupation 24

8. Triglycerides 25

9. HDL Cholesterol 26

10. LDL Cholesterol 27

11. Patients suffering from hypertension 27

12. Years suffering from hypertension 28

13. Patients suffering from obesity 28

14. Years suffering from obesity 29

 iv

15. Relationship between hypertension and obesity 29

16. Patients consuming fatty food 30

17. Patients consuming alcohol 30

18. Patients who smoke 30

19. Physical Exercise 30

20. Patients suffering from diabetes 31

21. Patients suffering from stress 31

22. Consumption of fish or fish related products 31

23. Consumption of fast food 32

24. Effect of blood pressure on daily activities 32

25. Patients who keep a regular check on their cholesterol 32

26. Patients aware of the hazards of high cholesterol level 33

27. Family history of high cholesterol level 33

28. Reasons for high cholesterol level 34

29. Patients who experienced heart attack 34

30. Was heart attack linked to high blood pressure 34

31. Lifestyle adjustment after hypercholesterolemia 35

 v

LIST OF FIGURES

SR. # TABLE NAME PAGE #

1. Gender 36

2. Age 37

3. Monthly income 38

4. Educational Status 39

5. Childhood Vaccination Status 40

6. Cholesterol 41

7. Occupation 42

8. Triglycerides 43

9. HDL Cholesterol 44

10. LDL Cholesterol 45

11. Patients suffering from hypertension 46

12. Years suffering from hypertension 47

13. Patients suffering from obesity 48

14. Years suffering from obesity 49

15. Relationship between hypertension and obesity 50

16. Patients consuming fatty food 51

17. Patients consuming alcohol 52

18. Patients who smoke 53

 vi

19. Physical Exercise 54

20. Patients suffering from diabetes 55

21. Patients suffering from stress 56

22. Consumption of fish or fish related products 57

23. Consumption of fast food 58

24. Effect of blood pressure on daily activities 59

25. Patients who keep a regular check on their cholesterol 60

26. Patients aware of the hazards of high cholesterol level 61

27. Family history of high cholesterol level 62

28. Reasons for high cholesterol level 63

29. Patients who experienced heart attack 64

30. Was heart attack linked to high cholesterol level 65

31. Lifestyle adjustment after hypercholesterolemia 66

 vii

LIST OF ABBREVIATIONS

HDL : High Density Lipoprotein

LDL : Low Density Lipoprotein

CHD : Coronary Heart Disease

HT : Hypertension

HC : Hypercholesterolemia
 1

ABSTRACT

BACKGROUND: The link between high blood pressure and high cholesterol
goes in both directions. When the body can’t clear cholesterol from the
bloodstream, that excess cholesterol can deposit along artery walls. When
arteries become stiff and narrow from deposits, the heart has to work overtime
to pump blood through them. This causes blood pressure to go up and up. Over
time, high blood pressure can damage arteries in its own way. It makes tears
in artery walls where excess cholesterol can collect.

OBJECTIVES: The aim of this research is to assess the association of

hypercholesterolemia with hypertension in patients of Medical Units of Allied
Hospital Faisalabad, Punjab, Pakistan.

METHODS: A cross sectional study will be conducted to assess the

association of hypercholesterolemia with hypertension from 15 March 2022
to 15 October 2022 in medical wards of Allied Hospital, Faisalabad, which
is a tertiary care teaching hospital, consisting of 1500 beds with two
Emergencies and 3 Medical Units affiliated with Faisalabad Medical
University, FMU and situated at Sargodha Road, Faisalabad, Punjab,
Pakistan. Allied Hospital Faisalabad also stands on top of the shortlisted
hospitals in respect of conducting various kinds of major and minor surgeries.
The study will be conducted on 60 patients admitted in Medical Wards, Allied
hospital Faisalabad. Convenient non-probability and sampling will be used.
Data will be collected through questionnaires. This study excludes those
patients who did not give consent and those patients who were in severe
condition. Data was collected, discussed and analyzed by using SPSS version
25.

RESULTS: It was seen that in almost all the patients with hypertension
hyperlipidemia was also seen. Moreover, there were many other contributing
factors such as obesity which was seen in 73.3% of the patients, having a
 2

sedentary life style which was seen in over half of the patients, stress which
was seen in 40 out of the 60 patients as well as lack of modification of lifestyle
which was seen in 25 out of the 60 patients all contributed to the prevalence
of hypertension and hyperlipidemia in these patients. This along with the lack
of consumption of fish related products as well as consumption of fatty food
as seen in 51 out of the 60 patients can be seen as on of the causative factors
for both hyperlipidemia and hypertension.

CONCLUSIONS AND RECOMMENDATIONS: There is an alarming

number of patients who have both hypertension as well as hyperlipidemia
present. This coupled with the lack of physical activity, consumption of fatty
food, obesity, lack of consumption of fish related products along side stress
are all contributing to make matters worse. Most people are not aware of the
hazards of hypertension and hyperlipidemia and are also not adjusting their
lifestyle in order to evade these harmful effects. There is a need to not only
provide health education regarding the ways to control hypertension and
hyperlipidemia as well as a need to make people aware of the harmfuleffects
of both these diseases so that people can live a healthy life and can spare
themselves from the most serious effects such as heart attack and stroke.

KEY WORDS: Hypertension, hyperlipidemia

 3

Chapter 1

INTRODUCTION
The aim of this review article is to summarize the current knowledge about
mechanisms that connect blood pressure regulation and hypercholesterolemia,
the mutual interaction between hypertension and hypercholesterolemia, and
their influence on atherosclerosis development. Most of the researches shows
that at least one-third of the population of Western Europe has hypertension
and hypercholesterolemia.1 Several bio humoral mechanisms could explain
the relationship between hypertension and hypercholesterolemia and the
association between these risk factors and accelerated atherosclerosis.

The most investigated mechanisms are the renin-

angiotensin- aldosterone system, oxidative stress, endothelial dysfunction,
and increased production of endothelin-1. Arterial hypertension is frequently
observed in combination with hypercholesterolemia, and this is related to
accelerated atherosclerosis.2 Understanding the mechanisms behind this
relationship could help explain the benefits of therapy that simultaneously
reduce blood pressure and cholesterol levels. At present many programs aim
to detect the presence of cardiovascular risk factors via population screening.
However, how often is detection followed by the start of active treatment with
adequate follow up of the subject at risk? Little attention is paid to the way
the participant and his/her general practitioner should be motivated to start
adequate risk factor treatment.3 Various intervention strategies are being
applied to influence prescription behaviour with the goal to obtain a higher
proportion of patients receiving treatment. These interventions are targeted to
either the patients, the general practitioners/health provider, or both .4 The
letter also can be used as intervention to improving drug use. Anintervention
 4

letter is relatively inexpensive, acceptable and successful at delivering the

message.5 In terms of global burden of disease, the World Health
Organization, WHO has identified obesity, hypertension,
hypercholesterolemia, and smoking among the top 10 risk factors for
premature death and disability.6 Over the last century, in most populations,
there has been a dramatic shift in the causes of death and disability with a
decrease in deaths from nutritional deficiencies and infectious diseases, and
an increase in deaths from noncommunicable diseases such as CVD.7 This
‘epidemiologic transition’ initially began in high-income countries, but has
now extended to many middle and low- income countries including those in
the Middle East region.8

These transitions are in part driven by decrease in childhood mortality from

malnutrition and infectious diseases, increase in tobacco consumption, and
urbanization leading to decrease in physical activity, and changes in diet
leading to obesity and increase in other risk factors.9

HT showed a higher content of organized collagen fibers and increased

intima-media thickness. Vasa vasorum density was increased in HC but not
in HT. Both HT and HC showed a pro angiogenetic biochemical milieu,
higher vascular endothelium growth factor, matrix metalloproteinases, and
lower endostatin, but this was more pronounced in HC.10 Both hypertension
and hypercholesterolemia induce endothelial dysfunction in the carotid artery.
However, hypertension is also associated with greater fibrosis and vascular
wall thickening, which might impair endothelium- independent
vasorelaxation and vasa vasorum growth. Hypercholesterolemia is, in turn,
associated with vasa vasorum neovascularization. These data suggest that
carotid atherosclerosis can evolve through different mechanisms in relation to
 5

different risk factors.11 Hypertension and hypercholesterolemia are well

known to induce functional and structural alteration in the vessel wall,
predisposing to atherosclerosis. Both risk factors are associated with increased
systemic and vascular oxidative stress, leading to a reduced NO
bioavailability and endothelial dysfunction.

The presence of similarly reduced vasorelaxation to acetylcholine in HC and

HT, associated with increased superoxide production in the endothelial layer
and increased systemic oxidative stress.12 On the contrary, the response to
calcium-ionophore was found impaired in HT, and was normal in HC,
consistent with previous results in hypercholesterolemic animals and
humans.13 Moreover, diversely from previous data in the pig coronary
circulation in HT a significant decreased response to sodium nitroprusside
was also detected, and this is consistent with that observed in the carotid
district of rodent models of hypertension.14 Although we cannot rule out the
possibility of a reduced responsiveness of HT smooth muscle cells to the
relaxant, the presence of structural modifications within the carotid arterial
wall of HT seems to be the most probable mechanism, by restraining smooth
muscle cells relaxation, because the vasorelaxation to sodium nitroprusside is
reversed by antifibrotic treatment. Conceivably, the observed increased
intima-media thickness and the adventitial fibrosis contribute to the arterial
stiffening and to the consequent impaired vasorelaxation. In particular, in the
Sirius red staining, HT showed an increased signal in the spectrum of the
orange-red wavelength, indicating accumulation of thick and more organized
collagen fibers.15

Hypertension causes many of the abnormalities observed in response to

 6

hypercholesterolemia, including changes in endothelial structure and

function, increased arterial permeability, stimulation of proliferation of
endothelial cells and smooth muscle cells, accumulation of macrophages and
smooth muscle cells in the intima, increased expression of a variety of growth
factors, connective tissue accumulation, and reduction in endothelium-
derived vasodilation.16

However, experimental studies on the effects of correction of hypertension

on atherosclerosis are complicated by the fact that hypertension by itself does
not promote experimental atherosclerosis unless plasma cholesterol levels are
raised.17 In rats, prolonged control of hypertension was shown to cause
reversal of some induced cellular abnormalities, although extracellular
changes including collagen deposition, were only minimally affected.18 In
prior studies performed in small groups of monkeys with combined
hypertension and hypercholesterolemia, lowering of blood pressure
appeared to have very little effect on coronary
atherosclerosis.19 Cholesterol is a risk factor that can be changed from
hypertension, so the higher the total cholesterol level, the higher the likelihood
of hypertension.20 The constriction and the rigidity of the blood vessel walls
resulting from the buildup of cholesterol in the blood vessels that can cause
increased blood pressure will have an impact on the increased risk of CHD.
High cholesterol levels in the blood cause cholesterol deposits on blood vessel
walls or the so called plaque cholesterol.21 The precipitation of calcium ions
in plaque cholesterol causes the soft plaque to become hard and rigid.

This causes the blood vessel wall to become stiff and not elastic. In addition,
in the presence of a hardened plaque cholesterol, this causes the inner walls
of blood vessels to become narrow and not slippery, so that blood supply to
 7

the organ becomes reduced.22 If hardening occurs in the arteries that supply
blood to the heart, coronary artery, then it causes CHD.23 Atherogenic
dyslipidemias could lead to hypertension by several mechanisms. First,
atherosclerosis can result in structural changes in large conduit arteries,
leading to reduced elasticity. Second, endothelial dysfunction due to lipid
abnormalities, resulting in reduced nitric oxide production, release, and
activity and abnormal vasomotor activity, could manifest as hypertension.24
Endothelium-dependent vasodilation is impaired by elevated total cholesterol,
TC levels. Third, lipid-mediated damage to the renal microvasculature could
manifest as hypertension, illustrated by an association between lipid
abnormalities and early renal dysfunction. Finally, dyslipidemia and
hypertension represent 2 of several components of the metabolic syndrome
that may share common mechanistic pathways.25

So finally, A close relationship between abnormalities of the lipid

metabolism and arterial hypertension has been observed in several
epidemiological studies.26 The aim of the present study was to investigate
whether serum cholesterol might affect blood pressure levels at rest, during
ambulatory monitoring or during sympathetic stimulation—independently of
other variables such as body weight or serum insulin—thus influencing the
outcome of hypertensive complications.27
 8

LITERATURE REVIEW

Analysis of the prevalence of CHD risk factors shows that there is a high
prevalence of smoking and hypertension in this population. Although the
prevalence of smoking is similar to previously reported studies, hypertension
is more prevalent. When WHO criteria are used for hypertension, the
prevalence of 7% in the present study is more than in previous studies.28 The
mean serum lipoprotein lipid levels are lower than those reported from the
Western countries, but are higher than a previously reported study from North
India.29 This may reflect a rising trend in lipid levels in the Indian population.
The prevalence of hypercholesterolemia in our subjects is not comparable to
any other Indian study because of the newer criteria used for classification.
However, while the prevalence of hypercholesterolemia is less than in USA,
as well as in several European countries, it is similar to the prevalence in
China. A low prevalence of diabetes could represent an artifact due to reliance
on self-reported diagnosis in our study.30
A study from USA has suggested that self-reported diagnosis of diabetes
accurately reflects the true prevalence. We used stricter criteria for grading
physical activity as compared with previous Indian studies. Low-grade
physical activity is universal in a rural agrarian population, and moderate or
high-grade physical activity is related to agricultural cycles.31 We used the
Paffenberger criteria for physical activity assessment, validated in studies
from USA and other developed countries. These criteria may not accurately
reflect physical activity in a semiliterate population. Univariate analyses
confirm the importance of classical coronary risk factors, age and smoking.
These factors are also independently associated with CHD prevalence in men
as confirmed by multivariate analysis. Systolic blood pressure positively
correlated with CHD in females.32 The significance of truncal obesity and
 9

hyper insulin states has recently been highlighted as an important coronary

risk factor among South Asians living in Britain. A precise relationship
between CHD with serum cholesterol, other lipoprotein lipids, obesity, and
truncal obesity has not been demonstrated in our study as the proportions
where such measurements were made was small. Sedentary lifestyle has not
emerged as an important risk factor.33 The absence of any significant
association may reflect the protective influence of intermittent physical
activity.
CHD prevalence was significantly greater among uneducated versus educated
persons. This observation is consistent with international data, which show
that CHD and coronary risk factors-smoking and hypertension are more
frequent among the uneducated. Men who engaged in regular prayer had a
significantly lower prevalence of CHD. Mental stress is important in the
genesis as well as the perpetuation of coronary atherosclerosis therefore
mentally relaxing activities may be relevant in CHD.34
The prevalence of isolated Systolic HTN in this study was 16.3%. This fact
also has to be taken seriously as previous studies have shown that increase in
Systolic hypertension alone itself interacts with other major risk factors such
as high cholesterol and diabetes, which also increase with age, to amplify the
age-related risk of cardiovascular events.35
Gender:
The prevalence among boys (31.75% n=211) was found to be much higher
than among girls (10.05%,n=189). The difference was highly significant (p
=0.000) and goes along with the study done in Allied Hospital Faisalabad. But
some other previous studies revealed the gender variation to be much
different. While the Mysore study found no gender predilection at all, few
other studies showed the prevalence high among girls.
Anyhow, the finding of the current study has to be taken as significant because
the prevalence among boys is strikingly high.
 10

Standard of study:
The prevalence of hypertension was increasing with the class of study, it was
the lowest among students of VIII standard and highest among X, XIand XII
students. It was also statistically very significant. Though there was no
previous data available in this regard, this higher prevalence may be attributed
to the high stress level among the students of X, XI and XII due to huge
academic burden and responsibilities.
Type of curriculum
No significant relationship between the type of curriculum followed by the
students and the prevalence of hypertension (p=0.340) could be found. It may
be taken as that irrespective of the difference in their curriculum, it seems all
the students face the same level of stress.
Academic performance and hypertension
There was no significant relationship between hypertension and academic
performance noticed. This maybe because hypertension in its earlier stage is
a silent condition without any symptoms and does not affect the studies and
day to day activities of the person.
Physical activity:
Current study could not find the any significant association between physical
activity and hypertension. Spending more time in physical activities plays an
important role in preventing and delaying the onset of hypertension. The
association between physical activity and Hypertension is an established fact.
A study done by Gang Hu on the relationship of physical activity and BMI to
the risk of hypertension proved the protective effect of physical activity was
observed in both sexes regardless of the level of obesity. Anyhow the It may
be perhaps due to the fact that only qualitative assessment was done. In depth
analysis of the level of physical activity of the students could have revealed
the association in a better way.
 11

Parents education, employment and income:

Details of parents’ education, employment status and income were asked, to
assess the socioeconomic status of the family. There is no influence of SES
with hypertension in this study. This is a contradiction to the result of an
analysis done by Tanya M.Spruill, which says prevalence of hypertension was
high among people belonging to low socio-economic status due to poor living
conditions and high stress.
Food habits:
The strong relationship between hypertension and diet habits has been well
proved through various studies. Still the current study does not show a
statistically significant relationship between food habits and HT. This may be
because only qualitative assessment of food consumption was done. Anyhow
nonsignificant relationship between diet and hypertension has also been
arrived in another study conducted by
M.R.Savitha.
Relationship between BMI and HTN:
There is an overwhelming evidence in this study that the prevalence of HT is
high among obese individuals, which is highly significant. This also confirms
results of done by Jonathan et al indicated obesity and overweight has major
risk factors in hypertension. John F Hall study also showed similar finding
that chronic obesity also causes marked structural changes in the kidneys that
eventually leads to a loss of nephron function, further increasing the arterial
pressure. This study results also coincides with an Indian study done by
Ruchika et al in Delhi among school children, published in 2010.
Hypertension causes many of the abnormalities observed in response
to hypercholesterolemia, including changes in endothelial structure and
function, increased arterial permeability, stimulation of proliferation of
 12

endothelial cells and smooth muscle cells, accumulation of macrophages and

smooth muscle cells in the intima, increased expression of a variety of growth
factors, connective tissue accumulation, and reduction in endothelium-
derived vasodilation. However, experimental studies on the effects of
correction of hypertension on atherosclerosis are complicated by the fact that
hypertension by itself does not promote experimental atherosclerosis unless
plasma cholesterol levels are raised. In rats, prolonged control of hypertension
was shown to cause reversal of some induced cellular abnormalities, although
extracellular changes, including collagen deposition, were only minimally
affected. In prior studies performed in small groups of monkeys with
combined hypertension and hypercholesterolemia, lowering of blood pressure
appeared to have very little effect on coronary atherosclerosis. Cholesterol is
a risk factor that can be changed from hypertension, so the higher the total
cholesterol level, the higher the likelihood of hypertension. The constriction
and the rigidity of the blood vessel walls resulting from the buildup of
cholesterol in the blood vessels that can cause increased blood pressure will
have an impact on the increased risk of CHD. High cholesterol levels in the
blood cause cholesterol deposits on blood vessel walls or the so called plaque
cholesterol. The precipitation of calcium ions in plaque cholesterol causes the
soft plaque to become hard and rigid.36
This causes the blood vessel wall to become stiff and not elastic. In
addition, in the presence of a hardened plaque cholesterol, this causes the
inner walls of blood vessels to become narrow and not slippery, so that blood
supply to the organ becomes reduced. If hardening occurs in the arteries that
supply blood to the heart (coronary artery), then it causes CHD. Atherogenic
dyslipidemias could lead to hypertension by several mechanisms. First,
atherosclerosis can result in structural changes in large conduit arteries,
 13

leading to reduced elasticity. Second, endothelial dysfunction due to lipid

abnormalities, resulting in reduced nitric oxide production, release, and
activity and abnormal vasomotor activity, could manifest as hypertension.
Endothelium-dependent vasodilation is impaired by elevated total cholesterol
(TC) levels. Third, lipid-mediated damage to the renal microvasculature could
manifest as hypertension, illustrated by an association between lipid
abnormalities and early renal dysfunction. Finally, dyslipidemia and
hypertension represent 2 of several components of the metabolic syndrome
that may share common mechanistic pathways.37
 14

OBJECTIVES
The aim of this research is to assess the association of hypercholesterolemia
with hypertension in patients of Medical Units of Allied Hospital
Faisalabad, Punjab, Pakistan.
 15

Chapter 2

METHODOLOGY

Study Design
A cross-sectional study was conducted for assessing the prevalence and
determinants of hypercholesterolemia with hypertension among known
patients.

Study Setting

Study will be conducted in medical wards of Allied Hospital, Faisalabad,

which is a tertiary care(teaching) hospital, consisting of 1500 beds with two
Emergencies and 3 Medical Units affiliated with Faisalabad Medical
University (FMU) and situated at Sargodha Road, Faisalabad, Punjab,
Pakistan. Allied Hospital Faisalabad also stands on top of the shortlisted
hospitals in respect of conducting various kinds of major and minor surgeries.

Study Population

The cross-sectional study will be conducted on patients of Medical Units in

Allied Hospital Faisalabad.

Data Collection Procedure

A detailed questionnaire was used for data collection. Written informed
consent will be obtained from all the respondents and face-to-face interviews
was conducted and close-ended questions will be asked. The questionnaire
was translated into the local language. The questionnaire was presented in
different settings. All the data was collected by the interviewer
himself/herself. The accuracy of the questionnaire was checked daily by the
researcher.
 16

Inclusion Criteria

All patients in medical wards who are suffering from hypertension and are
willing to take part in this study

Exclusion Criteria
• Patients who are not willing.

• Patients who are not suffering from hypertension

Ethical Consideration
The institutional ethics review board allowed the conduction of this study.
Respondents were fully explained about the study, along with care about
anonymization. Participation was voluntary and no modes of coercion were
used. Therefore, it was presumed that respondents gave informed consent. All
responses were kept anonymous and were treated confidentially.

Development of Survey Instrument

A questionnaire (supplement) was constructed with 2 parts. The three parts
were labeled as proforma A,and B. Performa A was made to gather
sociodemographic details. Proforma B was objectively developed to assess
the prevalence and determinants of hypertension with hypercholesterolemia.
The questionnaire was reviewed by faculty members for content. We invited
medical students (n=10) from the institution to fill the questionnaire as part of
pre-testing and asked them to rate it for general readability and
comprehension. The developed proforma was then finalized after addressing
the experiences of the pre-testing.
 17

Description of Survey Instrument

Demographic details collected include gender, age, residence (urban/rural),
occupation, salary, education level, vaccination status and mobile number.
Proforma B was structured to assess the various risk factors for relapse. 24
individual questions were listed and responses were obtained according to
dichotomous scale(yes/no).Participants filled the questionnaire and their data
was kept confidential.

Data Analysis
All statistical analysis for this study was done using SPSS version 26.

Descriptive Analysis
Frequency, percentage and mean of each question/variable were calculated.
The frequencies of those variable affecting relapse were compared .Different
plots were made to show influence of various risk factors on relapse in
psychiatric patients,

Inferential Analysis
We compared the differences of answers between different demographic
groups (male vs. female and urban vs. rural). The resultant mean of 'classes'
of different demographic groups was compared using the independent-
samples t-test. The significance level was set as 0.05 and any result having
p<0.05 was considered statistically significant. The calculated frequencies of
those having factors affecting relapse were similarly compared for different
demographic variables. The frequencies of predicted factors were compared
across demographic variables.
 18

OPERATIONAL DEFINITIONS

Hypertension is another name for high blood pressure. It can lead to severe
health complications and increase the risk of heart disease, stroke, and
sometimes death.
Types of Hypertensions:
1. Primary, or essential: high blood pressure is the most common type
of high blood pressure. For most people who get this kind of blood pressure,
it develops over time as you get older.
2. Secondary: high blood pressure is caused by another medical
condition or use of certain medicines. It usually gets better after you treat that
condition or stop taking the medicines that are causing it.
Blood pressure is the force that a person's blood exerts against the walls of
their blood vessels.
Hypercholesterolemia can be defined as the presence of high plasma
cholesterol levels, with normal plasma triglycerides, as a consequence of the
rise of cholesterol and apolipoprotein B (apoB)-rich lipoproteins, called low-
density lipoprotein (LDL).
Healthy Levels of Cholesterol as proposed by WHO fall in the range of 125
to 200 mg/dl.
Atherosclerosis is the thickening or hardening of the arteries. It is caused by
a buildup of plaque in the inner lining of an artery. Plaque is made up of
deposits of fatty substances, cholesterol, cellular waste products, calcium, and
fibrin. As it builds up in the arteries, the artery walls become thickened and
stiff.
 19

Chapter 3

Results
We researched the determinants of hypercholesterolemia in hypertensive
patients admitted to Medical Wards of Allied hospital Faisalabad. In this
study, we collected data from 60 patients. Among 60 patients, there were 29
Males(48.3%) and 31 Females(51.7%). Among these 60 patients, there were
20(33.3%) uneducated persons. Most of the patients were between 40 to 60
years of age. Among 60, 25 patients(41.66%) belong to low socio-economical
status. Concerning educational status, 20 patients were having no education
at all, and 40 were literate people. Among all the patients the average blood
cholesterol level falls to 250mg/dl. Average Triglyceride levels among these
patients are 170 mg/dl. If we see at HDL levels, the average value for HDL is
36 mg/dl. Average LDL levels fall at 141 mg/dl. Among all the 60 patients,
59 were suffering from hypertension on average for 10 years. According to
our research, 44(73.3%) patients were suffering from obesity which is the
major risk factor for hypertension and hypercholesterolemia. According to the
data we collected, most of the patients were suffering from hypertension after
they get obese. 51 of these patients were having fatty meals indicating it is a
major risk factor for obesity and hypercholesterolemia. We also analyze
alcohol consumption among these patients and most of them were
nonalcoholic indicating alcohol is a less risk factor for obesity among patients
in Pakistan. 23(38.33%) patients were smokers also indicates less effect of
smoking on our desired variables in this region. Most patients(33 out of 60)
were having a sedentary lifestyle which also contribute to obesity and
hypercholesterolemia in hypertensive patients.
40 patients were suffering from stress which indicates it is a contributing
factor to obesity. According to these patients, hypertension is affecting their
daily life activities. Most of the patients were not aware of the hazards of
cholesterol nor they were keeping a regular check on their cholesterol. Many
 20

patients indicated that they had a previous history of MI which they refer was
due to high cholesterol levels according to their doctor. Even then, only 25
out of 60 patients adjusted their lifestyle to prevent high cholesterol levels.
 21

TABULAR REPRESENTATION
OF RESULTS

TABLE NO. 1
GENDER
Response Frequency Percentage Cumulative
Percent
Male 29 48.3 48.3

Female 31 51.7 100.0

Total 60 100.0

TABLE NO. 2
AGE
Statistic Value
Mean 51.5167

Std. Error of Mean 1.59297

Median 51.0000
Mode 50.00
Std. Deviation 12.33912
Variance 152.254
Range 60.00
Minimum 15.00
Maximum 75.00
Sum 3091.00
25 45.0000
Percentiles 50 51.0000
75 60.0000
 22

TABLE NO. 3
MONTHLY INCOME
Statistic Value
Mean 56466.6667

Std. Error of Mean 4289.55285

Median 50000.0000
Mode 50000.00
Std. Deviation 33226.73350
1104015819.20
Variance
9
Range 170000.00
Minimum 5000.00
Maximum 175000.00
Sum 3388000.00
25 35000.0000
Percentiles 50 50000.0000
75 70000.0000

TABLE NO. 4
EDUCATIONAL STATUS
Response Frequency Percentage Cumulative
Percent
No 20 33.3 33.3
Formal 6 10.0 43.3
Primary 10 16.7 60.0

Secondary 11 18.3 78.3

Tertiary 13 21.7 100.0

Total 60 100.0
 23

TABLE NO. 5
CHILDHOOD VACCINATION STATUS
Response Frequency Percentage Cumulative
Percent
Yes 56 93.3 93.3
No 4 6.7 100.0
Total 60 100.0

TABLE NO. 6
CHOLESTEROL
Statistic Value

Mean 249.7167

Std. Error of Mean 7.25360

Median 255.0000
Mode 270.00

Std. Deviation 56.18616

Variance 3156.884
Range 282.00
Minimum 113.00
Maximum 395.00
Sum 14983.00

25 211.5000

Percentiles 50 255.0000

75 277.5000
 24

TABLE NO. 7
OCCUPATION
Response Frequency Percentage Cumulative
Percent
Agricultural
1 1.7 1.7
Officer
Army 2 3.4 5.0
Banker 1 1.7 6.7
Businessman 3 5 11.7
Clerk 2 3.4 15.0
Farmer 6 10.0 25.0
Freelancer 1 1.7 26.7
Head Clerk 1 1.7 28.3
Health worker 1 1.7 30.0
House wife 27 45.0 75.0
IT Department 1 1.7 76.7
Labourer 2 3.3 80.0
None 1 1.7 81.7
Police Man 1 1.7 83.3
Professor 1 1.7 85.0
School Teacher 1 1.7 86.7
Student 3 5.0 91.7
Tailor 1 1.7 93.3
College Teacher 4 6.7 100.0

Total 60 100.0
 25

TABLE NO. 8
TRIGLYCERIDES
Statistic Value
Mean 186.9167

Std. Error of Mean 5.86550

Median 183.5000
Mode 200.00
Std. Deviation 45.43399

Variance 2064.247
Range 220.00
Minimum 80.00
Maximum 300.00
Sum 11215.00

25 160.0000

Percentiles 50 183.5000

75 210.0000
 26

TABLE NO. 9
HDL CHOLESTEROL
Statistic Value
Mean 36.1333
Std. Error of Mean 1.48066
Median 35.0000
Mode 30.00a
Std. Deviation 11.46914
Variance 131.541
Range 60.00
Minimum 10.00
Maximum 70.00
Sum 2168.00
25 30.0000
Percentiles 50 35.0000
75 40.0000
 27

TABLE NO. 10
LDL CHOLESTEROL
Statistic Value

Mean 141.1833

Std. Error of Mean 5.92450

Median 147.5000
Mode 170.00
Std. Deviation 45.89099

Variance 2105.983
Range 188.00
Minimum 60.00
Maximum 248.00
Sum 8471.00
25 110.5000

Percentiles 50 147.5000

75 173.0000

TABLE NO. 11
ARE YOU SUFFERING FROM HYPERTENSION?
Response Frequency Percentage Cumulative
Percent
Yes 59 98.3 98.3
No 1 1.7 100.0
Total 60 100.0
 28

TABLE NO. 12
IF YES, THEN HOW MANY YEARS YOU
HAVE BEEN SUFFERING FROM HYPERTENSION?
Statistic Value

Mean 11.1500

Std. Error of Mean 1.11407

Median 9.0000
Mode 3.00
Std. Deviation 8.62952
Variance 74.469
Range 32.00
Minimum 1.00
Maximum 33.00
Sum 669.00
25 4.2500
50 9.0000
Percentiles
75 16.5000

TABLE NO. 13
ARE YOU SUFFERING FROM OBESITY?
Response Frequency Percentage Cumulative
Percent

Yes 44 73.3 73.3

No 16 26.7 100.0
Total 60 100.0
 29

TABLE NO. 14
IF YES, THEN HOW MANY YEARS
YOU HAVE BEEN SUFFERING FROM OBESITY?
Statistic Value
Mean 16.4444
Std. Error of Mean 1.99154
Median 10.0000
Mode 5.00
Std. Deviation 13.35963
Variance 178.480
Range 40.00
Minimum .00
Maximum 40.00
Sum 740.00
25 5.0000
Percentiles 50 10.0000
75 30.0000

TABLE NO. 15
WERE YOU SUFFERING FROM HYPERTENSION
BEFORE OR AFTER OBESITY?
Response Frequency Percentage Cumulative
Percent
Not suffering from obesity 16 26.7 26.7
Before 11 18.3 45.0
After 33 55.0 100.0
Total 60 100.0
 30

TABLE NO. 16
DO YOU EAT FATTY FOODS?
Response Frequency Percentage Cumulative
Percent
Yes 51 85.0 85.0
No 9 15.0 100.0
Total 60 100.0

TABLE NO. 17
DO YOU DRINK ALCOHOL?
Response Frequency Percentage Cumulative
Percent
Yes 1 1.7 1.7
No 59 98.3 100.0
Total 60 100.0

TABLE NO. 18
DO YOU SMOKE?
Response Frequency Percentage Cumulative
Percent
Yes 23 38.3 38.3
No 37 61.7 100.0
Total 60 100.0

TABLE NO. 19
DO YOU DO ANY PHYSICAL EXERCISE?
Response Frequency Percentage Cumulative
Percent
Yes 27 45.0 45.0
No 33 55.0 100.0
Total 60 100.0
 31

TABLE NO. 20
ARE YOU SUFFERING FROM DIABETES?
Response Frequency Percentage Cumulative
Percent
Yes 33 55.0 55.0
No 27 45.0 100.0
Total 60 100.0

TABLE NO. 21
ARE YOU SUFFERING FROM ANY KIND OF STRESS?
Response Frequency Percentage Cumulative
Percent

Yes 40 66.7 66.7

No 20 33.3 100.0
Total 60 100.0

TABLE NO. 22
HOW OFTEN DO YOU CONSUME FISH
OR FISH RELATED PRODUCTS?
Response Frequency Percentage Cumulative
Percent

Never 25 41.7 41.7

Rarely 28 46.7 88.3

Often 7 11.7 100.0

Total 60 100.0
 32

TABLE NO. 23
HOW OFTEN DO YOU CONSUME FAST FOOD?
Response Frequency Percentage Cumulative
Percent

Never 20 33.3 33.3

Rarely 18 30.0 63.3

Often 22 36.7 100.0

Total 60 100.0

TABLE NO. 24
DOES HIGH BLOOD PRESSURE AFFECT YOUR
DAILY ACTIVITIES
Response Frequency Percentage Cumulative
Percent

Yes 42 70.0 70.0

No 18 30.0 100.0

Total 60 100.0

TABLE NO. 25
DO YOU KEEP A REGULAR CHECK
ON YOUR CHOLESTEROL LEVEL?
Response Frequency Percentage Cumulative
Percent
Yes 12 20.0 20.0
No 48 80.0 100.0
Total 60 100.0
 33

TABLE NO. 26
ARE YOU AWARE OF THE HAZARDS
OF HIGH CHOLESTEROL LEVEL?
Response Frequency Percentage Cumulative
Percent

Yes 21 35.0 35.0

No 39 65.0 100.0
Total 60 100.0

TABLE NO. 27
DO YOU HAVE A FAMILY HISTORY
OF HIGH CHOLESTEROL LEVEL?
Response Frequency Percentage Cumulative
Percent

Yes 34 56.7 56.7

No 26 43.3 100.0
Total 60 100.0
 34

TABLE NO. 28
IF NO THEN WHAT DO YOU THINK
IS THE REASON FOR YOUR
HIGH CHOLESTEROL LEVEL?
Response Frequency Percentage Cumulative
Percent
Diet 27 45.0 45.0
Disease 3 5.0 50.0
Don't know 14 23.3 73.3
Family History 6 10.0 83.3
Lack of exercise 3 5.0 88.3
Work 1 1.7 90.0
Stress 2 3.3 93.3
Genetics 4 6.7 100.0
Total 60 100.0
TABLE NO. 29
HAVE YOU EVER EXPERIENCED AN
EPISODE OF HEART ATTACK BEFORE?
Response Frequency Percentage Cumulative
Percent
Yes 35 58.3 58.3
No 25 41.7 100.0
Total 60 100.0
TABLE NO. 30
IF YES DO YOU THINK IT WAS
LINKED TO YOUR HIGH CHOLESTEROL LEVEL?
Response Frequency Percentage Cumulative
Percent
Yes 25 41.7 41.7
No 35 58.3 100.0
Total 60 100.0
 35

TABLE NO. 31
DID YOU ADJUST YOUR LIFESTYLE
AFTER BEING DIAGNOSED WITH
HIGH CHOLESTEROL LEVEL?
Response Frequency Percentage Cumulative
Percent

Yes 25 41.7 41.7

No 35 58.3 100.0
Total 60 100.0
 36

GRAPHICAL REPRESENTATION
OF RESULTS

FIGURE NO. 1
GENDER
 37

FIGURE NO. 2
AGE
 38

FIGURE NO. 3
MONTHLY INCOME
 39

FIGURE NO. 4
EDUCATIONAL STATUS
 40

FIGURE NO. 5
CHILDHOOD VACCINATION STATUS
 41

FIGURE NO. 6
CHOLESTEROL LEVEL
 42

FIGURE NO. 7
OCCUPATION
 43

FIGURE NO. 8
TRIGLYCERIDE LEVEL
 44

FIGURE NO. 9
HDL CHOLESTEROL LEVEL
 45

FIGURE NO. 10
LDL CHOLESTEROL LEVEL
 46

FIGURE NO. 11
ARE YOU SUFFERING FROM HYPERTENSION?
 47

FIGURE NO. 12
IF YES HOW MANY YEARS HAVE YOU BEEN
SUFFERING FROM HYPERTENSION?
 48

FIGURE NO. 13
ARE YOU SUFFERING FROM OBESITY?
 49

FIGURE NO. 14
IF YES HOW MANY YEARS HAVE YOU BEEN
SUFFERING FROM OBESITY?
 50

FIGURE NO. 15
WERE YOU SUFFERING FROM HYPERTENSION
BEFORE OR AFTER OBESITY?
 51

FIGURE NO. 16
DO YOU EAT FATTY FOODS?
 52

FIGURE NO. 17
DO YOU DRINK ALCOHOL?
 53

FIGURE NO. 18
DO YOU SMOKE?
 54

FIGURE NO. 19
DO YOU DO ANY PHYSICAL EXERCISE?
 55

FIGURE NO. 20
ARE YOU SUFFERING FROM DIABETES?
 56

FIGURE NO. 21
ARE YOU SUFFERING FROM ANY KIND OF STRESS?
 57

FIGURE NO. 22
HOW OFTEN DO YOU CONSUME FISH OR FISH
RELATED PRODUCTS?
 58

FIGURE NO. 23
HOW OFTEN DO YOU CONSUME FAST FOOD?
 59

FIGURE NO. 24
DOES HIGH BLOOD PRESSURE AFFECT YOUR DAILY
ACTIVITIES?
 60

FIGURE NO. 25
DO YOU KEEP A REGULAR CHECK ON YOUR
CHOLESTEROL LEVEL?
 61

FIGURE NO. 26
ARE YOU AWARE OF THE HAZARDS OF HIGH
CHOLESTEROL LEVEL?
 62

FIGURE NO. 27
DO YOU HAVE A FAMILY HISTORY OF HIGH
CHOLESTEROL LEVEL?
 63

FIGURE NO. 28
IF NO THEN WHAT DO YOU THINK IS THE REASON
FOR YOUR HIGH CHOLESTEROL LEVEL?
 64

FIGURE NO. 29
HAVE YOU EVER EXPERIENCED AN EPISODE OF
HEART ATTACK BEFORE?
 65

FIGURE NO. 30
IF YES THEN DO YOU THINK IT WAS ALSO LINKED
TO YOUR HIGH CHOLESTEROL LEVEL?
 66

FIGURE NO. 31
DID YOU ADJUST YOUR LIFESTYLE AFTER BEING
DIAGNOSED WITH HIGH CHOLESTEROL LEVEL?
 67

DISCUSSION
According to WHO, A high intake of protein and pork, alcohol drinking and
overweight/obesity were positively associated with hypercholesterolemia.
Neither education nor fruit and vegetable intake were associated with
hypercholesterolemia.

Several epidemiological studies have already shown that hypertensive

subjects are very often characterized by elevated levels of serum cholesterol,
which increase the risk of cardiovascular diseases. It has been suggested that
only the contemporary treatment of both cardiovascular risk factors is able to
improve the individual cardiovascular risk profile even if, up to date, we still
have limited results from large clinical trials regarding the impact of multiple
therapeutic intervention in the prevention of cardiovascular diseases. More
scientific evidences came from the results of several clinical studies that have
investigate the preventive and therapeutic role of hypolipidemic drugs,
especially statins, in subjects with hypercholesterolemia and high blood
pressure, particularly when those diseases are associated with diabetes.
Indeed, this class of hypolipidemic agent has already shown to improve the
individual lipid profile and contemporary to reduce the blood pressure values
in the hypertensive hypercholesterolemic subjects acting synergistically with
some class of anti-hypertensive drugs.

Any alteration in the balance between serum lipids, platelets, hemodynamic

factors, and the blood vessel wall may lead to the development of
atherosclerosis. Hypertension and hypercholesterolemia are two major risk
factors that accelerate the development of coronary heart disease. The
mechanisms of the interactions of these two risk factors are examined in this
paper. First, hypertension may be associated with focal or generalized
endothelial injury or dysfunction. The altered endothelial functional integrity
 68

may predispose to platelet aggregation and altered vessel wall interaction,

which may stimulate proliferation and growth of vascular cells. Second,
elevated serum cholesterol levels may accelerate lipid deposition and
formation of atherosclerotic plaques. In hypertension the rate of clearance of
lipoprotein from the vessel wall may be reduced. Third, the sympathetic
nervous system may be involved in both the development of hypertension and
the alterations of lipid metabolism. Adrenergic activation, which increases
blood pressure may also adversely affect lipid metabolism. This is in part α1-
adrenoceptor mediated. Selective α1-inhibitors have been found to prevent or
reduce atherosclerosis in experimental animals. Selective α1-inhibitors may
act at a number of sites on lipoprotein metabolic pathways to favorably
influence serum lipids. Taken together, the relationship between hypertension
and atherosclerosis involves complex mechanisms. A complete understanding
of the mechanisms is of obvious importance.

There is good epidemiologic evidence that hypertension is associated with a

high risk of cardiovascular disease. However, primary intervention trials have
failed to demonstrate that a reduction in blood pressure in hypertensive
patients reduces morbidity and mortality from cardiac events. Since various
antihypertensive drugs adversely affect lipoprotein metabolism, these drugs
may increase associated coronary risk and offset the beneficial effects of
lowering blood pressure. This article reviews the effects of various
antihypertensive drugs on plasma lipids, lipoproteins, and apolipoproteins.
They can be summarized as follows: thiazide-type diuretics cause a marked
elevation of plasma triglycerides and very low-density lipoprotein (VLDL)
and minor increases in total cholesterol and low-density lipoprotein (LDL),
but have little effects on high-density lipoprotein (HDL). The nonselectiveβ-
blockers do not significantly affect total cholesterol and LDL, but increase
 69

total triglycerides and VLDL and decrease HDL. The changes in plasma lipids
and lipoproteins caused by cardioselective β-blockers and β-blockers with
intrinsic sympathomimetic activity are qualitatively similar but less
pronounced. Calcium antagonists and angiotensin-converting enzyme
inhibitors appear to have no significant effects on plasma lipids. α1-inhibitors
reduce total triglycerides, total cholesterol, VLDL, and LDL and increase
HDL. The possible mechanisms by which antihypertensive drugs affect
cellular lipid metabolism (e.g., LDL receptor, lipid synthesis, lipoprotein
lipase, lecithin cholesteryl acyltransferase, acylcholesteryl acyltransferase,
and cholesteryl ester hydrolase) are described. The clinical significance of
changes in blood lipids and cellular lipid metabolism caused by
antihypertensive drugs is not yet totally clear. Nevertheless, before
antihypertensive drug treatment is initiated, blood lipid levels should be
measured to identify preexisting hyperlipidemia. Blood lipoprotein levels
should be monitored during long-term antihypertensive therapy to reconsider
the therapeutic regimen if adverse lipid changes are observed.

We conducted research on patients of medical units in Allied hospital fsd

which is a tertiary care hospital located in Punjab Pakistan. The aim of this
research article is to summarize the data about mechanisms that connect the
mutual interaction between hypertension and hypercholesterolemia, and its
determinants. Our research shows that at least one-third of our sample
population has hypertension and hypercholesterolemia. Several biohumoral
mechanisms could explain the relationship between hypertension and
hypercholesterolemia. Arterial hypertension is frequently observed in
combination with hypercholesterolemia. Understanding the mechanisms
behind this relationship could help explain the benefits of therapy that
simultaneously reduce blood pressure and cholesterol levels.
 70

After data collection and analysis we compared the results with already done
and currently going on researches on the same topic. The Limitation of our
study is that our sample size is limited. Data collected from only onehospital
is another limitation including limited resources. Sample size was not large
enough to permit reliable comparison with WHO data.
 71

CONCLUSION

According to the data we collected, most of the patients were suffering from
hypercholesterolemia after they get obese. 51 of these patients were having
fatty meals indicating it is a major risk factor for obesity and
hypercholesterolemia. We also analyze alcohol consumption among these
patients and most of them were nonalcoholic indicating alcohol is a less risk
factor for obesity among patients in Pakistan. 23(38.33%) patients were
smokers also indicate less effect of smoking on our desired variables in this
region. Most patients (33 out of 60) were having a sedentary lifestyle which
also contributes to obesity and hypercholesterolemia in hypertensive patients.
 72

RECOMMENDATIONS

• There should be an effort made to inform the patients of the hazards of

high cholesterol level
• Patients at risk should undergo screening test along with regular checks
on lipid profile to prevent the potential hazards of hypertension and
hypercholesterolemia
• Saturated fat should be reduced in patient’s diet which can be done by
both providing awareness as well as government policies to ensure that
products are labelled with which contain saturated fat as well as reduce
the availability of such products in the market
• Trans fat should be eliminated from patient’s diet which can not only be
done by providing awareness as well government policies that ban the
selling of products with trans fat
• Awareness should be provided to improve life style including regular
exercise along with regular check on blood pressure and lipid profile to
prevent the harmful effects
• Patients who smoke should be encouraged to quit smoking by providing
counselling and therapy wherever necessary
• Patients who are obese should be encouraged to lose their weight
• Medicines to reduce cholesterol level and hypertension should be made
cheap and easily accessible to the public
 73

GANTT CHART

June July Aug Sep Oct Nov

Task We Wee Wee Wee Wee Week Week Week We Week Week
ek k3, k5,6 k7, k9, 11,12 13,14 15,16 ek 19,20 21,22
s 1, 4 8 10 17,
2 18
Synops
is
prepar
ation
Appro
val
proces
s
Revie
w&
feedba
ck
Prepar
ation
of
tools
Pretest
ing
tools
Finaliz
ation
of
tools
Data
collecti
on
Data
entry
&
cleanin
g
Report
writin
g
Report
review
 74

Chapter 4

ANNEXURE

Questionnaire
This questionnaire is about Prevalence and determinants of
hypercholesterolemia with HTN among patients of Medical Units of Allied
Hospital Faisalabad, Punjab, Pakistan.

A. Socio-Demographic Profile:

Name:

Father/Husband’s Name:

Gender: Male☐ Female ☐

Age:

Residence:

Monthly Income:

Educational status: No ☐ Formal ☐ Primary level ☐ Secondary level ☐

Tertiary level

Childhood Vaccination Status (EPI/Other):

Occupation:

Mobile Number:

Today’s Date:
 75

B. Information Regarding Study

1. Kindly fill the table given below according to your respective test results.
2. Are you suffering from hypertension?

Yes ☐ No ☐
3. If yes, then how many years have you been suffering from hypertension?

4. Are you suffering from obesity?

Yes ☐ No ☐
5. If yes, then how many years have you been suffering from obesity?

6. Were you suffering from hypertension before or after obesity?

Before ☐ After ☐
7. Do you eat fatty foods?

Yes ☐ No ☐
8. Do you think that fatty foods are the reason for your obesity?

Yes ☐ No ☐
9. Do you consume alcohol?

Yes ☐ No ☐
10. Do you smoke?

Yes ☐ No ☐
 76

11. Do you do any physical exercise?

Yes ☐ No ☐

12. Are you suffering from diabetes?

Yes ☐ No ☐
13. Are you suffering from any kind of stress?

Yes ☐ No ☐
14. How often do you consume fish or fish related products?

15. How often do you consume fast food?

16. Does high blood pressure affect your daily activities?

Yes ☐ No ☐
17. Do you keep a regular check on your cholesterol level?

Yes ☐ No ☐
18. Are you aware of the hazards of high cholesterol level?

Yes ☐ No ☐
19. Do you have a family history of high cholesterol level?

Yes ☐ No ☐
20. If no, then what do you think is the cause of your high cholesterol level?
 77

21. Have you ever experienced an episode of heart attack before?

Yes ☐ No ☐
22. If yes, then do you think it was linked to your high blood pressure?

Yes ☐ No ☐
23. If yes, then do you think it was also linked to high cholesterol level?

Yes ☐ No ☐
24. Did you adjust your lifestyle after being diagnosed with high cholesterol
level?

Yes ☐ No ☐
 78

REFERENCES
1. Sarrafzadegan N , Boshtam M , Mostafavi S , Rafiei M Prevalence of
hypertension and associated risk factors, East Mediterr Health J 1999; 5:992–
1001.
2. Stamler J, Liu K, Ruth KJ, Pryer J, Greenland P. Eight-year blood pressure
change in middle- aged men: relationship to multiple nutrients. Hypertension.
3. Azizi F , Rahmani M , Ghanbarian A , Emami H , Salehi P , Mirmiran P ,
Sarbazi N Serum lipid levels in an Iranian adults population: Tehran Lipid and
Glucose Study. Eur J Epidemiol 2003; 18:311–319.
4. Ibrahim MM , Rizk H , Appel LJ , Rizk HH , Helmy S , Mosley J et al. .
Hypertension prevalence, awareness, treatment, and control in Egypt. Results
from the Egyptian National Hypertension Project (NHP). NHP Investigative
Team. Hypertension 1995; 26:886–890
5. Sadeghi M , Roohafza HR , Kelishadi R Blood pressure and associated
cardiovascular risk factors in Iran: Isfahan Healthy Heart Programme. Med J
Malaysia 2004; 59:460–467.
6. Stamler J, Caggiula A, Grandits GA, Kjelsberg M, Cutler JA, MRFIT
Research Group Relationship to blood pressure of combinations of dietary
macronutrients: findings of the Multiple Risk Factor Intervention Trial
(MRFIT) Circulation.
7. Clarke R, Frost C, Collins R, Appleby P, Peto R. Dietary lipids and blood
cholesterol: quantitative meta-analysis of metabolic ward studies.
8. Stamler J. Established major coronary risk factors: historical overview. In:
Marmot M, Elliott P, editors. Coronary Heart Disease Epidemiology.
9. Jaddou HY , Batiehah AM , Ajlouni KM Prevalence and associated factors
of hypertension: results from a three community-based survey, Jordan. J Hum
Hypertens 1996; 10:815–821.
 79

10. Dennis B, Stamler J, Buzzard M, Conway R, Elliott P, Moag-Stahlberg

A, et al. INTERMAP: The dietary data -- Process and quality control. J Hum
Hypertens.
11. Schakel SF, Dennis BH, Wold AC, Conway R, Zhao L, Okuda N, et al.
Enhancing data on nutrient composition of foods eaten by participants in the
INTERMAP Study in China, Japan, the United Kingdom and the United
States.
12. Tobin MD, Sheehan NA, Scurrah KJ, Burton PR. Adjusting for treatment
effects in studies of quantitative traits: antihypertensive therapy and systolic
blood pressure.
13. Rouse IL, Beilin LJ, Armstrong BK, Vandongen R. Blood-pressure-
lowering effect of a vegetarian diet: controlled trial in normotensivesubjects.
14. Bener A , Al-Suwaidi J , Al-Jaber K , Al-Marri S , Dagash MH , Elbagi
IE The prevalence of hypertension and its associated risk factors in a newly
developed country. Saudi Med J 2004; 25:918–922.
15. Jenkins DJ, Kendall CW, Vuksan V, Vidgen E, Parker T, Faulkner D, et
al. Soluble fiber intake at a dose approved by the US Food and Drug
Administration for a claim of health benefits: serum lipid risk factors for
cardiovascular disease assessed in a randomized controlled crossover trial.
16. Appel LJ, Moore TJ, Obarzanek E, Vollmer WM, Svetkey LP, Sacks FM,
et al. A clinical trial of the effects of dietary patterns on blood pressure.
17. Sacks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray GA, Harsha D, et
al. Effects on blood pressure of reduced sodium and the Dietary Approaches
to Stop Hypertension (DASH) diet.
18. Chowienczyk PJ, Watts GF, Cockcroft JR, Ritter JM. Impaired
endothelium-dependent vasodilation of forearm resistance vessels in
hypercholesterolaemia.
 80

19. Wilkinson IB, Cockcroft JR. Cholesterol, endothelial function and

cardiovascular disease.
20. Wilkinson IB, Prasad K, Hall IR, Thomas A, MacCallum H, Webb DJ, et
al. Increased central pulse pressure and augmentation index in subjects with
hypercholesterolemia.
21. Ohara Y, Peterson TE, Harrison DG. Hypercholesterolemia increases
endothelial superoxide anion production. J Clin Invest.
22. Al-Shammari SA , Ali M , Al-Shammari A , Al-Maatouq MA , Tennier A
, Armstrong K Blood lipid concentrations and other cardiovascular risk factors
among Saudis. Fam Pract 1994; 11:153–158.
23. Warsy AS , el-Hazmi MA Diabetes mellitus, hypertension and obesity –
common multifactorial disorders in Saudis. East Mediterr Health J 1999;
5:1236–1242.
24. Wahid Saeed AA , al Shammary FJ , Khoja TA , Hashim TJ , Anokute
CC , Khan SB Prevalence of hypertension and sociodemographic
characteristics of adult hypertensives in Riyadh City, Saudi Arabia. J Hum
Hypertens 1996; 10:583–587.
25. Soyannwo MA , Gadallah M , Hams J , Kurashi NY , El-Essawi Khan
NA, Singh RG et al. Contrasting influence of the living environment and
gender on systemic hypertension in Saudi population of Gassim, Saudi
Arabia. Afr J Med Med Sci 1997; 26:145–152.
26. Stamler J, Rose G, Stamler R, Elliott P, Dyer A, Marmot M. INTERSALT
study findings: Public health and medical care implications. Hypertension.
27. Onat A , Surdum-Avci G , Senocak M , Ornek E , Gozukara Y Plasma
lipids and their interrelationship in Turkish adults. J Epidemiol Community
Health 1992; 46:470–476.
28. Kannel W.B. Fifty years of Framingham study contributions to
understanding hypertension. J Hum Hypertens. 2000; 14: 83-90
 81

29. Neaton J.D. Wentworth D. Multiple Risk Factor Intervention Trial

Research Group Serum cholesterol, blood pressure, cigarette smoking, and
death from coronary heart disease. Arch Intern Med. 1992; 152: 56-64
30. Eaton C.B. Feldman H.A. Assaf A.R. McPhillips J.B. Hume A.L. Lasater
T.M. Levinson P. Carleton P.A. Prevalence of hypertension, dyslipidemia,
and dyslipidemic hypertension. J Fam Pract. 1994; 38: 17-23
31. Johnson M.L. Pietz K. Battleman D.S. Beyth R.J. Prevalence of comorbid
hypertension and dyslipidemia and associated cardiovascular disease. Am J
Manag Care. 2004; 10: 926-932
32. NHANES 1999–2000 Laboratory/Medical Technologists Procedures
Manual. Rockville, MD: NCHS.
33. Hajjar I. Kotchen T.A. Trends in prevalence, awareness, treatment, and
control of hypertension in the United States, 1988–2000. JAMA. 2003; 290:
199-206
34. Ford E.S. Mokdad A.H. Giles W.H. Mensah G.A. Serum total cholesterol
concentrations and awareness, treatment, and control of hypercholesterolemia
among US adults. Circulation. 2003; 107: 2185-2189
35. John, Stefan; Schmieder, Roland E. Impaired endothelial function in
arterial hypertension and hypercholesterolemia: potential mechanisms and
differences. Journal of Hypertension. 18(4):363-374, April 2000.
36. Morrish N.J. Stevens L.K. Head J. et al. A prospective study of mortality
among middle-aged diabetic patients (the London cohort of the WHO
Multinational Study of Vascular Disease in Diabetics). II: Diabetologia. 1990;
33: 542-548
37. Andersson D.K.G. Svardsudd K. Long-term glycemic control relates to
mortality in type II diabetes. Diabetes Care. 1995; 18: 1534-1543