Pattern of Lipid Profile in Newly Detected Hypertensive Patients in Hypertension and Research Centre, Rangpur
Dr. Al Amin Md. Mamun Ibne Ashrafi
FCPS Internal Medicine part –II
Department of Medicine
Rangpur Medical College Hospital,
This primary data-based dissertation is submitted in partial fulfillment of the requirements of the Fellowship of College of Physicians and Surgeons (FCPS) Internal Medicine part–II Examinations of the Bangladesh College of Physicians and Surgeons (BCPS). This research work was done during 1st July 2010 to 30th June 2011 in Hypertension and Research Centre, Rangpur. No portion of the work referred to in this dissertation has been submitted in support of an application for another degree or qualification of this or any other institution of learning.
Certified that Dr. Al Amin Md. Mamun Ibne Ashrafi carried out this research work titled “Pattern of lipid profile in newly detected hypertensive patients in Hypertension and Research Centre, Rangpur” and prepared this dissertation under my direct supervision. I have found the work and dissertation satisfactory for partial fulfillment of the requirements of the fellowship of the College of Physicians and Surgeons (FCPS) Internal Medicine part –II Examinations of the Bangladesh College of College of Physicians and Surgeons (BCPS).
This study was conducted at Hypertension & Research Centre, Rangpur. The principle aim was to find out the relation between dyslipidemia and newly detected hypertension and target organ involvement in hypertensive patients with or without dyslipidemia.
Research design and methods
Study type: Descriptive and cross sectional study
Sample size: 253
During the study period a total 253 newly detected hypertensive patients (Patients who are diagnosed as hypertensive within six months) with or without dyslipidemia were studied. Staging of hypertension was done according to The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. A morning blood sample was taken after 9-12 hours fasting and laboratory values were interpretated according to Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Several other investigations were done to see the target organ involvement. Relationship among hypertension, Lipid profile, and Body Mass Index was assessed and target organ involvement was assessed considering dyslipidemia.
The patients are in between the age 20-85 years and majority are between 30-59 years of age (211; 83.4%). The mean age of them was 46.01 years with standard deviation (SD) 11.09. Out of 253 subjects, 151 (59.7%) patients are male and 102 (40.3%) are female. In this study 132 (52.2%) patients are urban and 121(47.8%) patients are rural dweller. Among the hypertensive patients 100 (39.5%) patients are service holder, 40 (15.8%) patients are businessman, 3 patients (1.2%) are farmer, 89 (35.2%) are housewife and 21(8.3%) patients are included in others group like retired person, student etc. Of the study group 84(33.2%) patients had stage-1 hypertension (systolic BP 140-159mmHg and or diastolic BP 90-99mmHg) and 169(66.8%) patients had stage-2 hypertension (systolic BP ≥160 mmHg and or diastolic BP ≥100 mmHg). Among 253 patients majority of patients have abnormal BMI (146; 57.7%). Dyslipidemia is also more in patients who have abnormal BMI (65 vs 38; 64.4% vs 35.6%) (p=0.037). Among 253 newly detected hypertensive patients, 103 (40.7%) patients have dyslipidemia of them 34(33%) are in stage I hypertension and 69(67%) patients are in stage II hypertension (p=0.03). 20 (7.90%) patients have IHD (p=0.51), of them 12 (4.74%) patients have dyslipidemia and 8 (3.16%) patients have no dyslipidemia. 4 (1.9%) patients have mild systolic dysfunction (p=0.16) of them 3 (2.9%) have dyslipidemia and 1 (0.7%) have no dyslipidemia. 6 (2.37%) patients have diastolic dysfunction (p=0.03), of them 5 (4.9%) patients have dyslipidemia and 1 (0.7%) patient have no dyslipidemia.. On Echocardiogram and ECG 14 (5.53%) patients have LVH (p=0.065) of them 9 (8.7%) patients have dyslipidemia and 5 (3.3%) patients have no dyslipidemia. On chest X-ray 12 (4.74%) patients have cardiomegaly (p=0.06) of them 8 (7.8%) patients have dyslipidemia and 4(2.7%) patients do not have dyslipidemia.
Among 253 patients total 12 (4.74%) patients have stroke (p=0.8) of them 5 (4.85%) patients have dyslipidemia and 7 (4.66%) patients have no dyslipidemia. The risk of stroke is increased slightly higher in hypertensive patients when concomitant dyslipidemia present (4.85% vs 4.66%). Among 103 dyslipidemic & hypertensive patients 6 (5.8%) patients have renal impairment and 150 non-dyslipidemic hypertensive patients 6 (4%) patients have renal impairment. 23 (9.09%) patients have proteinuria (p=0.027) of them 14 (13.6%) patients are dyslipidemic. 9(4.3%) patients have hypertensive retinopathy(p=0.028), of them 7(6.9%) patients are dyslipidemic.
Dyslipidemia is associated with increased blood pressure. Raised TCL, LDL-C & TG and low HDL-C all are associated with increased incidence of hypertension. Hypertensive patients with dyslipidemia are prone to develop target organ damage.
TABLE OF CONTENTS
TITLE OF THE CONTENTS PAGE NO.
CHAPTER ONE: INTRODUCTION 11
1.1 Background 12
1.2 Rationale of study 16
1.3 Aims and objective 17
1.4.0 Literature review 18
1.4.1 Epidemiology of Hypertension 18
1.4.2 Epidemiology of Dyslipidemia 19
1.4.3 Mechanism of Essential Hypertension 20
1.4.4 Measurement of Blood Pressure 22
1.4.5 Classification of Hypertension 23
1.4.6 Clinical features of Hypertension 24
1.4.7 Dyslipidaemia 26
1.4.8 Classification of Dyslipidaemia 28
1.4.9 Target organ involvement 32
1.4.10 Treatment of Hypertension 35
1.4.11 Treatment of Dyslipidemia 43
CHAPTER TWO: MATERIALS AND METHODS 50
2.1 Study design 51
2.2 Place of study 51
2.3 Period of study 51
2.4 Study population 51
2.5 Sample Size 51
2.6 Method of estimating sample size 51
2.7 Selection Criteria 53
2.8 Operational Definitions 54
2.9 Ethical measure 55
2.10 Data Collection and Sampling Technique 55
2.11 Methods of data processing and statistical analysis 55
CHAPTER THREE: RESULT 56
CHAPTER FOUR: DISCUSSION 80
LIMITATION OF STUDY 90
LIST OF THE TABLES
Table no. Title of the tables Page no.
Table 1.1: Classification of blood pressure 23
Table 3.1: Age frequency of the study subjects 57
Table 3.2 : Sex frequency of study subjects 57
Table 3.3: Residence frequency of the study subjects 58
Table 3.4: Frequency of religion of the study subjects 58
Table 3.5: Frequency of Educational qualification of the study subjects 59
Table3.6: Frequency of occupational of the study subjects 59
Table 3.7: Monthly income of family of the study subjects 60
Table 3.8: Marital status of the study subjects 60
Table 3.9: Number of family members of the study subjects 61
Table 3.10 : Family history of diseases of the study subjects 61
Table 3.11: Smoking status of the study subjects 62
Table 3.12: Duration of smoking of the study subjects 62
Table 3.13 : Duration of hypertension during presentation of the study subjects 63
Table 3.14: Stage of hypertension at presentation of the study subjects 63
Table 3.15: Systolic and diastolic blood pressure at presentation of the study subjects 63
Table 3.16: BMI evaluation of the study subjects 64
Table 3.17: Frequency of Dyslipidemia in different stages of BP 64
Table 3.18: Relation of Hypertension and BMI with Dyslipidemia 65
Table 3.19: Total cholesterol (TCL) estimation and evaluation 67
Low density lipoprotein cholesterol (LDL-C) estimation and evaluation.
Table 3.21: High density lipoprotein cholesterol (HDL-C) estimation and evaluation 71
Table 3.22: Triglyceride(TG) estimation and evaluation 73
Table 3.23: Relation of Blood pressure and Dyslipidemia with BMI 75
Table 3.24: Relationship among dyslipidemia, hypertension, sex and target organ damage 77
LIST OF FIGURES
Figure no. Title of figure Page no.
Figure 1.1 Algorithm for treatment of hypertension
Figure 1.2 Algorithm for treatment of dyslipidemia
At first I wish to express my gratitude to the almighty Allah, for his kindness to complete this article in time.
This is my great pleasure to express profound gratitude and in datedness to my respected teacher Professor Dr. Md. Zakir Hossain FCPS, MD, FACP (Internal Medicine), Professor of Medicine and Head of the Department of Medicine, Rangpur Medical College Hospital for his active guidance, constant supervision , constructive criticism and valuable suggestions which make this study possible.
I feel special pleasure to express my deep gratefulness to Professor Dr. Laique Ahmed Khan MD (Endocrinology), Professor of Endocrinology, Department of Endocrinology, Rangpur Medical College Hospital for his valuable suggestions.
It is my pleasant duty to thank Dr. Md. Ashraful Haque, Assistant Professor, Dept of Medicine, Rangpur Medical College Hospital, Dr. Md. Mahfuzer Rahman, Assistant Professor, Dept of Medicine, Rangpur Medical College Hospital and Dr. Md. Mokhlesur Rahman Sarker, MD student (Internal Medicine) Rangpur Medical College Hospital for their keen interest and assistance in my study.
Finally I would like to thank all the stuffs of Hypertension & Research Centre, Rangpur for their nice co-operation and hospitality.
Dr. Al Amin Md. Mamun Ibne Ashrafi
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 well1. Hypertension might be defined as that level of blood pressure at which the institution of therapy reduces blood pressure related morbidity and mortality. Current clinical criteria for defining hypertension are generally based on the average of two or more seated blood pressure readings during each of two or more outpatient visits2. According to Seventh report of Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure, Normal blood pressure is <120/80 mm of Hg. When systolic blood pressure (SBP) is 120-139 mm of Hg and diastolic blood pressure (DBP) is 80-89 mm of Hg it is called pre-hypertension. When SBP 140-159 mm of Hg and DBP 90-99 mm of Hg it is Stage-1 hypertension; and SBP >160 mm of Hg and DBP >100 mm of Hg it is Stage-2 Hypertension3.
Although several risk factors for the development of hypertension have been identified4 its etiology is still not fully understood3. About 80–95% of hypertensive patients are essential or primary or idiopathic hypertension. Remaining 5–20% of hypertensive patients are secondary hypertension2. Causes of secondary hypertension include alcohol, obesity, pregnancy, renal disease (i.e. chronic kidney disease, polycystic kidney disease) endocrine disease (i.e. phaeochromocytoma, primary hypothyroidism), coarctation of aorta, drugs etc5.
Hypertension is commonly associated with other cardiovascular risk factors, such as obesity, diabetes, and dyslipidemia6. The presence of these cardiovascular risk factors and the resulting endothelial dysfunction may play a role in the pathophysiology of hypertension7. Dyslipidemia, a strong predictor of cardiovascular disease8, causes endothelial damage9,10,11, and the loss of physiological vasomotor activity that results from endothelial damage may become manifested as increased blood pressure (BP). Therefore, factors like dyslipidemia that cause endothelial dysfunction may lead to hypertension. Cross-sectional studies have suggested a link between abnormal lipids and hypertension12,13. A few studies have prospectively examined the relationship between plasma lipids and the future development of hypertension, finding that there is an association between plasma lipids and development of hypertension12,13. Small trials have looked at the effect of lipid lowering on BP14,15.
One prospective study demonstrates that higher levels of plasma TC, non-HDL-C, and the TC/HDL-C ratio are independently associated with a subsequent increased risk of incident hypertension in apparently healthy men and that higher levels of HDL-C are associated with a decreased risk of incident hypertension. Elevated lipid levels appear to predate the onset of hypertension by years. The relationship between lipids and hypertension is preserved even after adjustment for multiple confounders and after the exclusion of men with diabetes and obesity16. Lipids and BP have been associated in several cross-sectional studies7,17,18. Castelli and Anderson17 found that BP and serum cholesterol were strongly correlated among hypertensive patients, which led to early recommendations to treat elevated cholesterol in patients with hypertension8,17. Gaziano et al19 also noted a potential interaction between elevated cholesterol and hypertension in the development of MI that suggested a direct relationship rather than the effect of 2 independent predictors.
Thus, plasma lipids may be useful in the identification risk for hypertension. Abnormalities in plasma lipoprotein metabolism play a central role in the pathogenesis of atherosclerosis and arterial hypertension.
Increased levels of atherogenic lipoproteins, especially LDL, but also IDL and possibly chylomicron remnants, contribute to the development of atherosclerosis. Increased plasma concentration and reduced diameter favor sub endothelial accumulation of these lipoproteins. Following chemical modifications such as oxidation, the lipoproteins are no longer cleared by normal mechanisms. They trigger a self-perpetuating inflammatory response during which they are taken up by macrophages to form foam cells-a hallmark of the atherosclerotic process. Low HDL cholesterol levels also predispose to atherosclerosis20. So there is correlation between abnormal lipids and hypertension16.
Hypertension is one of the 10 leading reported causes of death and about 4% deaths are due to hypertensive complications21. Cardiovascular disease risk doubles for every 20-mmHg increase in systolic and 10-mmHg increase in diastolic pressure, beginning at 115/75 mmHg2. The adverse effects of hypertension principally involve the blood vessels, central nervous system, retina, heart & kidneys and can often be detected clinically. Thus these organs are treated as target organ of hypertension 22. Manifestations of target organ damage are: in kidneys – proteinuria, nephrosclerosis, chronic kidney disease & end stage renal disease, in heart – left ventricular hypertrophy, coronary artery disease, angina, myocardial infarction, systolic dysfunction, diastolic dysfunction, chronic heart failure, atrial fibrillation & ventricular fibrillation, in brain- transient ischemic attack & stroke, in eye- retinopathy 23. Hypertension is a risk factor for stroke, myocardial infarction, renal failure, congestive cardiac failure, progressive atherosclerosis and dementia24.
1.2 Rationale of the study
Dyslipidemia, a strong predictor of cardiovascular disease and Elevated lipid levels appear to predate the onset of hypertension by years. Abnormalities in plasma lipoprotein metabolism play a central role in the pathogenesis of atherosclerosis and arterial hypertension. Current guidelines for the management of hypertension and dyslipidemia have focused on the need to set lipid targets to reduce the blood pressure and other cardiovascular risks25.
1.3 Aims and Objectives
To evaluate the status of lipid profile in newly detected Hypertensive patients.
1. To estimate Total Cholesterol (TC), High-density Lipoprotein Cholesterol
(HDL-C), Low-density Lipoprotein Cholesterol (LDL-C) and Triglyceride (TG)
in newly detected hypertensive patients.
2. To evaluate the target organ damage in newly detected hypertensive with
or without dyslipidemia.
1.4.1 Epidemiology of Hypertension
The National Health and Nutritional Examination Survey (NHANES), which has been studying the health of representative samples of Americans since 1960, have provided data on the changing prevalence of hypertension and its control. According to this, the prevalence of hypertension decreased somewhat between 1960 and 199126, but the latest published analysis by the Centres for Disease Control and prevention (CDC) 27, based on data obtained in the period 1991 to 2002, reported that the prevalence had increased by 3.6 percent, and that 28.6 percent of participants had hypertension.
Surveys in Europe show much higher rates of hypertension28. A comparison of seven European countries’ data found the highest rate in Germany (55 percent), and the lowest in Italy (38 percent) with France, England, Spane and Sweden ll showing a prevalence between these two extremes. The prevalence in Canada is very similar to that in the United States (27 percent) 28. The reasons for these wide differences are unknown, but do not appear to be because of differences in measurements or sampling rates. In Egypt the rate is also approximately 25%, whereas in China, the rate is lower (14 percent), but is increasing rapidly29.
In the United States, hypertension is significantly more prevalent in African Americans than in whites. In the more recent NHANES survey, 30 the prevalence in African American men was 38.6 percent whereas in white men it was 29.6 percent; in women the prevalence was 44 percent for African Americans and 29.6 percents for whites. The big issue here is whether the higher prevalence is genetic or environmental. Although the prevalence is higher than the other countries, for example, Brazil31, there is a large literature showing that the rate as of hypertension in Africans living in traditional rural societies are relatively low, but increase markedly when they move to the cities32.
There are also differences in the prevalence of hypertension in other ethnic groups. Hypertension tends to be relatively uncommon in Japanese Americans, while Philippines have rates approaching those of American Americans33. In American Indians the prevalence of hypertension is similar to that of American whites, despite a higher prevalence of obesity34.
The incidence of hypertension in India is 5- 15% in the adult population against 10- 12% in the west 35. In Bangladesh overall prevalence of Systolic & Diastolic Hypertension in a study were 14.4 & 9.1 percent respectively36.In other study overall prevalence of Hypertension is 11.3% 37.
1.4.2 Epidemiology of Dyslipidemia
One case-control study shows that 40.5% patients of essential hypertension have elevated level of lipoprotein a level38. Familial dyslipidemic hypertension occurs in 12% of subjects with essential hypertension39. The prevalence of coronary artery disease was often more than doubled among patients with concomitant dyslipidemia and hypertension compared with patients with either condition alone40. Current guidelines for the management of hypertension and dyslipidemia have focused on the need to set lipid targets to reduce the blood pressure and other cardiovascular risks38.
1.4.3 Mechanism of Essential Hypertension2
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 the long term. Sodium is predominantly an extracellular ion and is a primary determinant of the extracellular fluid volume. When Nacl intake exceeds the capacity of the kidney 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 reverts to normal. The effect of sodium on blood pressure is related to the provision of sodium with chloride; non-chloride salts of sodium have little or no effect on blood pressure.
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 factors, contributes to the long-term regulation of arterial pressure. The three endogenous catecholamines are epinephrine, norepinephrine and dopamine. All three play important roles in tonic and phasic cardiovascular regulation.
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 rennin secretion: 1. Decreased Nacl transport in the thick ascending limb of the loop of Henle (macula densa mechanism). 2. Decreased pressure or stretch within the renal afferent arteriole (baroreceptor mechanism), and 3. Sympathetic nervous system stimulation of rennin-secreting cells via β1 adrenoceptors. Once released into the circulation, active rennin cleaves a substrate, angiotensinigen, to form angiotensin I. A converting enzyme located primarily but not exclusively in the pulmonary circulation, converts angioten I to the active angioten II, Acting primarily through angiotensin II type I receptors located on cell membranes, angiotensin II is a potent pressor substance, the primary trophic factor for the secretion of aldosterone by the adrenal zona glomerulosa, and a potent mitogen stimulating vascular smooth-muscle cell and myocyte growth.
1.4.4 Measurement of blood pressure41
Blood pressure should be measured with a well-calibrated sphygmomanometer. The bladder width within the cuff should encircle 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 5 minutes and at least 30 minutes after smoking or coffee ingestion. 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 reading is not sufficient to establish the diagnosis if hypertension. The major exceptions to this rule are hypertensive presentations with unequivocal evidence of life-threatening end-organ damage, as seen in hypertensive emergency, or in hypertensive urgency where blood pressure is >220/125 mm of Hg but life threatening end organ damage is absent. In less severe cases, the diagnosis of hypertension depends on a series of measurements of blood pressure, since readings can vary and tend to regress toward the mean with time. Patients whose initial blood pressure is in the hypertensive range exhibit the greatest fall toward the normal range between the first and second encounters. Although blood pressure readings may still show variability after the third visit, these later changes are mostly random. However, the concern for diagnostic precision needs to be balanced by an appreciation of the importance of establishing the diagnosis of hypertension as quickly as possible, since a 3-month delay in treatment of hypertension in high risk patients is associated with a twofold increase in cardiovascular morbidity and mortality.
1.4.5 Classification of Hypertension3
Table 1 provides a classification of blood pressure for adults aged 18 years or older. The classification based on the mean of 2 or more properly measured seated blood pressure reading s on each of 2 or more office visits. This classification is provided in JNC 7 report.
Patients with prehypertension are at increased risk for progression to hypertension; those in the 130/80 to 139/89 mm of Hg BP range are at twice the risk to develop hypertension as those with lower values.
TABLE 1. Classification of blood pressure for adults aged 18 years or older3
Class Systolic blood pressure
(mm of Hg) Diastolic blood pressure
(mm of Hg)
Normal <120 <80 Prehypertension 120-139 80-89 Stage 1 hypertension 140-159 90-99 Stage 2 hypertension ≥160 ≥100 1.4.6 Clinical Features of Hypertension42 Most patients with hypertension are asymptomatic, the high blood pressure usually having been noted during an incidental clinical examination. A proportion of patients present with a major complication 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. Signs suggestive of secondary hypertension • Features of endocrine abnormalities, particularly Cushing’s syndrome • Multiple neurofibromatoma- present in 5 percent of patients with pheochromocytoma • Inappropriate tachycardia, suggesting catecholamine excess • Abdominal or lion bruits, suggesting renal artery stenosis. • Renal enlargement suggestive of polycystic kidney disease. • Radio femoral delay, due to coarctation of aorta. Signs suggestive of target organ damage: • A forcible and displaced apex beat due to left ventricular hypertrophy. • Accentuation of aortic component of the second heart sound • Added heart sounds: A fourth heart sound may be audible, reflecting decreased ventricular compliance. As failure develops a third sound may occur. • Fundal examination to detect hypertensive retinopathy. Investigations: Routine investigation of all hypertensive patients should include • Urinanalysis: Proteinurea, hyaline and granular cast may be found where there is renal disease or malignant hypertension. There is little or no protein in the urine if patients with benign essential hypertension. • Blood urea: A raised level of urea suggests renal failure • 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. 1.4.7 Dyslipidemia According to The National Cholesterol Education Program (NCEP) Adult Treatment Panel 3 (ATP III) guidelines LDL cholesterol optimal is <100mg/dl; near optimal or above optimal 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 desirable is <200mg/dl; borderline high is 200-239mg/dl; high is ≥240mg/dl. HDL cholesterol low is<40mg/dl; high is >60 mg/dl. Triglyceride level <150mg/dl is normal; 150-199mg/dl is borderline high; 200-499mg/dl is high; 500mg/dl is very high. Blood sample must be collected after 9-12 hours fasting43. Lipids and cardiovascular disease5 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. Increased plasma concentration and reduced diameter favour sub endothelial accumulation of these lipoproteins. Following chemical modifications such as oxidation, the lipoproteins are no longer cleared by normal mechanisms. They trigger a self-perpetuating inflammatory response during which they are taken up by macrophages to form foam cells-a hallmark of the atherosclerotic process. Atherogenic lipoproteins also have an adverse effect on endothelial function. Low HDL cholesterol levels also predispose to atherosclerosis. Lipid measurement5 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), triglyceride (TG) and HDL cholesterol (HDL-C) should be obtained after a 12-hour fast to permit the calculation of LDL cholesterol (LDL-C) according to the Friedewald formula (LDL-C = TC - HDL-C - (TG/2.2) mmol/l). (Before the formula is applied, lipid levels in mg/dl can be converted to mmol/l by dividing by 38 for cholesterol and 88 for triglycerides.) The formula becomes unreliable when TG levels exceed 4 mmol/l (350 mg/dl). Non-fasting samples are unaffected in terms of TC and measured LDL-C, but they differ in terms of TG and HDL-C, and hence the calculation of LDL-C is invalidated. Consideration must be given to confounding factors such as recent illness, after which cholesterol levels temporarily decrease in proportion to severity. Measurements that will affect major decisions, such as initiation of drug therapy, should be confirmed with a repeat measurement 1.4.8 Classification of Dyslipidaemia5 1. Predominant hypercholesterolemia • Familial hypercholesterolaemia • Hyperalphalipoproteinaemia 2. Predominant hypertriglyceridaemia • Lipoprotein lipase deficiency • Familial hypertriglyceridaemia 3. Mixed hyperlipidaemia • Familial combined hyperlipidaemia • Dysbetalipoproteinaemia Predominant hypercholesterolaemia: Polygenic hypercholesterolaemia 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 hypercholesterolaemia (FH) : Familial hypercholesterolaemia (FH) causes moderate to severe hypercholesterolaemia with a prevalence of at least 0.2% in most populations. Most patients with these abnormalities exhibit LDL levels that are approximately twice as high as in unaffected subjects of the same age and gender. Family history reveals that approximately 50% of each generation suffers hypercholesterolaemia, often with very premature cardiovascular disease. FH may be accompanied by xanthomas of the Achilles or extensor digitorum tendons, which are strongly suggestive (but not pathognomonic) for FH. The onset of corneal arcus before age 40 is also suggestive of this condition. Hyperalphalipoproteinaemia Hyperalphalipoproteinaemia refers to increased levels of HDL-C. In the absence of an increase in LDL-C, this condition does not cause cardiovascular disease, so it should not be regarded as pathological. Predominant hypertriglyceridaemia Polygenic hypertriglyceridaemia 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 manifestations of the insulin resistance syndrome. It is often accompanied by post-prandial hyperlipidaemia and reduced HDL-C, both of which may contribute to cardiovascular risk. Excessive dietary fat intake or other exacerbating factors may precipitate a massive increase in TG levels, which, if they exceed 10 mmol/l (880 mg/dl), may pose a risk of acute pancreatitis. Lipoprotein lipase deficiency: Lipoprotein lipase deficiency is an infrequent autosomal recessive disorder due to hereditary deficiency of lipoprotein lipase or its co-factor, apolipoprotein C2. It causes massive hypertriglyceridaemia that is resistant to drug treatment. It may commence in childhood and is associated with episodes of acute abdominal pain and pancreatitis. In common with other causes of severe hypertriglyceridaemia, it may result in hepatosplenomegaly, lipaemia retinalis and eruptive xanthomas. Familial hypertriglyceridaemia: Familial hypertriglyceridaemia refers to dominant inheritance of pure hypertriglyceridaemia. 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. On the other hand, it predisposes to levels of hypertriglyceridaemia that are sufficient to pose a risk of pancreatitis. Mixed hyperlipidaemia It is difficult to define the distinction between predominant hyperlipidaemias and mixed hyperlipidaemia quantitatively. The term 'mixed' usually implies the presence of hypertriglyceridaemia as well as an increase in LDL or IDL. Treatment of massive hypertriglyceridaemia may improve TG faster than cholesterol, thus mimicking mixed hyperlipidaemia. Primary mixed hyperlipidaemia is usually polygenic and, like predominant hypertriglyceridaemia, often occurs in association with type 2 diabetes, impaired glucose tolerance, central obesity or other manifestations of the insulin resistance syndrome. Both components of mixed hyperlipidaemia may contribute to the risk of cardiovascular disease Familial combined hyperlipidaemia: Familial combined hyperlipidaemia is a dominantly inherited disorder caused by overproduction of atherogenic apolipoprotein B-containing lipoproteins. It results in elevation of cholesterol, TG or both in different family members at different times. It is associated with an increased risk of cardiovascular disease but it does not produce any pathognomonic physical signs. In practice, this relatively common condition is substantially modified by factors such as age and weight. It may not be a monogenic condition, but rather one end of a heterogeneous spectrum that overlaps with the insulin resistance syndrome. Dysbetalipoproteinaemia: Dysbetalipoproteinaemia (also referred to as type 3 hyperlipidaemia, broad-beta dyslipoproteinaemia or remnant hyperlipidaemia) involves accumulation of roughly equal molar levels of cholesterol and TG. It is caused by homozygous inheritance of the apolipoprotein E2 allele, which is the isoform least avidly recognized by the LDL receptor. In conjunction with other exacerbating factors such as obesity and diabetes, it leads to accumulation of atherogenic IDL and chylomicron remnants. Premature cardiovascular disease is common and it may also result in the formation of palmar xanthomas, tuberous xanthomas or tendon xanthomas. Miscellaneous and rare forms of hyperlipidaemia • Tangier disease • Apo AI deficiency • Apo AI Milano • Fish eye disease • LCAT deficiency • Sitosterolaemia • Cerebrotendinous xanthomatosis Several rare disturbances of lipid metabolism have been described. They provide important insights into lipid metabolism and its impact on risk of cardiovascular disease. Fish eye disease and Apo A1 Milano demonstrate that very low HDL levels do not necessarily cause cardiovascular disease, but Apo A1 deficiency, Tangier disease and LCAT deficiency demonstrate that low HDL-C can be atherogenic under some circumstances. Sitosterolaemia and cerebrotendinous xanthomatosis demonstrate that sterols other than cholesterol can cause xanthomas and cardiovascular disease, while abetalipoproteinaemia and hypobetalipoproteinaemia suggest that low levels of apolipoprotein B-containing lipoproteins reduce the risk of cardiovascular disease at the expense of fat-soluble vitamin deficiency, leading to retinal lesions and peripheral neuropathy. 1.4.9 Target organ involvement Hypertension leads to adverse events in the brain, heart and kidneys through two related mechanisms, both of which involve the effects of increased pressure on the arteries. The first is the effects on the structure and function of the heart and arteries, and the second is the acceleration of the development of atherosclerosis. The former is directly the result of blood pressure, where as the latter requires an interaction with other risk factors for the cardiovascular disease, most importantly cholesterol. Thus strokes are closely related to the direct effects of blood pressure, whereas ischaemic heart disease is related to atherosclerosis, and the relationship between blood pressure and events is steeper for stroke than for ischaemic heart disease events. In countries where cholesterol levels are low, such as Japan, strokes are common, but ischaemic heart disease events are not44. Heart: Ischaemic heart disease: The prospective studies 45 Collaboration of 61 studies found strong log-liner relationships between systolic and diastolic pressure and the risk of ischaemic heart disease events in fives declines of age, ranging from 40-49 to 80-89, such that for each 20 mm increase of systolic pressure there was a twofold increase of risk over a range from 115 to 180. For diastolic pressure, the risk doubled with a 10 mm of Hg increase over a range of 75 to 100 mm of Hg. There is an interactive effect between the various risk factors; thus the relationship between systolic pressure and ischaemic heart disease risk is much steeper in patients whose cholesterols high than in patients whom it is normal46. This relationship has been reported in several countries, although the slop of the line relating blood pressure and risk is shallower in countries where the overall risk of ischaemic heart disease is low, such as Japan47. Although it is well recognized that blood pressure is one of the three major risk factors for the development of ischaemic heart disease( the other two being high cholesterol and smoking ), it has been claimed that ischaemic heart disease often occur in patients who lack all of those risk factors. An analysis of three large prospective studies found that for both fatal and nonfatal myocardial infarctions, at least one of the big three was present in more than 90 percent of cases48. Heart failure: Heart failure is now the leading cause of hospitalization for people age 65 years and older in the United States, and unlike other complications of hypertension, its prevalence has been increasing over the past 30 years49. For a 40 yrs old man or woman, the “remaining lifetime risk” of developing heart failure is approximately 20 percent, a surprisingly high number, if subjects with known ischaemic heart disease are excluded, the risk is 11 percent in men and 15 percent in woman50. Blood pressure is a major contributor to this : The risk is twice as high in hypertensive men as in normotensives, and three times as high in hypertensive women; 90 percent of new cases of heart failure in the Framingham Heart Study had a history of previous hypertension51.This risk is much more strongly related to systolic than diastolic pressure52. Treatment of hypertension in older people reduces the incidence of heart failure by approximately 50 percent53. The good news is that the incidence of heart failure is now decreasing in women (not in men), while survival has improved in both sexes54. Brain: Cerebrovascular disease: Stroke is the third most common cause of death throughout the world after ischaemic heart disease and cancer. Approximately 80 percent of strokes are ischaemic, 15 percents are hemorrhagic, and 5 percent are caused by subarachnoid hemorrhage55. As with coronary events, there is a strong long linear relationship between both systolic and diastolic pressure and stroke, although the relationship is steeper for strokes than ischaemic heart disease events, and much stronger for systolic than diastolic pressure56. Approximately 60 percent of patients who present with strokes have a past history of hypertension and in those who are hypertensive, approximately 78 percent have not had their blood pressure adequately controlled57. Kidney: Chronic kidney disease: A Japanese study of nearly 100,000 men and women found a progressive relationship between the height of the blood pressure and the risk of developing end-stage renal disease during a 17 year follow-up period, such that there was an increased risk even in patients with high normal blood pressure, in comparison with those whose pressure was optimal (less than 120/80 mm of Hg) 58. Hypertensive patients whose blood pressure is not well controlled are more likely to show a deterioration of renal function59. A prospective analysis of the MRFIT study also found that blood pressure was closely related to the likelihood of developing end-stage renal disease60. Hypertensive patients with mildly impaired renal function (estimated GFR <60 ml/min) have an increased prevalence of target organ damage such as left ventricular hypertrophy, increased carotid intima-media thickness, and microalbuminuria61. Peripheral Vascular Disease: Hypertension is a major risk factor for peripheral vascular disease. This is important for two reasons: first, it causes debilitating symptoms, and second, it is a marker of high risk for cardiovascular events62. It is strongly associated with the risk factors of atherosclerotic disease-blood pressure, smoking, cholesterol, diabetes and most importantly, age. In a study of the Framingham Offspring the strongest risk factor for peripheral vascular disease was age, followed by hypertension, and smoking63. Retina: The optic fundi reveal a gradation of changes linked to the severity of hypertension; fundoscopy can, therefore, provide an indication of the arteriolar damage elsewhere. Cotton wool exudates are associated with retinal ischaemia or infarction, and fade in a few weeks. Hypertension is also associated with central retinal vein thrombosis22. 1.4.10 Treatment of Hypertension Goals of therapy: The ultimate public health goal of antihypertensive therapy is the reduction of cardiovascular and renal mortality and morbidity. Because most patients with hypertension, especially those aged at least 50 years, will reach the diastolic blood pressure goal once systolic blood pressure is at goal, the primary focus should be on achieving the systolic blood pressure goal. Treating systolic and diastolic blood pressure to targets that are less than 140/90 mm of Hg is associated with a decrease in cardiovascular complications. In patients with hypertension with diabetes or renal disease, the blood pressure goal is less than 130/80 mm of Hg. The goal may be achieved by life style modification, alone or with pharmacological treatment. FIGURE 1: Algorithm for treatment of hypertension3 Life style modification: Recent controlled trials have confirmed that lifestyle changes can lower blood pressure64-67. Lifestyle interventions reduce the need for drug therapy, enhance the antihypertensive effects of drugs, and favorably influence overall CVD risk3. A DASH (Dietary Approach to stop Hypertension) diet, rich in fruits, vegetables, and low-fat dairy products with a reduced content of dietary cholesterol as well as saturated and total fat is helpful in lowering blood pressure69. It is also rich in potassium and calcium. Patients should be instructed in methods to reduce dietary salt to <6 gm/day70. Regular aerobic physical activities such as brisk walking at least 30 minutes per day most days of the week should become part of the hypertensive patient’s life. Alcohol intake should be limited to no more than 30 ml of ethanol, the equivalent of two drinks, per day in most men, and no more than 15 ml of ethanol ( one drink) per day in women and lighter weight persons. For overall cardiovascular risk reduction, patients should be strongly counseled to stop smoking. Pharmacological treatment3: Excellent clinical trial outcome data prove that lowering BP with several classes of drugs including ACE inhibitors, ARBs, β-blockers, CCBs and thiazide-type diuretics, will all reduce the complications of hypertension. Diuretics enhance the antihypertensive efficacy of multidrug regimens, can be useful in achieving BP control, and are more affordable than other antihypertensive agents. Despite these findings, diuretics remain underused. Thiazide-type diuretics should be used as initial therapy for most patients with hypertension, either alone or in combination with one of the other classes (ACE inhibitors, ARBs, β-blockers, CCBs) demonstrated to be beneficial in randomized controlled outcome trials. If a drug is not tolerated or is contraindicated, then one of the other classes proven to reduce cardiovascular events should be used instead. If a drug is not tolerated or is contraindicated, then one of the other classes proven to reduce cardiovascular events should be used instead. Achieving BP control in individual patients: Most patients with hypertension will require two or more antihypertensive medications to achieve their BP goals. Addition of a second drug from a different class should be initiated when use of a single drug in adequate dose fail to achieve the BP goal. When BP is more than 20/10 mm of Hg above the goal, consideration should be to initiating therapy with two drugs, either as separate prescriptions or infixed dose combinations. The initiation of drug therapy with more than one agent may increase the likelihood of achieving the BP goal in a more timely fashion, but particular caution is advised in those at risk for orthostatic hypotension, such as patients with diabetes, autonomic dysfunction, and some older persons. Use of generic drugs or combination drugs should be considered to reduce prescription costs. Follow- up and monitoring: Once antihypertensive drug therapy initiated, most patients should return for follow-up and adjustment of medication at approximately monthly interval until the BP goal is reached. More frequent visit will be necessary for patients with stage two hypertension or with complicating co morbid conditions. Serum potassium and creatinine should be monitored at least one or two times per year. After BP is at goal and stable, follow up visit usually be at three to six months intervals. Co morbidities, such as heart failure, associated diseases, such as diabetes and the need for laboratory tests influence the frequency of visits. Other cardiovascular risk factors should be treated to their respective goals, and tobacco avoidance should be promoted vigorously. Low dose aspirin therapy should be considered only when BP is controlled, because the risk of haemorrhagic stroke is increased in patients with uncontrolled hypertension. Special considerations: The patient with hypertension and certain co morbidities requires special attention and follow-up by the clinician. Compelling indication of drugs: Ischaemic heart disease: Ischaemic heart disease is the most common form of target organ damage associated with hypertension. In patient with hypertension and stable angina pectoris, the first drug of choice is usually a β-blocker; alternatively, long-acting CCB can be used. In patient with acute coronary syndrome (unstable angina or acute myocardial infarction), hypertension should be treated with β-blockers and ACE inhibitors, with addition of other drugs as needed for BP control. In patient with post myocardial infarction, ACE inhibitors, β-blockers and aldosteron antagonists have proven to be most beneficial. Intensive lipid management and aspirin therapy are also indicated. Heart failure: Heart failure is the form of systolic or diastolic ventricular dysfunction, results primarily from systolic hypertension and ischaemic heart disease. Fastidious BP and cholesterol controls are the primary preventive measures for those at high risk for heart failure. In asymptomatic individual with demonstrable ventricular dysfunction ACE inhibitors β-blockers, are recommended. For those with symptomatic ventricular dysfunction or end-stage heart disease, ACE inhibitors, β-blockers, ARBs, and aldosteron antagonists are recommended along with loop diuretics. Diabetic hypertension: Combination of two or more drugs are usually needed to achieve the target BP of less than 130/80 mm of Hg. Thiazide diuretics, β-blockers, ACE inhibitors , ARBs and CCBs are beneficial in reducing CVD and stroke incidence in patients with diabetes. The ACE inhibitors or ARB-based treatments favorably affect the progression of diabetic nephropathy and reduce albuminuria and ARBs have been shown to reduce the progression to macroalbuminuria. Chronic kidney disease: In patients with chronic kidney disease, defined by either (1) reduced excretory function with an estimated glomerular filtration rate of <60 ml/min per 1.73 squire meter (Corresponding approximately to a creatinine of >1.5 mg/dl) or (2) the presence of albuminuria (> 300 mg/day or 200mg albumin per gram of creatinine), therapeutic goals are to slow deterioration of renal function and prevent CVD. Hypertension appears in the majority of these patients and they should receive aggressive BP management, often with three or more drugs to reach target BP values of <130/80 mm of Hg. The ACE inhibitors and ARBs have demonstrated favorable effect on the progression of diabetic and non-diabetic renal disease. A limited increase in serum creatinine of as much as 35% above baseline with ACE inhibitors or ARBs is acceptable and not a reason to withhold treatment unless hyperkalaemia develops. With advanced renal disease (estimated glomerular filtration rate <30 ml/min per 1.73 square meter, corresponding to a serum creatinine of 2.5-3.0mg/dl), increasing doses of loop diuretics are usually needed in combination with other drug classes. Cerebrovascular disease: The risk and benefits of acute lowering of BP during an acute stroke are still unclear; control of BP at intermediate levels (approximately 160/100 mm of Hg) is appropriate until the condition has stabilized or improved. Recurrent stroke rates are lowered by the combination of an ACE inhibitors and thiazide-type diuretic. Other special situations Left ventricular hypertrophy: Left ventricular hypertrophy is an independent risk factor that increases the risk of subsequent CVD. Regression of left ventricular hypertrophy occurs with aggressive BP management, including weight loss, sodium restriction and treatment with all classes of anti-hypertensive agents except the direct vasodilators, hydralazine and minoxidil. Peripheral arterial disease: Peripheral arterial disease is equivalent risk to ischaemic heart disease. Any class of antihypertensive drugs can be used in most patients with peripheral arterial disease. Other risk factors should be managed aggressively and aspirin should be used. Hypertension in older individuals: Hypertension occurs in more than two thirds of individuals after 65 years. This is also the population with the lowest rates of BP control. Treatment recommendation for older individuals with hypertension, including those who have isolated systolic hypertension, should follow the same principles outline for the general care of hypertension. Many individuals lower initial drug doses may be indicated to avoid symptoms; however, standard doses and multiple drugs are needed in the majority of older individuals to reach appropriate BP targets. Postural hypotension: A decrease in standing systolic BP of more than 10 mm of Hg , when associated with dizziness or fainting, is more frequent in older patients with systolic hypertension , diabetes and those taking diuretics, venodilators (e.g. nitrates, α-blockers and sindenafil like drugs), and some psychotropic drugs. Blood pressure in these individuals should also be monitored in the upright position. Caution should be taken to avoid volume depletion and excessively rapid dose titration of antihypertensive drugs. Hypertension in women: Oral contraceptives may increase BP and the risk of hypertension increases duration of use. Women taking oral contraceptives should have their BP checked regularly. Development of hypertension is a reason to consider other forms of contraception. In contrast, hormone replacement therapy dose not raise BP. Women with hypertension who become pregnant should be followed carefully because of increased risk to mother and fetus. Methyl-dopa, β-blockers, and vasodilators are preferred medications for the safety of the fetus. Angiotensin converting enzyme inhibitors and ARBs should not be used during pregnancy because of the potential for fetal defects and should be avoided in women who are likely to become pregnant. Pre-eclampsia, which occurs after the 20th gestation weeks of pregnancy, is characterized by new onset or worsening hypertension, albuminura and hyperureceamia, sometimes with coagulation defects. In some patients, preeclampsia may develop into a hypertensive emergency or urgency and may require hospitalization, intensive monitoring, early fetal delivery and parenteral antihypertensive and anticonvulsant therapy. Hypertensive urgencies and emergencies: Patients with marked BP elevations and acute target organs damage (e.g. encephalopathy, myocardial infarction, unstable angina, eclampsia, pulmonary oedema, stroke, head trauma, life threatening arterial bleeding or aortic dissection) require hospitalization and parenteral drug therapy. Patients with markedly elevated BP but without acute target organs damage usually do not require hospitalization but they should receive immediate combination oral antihypertensive therapy. They should be carefully evaluated and monitored for hypertension induced heart and kidney damage and for identifiable causes of hypertension. Additional consideration in antihypertensive drugs choices: Antihypertensive drugs can have favorable or unfavorable effects on other co morbidities. Potential favorable effects: Thiazide type diuretics are useful in slowing demineralization in osteoporosis. Β-blockers can be useful in the treatment of tachyarrhythmias/fibrillation, migraine, thyrotoxicosis (short term), essential tremor, or perioperative hypertension. . Calcium channel blockers may be useful Reynaud’s syndrome and certain arrhythmias, and α-blockers may be useful in prostatism. Potential unfavorable effects: Thiazide diuretics should be used cautiously in patients who have gout, or who have a history of significant hyponatraemia. Β-blockers should generally be avoided in individual who have asthma, reactive airway disease, or second or third degree heart block. Angiotensin converting enzyme inhibitors and ARBs should not be given to woman likely to become pregnant and are contraindicated in individuals with history of angioedema. Aldosterone antagonists and potassium sparing diuretics can cause hyperkalaemia and generally be avoided in patients who have serum potassium values of more than 5.0 mEq/L, while not taking medications. 1.4.11 Treatment of dyslipidemia5 Lipid-lowering therapies have a key role in the secondary and primary prevention of cardiovascular diseases. Assessment of absolute risk, treatment of all modifiable risk factors and optimization of lifestyle factors, especially diet and exercise, are central to management in all cases. Non-pharmacological treatment Patients with lipid abnormalities should receive medical advice and, if necessary, dietary counseling to: • reduce intake of saturated and trans-unsaturated fat to less than 7-10% of total energy • reduce the intake of cholesterol to less than 250 mg/day • replace sources of saturated fat and cholesterol with alternative foods such as lean meat, low-fat dairy products, polyunsaturated spreads and low glycaemic index carbohydrates • reduce energy-dense foods such as fats and soft drinks, whilst increasing activity and exercise to achieve stable or negative energy balance (i.e. weight maintenance or weight loss) • increase consumption of cardioprotective and nutrient-dense foods such as vegetables, unrefined carbohydrates, fish, pulses, legumes, fruit etc. • adjust alcohol consumption, reducing intake if excessive or if associated with hypertension, hypertriglyceridaemia or central obesity • achieve additional benefits with supplementary intake of foods containing lipid-lowering nutrients such as n-3 fatty acids, dietary fibre and plant sterols. Response to diet is usually apparent within 3-4 weeks but dietary adjustment may need to be introduced gradually. Hyperlipidaemia in general and hypertriglyceridaemia in particular, can be very responsive to these measures. Explanation, encouragement and other measures should be undertaken to reinforce patient compliance. Even minor weight loss can substantially reduce cardiovascular risk, especially in centrally obese patients All other modifiable cardiovascular risk factors should be assessed and treated. Where possible, intercurrent drug treatments that adversely affect the lipid profile should be replaced. Pharmacological management The main diagnostic categories provide a useful framework for management and the selection of first-line pharmacological treatment FIGURE 2: Algorithm for treatment of dyslipidemia *Interrupted treatment if CK >5-10 times the upper limit of normal, or if elevated with muscle symptoms, or if ALT > 2-3 times the upper limit.
Predominant hypercholesterolaemia is treated with one or more of the cholesterol-lowering drugs.
HMG Co A reductase inhibitors (statins):
Statins inhibit cholesterol synthesis, thereby up-regulating activity of the LDL receptor. This increases clearance of LDL and its precursor, IDL, thereby causing a secondary reduction in LDL synthesis. As a result, statins reduce LDL-C by up to 60%, reduce TG by up to 40% and increase HDL-C by up to 10%. They also reduce the concentration of intermediate metabolites such as isoprenes, which may lead to other effects such as suppression of the inflammatory response. There is clear evidence of protection against stroke, and total and coronary mortality, as well as a reduction in cardiovascular events in high-risk patients.
Statins are generally well tolerated and serious side-effects are rare (well below 2%). Myalgia, asymptomatic increase in creatine kinase (CK), myositis and, infrequently, rhabdomyolysis are the most important category, along with liver function test abnormalities. Side-effects are more likely in patients who are elderly, debilitated or receiving other drugs that interfere with statin degradation, which usually involves cytochrome P450 3A4.
Cholesterol absorption inhibitors, such as ezetimibe
These inhibit the intestinal mucosal transporter NPC1L1 that absorbs dietary and biliary cholesterol. Depletion of hepatic cholesterol up-regulates hepatic LDL receptor activity. This mechanism of action is synergistic with the effect of statins. Monotherapy with the standard 10 mg/day dose reduces LDL-C by 15-20%. Slightly greater (17-25%) incremental LDL-C reduction occurs when ezetimibe is added to statins. Experience with ezetimibe is limited but it seems to be well tolerated. Its effect on cardiovascular disease endpoints is yet to be determined. Plant sterol-supplemented foods, which also reduce cholesterol absorption, lower LDL-C by 7-15%.
Bile acid sequestering resins, such as colestyramine and colestipol
These prevent the reabsorption of bile acids, thereby increasing de novo bile acid synthesis from hepatic cholesterol. As with ezetimibe, the resultant depletion of hepatic cholesterol up-regulates LDL receptor activity and reduces LDL-C in a manner that is synergistic with the action of statins. High doses (24 g/day colestyramine) can achieve substantial reductions in LDL-C and modest increases in HDL-C, but TG may rise. Resins are safe, but they are poorly tolerated because of their gastrointestinal effects and they may interfere with bio-availability of other drugs. New formulations and specific inhibitors of the intestinal bile acid transporter may improve tolerability and rekindle interest in this class of agents.
Nicotinic acid (vitamin B3)
In pharmacological doses, this reduces peripheral fatty acid release with the result that cholesterol and TG decline whilst HDL-C increases. Flushing occurs universally, and other side-effects include gastric irritation, liver function disturbances and exacerbation of gout and hyperglycemia. Slow-release formulations and low-dose aspirin may reduce flushing. Trials suggest a beneficial effect on atherosclerosis and cardiovascular events.
Routine treatment of predominant hypercholesterolaemia generally requires continuation of diet plus the use of a statin in sufficient doses to achieve target LDL-C levels. Therapy may have to be interrupted or ceased if there are clear-cut muscle side-effects, CK elevation beyond 10 times the upper limit of normal, or sustained ALT elevation beyond 2-3 times the upper limit of normal (and not accounted for by fatty liver. Patients who do not reach LDL targets on the highest tolerated statin dose may receive ezetimibe, plant sterols, nicotinic acid or resins, and these agents may also be added when patients are intolerant of statins. Nicotinic acid may also be used as an alternative in statin intolerance. It is also very effective in combination with a statin, but caution is required because the risk of side-effects is increased. Post-menopausal oestrogen replacement therapy, which may reduce LDL-C and increase HDL-C and TG, is no longer recommended for cardiovascular disease prevention.
Predominant hypertriglyceridaemia is treated with one of the triglyceride-lowering drugs.
These stimulate peroxisome proliferator activated receptor (PPAR)-alpha, which controls the expression of gene products that mediate the metabolism of
Fewer large-scale trials have been conducted with fibrates than with statins, but reduced rates of cardiovascular disease have been reported in studies amongst patients with low HDL-C levels and in subgroups of patients with the clinical picture of insulin resistance. The FIELD trial suggests that fibrates represent selective adjuvant therapy rather than first-line lipid-lowering therapy in most patients with type 2 diabetes. Fibrates are generally well tolerated but they exhibit a similar profile and frequency of side-effects as statins, including myalgia, myopathy and abnormal liver function tests. In addition, they may increase the risk of cholelithiasis and prolong the action of anticoagulants.
Highly polyunsaturated long-chain n-3 fatty acids
Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) comprise approximately 30% of the fatty acids in fish oil. EPA and DHA are potent inhibitors of VLDL TG formation. Intakes of greater than 2 g n-3 fatty acid (equivalent to 6 g of most forms of fish oil) per day lower TG in a dose-dependent fashion. Up to 50% reduction in TG may be achieved with 15 g fish oil per day or fish oil concentrates. Changes in LDL-C and HDL-C are variable. Fish oil fatty acids have also been shown to inhibit platelet aggregation and improve models of ventricular arrhythmia. Dietary and pharmacological trials indicate that n-3 fatty acids reduce mortality from coronary heart disease. Fish oils appear to be safe and well tolerated.
Patients with predominant hypertriglyceridaemia who do not respond to lifestyle intervention can be treated with fibrates, fish oil or nicotinic acid, depending on individual response and tolerance. If target levels are not achieved, the fibrates or nicotinic acid and fish oil can be combined. Massive hypertriglyceridaemia may require more aggressive limitation of dietary fat intake (< 10-20% energy as fat). Any degree of insulin deficiency should be corrected because insulin is required for optimal activity of lipoprotein lipase. The initial target for patients with massive hypertriglyceridaemia is TG < 10 mmol/l (880 mg/dl), to reduce the risk of acute pancreatitis. Mixed hyperlipidaemia Mixed hyperlipidaemia can be difficult to treat. Statins alone are less effective first-line therapy once fasting TG exceeds approximately 4 mmol/l (∼350 mg/dl). Fibrates alone are first-line therapy for dysbetalipoproteinaemia, but they may not control the cholesterol component in other forms of mixed hyperlipidaemia. Combination therapy is often required. Statin plus fish oil is relatively safe and effective when TG is not too high and in future fibrate plus ezetimibe may be effective. Statin plus nicotinic acid or statin plus fibrate is effective, but the risk of myopathy is greater. Monitoring of therapy The effect of drug therapy can be assessed after 6 weeks (12 weeks for fibrates), and it is prudent to review side-effects, lipid response, CK and liver function tests at this stage. Follow-up should encourage continued compliance (especially diet and exercise), monitoring for side-effects and cardiovascular symptoms or signs, measurement of weight, blood pressure and lipids as well as review of absolute cardiovascular disease risk status. Some special issues relevant to treating hyperlipidaemia in the elderly are given in. 2.1 Study design: Descriptive and cross sectional study 2.2 Place of study: Hypertension and Research centre, Rangpur 2.3 Period of study: 1st July 2010 to 30th June 2011 2.4 Study Population: Hypertensive patients attending in outpatient department of Hypertension and Research centre, Rangpur. 2.5 Sample Size: 253 2.6 Method of estimating sample size: Sample size calculation: Sample size is calculated by following equation n=Z2 (p×q)/d2 Here, n=Sample size Z=Standard normal deviation at 95% confidence limit. It is1.96 p=Proportion of patients with hypertension having dyslipidemia =20.7(=20.7/100=0.207) In Bangladesh the prevalence of dyslipidemia in hypertensive patients is 20.7% according to NCEP Adult Treatment Panel 3 (ATP III) criteria for dyslipidemia43. q=1-p =1-0.207=0.793 d=Degree of precision=5 %( =5/100=0.05) So sample size is = [(1.96)2 (0.207× 0.793)] / (0.05)2 = (3.8416×0.164151)/0.0025 =0.6306024816/0.0025 =252.2409926 =253 2.7 Selection Criteria Inclusion Criteria: 1. Newly detected hypertensive patients attending in outpatient department of Hypertension and Research centre, Rangpur 2. Age ≥18 years. 3. Both sexes. 4. Patient who gives informed consent for the study 5. Patient who fulfils the diagnostic criteria for the study. Exclusion criteria: 1. Patient refuses to take part in the study. 2. Patients below 18 years 3. Patients with incomplete data. 2.8 Operational Definitions Newly detected hypertensive patient: There is no definition of newly detected hypertensive patient .But there are some evidence that a 3-month delay in treatment of hypertension in high-risk patients is associated with a two-fold increase in cardiovascular morbidity and mortality41.According to JNC-7 we may have a trial of life style modification alone for an unspecified time (6 to 12 months) before antihypertensive medication is prescribed, even for high-risk patients3. So we have defined those patients as newly detected hypertension patients who has diagnosed first time or within the last six months with or without taking drug. Dyslipidemia: Dyslipidemia is the term given to abnormalities in blood lipid levels71. According to The National Cholesterol Education Program (NCEP) Adult Treatment Panel 3 (ATP III) guidelines LDL cholesterol optimal is <100mg/dl; near optimal or above optimal 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 desirable is <200mg/dl; borderline high is 200-239mg/dl; high is ≥240mg/dl. HDL cholesterol low is<40mg/dl; high is >60 mg/dl. Triglyceride level <150mg/dl is normal; 150-199mg/dl is borderline high; 200-499mg/dl is high; 500mg/dl is very high. Blood sample must be collected after 9-12 hours fasting43. Body mass index (BMI): Body mass index (BMI) is calculated as the person's weight in kilograms divided by the square of his or her height in meters (kg/m2). For example, an adult weighing 70 kg with a height of 1.75 meters has a BMI of 70/1.752 = 22.9. This adjusts crudely for differences in body habitus, and provides the usual definition of severity of obesity. Normal BMI range is 18.5-24.9. When it is 25.0-29.9 person is overweight. BMI above 30 is considered obese. When 30.0-34.9 it is class I or moderate obesity, when 35.0-39.9 it is class II or severe obesity, when > 40.0 it is class III or very severe obesity72.
2.9 Ethical measure
All patients were given an explanation of the study, and informed consent was taken. The study did not involve any additional investigation procedures and significant risk as well as economic burden to the patients.
2.10 Data collection and sampling technique
Data was collected using a structured research instrument (data collection Format) containing the variables of interest. Purposive sampling method was followed as per inclusion and exclusion criteria. Evaluation of patient was based on history, physical examinations and investigations.
2.11 Methods of data processing and statistical analysis
All the data will be appropriately recorded in a computer in a tabulated form. After final scrutiny data will be processed and analyzed statistically using computer software SPSS (Statistical Package for Social Sciences) windows version 15. The test statistics to be used for analysis of data are descriptive statistics, Chi-square Test. The level of significance is 0.05 and p-value <0.05 was considered significant. Table 3.1: Age frequency of the study subjects Age(yrs) Frequency Percent Maximum(yrs) Minimum(yrs) Mean(yrs) (±SD) 20-29 13 5.1 30-39 58 22.9 40-49 93 36.8 85 20 46.01(11.09) 50-59 60 23.7 60-69 17 6.7 ≥70 12 4.7 All ages 253 100 This study shows 253 newly detected hypertensive patients who are between 20 to 85 years of age. The mean age of them is 46.01 years with SD 11.09. Among them majority are 30 to 59 years of age (211, 83.4%) that is majority are younger and middle aged. Table 3.2 : Sex frequency of the study subjects Sex Frequency Percent Male 151 59.7 Female 102 40.3 All 253 100 In this study out of 253 newly detected hypertensive patients 151 (59.7%) are male and 102(40.3) were female. The percentage of male patients is higher than female both stage I and stage II. Of 103 (40.7%) dyslipidemic patients 66 (64.1%) patients are male and 37(35.9%) patients are female. Table 3.3: Residence frequency of the study subjects Residence Frequency Percent Urban 132 52.2 Rural 121 47.8 All 253 100 Among the 253 patients 132(52.2%) patients are urban dweller and 121(47.8%) patients are rural dweller. Table 3.4: Frequency of religion of the study subjects (n=253) Religion Frequency Percent Muslim 237 93.7 Hindu 16 6.3 All 253 100 This study shows that among 253 participant 237(93.7%) are Muslim and remaining 16(6.3%) patients are Hindu. Majority are Muslim participants. Table 3.5: Frequency of Educational qualification of the study subjects Educational status Frequency Percent No education 9 3.6 Primary 56 22.1 Secondary 63 24.9 Higher secondary 27 10.7 Graduate 78 30.8 Postgraduate 20 7.9 All 253 100 Among the 253 patients 9 (3.6%) patients have no education, 56 (22.1%) completed primary education, 63(24.9%) completed secondary education 27(10.7%) completed higher secondary education, 78(30.8%) patients are graduate, 20(7.9%) patients completed post graduation. Majority of patients are educated. Table3.6: Frequency of occupational of the study subjects Occupation Frequency Percent Farmer 3 1.2 Service 100 39.5 Business man 40 15.8 House wife 89 35.2 Others 21 8.3 All 253 100.0 Among the 253 patients 3(1.2%) patients are farmer, 100(39.5%) patients are service man, 40(15.8%) patients are business man, 89(35.2%) patients are housewife, 21 (8.3%)patients are included in others group that is they are retired person, student etc. Table 3.7: Monthly income of family of the study subjects (n=253) Monthly Income(Taka) Frequency Percent < 5000 9 3.6 5,001-10,000 54 21.3 10,001-15,000 124 49.0 >15,000 66 26.1
Among 253 patients majority of patients’ family income is between 10,001 taka to 15,000 taka.
Table 3.8: Marital status of the study subjects
Marital status Frequency Percent
Married 250 98.8
Unmarried 2 0.8
Widow 1 0.4
All 253 100
Among 253 patients 250 (98.8%) patients are married 2 (0.8%) patients are unmarried, and 1(0.4%) patient is widow.
Table 3.9: Number of family members of the study subjects
Minimum Maximum Mean Standard Deviation(SD)
Among 253 patients 223(88.14%) patients have family members between 3-7. Maximum family member is 11 and minimum family member is 2.
Table 3.10 : Family history of diseases of the study subjects (n=253)
Family history of disease Family history of HTN Family history of Cardiac disease Family history of stroke Family history of DM Family history of Blindness
Present 177(70%) 56(22.1%) 60(23.7%) 73(28.9%) 2(0.8%)
Absent 76(30%) 197(77.9%) 193(76.3%) 180(71.1%) 251(99.2%)
Among 253 patients 177(70%) patients have family history of hypertension, 56 (22.1%) patients have family history of cardiac disease especially IHD, 60 (23,7%) patients have family history of Stroke, 73(28.9%) patients have family history of Diabetes mellitus and 2(0.8%) patients have family history of blindness due to hypertensive retinopathy.
Table 3.11: Smoking status of the study subjects (n=253)
Smoking status Frequency Percent
Non-smoker 179 70.8
Ex-smoker 7 2.8
Irregular smoker 7 2.8
Regular smoker 60 23.7
Table 3.12: Duration of smoking of the study subjects (n=253)
Duration of smoking Frequency Percent
No 179 70.8
≤ 10 pack years 40 15.8
11-20 pack years 31 12.3
21-30 pack years 3 1.2
In this study among 253 newly detected hypertensive patients 74 (29.2%) patients are smokers. Among them 40 (15.8%) patients smoked ≤ 10 pack years, 31 (12.3%) patients smoked 11-20 pack years and 3 (1.2%) patients smoked 21-30 pack years. 7 (2.76%) patients are considered ex-smoker that is they gave up smoking at least 2 years back. 67 (26.48%) patients are current smokers and of them 60 (23.71%) patients smoke regularly and 7 (2.76%) patients smoke irregularly.
Table 3.13 : Duration of hypertension during presentation of the study subjects
Duration Frequency Percent
<2 months 74 29.2 2months 1day-4 months 77 30.4 4months 1 day-6 months 102 40.3 All 253 100 Table 3.14: Stage of hypertension at presentation of the study subjects (n=253) BP on first detection Frequency Percent Stage 1 HTN 84 33.2 Stage 2 HTN 169 66.8 Table 3.15: Systolic and diastolic blood pressure at presentation of the study subjects Blood pressure Maximum (mm of Hg) Minimum (mm of Hg) Mean (mm of Hg) Standard Deviation Systolic BP 220 125 157.92 18.52 Diastolic BP 140 40 96.98 11.81 In this study among 253 newly detected hypertensive patients(Diagnosed as hypertension within six months) 74(%) patients are diagnosed as hypertension within 2 months, 77(%) patients are diagnosed as hypertension between 2-4 months and remaining 102(%) patients are Diagnosed as hypertension between 4-6 months. 84 (33.2%) patients are in stage I HTN and remaining 169 (66.8%) are in Stage II. Maximum Systolic blood pressure (SBP) is 220 mm of Hg, minimum SBP is 125 mm of Hg and mean SBP is 157.92 mm of Hg with standard deviation 18.52. Maximum Diastolic blood pressure (DBP) is 140 mm of Hg, minimum DBP is 40 mm of Hg and mean DBP was 96.98 mm of Hg with standard deviation 11.81. Table 3.16: BMI evaluation of the study subjects (n=253) BMI Frequency Percent Maximum Minimum Mean (±SD) Normal 107 42.3 25.50 (4.02) Overweight 109 43.1 Moderate obese 25 9.9 39.18 12.38 Severe obese 7 2.8 Underweight 5 2.0 Total 253 100 Among 253 hypertensive patients 107 (42.3%) patients have normal BMI, 109 (43.1%) patients are overweight or mild obese, 25 (9.9%) patients are moderately obese, 7 (2.8%) patients are severely obese, and surprisingly 5 (2.0%) patients are underweight. Maximum BMI is 39.18, minimum BMI is 12.38 and mean BMI is 25.50 with standard deviation 4.02. Majority of patients have BMI above normal (and most of them are in stage II HTN). Table 3.17: Frequency of Dyslipidemia in different stages of BP (n=253) Dyslipidemia status Frequency (%) Level of BP P value Stage I (%) Stage II (%) Present 103 (40.7%) 34(33) 69(67) P= 0.03 Absent 150 (59.3%) 50(33.3) 100(66.7) In this study among 253 newly detected hypertensive patients, 103 (40.7%) patients have dyslipidemia (p=0.03) and remaining 150(59.3%) patients have no dyslipidemia. Among 103 dyslipidemic patients 34(33%) are in stage I hypertension and 69(67%) patients are in stage II hypertension. Among 150 non-dyslipidemic patients 50(33.3%) are in stage I hypertension and 100(66.7%) patients are in stage II hypertension Among 103 dyslipidemic patients 34(33%) are in stage I hypertension and 69(67%) patients are in stage II hypertension. Their maximum systolic BP is 220 mm of Hg and minimum systolic BP is 130 mm of Hg with mean SBP is 158.34 with standard deviation 18.04. Maximum diastolic BP is 140 mm of Hg and minimum diastolic BP is 40 mm of Hg with mean DBP is 96.41mm of Hg with standard deviation 12.56. Maximum BMI is 36.68, minimum BMI is 16.39 and mean BMI is 25.88 with standard deviation 4.16. Among 150 dyslipidemic patients 50(33.3%) are in stage I hypertension and 100(66.7%) patients are in stage II hypertension. Their maximum systolic BP is 220 mm of Hg and minimum systolic BP is 125 mm of Hg with mean SBP is 157.63 with standard deviation 18.66. Maximum diastolic BP is 140 mm of Hg and minimum diastolic BP is 70 mm of Hg with mean DBP is 97.37mm of Hg with standard deviation is (11.29). Maximum BMI is 39.18, minimum BMI is 12.38 and mean BMI is 25.24 with standard deviation 3.92. Among 253 newly detected hypertensive patients, 182 (71.9%) patients have normal/desirable TCL level, 40 (15.8%) patients have borderline high and 31 (12.3%) patients have high TCL(p=0.45). Maximum TCL is 410 mg/dl; minimum TCL is 120 mg/dl and mean TCL is 193.12 mg/dl with standard deviation 38.80. Mean TCL level do not vary significantly between stages I and stage II groups. Among 253 newly detected hypertensive patients, 93 (36.8%) patients have optimal LDL-C, 116(45.8%) patients have near optimal or above optimal LDL-C, 30(11.9%) patients have borderline high LDL-C, 9 (3.6%) patients have high LDL-C and 5 (2%) patients have very high LDL-C (p=0.91). Maximum LDL-C level is 255 mg/dl, minimum LDL-C level is 50 mg/dl and mean LDL-C is 111.48 mg/dl with standard deviation 30.18. Among 253 hypertensive patients 44 (17.5%) patients have increased LDL-C level. Maximum and mean LDL-C levels are seen higher in stage II hypertensive patients. Among 253 newly detected hypertensive patients, 62 (24.5%) patients have low HDL-C level, 9 (3.6%) patients have high HDL-C level and 182 (71.9%) patients have normal HDL-C (p=0.52). Maximum HDL-C level is 67 mg/dl and minimum HDL-C level is 24 mg/dl and mean HDL-C level is 43.60 mg/dl with standard deviation 8.58. Mean HDL-C level is seen higher in stage I hypertensive group patients. Among 253 newly detected hypertensive patients, 144 (56.9%) patients have normal TG, 26 (10.3%) patients have borderline high TG, 74 (29.2%) patients have high TG and 9 (3.6%) patients have very high TG(p=0.1). Maximum TG level is 810 mg/dl, minimum TG level is 69 mg/dl and mean TG level is 194.96 mg/dl with standard deviation 112.68. Mean TG level is seen higher in Stage I hypertensive group patients. Among 253 hypertensive patients 107(42.3) patients have normal BMI, 109 (43.1%) patients are overweight or mild obese, 25(9.9%) patients are moderately obese, 7(2.8%) patients are severely obese, Surprisingly 5(2.0%) patients are underweight. Obviously majority of patients have BMI above normal. Again most of them are in stage II HTN. Dyslipidemia is also more in patients who had abnormal BMI (65 vs 38). Abnormal TCL level seen in 27(25.23%) patients among 107 patients who have normal BMI, 31(28.44%) patients among 109 patients who are overweight or mildly obese, 8(32%) patients among 25 patients who are moderately obese, 4(57.14%) patients among 7 patients who are severely obese, and 1(20%)patient among 5 patients who are underweight. High LDL level seen in 16(14.9%) patients among 107 normal BMI patients, 18(16.51%) patients among 109 overweight patients, 5(20%)patients among 25 moderately obese patients, 4 (57.14%)patients among 7 severely obese patients, and 1 (20%)patients among 5 underweight patients. HDL level seen low in 24(22.4%) patients among 107 normal BMI patients, 31(28.4%) patients among 109 overweight patients, 5(20%) patients among 25 moderately obese patients and 1 (20%) patients among 5 underweight patients. TG level is seen high in 41(38.31%) patients among 107 normal BMI patients, 51(46.78%) patients among 109 overweight patients, 11(44%) patients among 25 moderately obese patients 5(71%) patients among 7 severely obese patients and 1(20%) patients among 5 underweight patients. In this study, among 253 newly detected hypertensive patients 20 (7.90%) patients have IHD (p=0.51), of them 12 (4.74%) patients have dyslipidemia and 8 (3.16%) patients have no dyslipidemia. Among the 12 (11.6%) dyslipidemic patients 9 (8.7%) patients have anterior ischemia and 3 (2.9%) patients have inferior ischemia. Among 8 (5.3%) non-dyslipidemic patients 2 (1.3%) patients have anterior ischemia, 1 (0.7%) patient has lateral ischemia and 5 (7.3%) patients have inferior ischemia. 4 (1.9%) patients have systolic dysfunction (p=0.16) of them 3 (2.9%) have dyslipidemia and 1 (0.7%) have no dyslipidemia, All of them have mild systolic dysfunction. 6 (2.37%) patients have diastolic dysfunction (p=0.032), of them 5 (4.9%) patients have dyslipidemia and 1 (0.7%) patient have no dyslipidemia. On Echocardiogram and ECG 14 (5.53%) patients have LVH (p=0.065) of them 9 (8.7%) patients have dyslipidemia and 5 (3.3%) patients are not dyslipidemic. On chest X-ray 12 (4.74%) patients have cardiomegaly (p=0.06) of them 8 (7.8%) patients have dyslipidemia and 4(2.7%) patients do not have dyslipidemia. In this study, Of 253 patients total 12(4.74%) patients have stroke (p=0.8). Among 103 dyslipidemic hypertensive patients 5 (4.85%) patients have stroke, all of them have ischaemic stroke. Among 150 non-dyslipidemic hypertensive patients 7 (4.66%) patients have stroke, of them 5 (3.3%) patients have ischaemic stroke and 2(1.3%) patients have haemorrhagic stroke. Cumulatively among 253 patients total 12 (4.74%) patients have stroke of them 5 (4.85%) patients have dyslipidemia and 7(4.66%) patients have no dyslipidemia. So the risk of stroke is increased slightly higher in hypertensive patients when concomitant dyslipidemia present (4.85% vs 4.66%). In this study, among 103 dyslipidemic hypertensive patients 6(5.8%) patients have renal impairment and 150 non-dyslipidemic hypertensive patients 6(4%) patients have renal impairment. Cumulatively among 253 patients 12 (4.74%) patients have renal impairment (p=0.5). 23 (9.09%) patients have proteinuria (p=0.027)of them 14(13.6%) patients are dyslipidemic, of them 13 (%) patients have mild(+) proteinuria and 1(1%) patient has massive(+++) proteinuria and 9(6%) patients have proteinuria who are not dyslipidemic. Proteinuria is also more seen in dyslipidemic patients. In this study, 9(4.3%) patients have hypertensive retinopathy (p=0.028), Of them 7 patients are dyslipidemic. Among dyslipidemic patients 1(1%) patient have grade I retinopathy, 5(4.9%) patients have grade II hypertensive retinopathy and 1(1%) patient have grade III retinopathy. 2(1.3%) non-dyslipidemic patients have grade II retinopathy. 1 patient has diabetic retinopathy. Age frequency: This study shows 253 newly detected hypertensive patients who are between 20 to 85 years of age. The mean age of them is 46.01 years with SD 11.09. Among them majority are 30 to 59 years of age (211, 83.4%) that is majority are young and middle aged. When for the first time they are diagnosed as hypertensive 84 (33.2%) patients are in stage I HTN and remaining 169(66.8%) are in Stage II. In both stages majority of patients are in between 30 to 59 years of age. Dyslipidemia is more common in 30 to 59 years age groups 87 patients (84%). Obesity is more in this age group 129 (91.5%). The result of a study shows that increased age is associated with a significant increase in the prevalence of hypertension and especially systolic hypertension after aged 60 years. Increased obesity between age 30-50 years is associated with significant increased in diastolic blood pressure73. Another study shows the prevalence of hypertension among individuals aged >60, is 65.4 percent2. In this study, total 253 of newly detected hypertensive patients, most are in 30 to 60 years age group. The discrepancy may be due to the increased awareness of hypertension in middle aged people. And aged people are neglected in our society because of low socio-economic condition. But obesity in 30-59 age group matches with the hypertension in this study.
In this study out of 253 newly detected hypertensive patients 151 (59.7%) are male and 102(40.3) were female. The percentage of male patients is higher than female both stage I and stage II. Of 103 (40.7%) dyslipidemic patients 66 (64.1%) patients are male and 37(35.9%) patients are female.
Hypertension is more common in men than in women of same age. Sex differences in the prevalence of hypertension may be mainly attributed to the differences in dietary habits, lifestyle choices, sodium and potassium intakes, physical activity level, and some genetic polymorphisms74.
Smoking and hypertension:
In this study among 253 newly detected hypertensive patients 74 (29.3%) patients are smoker. Among them 40 (15.8%) patients smoked ≤ 10 pack years, 31 (12.3%) patients smoked 11-20 pack years and 3 (1.2%) patients smoked 21-30 pack year. 7 (2.76%) patients are considered ex-smoker that is they gave up smoking at least 2 years back. 67 (26.48%) patients are smoker and of them 60 (23.71%) patients smoke regularly and 7 (2.76%) patients irregularly.
A prospective study shows that cigarette smoking is modestly associated with an increased risk of developing hypertension.75,76
Family history of hypertension:
In a screening program, blood pressure measurements, family (parental) histories of hypertension and self evaluations of weight class are obtained for more than a half million people. Positive family history is associated with hypertension prevalence double that found in persons with negative history and is independent of weight. When overweight is also present, however hypertension prevalence is three to four times as high77.
In this study among 253 newly detected hypertensive patients, 177 (70%) patients have a family history of hypertension. So there is a strong association of hypertension with family history.
BMI and hypertension:
Higher BMI is associated with a higher prevalence of hypertension in all ethnic group78.
In this study among 253 newly detected hypertensive patients, 107 (42.3%) patients have normal BMI, 109 (43.1%) patients are overweight and only 32 (12.7%) patients are obese. Interestingly 5 (2%) patients are underweight, that is BMI <18.5. BMI and dyslipidemia Among 253 hypertensive patients 107 (42.3%) patients have normal BMI, 109 (43.1%) patients are overweight or mild obese, 25 (9.9%) patients are moderately obese, 7 (2.8%) patients are severely obese, and surprisingly 5 (2.0%) patients are underweight. Obviously majority of patients have BMI above normal and most of them are in stage II HTN. Dyslipidemia is also more in patients who have abnormal BMI (65 vs 38) (p= 0.037). Abnormal TCL level seen in 27 (25.23%) patients among 107 patients who have normal BMI, 31 (28.44%) patients among 109 patients who are overweight or mildly obese, 8 (32%) patients among 25 patients who are moderately obese, 4 (57.14%) patients among 7 patients who are severely obese, and 1 (20%) patient among 5 patients who are underweight. High LDL level seen in 16 (14.95%) patients among 107 normal BMI patients, 18 (16.51%) patients among 109 overweight patients, 5 (20%)patients among 25 moderately obese patients, 4 (57.14%)patients among 7 severely obese patients, and 1 (20%)patients among 5 underweight patients. HDL level seen low in 24 (22.4%) patients among 107 normal BMI patients, 31 (28.4%) patients among 109 overweight patients, 5 (20%) patients among 25 moderately obese patients and 1 (20%) patients among 5 underweight patients. TG level is seen high in 41 (38.31%) patients among 107 patients with normal BMI, 51 (46.78%) patients among 109 patients who are overweight, 11 (44%) patients among 25 patients who are moderately obese, 5 (71%) patients among 7 patients who are severely obese and 1 (20%) patients among 5 underweight patients. In recent findings from the Framingham Offspring79, indicate that BMI is linearly related to the total cholesterol, LDL cholesterol and triglyceride concentrations and is, however, inversely related with HDL cholesterol, especially in non-smoking men and women. It has been found that most of the co morbidities, which relates obesity to coronary artery disease, increases as BMI increases, and in this way they are associated to body fat distribution80. In this study, correlation between dyslipidemia and BMI is found and p value is statistically significant. Stage of hypertension at presentation: In this study among 253 newly detected hypertensive patients 84 (33.2%) patients are in stage I HTN and remaining 169 (66.8%) are in Stage II. Maximum Systolic blood pressure (SBP) is 220 mm of Hg, minimum SBP is 125 mm of Hg and mean SBP is 157.92 mm of Hg with standard deviation 18.52. Maximum Diastolic blood pressure (DBP) is 140 mm of Hg, minimum DBP is 40 mm of Hg and mean DBP was 96.98 mm of Hg with standard deviation 11.81. 27 (10.7%) patients did not take any treatment as they were diagnosed as hypertensive for the first time. 77 (30.4%) patients took irregular treatment and remaining 149 patients took regular treatment and they are diagnosed as hypertensive patient within six months. These findings are consistent with other data, such as those from a study involving patients with hypertension who are followed up regularly at Veterans Affairs Clinics, where free care and medications are provided. Only 25% of patients have well controlled blood pressure, and 40% have levels below 160/90 mm of Hg after three year follow up81. Dyslipidemia and hypertension: In this study among 253 newly detected hypertensive patients, 103 (40.7%) patients have dyslipidemia (p=.03) and remaining 150(59.3%) patients have no dyslipidemia. Among 103 dyslipidemic patients 34(33%) are in stage I hypertension and 69(67%) patients are in stage II hypertension. One case-control study shows that 40.5% patients of essential hypertension have elevated level of lipoprotein a level38. Familial dyslipidemia occurs in 12% of subjects with essential hypertension39. This data is consistent with this study and p value is statistically significant. Total cholesterol (TCL) and hypertension: Among 253 newly detected hypertensive patients, 182 (71.9%) patients have normal/desirable TCL level, 40 (15.8%) patients have borderline high and 31 (12.3%) patients have high TCL(p=0.45). Maximum TCL is 410 mg/dl, minimum TCL is 120 mg/dl and mean TCL is 193.12 mg/dl with standard deviation 38.80. Mean TCL level do not vary significantly between stages I and stage II groups. In this study TCL level is high in 28.1% (71) patients which is in between the above two studies. Low density lipoprotein cholesterol (LDL-C) and hypertension: Among 253 newly detected hypertensive patients, 93 (36.8%) patients have optimal LDL, 116(45.8%) patients have near optimal or above optimal LDL, 30(11.9%) patients have borderline high LDL, 9 (3.6%) patients have high LDL and 5 (2%) patients have very high LDL(p=0.91). Maximum LDL level is 255 mg/dl, minimum LDL level is 50 mg/dl and mean LDL is 111.48 mg/dl with standard deviation 30.18. Among 253 hypertensive patients 44 (17.5%) patients have increased LDL level. Maximum and mean LDL-C levels are seen higher in stage II hypertensive patients. High density lipoprotein cholesterol (HDL-C) and hypertension: 62 (24.5%) patients have low HDL level, 9 (3.6%) patients have high cholesterol level and 182 (71.9%) patients have normal HDL (p=0.52). Maximum HDL level is 67 mg/dl and minimum HDL level is 24 mg/dl and mean HDL level is 43.60 mg/dl with standard deviation 8.58. Mean HDL-C level is seen higher in stage I hypertensive group patients Triglyceride (TG) and hypertension: 144 (56.9%) patients have normal TG, 26 (10.3%) patients have borderline high TG, 74 (29.2%) patients have high TG and 9 (3.6%) patients have very high TG (p=0.1). Maximum TG level is 810 mg/dl, minimum TG level is 69 mg/dl and mean TG level is 194.96 mg/dl with standard deviation 112.68. Individual lipoprotein levels and their association with hypertension are not significant statistically except HDL-C, but as a whole dyslipidemia correlates with hypertension. Target organ damage: Hypertension and heart disease: For adults aged 40-69 years each 20 mm of Hg rise in usual systolic blood pressure or 10 mm rise in diastolic blood pressure doubles the risk of death from ischemic heart disease82. The INTERHEART study shows that 22% of heart attack in Western Europe are due to a history of high blood pressure and those with hypertension have almost twice the risk of a heart attack83. One study shows that, the percentage of IHD is higher in patients with hypertension and dyslipidemia84. In this study, among 253 newly detected hypertensive patients 20 (7.90%) patients have IHD (p=0.51), of them 12 (4.74%) patients have dyslipidemia and 8 (3.16%) patients have no dyslipidemia. Among the 12 (11.6%) dyslipidemic patients 9 (8.7%) patients have anterior ischemia and 3 (2.9%) patients have inferior ischemia. and among 8 (5.3%) non-dyslipidemic patients 2 (1.3%) patients have anterior ischemia, 1 (0.7%) patient has lateral ischemia and 5 (7.3%) patients have inferior ischemia. 4 (1.9%) patients have systolic dysfunction(p=0.16) of them 3 (2.9%) have dyslipidemia and 1 (0.7%) have no dyslipidemia, All of them have mild systolic dysfunction. 6 (2.37%) patients have diastolic dysfunction (p=0.032), of them 5 (4.9%) patients have dyslipidemia and 1 (0.7%) patient have no dyslipidemia.. On Echocardiogram and ECG 14 (5.53%) patients have LVH (p=0.065) of them 9 (8.7%) patients have dyslipidemia and 5 (3.3%) patients are not dyslipidemic. On chest X-ray 12 (4.74%) patients have cardiomegaly (p=0.06) of them 8 (7.8%) patients have dyslipidemia and 4(2.7%) patients do not have dyslipidemia. The discrepancy between INTERHEART study and this study probably patients are newly detected and have not got enough time for cardiac damage up to the mark. Another cause may be that study is done in European population, not in Asian. Another interesting point is that cardiac involvement is more in dyslipidemic hypertensive patients. Hypertension and stroke: Some author compared risk factors, clinical features, neuro-imaging, and outcome between hypertensive and non hypertensive ischaemic stroke patients. Atherothrombotic infarction and lacunar infarct were significantly more common in the hypertensive group, in which older age and a higher occurrence of previous cerebral infarction, hyperlipidemia, acute stroke onset, lacunar syndrome, and pons topography was also observed. Age of 85 years or older, valvular heart disease, and decreased consciousness were more common in non hypertensive patients. Hypertension was the main cardiovascular risk factor only for lacunar and atherothrombotic infarction, that is ischaemic stroke associated with small and large-artery disease85. Untreated hypertension is an important risk factor for hemorrhagic stroke. Study shows that among hypertensive subjects, approximately one fourth of hemorrhagic strokes would be prevented if all hypertensive subjects receive treatment86. In this study, among 253 patients total 12(4.74%) patients have stroke (p=0.8). Among 103 dyslipidemic hypertensive patients 5 (4.85%) patients have stroke, all of them have ischaemic stroke. Among 150 non-dyslipidemic hypertensive patients 7 (4.66%) patients have stroke, of them 5 (3.3%) patients have ischaemic stroke and 2(1.3%) patients have haemorrhagic stroke. Cumulatively among 253 patients total 12 (4.74%) patients have stroke of them 5 (4.85%) patients have dyslipidemia and 7(4.66%) patients have no dyslipidemia. So the risk of stroke is increased slightly higher in hypertensive patients when concomitant dyslipidemia present (4.85% vs 4.66%). Kidney diseases and hypertension: Chronic kidney disease (CKD) occurs commonly in patients with cardiovascular disease. In addition, CKD is a risk factor for the development and progression of cardiovascular disease87. Study shows, After adjusting for age, sex, smoking status and baseline glomereular filtration rate (GFR), hypertensive patients without other metabolic risk factors have a double relative risk of CKD(Versus normotensive patients)88. In this study, among 103 dyslipidemic hypertensive patients 6(5.8%) patients have renal impairment and 150 non-dyslipidemic hypertensive patients 6(4%) patients have renal impairment. Cumulatively among 253 patients 12 (4.74%) patients have renal impairment (p=0.5). 23 (9.09%) patients have proteinuria (p=0.027)of them 14(13.6%) patients are dyslipidemic, of them 13 (%) patients have mild(+) proteinuria and 1(1%) patient has massive(+++) proteinuria and 9(6%) patients have proteinuria who are not dyslipidemic. Proteinuria is also more seen in dyslipidemic patients. Retinopathy and hypertension: Both the presence89 and development of new hypertensive retinopathy signs90 are strongly related to elevated blood pressure. Prevalence rate ranges from2-15% for various signs of retinopathy91-96, in contrast to the earlier report from the Framingham Eye Study that found a prevalence of less than 1 percent among participants who underwent an opthalmoscopic examination with dilatation97. In this study, 9(4.3%) patients have hypertensive retinopathy (p=0.028), of them 7(6.9%) patients are dyslipidemic. Among dyslipidemic patients 1(1%) patient have grade I retinopathy, 5(4.9%) patients have grade II hypertensive retinopathy and 1(1%) patient have grade III retinopathy. 2(1.3%) non-dyslipidemic patients have grade II retinopathy. 1 patient has diabetic retinopathy. Peripheral arterial disease and hypertension: In the SHEP study, it is shown that 2-5% hypertensive patients also experience sign or symptoms of peripheral arterial disease at presentation such as intermittent claudication, the prevalence increases with age98. Conversely, in PARTNERS study, 35 to 65 patients with peripheral arterial disease have elevated blood pressure at presentation99. In this study, no patient is found with peripheral arterial disease. In 253 hypertensive patients cardiac, cerebral and renal involvement as target organ damage is not significant statistically. The cause may be, the patients are newly detected and have not got enough time for organ damages to be significant statistically. But their association with dyslipidemia is present. Proteinuria and hypertensive retinopathy are statistically significant and probably these patients were undiagnosed as hypertensive for long time. CONCLUSION Dyslipidemia is an important risk factor for hypertension and in this study association between dyslipidemia and increased blood pressure is observed. Raised TCL, LDL-C & TG and low HDL-C are associated with increased incidence of hypertension. Hypertensive patients with dyslipidemia are prone to develop target organ damage. 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New England Journal of Medicine 2002; 347(18):1397-1402. 55. Warlow C, Sudlow C, Dennis M, Wardlaw J, Sandercock P, Stroke. Lancet 2003;362(939):1211-1224. 56. Neilsen WB, Lindenstrom E, Vestbo J, Jensen GB, Is diastolic hypertension an independent risk factor for stroke in the presence of normal systolic blood pressure in the middle aged elderly ? Am J Hypertens 1997; 10(6):634-639. 57. Droste DW, Ritter MA, Dittrich R, Arterial hypertension and ischaemic stroke. Acta Neurol Scand 2003; 107(4):241-251. 58. Tozawa M, Iseki K, Iseki C, Kinjo K, Ikemiya Y, Takishita S. Blood pressure predicts risk of developing end-stage renal disease in men and women. Hypertension 2003; 42(6):1144-1149. 59. Vupputuri S, Btuman V, Muntner P, Effect of Blood oressure on early decline in kidney function among hypertensive men. Hypertension 2003; 42(6):1144-1149. 60. Klag MJ, Whelton PK, Randall BL, Neaton JD, Brancati FL, Stamler J, End-stage renal disease in African- American and white men. 16 year MRFIT findings JAMA 1997; 227(16):1293-1298. 61. Leoncini G, Viazzi F, Paeodi D. Mild renal dysfunction and subclinical cardiovascular damage in primary hypertension. Hypertension 2003; 42(1):14-18. 62. Criqui MH, Langer RD, Fronek A. Mortality over a period of 10 years in patients with peripheral arterial disease. New England Journal of Medicine 2001992;326(6):381-386. 63. Murabito JM, Evans JC, Nieto K, Larson MG, Levy D, Wilson PW. Prevalence and clinical correlates of peripheral arterial disease in the Fremingham OffspringStudy. Am Heart J 2002: 143(6):961-965. 64. Sacks FM, Svetkey LP, Volmer WM, Effects on blood pressure of reduced dietary sodium and the Dietary Approachto Stop Hypertension (DASH) diet. Dash-sodium Collaborative Research Group. New England Journal of Medicine 2001; 344(1):3-10. 65. Hagberg JM, Park JJ, Brown MD, The role of exercise training in the treatment of hypertension: an update. Sport Med 2000;30(3):193-206. 66. Xin X, He J, Frontini MG, Ogden LG, Motsamai OI, Whelton PK, Effects of alcohol reduction on blood pressure : a meta-analysis of randomized controlled trials. Hypertension 2001; 38(5):1112-1117. 67. He J, Whelton PK, Effect of dietary fibre and protein intake on blood pressure: a review of epidemiologic evidence. Clin Exp Hypertens 1999; 21(5-6):785-796. 68. Chobanian AV, Bakris GL, Black HR, Seventh report of the Joint National Committee on prevention, Detection, Evaluation and Treatment of Hogh Blood Pressure. Hypertension 2003; 42(6):1206-1252. 69. Appel LJ, Moore TJ, Obarzanek E. A clinical trial of effects of dietary patterns on blood pressure. DASH Collaboration Research Group. New England Journal of Medicine 1997; 336(16):1117-1124. 70. Appel LJ, Espeland MA, Easter L, Wilson AC, Folmar S, Lacy CR. Effects of reduced sodium intake on hypertension control in older individuals: results from the Trial of Nonpharmacological Interventions in the Elderly (TONE). Arch Intern Med 2001; 161(5):685-693. 71. Leiter LA, Genest J, Harris SB et al., Dyslipidemia in Adults with Diabetes. Canadian Journal of Diabetes. 2006;30(3):230-240. 72. Hanlon P, Byers M, Walker BR, Macdonald HM. Environmental and nutritional factors in disease, In: Colledge NR, Walker B R, Ralstone S H Davidson’s Principles & Practice of Medicine, 21th edition, Churchill Livingstone Elsevier, 2010;115-117. 73. Gunnar HA. Effect of age on Hypertension. Analysis of Over 4800 Referred Hypertensive Patients. Saudi journal of kidney diseases and transplantation 1999;10(3):286-297. 74. Ruixin Y, Jinzhen W, Shangling P, Weixiong L, Dezhai Y, Yuming C. Sex differences in environmental and genetic factors for hypertension. The American journal of medicine2008;121(9):811-819. 75. Bowman TS, Gaziano M, Buring JE, Sesso HD. A prospective study of cigarette smoking and risk of incident hypertension in women. Journal of the American College of Cardiology 2007;50(21):2085-2092. 76. Halperin RO, Gaziano M, Sesso HD. Smoking and the risk of incident hypertension in middle aged and older men. American journal of hypertension 2008;21(2):148-152. 77. Stamler R, Stamler J, Reidlinger WF, Algera G, Roberts RH. Family (Parentaral ) history and prevalence of hypertension. JAMA 1979; 241(1): 43-46. 78. Bell Ac, Adair LS, Popkin BM, Ethnic Differences in the Association between Body Mass Index and Hypertension. American Journal of Epidemiology 2002; 155(4):346-353. 79. Kannel WB. Risk stratification of dylipidemia: Insight from the framingham Study. Curr Med Chem Cardivasc Hematol Agents 2005;3(3):187–93. 80. Narayan KM, Boyle JP, Thompson TJ, Gregg EW, Williamson DF.. Effect of BMI on lifetime risk for diabetes in the U.S. Diabetes Care 2007;30:1562–6. 81. Berlowitz DR, Ash AS, Hickey EC, Inadequate management of blood pressure in a hypertension population . New England Journal of Medicine1998; 339:1957-1963. 82. Lewington S, Clarke R, Quizilbash N. Age specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies. Lancet. 2002 Dec 14;360(9349):1903-13. 83. Yusuf S, Hawken S, Ounpuu S. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study) case-control study. Lancet 2004;364(9438):937-952. 84. Tseng CH, Chong CK, Tseng CP, Shau WY, Tai TY. Hypertension, the most important component of metabolic syndrome in the association with ischemic heart disease in Taiwanese type 2 diabetic patients; Circulation journal, september 2008; 72: 1419–1424. 85. Arboix A, Roig H, Rossich R, Martinez EM, Garcia-eroles L. Differences between hypertensive and non-hypertensive ischaemic stroke. Europian journal of neurology 2004;11(10):687-692. 86. Woo D, Haverbusch M, Sekar P, Kissela B, Khoury J, Schneider A, et al.Effect of untreated hypertension on haemorrhagic stroke. Stroke 2004;35:1703-1708. 87. Brosious FC, Hostetter TH, Kelepouris E, Mitsnefes MM, Moe SM, Moore MA et al. Detection of Chronic Kidney Disease in Patients With or at Increased Risk of Cardiovascular Disease. Circulation 2006;114:1083-1087. 88. Weycker D, Nichols GA, O’Keeffe-Rosetti M, Edelsberg J, Vincze G, Khan ZM, et al. Risk of chronic kidney disease in hypertensive patients with other metabolic conditions. Journal of human hypertension 2008;22:132-134. 89. Klein R, Klein BEK, Moss SE, Wang Q. Hypertension and retinopathy, arteriolar narrowing and arteriovenous nipping in a population. Arch Opthalmol 1994;112:92-98. 90. Klein R, Klein BEK, Moss SE. The relation of systemic hypertension to changes in the retinal vasculature. The Beaver Dam Eye Study. Trans Am Opthalmol Soc 1997;95:329-350. 91. Klein R, Klein BEK, Moss SE, Wang Q. Hypertension and retinopathy, arteriolar narrowing and arteriovenous nipping in a population. Arch Opthalmol 1994;112:92-98. 92. Sharp PS, Chaturvedi N, Wormald R, McKeigue PM, Marmot MG, Young SM. Hypertensive retinopathy in Afro-Caribbeans and Europeans: prevalence and risk factor relationships. Hypertension 1995;25:1322-1325. 93. Stolk RP, Vingerling JR, de Jong PT. RAtinopathy, glucose, and insulin in an elderly population: the Rotterdam Study. Diabetes 1995;44:11-15. 94. Yu T, Mitchell P, Berry G, Li W, Wang JJ. Retinopathy in older persons without diabetes and its relationship to hypertension. Arch Opthalmol 1998; 116: 83-89. 95. Klein R, Sharret AR, Klein BEK, Are retinal arteriolar abnormalities related to atherosclerosis ? The Atherosclerosis Risk in Communities Study. Arterioscler Thromb Vasc Biol 2000;20:1644-1650. 96. Wong TY, Klein R, Sharrett AR. The prevalence and risk factors of retinal microvascular abnormalities in older people: the Cardiovascular Health Study. Ophthalmology2003;110:658-666. 97. Leibowitz HM, Krueger DE, Maunder LR. The Framingham Eye Study Glucoma, diabetic retinopathy, macular degeneration and visual acuity in a general population of 2631 adults, 1973-1975. Surv Ophthalmol 1980; 24:Suppl:335-610. 98. Newman AB. The unsung perils of peripheral arterial disease: Concomitant atherosclerotic vascular disease. Journal of American Geriatric Sosiety 1997;45:1472-1478. 99. Rosei EA, Ambrosio G, Badimon L, Bassand JP, Luna ABD, Bertrand AD, et al. Management of peripheral Arterial Disease: Are we doing better? Partners Study JAMA 2001;286:317-324. APPENDICES Data Collection Format Hypertension and Research centre, Rangpur Title: Pattern of lipid profile in newly detected hypertensive patients in Hypertension and Research centre, Rangpur. IDNo………. Date…………… 1) Name 2) Age <40 years-1, 40-60 years-2, >60years-3
3) Sex Male-1, Female-2
4) Father’sname/ Husband’s name
5) Present address(with mob/phone no)
6) Marital status Unmarried-1, Married-2, Widow-3, Widower-4,Divorced-5, Separated-6
7) Educational Qualification No education-1, Primary-2, Secondary-3, Higher secondary-4, Graduate-5, Post Graduate-6, Madrasa education-7
8) Occupation Farmer-1, Service-2, Businessman-3, Others-4
9) Family members
10) Monthly income(Tk) <5000-1, 5001-10000-2, 10001-15000-3, >15001-4
11) Smoking status Number of stick/day….. Duration in days….. Pack years…. No-1, ≤10-2, 11-20-3, 21-30-4, >30-5
12) History of other addiction No-1, Jarda, Gul, other tobacco derived substances-2, Alcohol-3, Other addiction-4
13) Obey religious culture Regular-1, Irregular-2, No-3
14) Regular walking/ exercise Yes-1, No-2
15) For how long exercise done 30 minutes-1, 30-60 minutes-2, >60 minutes-3
16) Family history of diseases(Father ,Mother, Brother, Sister, Blood related relatives): High Blood Pressure-1, Cardiac Disease-2, Brain Stroke/Paralysis-3, Diabetes-4, Blindness-
17) Chief complaints:
18) History of Hypertension in Details:
a) First detection –when: b) BP level on first detection:
c) Previous highest record of BP:
d) Complications detected if any: No-1, Cardiac-2, Cerebral3, Visual-4, Renal-5,
Others-6 (please specify…..) (…….)
19) History of treatment: Drugs …….Regular-1, Irregular-2 (……..)
20) Other Associated diseases: No-1, Diabetes mellitus-2, IHD-3, Stroke-4, Bronchial Asthma/COPD-5, Others-6 (please specify……..) (…….)
21) Drugs: Oral contraceptive pills-1, Steroids-2, NSAIDs-3, Sympathomimetic drugs-4, Others-6(please specify….) (…….)
22) Dietary habit- vegetarian/non-vegetarian
23) Physical examination
a. Height (cm): b. Weight (Kg):
c. BMI: Normal-1, overweight -2, Obese-3 (…….)
d. Oedema: Absent-1, Present-2 (…….)
e. Neck Vein: Engorged-1,Not engorged-2 (…….)
f. Pulse: ..…./min; Normal-1, Abnormal-2 (…….)
g. Respiratory rate:…../min; Normal-1, Abnormal-2 (…….)
h. B.P. :
Right arm: Sitting Standing
Left arm: Sitting Standing
i. Peripheral pulses: Absent-1, Present-2 (……)
m. Nervous system
o. Signs of hyplerlipidemia:Xanthelasma-1, Corneal arcus-2, Tendon xanthoma-3 (…….)
p. Other findings:
2) Blood sugar: Random
2hours after 75 gm glucose intake Normal-1, IGT-2, DM-3.
3) Serum creatinine: Normal-1, Abnormal-2
4) Lipid profile(mg/dl):
Total Cholesterol: Desirable-1,Borderline high-2,High-3
High-density lipoprotein (HDL) cholesterol:Low-1, High-2
LDL-Cholesterol: optimal-1, above optimal-2, borderline-3, high-4,very high-5
Triglyceride(TG):Normal-1,Bordreline High-2, High-3, Very high-4
5) ECG: Normal-1,Abnormal-2
6) X-ray chest P/A view: Normal-1, Cardiomegaly-2,Aortic unfolding-3,Others-4
7) Echocardiogram: LVH: Present-1, Absent-2
RWMA: Present-1, Absent-2
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