ejbps, 2015, Volume 2, Issue 3, XX-XX. Research Article SJIF Impact Factor 2.

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Rafiqa et al. European Journal

European Journal of Biomedical
of Biomedical ISSN 2349-8870
and Pharmaceutical Sciences
Volume: 2
AND Issue: 3
Pharmaceutical sciences XX-XX
http://www.ejbps.com Year: 2015

PREVALENCE OF DYSLIPIDEMIC HYPERTENSION IN A SUBSET

OF KASHMIRI (NORTH INDIA) POPULATION

Hakim Ali Qanoon1 and Rafiqa Eachkoti2*

1
Departments of Medicine Sher-i-Kashmir Institute of Medical Sciences, Srinagar, Kashmir
India.
2
Departments of Biochemistry Sher-i-Kashmir Institute of Medical Sciences, Srinagar,
Kashmir India.
Article Received on 04/05/2015 Article Revised on 26/05/2015 Article Accepted on 18/06/2015

ABSTRACT
*Correspondence for
Worldwide studies conducted on different populations have suggested
Author
Rafiqa Eachkoti a positive association between dyslipidemia and hypertension, with
Departments of significant proportion of populations suffering from both ie
Biochemistry Sher-i- dyslipidemic hypertension, most often possible mechanism being
Kashmir Institute of Medical
insulin resistance and endothelial dysfunctioning. The present study
Sciences, Srinagar, Kashmir
aimed to determine prevalence of dyslipidemic hypertension and to
India.
rafiqahaq@gmail.com establish, if any, relationship between blood pressure and serum lipid
levels across the range of blood pressure categories including
prehypertension in a subset of Kashmiri population. A total of 100 patients and 50 control
subjects from Kashmiri population were included in the present study. The level of TG and
total cholesterol, LDL, HDL and VLDL in serum samples was estimated by enzymatic
colorometric method on Hitachi 912 (Boehringer Mannhum system). Statistical analysis was
carried out by students “t” test using ANOVA software and the results were considered
statistically significance when p value ≤0.05. In our study overall 14.4% of total kashmiri
population (i.e.72% of hypertensive kashmiri population) suffer from dyslipidemic
hypertension. Significantly elevated total levels of serum TG (204.9mg/dl Vs 139.2mg/dl
(p=000), total Cholesterol (175.1mg/dl Vs 147.2 mg/dl) (p=0.002), VLDL-cholesterol
(41.0mg/dl Vs 28.9mg/dl) (p≤0.0001) LDL-cholesterol (181.3 mg/dl Vs 130.0 mg/dl)
(p≤0.0001) and decreased level of HDL-cholesterol (34.8mg/dl Vs 46.1 mg/dl) (p≤0.0001)
were found in hypertensive’s when compared with normotensive’s. Within lipid profile,

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Rafiqa et al. European Journal of Biomedical and Pharmaceutical Sciences

greater percentage of hypertensive’s compared to normotensives show elevated levels of TG

(51% Vs 18%) followed by cholesterol (49%\ Vs 21%) or LDL cholesterol(45% Vs 22%).
Low HDL was also found in 44% of hypertensives compared to only 12% in normotensive’s.
The findings of the present study show slight variations when compared with rest of the India
but is in complete agreement with certain Muslim dominant areas with which we share
common dietary habits and cultural practices. Conclusion: Our study reveals a positive
association between blood pressure and dyslipidemia in Kashmiri population.72% of the
hypertensive in our population shows dyslipidemia too. Since the treatment of dyslipidemia
and hypertension alone is different from the treatment of dyslipidemic hypertension which
may involve reversal of insulin resistance. The findings of the present study, therefore, may
provide a rationale for pharmacotherapy in a subset of hypertensive people with dyslipidemic
hypertension.

ABBREVIATION: LDL=low density lipoproteins; HDL=high density lipoprotein;

VLDL=very low density lipoprotein TG=Triglycerides.

INTRODUCTION
Hypertension is a common, asymptomatic, readily detectable usually easily treatable disease
that leads to lethal complications if left untreated.[1] A recent estimate suggests that world
over approximately 1 billion adults have hypertension (333 million in economically
developed and 639 million in economically developing countries).[2] Hypertension is
probably the most important public health problem in developed countries with over 50
million adults (29%) having hypertension (defined BP=140/90) in United States alone[1,2] The
prevalence of hypertension in India ranges from 20-40% in urban adults and 12-17% among
rural adults.[3] Hypertension can be classified as essential (primary) (unknown medical cause)
or secondary (such as Renal Artery Stenosis or tumors pheochromocytoma, paraganglioma).

Hypertension is a multifactorial trait that results from the net effect of environmental and
genetic factors.[2] Factors that may contribute to hypertension include excess dietary salt or
alcohol intake, stress, aging, genetic susceptibility, physical inactivity, diet rich in saturated
fats and family history. Dyslipidemia or disordered lipid profile characterized by elevated
total cholesterol >200mg/dl, LDL Cholesterol >130mg/dl, TG >200mg/dl, Total
cholesterol/HDL =4.5 and low HDL =<40mg/dl) has been associated with hypertension.[4]
The interrelationship of elevated circulating triglycerides, low HDL cholesterol, central body
fat distribution, diabetes mellitus, and hypertension is postulated to be explained by insulin

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Rafiqa et al. European Journal of Biomedical and Pharmaceutical Sciences

resistance and grouped as Syndrome X.[5-7] Insulin resistance by promoting fat utilization for
energy increases fatty acid accumulation, causing dyslipidemia.[7,8]

A growing body of evidences indicates a positive relation between disordered lipid profile,
marked by increased lipid peroxides like manoldialdehyde, and endothelial dysfunction [9].
Dysordered lipid profile has been also reported in pregnancy induced hypertension (PIH)
with a prevalence of 15.2%. The finding that serum lipids increases during pregnancy with 2
fold further increase during pregnancy induced hypertension (PIH), suggests a positive
association between dyslipidemia and hypertension.[9]

The relevance of persistent elevated hypertension and hyperlipidemia/dyslipidemia,

especially in younger age group, in predicting cardiovascular risk is gaining increasing
recognition and in that respect lipid profile has been the most intensively investigated in
hypertensive patients in clinical studies.[8] The present study is a preliminary attempt to
establish the prevalence of dyslipidimic hypertension (ie patient suffering from both
hypertension and dyslipidemia) in the Kashmiri population which indirectly reflects the
individuals or the proportion of our population that eventually are at risk of developing
cardiovascular disease.

MATERIALS AND METHODS

Patients attending the Cardiology Clinic of Sher-i-Kashmir Institute of Medical Sciences
(SKIMS) for the management of hypertension were recruited for this study with prior
informed consent. The acceptance for the present work was taken from our Institutional
(SKIMS) ethical committee and the procedures adopted in the study were in accordance with
Helsinki Declaration (1964) of the World Medical Association. In total, 100 patients and 50
healthy control subjects with descriptive features given in Table 1 were included in the
present study. Patients with stroke, and renal diseases were excluded from this study. The
patients under study were grouped according to JNC 7 classification of hypertension (2003)
as pre-hypertensive [defined BP=130-139/85-89mmHg], hypertensive stage I [defined
BP=140-159/90-99 mmHg] and hypertensive Stage II [defined BP =160/>100mmHg].[10] The
patients under study were grouped as Dyslipidemic whose lipid profile is characterized by
either elevated total cholesterol>200mg/dl or LDL Cholesterol>130mg/dl or TG>200mg/dl or
Total cholesterol/HD =4.5 or lowHDL =<40mg/dl or combination of these parameters. The
controls subjects under study were randomly selected age and sex matched healthy people

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Rafiqa et al. European Journal of Biomedical and Pharmaceutical Sciences

from the Kashmir population that clinically were found devoid of hypertension or
dyslipidemia or any other disease that affect these parameters.

Serum was separated from the blood samples drawn from patient and control subjects by
centrifugation at 3000rpm, and stored frozen at -700C until analysis. The level of TG and
total cholesterol in serum samples was estimated by enzymatic colorometric method on
Hitachi 912 (Boehringer Mannhum system). The assay for TG estimation is based on
principle where complete enzymatic hydrolysis of TG by lipase produces glycerol, which in
presence of ATP and enzyme glycerol kinase is converted to glycerol-3-phosphate which in
presence of molecular O2 and glycerol phosphate oxidase (GPO) is converted to H 2O2. The
H2O2 produced in presence of 4amino-phenazone and chlorophenol is converted to a
chromogen (4-p-benzaquinone-mono iminophenazone) read at 700nm.[11] The calibration was
carried out using quality control sera.

Total cholesterol in serum samples was estimated by enzymatic colorometric method on

Hitachi 912 (Boehringer Mannhum system).[12] The assay involves enzymatic conversion of
cholesterol esters and cholesterol in presence of molecular O2 to the production of H2O2,
which in presence of 4amino-phenazone and chlorophenol is converted to a chromogen ( 4-
p-benzaquinone-mono iminophenazone) read at 700nm. The calibration was carried out using
quality control sera.

The level of HDL cholesterol in serum samples was estimated by phosphotungtic acid and
magnesium chloride method.[13] LDL cholesterol, VLDL and chylomicrons was precipitated
from the serum using phosphotungstic acid and MgCL2, leaving HDL in the supernatant. The
HDL from the supernatant was estimated as total cholesterol estimation. The quality control
was established using precilip EL and precinorm. The level of LDL and VLDL was
calculated by Friedwalds formulae: LDL=TOTAL Cholesterol-[HDL+TG/5], where TG/5
represents cholesterol contained in VLDL.[14]

Statistical Analysis
The total serum lipid profile were expressed as mean ±SD. Standard unpaired students “T”
test was used for comparison of lipid levels between prehypertensives ,hypertensives and
normotensive control subjects. Statistical analysis was carried out by ANOVA software and
results were considered significant when p<0.05.

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Rafiqa et al. European Journal of Biomedical and Pharmaceutical Sciences

RESULTS
Total 80 hypertensive (42.5% M and 57.5%F) mean age group of 54.5+11.2yrs; 20 pre-
hypertensive (50%M and 50% F) mean age group of 50.7 ±11.1yrs and 50 normotensive
mean age group of 50±10.8 years were included in the study (Table: 1). The mean total
cholesterol, TG, LDL and HDL in hypertensive, prehypertensive and normotensive subjects
is given in (Table 2). In our study 72% (72/16,00000x100=115200) of hypertensive’s show
dislipidemic too characterized by either cholesterol >200mg/dl or LDL >100mg/dl or
TG>150mg/dl or HDL <40mg/dl or combination of them compared to only 23.3% among
normotensives. Assuming a prevalence of hypertension 20% in Kashmir (Northern India),
with a total population of 80 lakhs, the present study reveals dyslipidemic hypertention in
72% of hypertemnsives (72/16,00000x100=115200) which amounts to overall 14.4%
(115200/80,00000x100) of a subset of Kashmiri population.

The estimation of cholesterol level in 100 patients and 50 control subjects, revealed
significantly high level of mean total cholesterol in hypertensives (175±40.6mg/L) compared
to control subjects (147.2±61.9 mg/dl) (p<0.002) (Table 2). Also the total cholesterol mean
was found higher, though not statistically significant, in prehypertensive subjects
(166.9±57.8mg/dl) as compared to normotensive (147.2±61.9mg/dl) (p=0.147) subjects. The
overall total cholesterol mean was significantly different between hypertensive,
prehypertensive and normotensive (p=0.011) (Table 2). The serum cholesterol was
>200mg/dl in 49% of hypertensives, 37% of prehypertensives as compared to only 21% of
normotensive subjects, which is statistically significant (p=0.011).

Similarly statistically significant difference in levels of TG was found in hypertensive (204-

9±125.1 mg/dl) (p<0.0001) when compared with normotensive subjects (139.2±62 mg/dl).
But was found insignificant when compared between hypertensive (204.9±125.1) and
prehypertensive (186.2±121mg/dl) (p=0.487) and between pre- hypertensive (186.2±121
mg/dl) and normotensive subjects (139.2±62 mg/dl) (p=0.100). The overall mean total TG
levels is significantly different in hypertensive, prehypertensives and normotensives
(p=0.003). TG levels >200mg/dl was found in 51% of hypertensive’s, 39% of
prehypertensives as compared to only 18% of normotensive subjects, which is again
statistically significant (p=0.003).

The difference in mean total level of VLDL between hypertensive (41.0±25.1 mg/dl) and
normotensive (28.9±14.8 mg/dl) was found significant (p=0.002). Difference in levels of

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VLDL, though not statistically significant, was also found between prehypertensive and
normotensive subjects (p=0.154) and between hypertensive and prehypertensives (p=0.496).
The overall mean total VLDL level between hypertensive, prehypertensive and normotensive
subjects is statistically significant (p=0.011).

Statistically significant difference was also found in mean total LDL level between
hypertensives (181.3±62.4 mg/dl) and normotensives (130±74.2 mg/dl) (p=0.00) as well as
between prehypertensive (169.8±80.3 mg/dl) and normotensives (130±74.2) (p=0.030). The
overall mean total LDL levels between three group is statistically significant (p=0.000).
Serum LDL was found >130mg/dl in 45% of hypertensives, in 31% of prehypertyensives
while as only 22% of normotensives had LDL>130mg/dl, which is statistically significant
(p=0.00).

Statistically significant difference in levels of HDL was also found between hypertensive
(34.8±8.4mg/dl) and normotensives (46.1±8.4 mg/dl) (p=0.000) as well as between
prehypertensives (37.0±9.7 mg/dl) and normotensives (46.1±8.4 mg/dl) (p=0.000).The
overall mean total HDL levels between three groups is statistically significant (p=0.000).
Low HDL level (<40mg/dl) was found in 44% of hypertensives, 29% of prehypertensives
compared to only 12% of normotensives.

Table 1: Descriptive characteristics of patients and control groups

Patient Control t P-value
Hypertensive Prehypertensive
n=80 n=20 n=50
Male 34 (42.5%) 10(50%) 26 (52%)
Gender
Female 46(57.5%) 10(50%) 24(48%) 0.544(NS)
Age in Years 54.5±11.2 50.7±11.1 50±10.8
Mean ±SD
≤35 17(% 7 28
≥35 63(% 13 22
SBP (mmHg)
143.3±10.15 132±8.15 118.41±5.42 1.385 0.168
Mean ±SD
2.244 0.026b
DBP(mmHg)
85.21±4.15 85.56±4.32 77.43±3.40 0.227 0.824
Mean ±SD
JNC 7 classification of hypertension,(2003).
Values are expressed as mean±1 SD or percent, unless otherwise specified.
“n” Represents the number of Subjects; SD= Standard Deviation; SBP= Systolic Blood
Pressure. DBP= Diastolic Blood Pressure. Superscripted alphabets a, b, and c represents the
respective significant differences determined by students t-test between hypertensives and
prehypertensives; hypertensives and normal and prehypertensives and normal subjects.

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Table: 2 Lipid profile (in mg/dl) in patients with different grades of Hypertension
compared to controls
Patient Control t P-value ANOVA
Investigation Hypertensive Prehypertensive
n=50
n=80 n=20
8.287 0.516
Cholesterol(mg/dl) F=4.6
175.1±40.6 166.9±57.8 147.2±61.9 27.91 0.002b
Mean ±SD P=0.01
19.83 0.147
Triglycerides 18.73 0.487
F=5.77
(TG)(mg/dl) Mean 204.9±125 186.2±121 65.73 0.000 b
139.2±62 P=0.003
±SD 47.00 0.100
3.76 0.496
VLDL(mg/dl) F=4.65
41.0±25.1 37.2 ±24.2 28.9±14.8 12.14 0.002b
Mean ±SD P=0.01
8.37 0.154
11.52 0.505
LDL(mg/dl) Mean F=8.62
181.3±62.4 169.8 ±80.3 130.0±74.2 51.30 0.000 b
±SD P≤0.0001
39.78 0.030 c
2.187 0.307
HDL(mg/dl) Mean F=27.39
34.8±8.4 37.0±9.7 46.1±8.4 11.29 0.000 b
±SD P≤0.0001
9.11 0.000 c
Values are expressed as mean±1 SD or percent, unless otherwise specified.
“n” Represents the number of Subjects; SD= Standard Deviation; Superscripted alphabets a,
b, and c represents the respective significant differences determined by students t-test
between hypertensives and prehypertensives; hypertensives and normal and prehypertensives
and normal subjects.

DISCUSSION
In the present study the estimation of serum lipid levels in hypertensives, prehypertensives
and normotensives revealed dyslipidemic hypertension in 72% of hypertensive which
amounts to overall 14.4% of a subset of Kashmiri population. This prevalence is comparable
to that found in two communities of southeastern New England.[15] Further the difference in
lipid profile was higher among hypertension than pre-hypertensives when compared with
normotensives. Similar Association between hypertension and lipid levels were also reported
in a large age adjusted case control studies carried out by Karee etal (1991).[4] Rajeev Gupta
(2001)[8] Catherine E,[16] Johnson M .L (2004).[17] The result of our study is also in good
agreement with the studies carried out in Stockholm[18]; in US[19]; in Nigeria.[20] Within lipid
profile, maximum percentage deviation in hypertensives Vs normotensives was observed in
TG levels (51% Vs 18% ) and HDL (45% Vs 12%) followed by Cholesterol (49% Vs 21%)
and LDL (45% Vs 22%). Similar association, except for TG levels, was also reported in a
large retrospective study carried out by Jogleker, S.J and Nanivadekar A.S (1996)[9] in India

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Rafiqa et al. European Journal of Biomedical and Pharmaceutical Sciences

on patients who attended Apollo hospital for the management of hypertension where 51% of
patients showed cholesterol >200mg/dl, 37% had LDL>130mg/dl , 11% had elevated ratio of
total cho/HDL >4.5, 30% TG>200mg/dl.

The findings of the present study, ie greater proportion of hypertensive patients from our
population having higher TG levels compared to rest of India where Cholesterol levels are
higher in significant proportion of hypertensive population, could be associated to different
ethnicity, dietary habits and cultural practices of kashmiri population from rest of India.
However, this finding of our study, is in good agreement with the study carried out in
Bangladesh, a Muslim dominated area, by Shahadat H, et al.,(1999) ; .and by Saha M S
(2006).[21,22] Kashmir being Muslim dominated area, share dietary habits (like heavy
consumption of red meat) and cultural practices (marriage/functional ceremonies) with
Muslim dominated populations of Southeast Asia, as substantiated by the findings of the
present study which is in good agreement with other Muslim dominated populations.

Various studies conducted worldwide including present one suggest a possible biological
interaction between hypertension and dyslipidemia.[19] However the exact mechanisms that
may account for the observed relationship between hypertension and dislipidemia are obscure
but certainly include insulin resistance (also grouped as Syndrome X)[6,7] and endothelial
dysfunction, common features in the pathogenesis of both the conditions.[4] Insulin resistance
causes dislipidemia by promoting fat utilization for energy purposes, and hypertension may
decrease insulin sensitivity by affecting sympathetic nervous activity, or alternatively
influencing function of biological membranes depending upon plasma fatty acid and
lipoprotein concentrations.[5-7, 23, 24] The correlation between the two is further supported by
the fact that lipid lowering agents like statins and fibrates also lowers blood pressure by
affecting arterial wall structure and hence pulse wave velocity.[25,26] Hypertension and
dislipidemia may be, therefore, considered independent risk factors that contribute
synergistically to the development of Cardiovascular disease. Further, the life style strategies
employed for the management of hypertension and dislipidemia alone share remarkable
similarities. Both aim to reduce saturated fat intake, increase fruit and fiber intake, improve
exercise tolerance and stop smoking. However the treatment of dyslipidemia and
hypertension alone is different from the treatment of dyslipidemic hypertension which may
involve insulin resistance as well. The finding of this study, therefore, may provide a
rationale for pharmacotherapy, in a broader subset of people with dyslipidemic hypertension.

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Rafiqa et al. European Journal of Biomedical and Pharmaceutical Sciences

CONCLUSION
The findings of the present study suggest estimation of lipid levels in hypertensives as an
essential/potential tool for early identification of individuals with dyslipidemic hypertension.
Since treatment of dyslipedemia and hypertension alone is different from treatment of
dyslipidemic hypertension, the finding of this study, prevalence of dyslipidemic
hypertension, therefore, provide a rationale for pharmacotherapy, in a broader subset of
people with dyslipidemic hypertension.

ACKNOWLEDGEMENT
We are thankful to Mr. B. A. Pathan, M.A Malik for providing technical assistance and Mr.
Tariq Ahmed for statistical analysis of data.

REFERENCES
1. Fisher NDL, Williams G H, Hypertensive Vascular Disease. Harrison’s Principles of
Internal Medicine. 16thEdition. Part Eight; Section Four; Chapter 246; 1463-1470.
2. Whelton P K, Epidemiology and the Prevention of Hypertension. J Clin Hypertens, 2004;
6(11): 636-642.
3. Gupta R. Trends in hypertension epidemiology in India. J Hum Hypertens 2004; 18: 73-8.
4. Kaare H, Bonaa M D, and Thella M D, Association between blood pressure and serum
lipids in population. The Troms study, Circulation 1991; 83: 1305-1314.
5. Krauss R M., The tangled web of coronary risk factors. Am Jed Med, 1991; 90(supply
2A): 365-415.
6. Reaven GM, Insulin resistance, hyperinsulinemia, and hypertriglyceridemia in the
etiology and clinical course of hypertension. Am J Med 1991; 90(suppl 2A): 75-125.
7. Reaven GM, Banting lecture. Role of insulin resistance in human disease. Diabetes, 1988;
37: 1595-607.
8. Gupta R, Kaul V, Prakash H, et al. Lipid abnormalities in coronary heart diseases. A
population based case control study. Indian Heart J, 2001; 53: 332-336.
9. Joglekar S J, Nanivadekar A S, Prevalence of lipid and glycemic abnormalities in
Hypertensive patients: a retrospective survey. Indian Heart J 1996; 48: 371-374.
10. Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL Jr, et al. The
Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation,
and Treatment of High Blood Pressure: the JNC 7 Report. JAMA 2003; 289: 2560-72.

www.ejbps.com
Rafiqa et al. European Journal of Biomedical and Pharmaceutical Sciences

11. Jacobs N J, and Van Denmark P J, Enzymatic determination of serum triglyceride.ch.

Biochem. Biophys. 1960; 88: 250-255.
12. Allain CC, Poon I S, Chan C H G, Richmond W, and Fu PC., Enzymatic determination of
serum total cholesterol. Clin. Chem. 1974; 20: 470-471.
13. Gordon T, and Gordon M. Enzymatic method to determine the serum HDL-cholesterol.
Am. J. Med. 1977; 62: 707-708.
14. Friedewald W T, Levy RI, Fredrickson D S. Estimation of plasma low density lipoprotein
cholesterol concentration without use of the preparative ultracentrifuge. Clin Chem 1972;
18: 499-512.
15. Eaton C B, Feldman H A, Assaf AR, McPhillips JB, Hum A., Lasater T M, Levinson
P, Carleton RA, Prevalence of hypertension, dyslipidemia, and dyslipidemic
hypertension. Journal of Family Practice, 1994.
16. Catherine E Cooke, Pharm D, BCPS, PAHM; Teisha A Robertson, Pharm.D, MBA
Retrospective analysis of comorbid hypertension and dyslipidemia management in a
primary care practice.
17. Johnson M L, Pietz K, Battleman DS., et al. Prevalence of Comorbid Hypertension and
Dyslipidemia and Associated Cardiovascular Disease. American Journal of Managed
Care. 2004; 10: 926-32.
18. Carlson L A., and Bottiger L E., Ischemic heart disease in relation to fasting values of
plasma triglycerides and cholesterol in Stockholm prospective study. Lancet. 1972; 1:
865-868.
19. Battleman DS, Peterson ED., Estimated prevalence of comorbid hypertension and
dyslipidemia and therapeutic goal attainment among US adults in 2000, utilizing data
from the National Health and Nutrition Examination Survey (NHANES III). Journal of
Managed Care Pharmacy, 2004; 10: 186.
20. Adedeji O O, and Onitiri AC., Lipids in Nigerian hypertensives. Afr. J. Med. Sci. 1990;
19: 281-284.
21. Shahadat H, Maliha R, Iqbal A and Suhrab A, Study of serum lipid profile in essential
hypertensive patients. Mym. Med. J. 1999; 8(1): 22-25.
22. Saha M S, Sana NK, Shaha RK,. Serum Lipid Profile of Hypertensive Patients in the
Northern Region of Bangladesh. Journal of Bio-Science, 2006; 14.
23. Salonen J T, Lakka TA, Lakka H M, Valkonen V P., Everson S A., Kaplan G A,
Hyperinsulinemia is associated with the incidence of hypertension and dyslipidemia in
middle-aged men. Diabetes. 1998; 47(2): 270-5.

www.ejbps.com
Rafiqa et al. European Journal of Biomedical and Pharmaceutical Sciences

24. Misra A, Cherukupalli R, Reddy K S, Mohan A, Bajaj J S., Hyperinsulinemia and

dyslipidemia in non-obese, normotensive offspring of hypertensive parents in northern
India. Blood Press. 1998; 7(5-6): 286-90.
25. Avorn J, Monette J, Lacour, A, et al. Persistence of use of lipid lowering medications: a
cross-national study. Journal of the American Medical Association. 1998; 279: 1458-62.
26. Benner J S., Glynn R J , Mogun H , et al. Long-term persistence in use of statin therapy in
elderly patients. Journal of the American Medical Association. 2002; 288: 455-61.

www.ejbps.com