Background: By the dawn of this modern era of science, the prime challenge of physician is cardiovascular disease (CVD). The most important modifiable risk factors of CVDs are unhealthy diet, physical inactivity and tobacco use. The effects of unhealthy diet and physical inactivity include abnormal blood lipid, obesity and hypertension. We tried to evaluate and correlate the pattern of lipid profile in obese and non-obese hypertensive patients. Objectives: This study was conducted at medicine department of Cumilla Medical College Hospital. The principal aim was to evaluate the lipid profile in obese and non-obese adult hypertensive patients. Methodology: During this cross sectional analytical study, a total of 100 adult hypertensive patients were taken by purposive sampling. Among them 50 (group 1) patients were taken those were obese and 50 (group 2) patients taken those were non-obese according to BMI measurement on operational definition. Diagnosis of hypertension would be established with the help of ambulatory BP measurements two occasions few minutes apart. The staging of hypertension was done according to JNC7 Criteria. Morning blood samples were taken after 8 - 12 hours of fasting and lipid profiles were done on authentic laboratories. The laboratory values were interpreted according to the operational definition of dyslipidaemia. The ethical research and review committee approved the study protocol and signed informed consent was obtained from the participants. The statistics was analyzed using the IBM SPSS software of version 19.0. Statistical significance was set at p < 0.05. Results: Among the two groups, there were 56 (56%) males and 44 (44%) females. The mean age of group 1 (46.10 ± 11.09) was compared to that of group 2 (45.5 ± 10.6). Lipid profile abnormalities were significantly higher in the stage 2 hypertension (59.62%) and stage 3 hypertension (66.66%), higher in class 2 obese (100%) and class 3 obese subjects (100%), female hypertensive patients had significantly higher BMI than their male counterparts (27.24 ± 3.63 kg/m2 versus 29.29 ± 3.99 kg/m2), lipid profiles were higher in the female than male hypertensive patients (63.33% vs 55.35%) but only TC was statistically significant (4.45 ± 1.19 mmol/l versus 4.86 ± 1.29 mmol/l, p < 0.05). Those who were obese had significant high TG (p < 0.001), high TC (p < 0.001) and high LDL-C (p < 0.001). 38 (76%) of the obese hypertensive patients had dyslipidaemia whereas 21 (42%) of non-obese hypertensive patients had dyslipidaemia. In multivariate regression, TG was significantly and directly associated with BMI of subjects. Dyslipidaemia was more prevalent in the age group 30 - 59 of adult hypertensive patients. It showed that obese hypertensive patients had significantly higher SBP (p < 0.001), DBP (p < 0.001) than non-obese subjects. The mean TC (4.83 ± 0.95 mmol/l versus 4.15 ± 0.57 mmol/l, t = -9.70, p < 0.001), TG (2.64 ± 0.67 mmol/l versus 2.10 ± 0.45 mmol/l, t = -5.37, p < 0.001) and LDL-C (3.00 ± 0.82 mmol/l versus 2.44 ± 0.53 mmol/l, t = -9.11, p < 0.001) were also significantly higher among the hypertensive obese subjects. The mean HDL-C was however comparable in the two groups (1.25 ± 0.27 mmol/l versus 1.24 ± 0.57 mmol/l, t = -0.25, p = 0.08)...
Among the common non-communicable disorders, hypertension is emerging as a public health problem worldwide. It is now spreading in epidemic fashion in developing countries as well [
Abnormalities of serum lipid and lipoprotein levels (dyslipidaemia) are considered as major modifiable cardiovascular disease risk factors and identified as independent risk factors for essential hypertension [
They trigger a self perpetuating inflammatory response during which they are taken up by macrophage to form foam cells-a hallmark of the atherosclerosis process. Low HDL cholesterol also predisposes to atherosclerosis [
Hypertension is defined as trait as opposed to a specific disease and represents a quantitative rather than qualitative deviation from the normal [
Obesity is noticed among all strata of the population in developing countries. It is one of the conventional risk factors for cardiovascular disease [
Hypertension is a common disease with serious consequences [
1) What is the pattern of lipid profile in obese and non-obese hypertensive patients?
2) Whether dyslipidaemia is related with obesity or hypertension?
General objectives:
· To evaluate and correlate the lipid profile between obese and non-obese adult hypertensive patients.
Specific objectives:
1) To see the pattern of lipid profile in obese and non-obese hypertensive patients.
2) To evaluate the relation of lipid profile with obese and non-obese person.
3) To determine whether dyslipidaemia is related with obesity or hypertension.
4) To see the socio-demographic distribution of obesity.
5) To evaluate the lipid profile on different stages of hypertension.
The National Health and Nutritional Examination Survey (NHANES) which has been studying the health of representative samples of Americans since 1960 has provided data on the changing prevalence of hypertension and its control. According to this, the prevalence of hypertension decreased somewhat between 1960 and 1991 [
Surveys in Europe show much higher rates of hypertension [
One case control study shows that 30% patients of essential hypertension have elevated level of lipoprotein [
Cardiac output and peripheral vascular resistance are the two determinants of arterial pressure. Cardiac output is determined by stroke volume and heart rate; stroke volume is related to myocardial contractility and to the size of the vascular compartment. Peripheral resistance is determined by functional and anatomic changes in small arteries and arterioles.
Intravascular volume: Vascular volume is a primary determinant of arterial pressure over long term. Sodium is predominantly an extracellular fluid volume. When NaCl intake exceeds the capacity of the kidneys to excrete sodium, vascular volume initially expands and cardiac output increases. The initial elevation of blood pressure in response to vascular volume expansion is related to an increase of cardiac output revert to normal.
Autonomic nervous system: The autonomic nervous system maintains cardiovascular homeostasis via pressure, volume and chemoreceptor signals. Adrenergic reflexes modulate blood pressure over the short term and adrenergic function, in concert with hormonal and volume related effort contributed to the long term regulation of arterial pressure. The three endogenous catecholamines are epinephrine, nor epinephrine and dopamine. All three play an important role in cardiovascular volume.
Renin-angiotensin-aldosterone system: The renin-angiotensin-aldosterone system contributes to the regulation of arterial pressure primarily via the vasoconstrictor properties of angiotensin II and sodium retaining properties of aldosterone. There are three primary stimuli for renin secretion [
Blood pressure should be measured with a well calibrated sphygmomanometer. The bladder width within the cuff encircles at least 80% of the arm circumference. Reading should be taken after the patient has been resting comfortably back supported in the sitting or supine position for at least 30 minutes after smoking or coffee intake. Hypertension is diagnosed when systolic blood pressure is consistently elevated above 140 mm of Hg or diastolic blood pressure is above 90 mm of Hg, a single elevated blood pressure is not sufficient for diagnosis. The major exceptions of the rule are hypertensive presentation with equivocal evidence of life threatening end organ damage as seen in hypertensive emergency or in hypertensive urgency where blood pressure is >220/120mm of Hg but life threatening end organ damage is absent. In less severe cases, the diagnosis of hypertension depends on a series of measurement of blood pressure since reading can vary and to regress toward the mean with time.
The following table provides a classification of blood pressure for adults aged 18 years of age or older. The classification based on the mean of 2 or more properly measured seated blood pressure reading on each of 2 or more office visits.
Most patients with hypertension are asymptomatic. The high blood pressure usually has been noted during an incidental clinical examination. A proportion of patients present with a major complications of hypertension such as stroke or myocardial infarction but only a small number present with symptoms directly attributable to hypertension such as breathlessness or headache. Symptoms also have according to secondary causes of hypertension.
Investigations: Routine investigations of all hypertensive patients should include Urinalysis: Proteinuria, hyaline and granular cast may be found where there is renal disease of malignant hypertension. There is little or no protein in urine if patient with benign essential hypertension.
Blood urea: A raised level of urea suggests renal failure.
S. Creatinine: reflects the renal function.
ECG: This is usually normal in patients with mild hypertension but may show evidence of left ventricular hypertrophy.
Lipids: Although not directly related to blood pressure, an increased level of cholesterol is a risk factor for cardiovascular events.
According to The National Cholesterol Education Programme (NCEP) Adult Treatment Panel (ATP III) guidelines LDL cholesterol optimal is <100 mg/dl; near optimal or above normal is 100 - 129 mg/dl; borderline is 130 - 159 mg/dl, high is 160 - 189 mg/dl; very high is >190 mg/dl. Total cholesterol is desirable is <200 mg/dl; borderline high is 200 - 239 mg/dl; high is >240 mg/dl.HDL cholesterol low is <40 mg/dl; high is >60 mg/dl. Triglycerides level < 150 mg/dl is normal; borderline high is 150 - 199 mg/dl; high is 200 - 499 mg/dl; very high is >500 mg/dl. Blood sample must be collected after 09 - 12 hours of fasting [
Lipids and cardiovascular disease [
Plasma lipoprotein levels are major modifiable risk factors for cardiovascular disease. Increased levels of atherogenic lipoproteins especially LDL but also IDL and possibly chylomicron remnants contribute to the development of atherosclerosis [
Lipid measurement [
Abnormalities of lipid metabolism most commonly come to light following routine blood testing. Measurement of plasma cholesterol alone is not sufficient for comprehensive assessment. Levels of total cholesterol (TC), triglycerides (TG) and HDL cholesterol (HDL-C) should be obtained after an 8 - 12 hour fast to permit the calculation of LDL cholesterol (LDL-C) according to Friedewald formula (LDL-C = TC-HDL-C-(TG/2.2) mmol/l). The formula becomes unreliable when TG level exceeds 4 mmol/l (350 mg/dl). Nonfasting samples are unaffected in terms of TC and measured LDL-C but they differ in terms of TG and HDL-C.
· Predominant hypercholesterolemia
· Familial hypercholesterolemia
· Hyper alphalipoproteinemia
· Predominant hypertriglyceridemia
o Lipoprotein lipase deficiency.
o Familial hypertriglyceridemia.
· Mixed hyperlipidaemia
o Familial combined hyperlipidaemia.
o Dys betalipoproteinemia.
Predominant hypercholesterolaemia
Polygenic hypercholesterolemia is the most common cause of mild to moderate increase in LDL-C. Physical signs such as corneal arcus and xanthelasma may be found in this as well as other forms of lipid disturbance. Risk of cardiovascular disease is proportional to the degree of LDL-C elevation, together with other major risk factors particularly HDL-C.
Familial hypercholesterolemia (FH):
Familial hypercholesterolemia causes moderate to severe hypercholesterolemia with a prevalence of at least 0.2% in most populations. It is usually caused by a loss of function mutations in the LDL receptor gene, which results in an autosomal dominant pattern of inheritance. A similar syndrome can arise with loss of functions mutations in the legend-binding domain of Apo B100 or gain of function mutations in the ligand-binding domain of Apo B100 or gain of function mutations in the PCSK9 gene. The latter increases the activity of the PCSK9 protein, which is a sterol sensitive protease that targets the LDL receptor for degradation. Causative mutations can be detected in one of these three genes by genetic testing in about 70% of patients with FH. Affected subjects suffer from severe hypercholesterolemia and premature cardiovascular disease.
Hyperalphalipoproteinemia
Hyperalphalipoproteinemia refers to increased levels of HDL-C. In the absence of an increase in LDL-C, this condition does not cause cardiovascular disease.
Predominant hypertriglyceridemia
Polygenic hypertriglyceridemia is the most common primary cause of TG elevation. It also commonly occurs secondary to excess alcohol, medications, type 2 diabetes, impaired glucose tolerance, central obesity or other manifestation of the insulin resistance syndrome. It is often accompanied by postprandial hyperlipidaemia and reduced HDL-C both of which may contribute to cardiovascular risk.
Lipoprotein lipase deficiency
Lipoprotein lipase deficiency is an infrequent autosomal recessive disorder due to hereditary deficiency of lipoprotein lipase or its co-factor. It causes massive hypertriglyceridemia that is resistant to drug treatment. It may result in hepatosplenomegaly, lipaemia retinitis and eruptive xanthoma.
Familial hypertriglyceridemia
Familial hypertriglyceridemia refers to dominant inheritance of pure hypertriglyceridemia. It has been suggested that it may represent a secondary response to impaired bile acid resorption and that it seems not to increase the risk of cardiovascular disease.
Mixed hyperlipidaemia
It is difficult to define the distinction between predominant hyperlipidaemia and mixed hyperlipidaemia quantitatively. The term mixed usually implies the presence of hypertriglyceridemia as well as increase in LDL or IDL. Treatment of massive hypertriglyceridemia may improve TG faster than cholesterol thus mimicking mixed hyperlipidaemia. Both components of hyperlipidaemia may contribute to the risk of cardiovascular disease.
Dysbetalipoproteinaemia
Dysbetalipoproteinaemia involves accumulation of roughly equal molar levels of cholesterol and TG. It is caused by homozygous inheritence of the apolipoprotein E2 alles which is the isoform least avidly recognized by the LDL receptor. Premature cardiovacular disease is common and it may result in the formation of palmar xanthoma, tuberous xanthoma or tendon xanthoma.
Miscellaneous and rare forms of hyperlipidaemia.
Tangier disease.
Apo A1 deficiency.
Fish eye disease.
LCAT deficiency.
Sitosterolemia.
Obesity is widely regarded as a pandemic with potentially disastrous for human health. Over one quarter of adults in the UK were obese (BMI > 30 kg/m2) in 2010. In developing countries, average national rates of obesity are low but these figures may disguise high rates of obesity in urban communities for example nearly one quarter of women in urban India are overweight. There is increasing public awareness of the health implications of obesity.
Obesity has adverse effects on both mortality and morbidity. Changes in mortality are difficult to analysis due to the confounding effects of lower body weight in cigarette smokers and those with other illnesses. It is suggested that obesity at age 40 years can reduce life expectancy by up to 7 years for non-smoker and by 13 years for smokers [
Classification of obesity [
The western pacific region office of WHO recommends that, amongst Asians the classification of obesity [
Cross sectional type of analytical study.
Department of Medicine, Cumilla Medical College Hospital, Cumilla.
Nine months.
Adult Obese and non-obese patients suffering from hypertension.
Sampling method: Sample size calculation—it is calculated by using Cochran’s formula which considering 95% level of significance at 5% precision level and prevalence of dyslipidaemia is 30%.
The formula is using N = Z 2 ( p × q ) d 2 , here N = minimum number of sample to be studied.
Z = Standardized normal value usually set at 1.96 which corresponds to 95% confidence interval.
P = Prevalence of dyslipidaemia is 30% = 0.30
q = 1 − p = 1 − 0.30 = 0.69
d = degree of accuracy, 0.05 at 5% confidence level.
So, N = 327
But due to limitation of budget and study period, my sample size was 100.
Inclusion criteria:
1) Hypertensive patients of age > 18 years.
2) Patients who gave informed written consent.
Exclusion criteria:
1) Known case of secondary hypertension.
1) Patients taking lipid lowering drugs.
3) Pregnancy.
1) Hypertension
Hypertension is said when SBP is > 140 mm of Hg & DBP is >90 mm of Hg. It is again graded into three stages. Grade 1 (mild) hypertension is SBP is 140 to 159 mm of Hg & DBP is 90 to 99 mm of Hg. Grade 2 hypertension (moderate) is SBP is 160 to 179 mm of Hg & DBP is 100 to 109 mm of Hg. Grade 3 hypertension (severe) hypertension is SBP is >180 mm of Hg & DBP is >110 mm of Hg [
2) Obesity
The western pacific region office of WHO recommends that amongst Asians, normal BMI (reference range-non obese) is 18.5 - 23 kg/m2 BMI > 23.0 - 24.9 kg/m2 is overweight and BMI > 25.0 kg/m2 is obesity. Class 1 obesity is BMI 25 - 29.9 kg/m2, Class 2 obesity is BMI 30 - 34.9 kg/m2, Class 3 obesity is BMI > 35 kg/m2 [
3) Dyslipidaemia
Dyslipidaemia is the term given to abnormalities in blood lipid levels. According to the National Cholesterol Education Program (NCEP) Adult Treatment Panel 2 (ATP III) guidelines LDL cholesterol optimal is <100 mg/dl; near optimal or above normal is 100 - 129 mg/dl (2.59 - 3.34 mmol/l); borderline is 130 - 159 mg/dl (3.37 - 4.12 mmol/l); high is 160 - 189 mg/dl (4.15 - 4.90 mmol/l); very high is >190 mg/dl (>4.90 mmol/l). Total cholesterol is desirable is < 200 mg/dl (5.18 mmol/l); borderline high is 200 - 239 mg/dl (5.18 - 6.18 mmol/l); high is >240 mg/dl (>6.22 mmol/l). HDL cholesterol low is <40 mg/dl (1.00 mmol/l); average is 40 - 50 mg/dl (1.00 - 1.3 mmol/l) high is >60 mg/dl (> 1.55 mmol/l). Triglyceride level is <150 mg/dl (<1.7 mmol/l) is normal; 150 - 199 mg/dl (1.7 - 2.2 mmol/l) is borderline high; 200 - 499 mg/dl (2.3 - 5.6 mmol/l is high. > 500 mg/dl (>5.6 mmol/l) is very high. Blood sample collected after 9 - 12 hours fasting [
Selection of cases (according to inclusion & exclusion criteria) → Data collection → Data entry & analysis by computer & statistical software.
100 adult hypertensive patients were taken by purposive sampling method. Among them 50 were obese (group 1) and 50 are non-obese (group 2). Diagnosis of hypertension would be established with the help of ambulatory BP measurement on different occasions. Informed written consent would be obtained from the patients after full explanation of the details of the disease process. Lipid profile would be done from authentic laboratories. Findings of observation would be recorded or prescribed data collection form and compare them by statistical methods.
Adult Sphygmomanometer, Stethoscope, weight measuring machine, height measuring machine, measuring tape, Computer with internet access & printer etc.
After collection, data would be edited, analyzed in a computer by Statistical package for social science (SPSS version-19). Assistance of a statistician would be taken.
January 2018 to September 2018.
Implement research finding in practice both because of a growing awareness of the gap between clinical practice and the findings of research and also because of the need to show that investment in research results in benefits for patients.
The aims and objectives of the study along with its procedure, method risks and benefits of the study would be explained to the patients in easily understandable local language and the informed consent would be taken from the patient or legal guardian. It would be assured that all information and records would be kept confidential and the procedure would be helpful for both the physicians and the patients in making rational approach of case management. Permission from ethical committee of Comilla Medical College Hospital was taken.
Among the two groups, there were 56 (56%) males and 44 (44%) females. The mean age of group 1 (46.10 ± 11.09) was compared to that of group 2 (45.5 ± 10.6). Lipid profile abnormalities were significantly higher in the stage 2 hypertension (59.64%) and stage 3 hypertension (66.66%), higher in class 2 obese (100%) and class 3 obese (100%) subjects, female hypertensive patients were significantly higher BMI than their male counterparts (27.24 ± 3.62 kg/m2 versus 29.29 ± 3.99 kg/m2), lipid profile were higher in the female than male hypertensive patients (63.33% vs 55.35%) but only TC was statistically significant (4.45 ± 1.19 versus 4.86 ± 1.29, p < 0.05),among female patients higher in the housewife. Those who are obese had significant high TG (p < 0.001), high TC (p < 0.001) and high LDL-C (p < 0.001). 38 (76%) of the obese hypertensive patients had dyslipidaemia and 12 (24%) of the obese hypertensive patient had no dyslipidaemia. 21 (42%) of non-obese hypertensive patients have dyslipidaemia and 29 (58%) of nonobese hypertensive patient had no dyslipidaemia. In multivariate regression, TG was significantly and directly associated with BMI of subjects. Dyslipidaemia was more prevalent in the age group 30 - 59 of adult hypertensive patients. It showed that obese hypertensive patients had significantly higher SBP (p < 0.001), DBP (p < 0.001) than non-obese subjects. The mean TC (4.83 ± 0.95 mmol/l versus 4.15 ± 0.57 mmol/l, t = −9.70, p < 0.001), TG (2.64 ± 0.67mmol/l versus 2.10 ± 0.45 mmol/l, t = −5.4, p < 0.001) and LDL-C (3.00 ± 0.82 mmol/l versus 2.44 ± 0.53 mmol/l, t = −9.1, p < 0.001) were also significantly higher among the hypertensive obese subjects. The mean HDL-C was however comparable in the two groups (1.25 ± 0.27 mmol/l versus 1.24 ± 0.57 mmol/l, t = −0.3, p = 0.08). Among the obese adult hypertensive subjects 38 (76%) had at least one abnormal lipid parameter while 21 (42%) of the non-obese hypertensive subjects had at least one lipid abnormalities. Elevated TG was therefore most frequent individual abnormality among both obese and non-obese adult hypertensive subjects.
In this study, serum TC, TG, LDL-C concentrations are significantly higher in hypertensive obese than in hypertensive non-obese subjects.
| Age (yrs) | Frequency | Percent | Maximum (yrs) | Minimum (yrs) | Mean (yrs) SD |
|---|---|---|---|---|---|
| 20 - 29 | 04 | 08 | |||
| 30 - 39 | 07 | 14 | |||
| 40 - 49 | 17 | 34 | |||
| 50 - 59 | 14 | 28 | 85 | 20 | 46.01 ± 11.09 |
| 60 - 69 | 05 | 10 | |||
| >70 | 03 | 06 | |||
| All ages | 50 | 100% |
Among them majority are 30 to 59 years of age (76%) that is majority are middle aged.
| Age (yrs) | Frequency | Percent | Maximum | Minimum | Mean (yrs) SD |
|---|---|---|---|---|---|
| 20 - 29 | 04 | 08 | |||
| 30 - 39 | 06 | 12 | |||
| 40 - 49 | 15 | 30 | |||
| 50 - 59 | 13 | 26 | 78 | 20 | 45.5 ± 10.6 |
| 60 - 69 | 07 | 14 | |||
| >70 | 05 | 10 | |||
| All ages | 50 | 100% |
Among them majority are 30 to 59 years of age (68%) that is majority are middle aged.
and 45.5 ± 10.6. Dyslipidaemia is more common in 30 to 59 years of age group. In both obese and non-obese hypertensive group, 37 (37%) patients are in stage 1 hypertension, 57 (57%) are in stage 2 hypertension and 6 (6%) patients are in stage 3 hypertension. In all stage majority of the patient are in between 30 to 59 years of age. The results of a study show that increased age is associated with a significant increase in the prevalence of hypertension [
Another study shows the prevalence of hypertension among individual aged > 60 is 65.4% [
female in both obese and non-obese hypertensive group (56% vs 44%). But in this study, dyslipidaemia is more common in women than in men of same age (63.33% vs 55.35%). Rulixin Y et al. showed that sex difference in the prevalence of hypertension and dyslipidaemia may be mainly attributed to the differences in dietary habits, life style choices, sodium and potassium intake, physical activity level and some genetic polymorphism [
wife and 1 (4.8%) patient is from other professions. Those 29 (58%) patients have no dyslipidaemia of them 12 (41.38%) patient are serviceman, 7 (24.14%) patient are businessman, 6 (20.68%) patients are housewife and 4 (13.80%) from other professions. So it showed that service holder and housewife have more prevalence of dyslipidaemia (74%). In one study conducted in Bangladesh showed that sedentary workers have more prevalence of obesity as well as hypertension [
| BP | Group 1 (Obese hypertensive) Mean ± SD | Group 2 (Non-obese hypertensive) Mean ± SD | t | p-value |
|---|---|---|---|---|
| SBP | 163.77 ± 18.88 | 160.50 ± 14.60 | −32.9 | <0.001 |
| DBP | 99.1 ± 11.45 | 98.44 ± 10.45 | −28 | <0.001 |
| BMI (kg/m2) | Number | Percent | Maximum | Minimum | Mean (SD) |
|---|---|---|---|---|---|
| Class I | 40 | 80 | |||
| Class II | 9 | 18 | 38 | 25.8 | 28.50 (6.02) |
| Class III | 1 | 2 | |||
| Total | 50 | 100 |
| Dyslipidaemia status | Frequency (%) | Stage I HTN (%) | Stage II HTN (%) | Stage III HTN (%) | P value |
|---|---|---|---|---|---|
| Present | 38 (76%) | 11 (28.94%) | 23 (60.53%) | 04 (10.53%) | 0.04 |
| Absent | 12 (24%) | 04 (33.34%) | 08 (66.66%) | 00 |
| Dyslipidaemia status | Frequency (%) | Stage 1 HTN (%) | Stage 2 HTN (%) | Stage 3 HTN (%) | P value |
|---|---|---|---|---|---|
| Present | 21 (42%) | 10 (47.61%) | 11 (52.38%) | 0.06 | |
| Absent | 29 (68%) | 12 (41.37%) | 15 (51.72%) | 02 (6.89%) |
| Stage 1 HTN (n = 37) | Stage 2 HTN (n = 57) | Stage 3 HTN (n = 6) | |
|---|---|---|---|
| Dyslipidaemia | 21 (56.75%) | 34 (59.64%) | 04 (66.66%) |
dyslipidaemia and remaining 41 (41%) patients have no dyslipidaemia. Among patients of dyslipidaemia, 21 (56.75%) patients in stage 1 hypertension, 34 (59.64%) patients in stage 2 hypertension and 4 (66.66%) patients in stage 3 hypertension. One case control study Bhavani BA et al. showed that 40.5% patients of hypertension have elevated level of lipoprotein and lipoprotein abnormalities tend to be more in patients with increase level of hypertension [
| Class 1 obesity (n = 40) | Class 2 obesity (n = 9) | Class 3 obesity (n = 1) | |
|---|---|---|---|
| Dyslipidaemia | 28 (70%) | 9 (100%) | 1 (100%) |
| Male (n = 56) | Female (n = 44) | p-values | |
|---|---|---|---|
| BMI (kg/m2) | 27.24 ± 3.62 | 29.29 ± 3.99 | <0.05 |
| TC (mmol/l) | 4.45 ± 1.19 | 4.86 ± 1.29 | <0.05 |
| TG (mmol/l) | 1.61 ± 0.71 | 1.69 ± 0.63 | >0.05 |
| HDL-cholesterol | 1.23 ± 0.48 | 1.38 ± 0.53 | >0.05 |
| LDL-cholesterol | 2.49 ± 0.93 | 2.71 ± 0.98 | >0.05 |
This table shows female hypertensive patients were significantly higher BMI than their male counterparts (27.24 ± 3.62 vs 29.29 ± 4.79). Although the lipid profile was higher in the female than male hypertensive patients only total cholesterol was statistically significant (4.86 ± 1.29 mmol/l vs 4.45 ± 1.19 mmol/l, p < 0.05).
| Variable | Hypertensive obese Mean ± SD | Hypertensive (non-obese) | t | P value |
|---|---|---|---|---|
| BMI (kg/m2) | 28.5 ± 6.02 | 20.5 ± 3.4 | −4.1 | <0.001 |
| TG | 2.64 ± 0.67 | 2.10 ± 0.45 | −5.4 | <0.001 |
| HDL-C | 1.25 ± 0.27 | 1.24 ± 0.57 | −0.3 | =0.8 |
| LDL-C TC | 3.00 ± 0.82 4.83 ± 0.95 | 2.44 ± 0.53 4.15 ± 0.57 | −9.1 −9.7 | <0.001 <0.001 |
The mean TC (4.83 ± 0.95 versus 4.15 ± 0.57, t = −9.70, p < 0.001), TG (2.64 ± 0.67 versus 2.10 ± 0.45, t = −5.4, p < 0.001) and LDL-C (3.00 ± 0.82 versus 2.44 ± 0.53, t = −9.11, p < 0.001) were also significantly higher among the hypertensive obese subjects. The mean HDL-C was however comparable in the two groups (1.25 ± 0.27 versus 1.24 ± 0.57, t = −0.3, p = 0.08).
with the earlier observation in other parts of the world [
· Dyslipidaemia is an important risk factor for hypertension and in this study association between dyslipidaemia and hypertension was observed.
· TC, TG and LDL-C were significantly higher among the obese hypertensive than non-obese hypertensive.
· Raised TC, LDL-C & TG and low HDL are associated with increased incidence of hypertension.
· Dyslipidaemia is more prevalent among the patients having higher BMI.
· Isolated high TG is the most common abnormality in both obese and non-obese hypertensive patients.
| Lipid abnormalities | Hypertensive obese (%) | Hypertensive non-obese (%) |
|---|---|---|
| Elevated TC | 24 (48%) | 17 (34%) |
| Elevated LDL-C | 29 (58%) | 14 (28%) |
| Elevated TG | 35 (70%) | 18 (36%) |
| Low HDL-C | 32 (64%) | 18 (36%) |
| No lipid abnormality | 12 (24%) | 29 (58%) |
| One lipid abnormality | 16 (32%) | 07 (14%) |
| >2 lipid abnormality | 22 (44%) | 14 (28%) |
Elevated TG was therefore most frequent lipid abnormality among both hypertensive obese and non-obese subjects.
· Dyslipidaemia is major risk factor of atherosclerotic cardiovascular disease and also risk factor or association with other co-morbidities such as hypertension which is also another major modifiable risk factor of atherosclerotic cardiovascular disease. Dyslipidaemia presents among persons with higher BMI (obese) than non-obese persons.
· The study is conducted in one center only.
· Small sample size.
· Risk factors other than dyslipidaemia are not considered.
As dyslipidaemia is an important risk factor for hypertension, lipid profile should be investigated thoroughly in hypertensive patients in medical practice.
· To control hypertension concomitant dyslipidaemia should be treated with appropriate lipid lowering drugs.
· As hypertension and dyslipidaemia are common in patients with having increased BMI. Weight reduction should be encouraged in hypertensive as well as normotensive patients.
· Doing the paper on a large scale multi-centric basis and maybe adding other risk factors of ischaemic heart disease in the study.
The authors declare no conflicts of interest regarding the publication of this paper.
Chowdhury, MdR.U., Akter, K.S., Bhuiyan, S.I., Sohel, M., Majumder, M., Sohan, A.M., Rahman, M., Kabir, M.A. and Ahmed, Z. (2020) Evaluation of Lipid Profile in Obese and Non-Obese Hypertensive Adult Patients Attended in Medicine Department of a Medical College Hospital of Bangladesh. World Journal of Cardiovascular Diseases, 10, 520-544. https://doi.org/10.4236/wjcd.2020.108052
· TC = Total cholesterol.
· TG = Triglycerides.
· LDL-C = Low density lipoprotein-cholesterol.
· HDL-C = High density lipoprotein-cholesterol.
· BMI = Body mass index.
· HTN = Hypertension.
· BP = Blood pressure.
· SBP = Systolic blood pressure.
· DBP = Diastolic blood pressure.
· CVD = Cardiovascular disease.
· NHANES = National health and nutritional examination survey.
· ATP = Adult treatment panel.
· NCEP = National cholesterol education programme.
· CuMch = Cumilla Medical College Hospital.
1) ID:
2) Evaluation of Lipid Profile in Obese and Non-obese Adult Hypertensive Patients Attended in Medicine Department of Cumilla Medical College Hospital.
3) Investigator’s name: Dr. MD REAZ UDDIN CHOWDHURY
4) Institute: Cumilla Medical College Hospital, Cumilla.
5) Purpose of the study: This study is doing to correlate the lipid profile in obese and non-obese Hypertensive Adult patients presented to Medicine department of Comilla medical college hospital.
6) Selection of the participant: This study includes all adult hypertensive obese and non-obese Patients attended at Cumilla Medical College Hospital.
7) Expectation from and involvement of the participant: You will be asked some question according you are giving all will be correct
8) Risk and benefit: There is no risk of you as it will collect only verbal information and small amount of fasting venous blood.
9) Privacy, anonymity and confidentiality: You are ensured that all information should be kept confidential and you are labile to choose time and place which will be suitable for you.
10) Right to withdraw: You are free to take part or refuse any part of the study. If you agree to our proposal of enrolling you/your patient in our study, Please indicate that by putting your signature at the specified below
Signature of the participant signature of investigator