Hypertension and the influence of the waist circumference and the body mass index

CONTENTS

ACKNOWLEDGEMENT

ABBREVIATIONS

ABSTRACT

1 INTRODUCTION

2 REVIEW OF LITERATURE

3 NEED FOR THE STUDY

4 AIMS AND OBJECTIVES OF THE STUDY

5 METHODOLOGY

6 RESULTS

7 DISCUSSION

8 CONCLUSION

9 REFERENCES

10 APPENDIX

a.HUMAN ETHICS COMMITTEE

b. PRO FORMA

c. PUBLICATIONS

ACKNOWLEDGEMENT

I take the privilege to acknowledge all those who helped me in the completion of my work.

At first, I put forward my sincere thanks to Mr. Devendar Reddy BE., Secretary, Vishwambhara Educational Society for providing me the opportunity for my higher studies. His help and support have been of genuine assistance to me during this course.

I express my deepest gratitude and indebtedness to my research guide S. Vijaya Kumar, M. pharm (Ph.D.), Head, Department of Pharmacy practice, under whose untiring and invaluable guidance, support and inspiration I have pursued my research work.

Deep sense of gratitude and special thanks to Dr. A.N.R. Laxmi, Ex. Superintendent, M.G. M. Hospital, Warangal for allowing me to work there in this hospital

I am also thankful to my principal , Dr. Ch. Srinivas Reddy and also the nursing staff of cardiology departments for helping me to collect the relevant data of the patients.

I would also like to extend my sincere thanks to Mrs. M. Leena, Assistant professor, Department of Pharmacy practice without whose guidance, patience and valuable suggestions my work would be impossible.

I am extremely thankful to Miss. A. Shailaja, Lab technician, for their help and support whenever required.

I also would like to acknowledge all the teaching and non- teaching staff of Vaagdevi college of Pharmacy and Mahatma Gandhi Memorial Hospital who have directly or indirectly helped me in my project work.

My thanks also goes out to all my friends, Mahamood Ali, kavya adepu, Rasaad Mahamood, Shilpa Sirimalle, Santosh Peraveni, Surya prakash singh, Ram mohan, Rajender, Kishore and Nitesh for their help, love and moral support throughout.

I am very thankful to the participants who had came forward and readily participated in this project. It would have been impossible to complete this work without their co-operation and participation. Their noble contribution shall ever be remembered.

My heartful thanks to my parents Laxmaih Pasula, Ialamma Pasula, Friends Anil Gade, Sujith Kadari, sisters and brothers too for their unconditional love and support for me and without whose blessings I would not have been at this memorable stage of my life.

I thank dear God for His love and blessings.

I also would like to acknowledge all the teaching and non- teaching staff of schools and colleges of Warangal district who have directly or indirectly helped me in my project work.

Place: Warangal, India SRINIVAS PASULA

Date:

ABBREVIATIONS

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ABSTRACT:

Hypertension is a major public health problem world-wide and is one of the risk factors for coronary artery disease. The objective of the present study was to determine the relative role of abdominal fat accumulation on the relationship between excess body weight, and high blood pressure among men and women of non-teaching staff members of public school of Warangal. This study was performed in the department of pharmacy practice clinical research centers of MGM hospitals; Warangal in 2013. We had a study group which includes 150 subjects of non-teaching staff members of government and private school of Warangal. There were 44 women and 106 men. At the point of entry into the study group of all the study subjects written informed consent from before stating of research work. Data were collected by trained Pharm D and M. Pharmacy paramedical students. The exclusion criterion was the co-existence of any other serious elements. A total number of 32 subjects were found to be normotensive in which 25 (17%) were men and 7 (5%) were women. Overall, 26 subjects were found to be pre-hypertensives whereas, 20 (13%) were men. A total number of 8 (5%) subject were found to be hypertensive of which 6(4%) men and 2 (1.3%) women. Our results highlighted that the waist circumference seems to have a strong association with the risk of hypertension, especially among men than women. In future studies should investigate lipid profile of study subjects to correlate hypertension management regardless of gender or age.

Key words: Hypertension, Non-teaching staff, Men and Women.

1. INTRODUCTION

1.1 BACKGROUND

South East Asian – Americans are disproportionately impacted by hypertension and its related morbidity and mortality compared to Caucasian. C-Americans have almost twice the fatal stroke, 1.5> rate of cardiac mortality and 4 time greater rate of young stage renal disease. Hypertension is an important public health problem in different regions of the world because of its high prevalence and concomitant risk of cardiovascular and renal disease. A recent analysis of worldwide data from different regions estimated that the total number of adults with hypertension in 2000 was 972 million: 333 million in countries with established market economies and 639 million in economically developing countries. This proportion will increase by 60%-1.56 billion-by 2025. The magnitude of the hypertension burden countries to predict a worldwide cardiovascular disease epidemic. The increasing prevalence of hypertension occurred in conjunction with a dramatic increase in the prevalence of overweight and obesity. The international obesity task force has estimated that at present at least 1.1 billion adults are overweight including 312 million who are obese.Although the USA is world leader concerning overweight, several Latin American countries are only a decade is less behind. In Brazil a national survey conducted in 2002-2003 is 9.5 million adults over the age of 20 years indicated that overweight was 8times greater than weight deficit. In that survey 38.8million (40.6 %) were overweight of whom 10.5 million were obese (BMI >30kg/m[2]). Those changes clearly reflect the nutritional transition that has also been observed in other emerging economies at a rate never seen before. As a consequence, diabetes will become an increasingly common problem in developing countries. Obesity is independently associated with numerous adverse cardiovascular, renal and metabolic outcomes, including coronary heart disease, heart failure and type 2 diabetes mellitus. Roughly 60% of all cases of diabetes can be directly attributed to weight gain. And the risk of death from all causes also rises as BMI increases for both men and women at all age groups.

1.2 EPIDEMIOLOGY

1.2.1 GLOBAL:

As per the Health Statistics 2012, of the estimated 57 million global deaths in 2008, 36 million (63%) were due to non-communicable disease (NCDs). The largest proportion of NCD deaths is caused by cardiovascular diseases (48%). In term of attributable deaths raised blood pressure is one of the leading behavioral and physiological risk factors to which 13% of the global deaths are attributed. Hypertension is reported to be fourth contributor to premature death in developed countries and the seventh in developing countries.

Recent reports indicate that nearly one billion adults (more than a quarter of the world’s population) had hypertension in 2000 and this is predicted to increase to 1.56 billion by 2025. Earlier reports also suggest that the prevalence of hypertension is rapidly increasing in developing countries and is one of the leading causes of death and disability. While mean blood pressure has decreased in nearly all high income countries, it has been stable or increasing in most African countries. Today, mean blood pressure remains very high in many African and some European countries. The prevalence of raised blood pressure in 2008 was highest in the WHO African Region at36.8% (34.0-39.7).

The Global Burden of Disease; Chronic Disease Risk Factors collaborating group has reported 35-years (1980-2005) trend in mean levels of body mass index (BMI),systolic BP and cholesterol in 199 high income, middle income and low income countries. Mean systolic BP decline in high and in low income countries but increased in low income countries and is now more than in high income counties. The India specific data are similar to the overall trends in low income countries.

1.2.2 NATIONAL:

The prevalence of hypertension in the late nineties and early twenties century varied among different studies in India, ranging from 2-15% in Urban India and 2-8% in Rural India. The historic studies on the prevalence of hypertension in urban and rural India are depicted in (Table1).

Review of epidemiological studies suggests that the prevalence of hypertension has increased in both urban rural subjects and presently is 25% in urban and 10-15% among rural adults (Table2).

As per the Register General of India and Million Death study investigated (2001-2003), CVD was the largest cause of deaths in males (20.3%) as well as female (16.9%) and led to about 2 million deaths annually. Mortality data from CVD in India are reported by the WHO. The Global status on Non-Communicable Disease Report (2011) has reported that there were more than 2.5 million deaths from CVD in India in 2008, two-thirds due to coronary artery disease and one third to stroke. These estimates are significantly greater than those reported by the Register General of India shows that CVD mortality is increasing rapidly in the country. CVD is the largest cause of mortality in all region of the country. (Table 3) shows the top 5 causes of deaths in rural and urban population. There are large regional differences in cardiovascular mortality in India among both men and women. The mortality is highest in south Indian states, eastern and north eastern states and Punjab in both men and women, while mortality is the lowest in the central Indian sates of Rajasthan, Uttar Pradesh, and Bihar. Deaths study from 2004-2013 shall provide data on regional variation and trends in CVD mortality in India.

The prevalence of hypertension in the six decades has increased from 2% to 25% among urban residents and from to 2% to 15% among the rural residents in India. According to Directorate General of Health Services, Ministry of Health and Family Welfare, Government of India , the overall prevalence of hypertension in India by 2020 will be 159.46/. Various factors might have contributed to this rising trend, attributable to several indicators of economic progress such as increased life expectancy, urbanization and its attendant lifestyle changes including increasing salt intake and the overall epidemiologic transition, India is experiencing currently. Another factor that may contribute is the increased awareness.

The prevalence of high normal blood pressure (also called pre hypertension in JNC-7) has been seen in many recent studies and was found to be 32% in a recent urban study from Central India. In last two decades the prevalence of hypertension has been seen to be static in some urban areas. The prevalence of smoking has declined while that of diabetes, metabolic syndrome, hypercholesterolemia and obesity has been increasing. Preventive measure are required so as to reduce obesity, increasing physical activity, decreasing the salt intake of the population and a connected effort to promote awareness about hypertension related risk behaviors.

Table 1. Previous Studies (1963 - 1999) on prevalence of hypertension in Urban and Rural Indian population

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Table 2. Recent studies (2000 - 2012) on prevalence of hypertension in urban and rural Indian population

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Table 3. Top five causes of deaths in India classified according to areas of residence and gender

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(Adapted from Registrar General of India Report.Supplement to JAPI 2013.61).

COPD: Chronic obstructive pulmonary disease.

1.3 ETIOLOGY

1.3.1 Primary hypertension

Primary (essential) hypertension is the most common form of hypertension, accounting for 90–95% of all cases of hypertension. In almost all contemporary societies, blood pressure rises with aging and the risk of becoming hypertensive in later life is considerable. Numerous common genetic variants with small effects on blood pressure have been identified as well as some rare genetic variants with large effects on blood pressure but the genetic basis of hypertension is still poorly understood. Several environmental factors influence blood pressure. Lifestyle factors that lower blood pressure include reduced dietary salt intake, increased consumption of fruits and low fat products (Dietary Approaches to Stop Hypertension (DASH diet), exercise, weight loss and reduced alcoholintake. Insulin resistance, which is common in obesity and is a component of syndrome X(or the metabolic syndrome), is also thought to contribute to hypertension.

1.3.2 Secondary hypertension

Secondary hypertension results from an identifiable cause of hypertension. Hypertension can also be caused by endocrine conditions, such as Cushing’s syndrome, Hyperthyroidism, hypothyroidism, acromegaly, conn’s syndrome (or) hyperaldosteronism, hyperparathyroidism and pheochromacytoma. Other causes of secondary hypertension include obesity, sleep apnea, pregnancy, Coarctation of aorta, excessive liquorice consumption and certain prescription medicines, herbal medicines and illegal drugs.

A. PRIMARY (ESSENTIAL) HYPERTENSION

Primary (essential) hypertension is the term applied to the 95% of cases in which no cause for hypertension can be identified. This occurs in 10-15% of white adults and 20-30% of black adults in the United States. The onset is usually between ages 25 and 55 years; it is uncommon before age 20 years. Much less commonly, hypertension arises from an identifiable cause, in which case it is called secondary hypertension (see below). The secondary form should be suspected in children or young adults and in older persons in whom onset of hypertension is new or in whom hypertension suddenly worsens. Genetic factors play an important role. Children have higher blood pressure when one parent is hypertensive (and more so when both parents are hypertensive). Environmental factors also are significant. Increased salt intake and obesity have long been incriminated. Other factors that may be involved in the pathogenesis of primary (essential) hypertension are sympathetic nervous system hyperactivity, abnormal cardiovascular development, renin-angiotensin system activity, defect in natriuresis, intracellular sodium and calcium, as well as exacerbating factors (including obesity, alcohol, cigarette smoking, and polycythemia).

1. Sympathetic nervous system hyperactivity

This is most apparent in younger persons with hypertension, who may exhibit tachycardia and an elevated cardiac output. However, correlations between plasma catecholamine’s and blood pressure are poor. Insensitivity of the baroreflexes may play a role in the genesis of adrenergic hyperactivity.

2. Abnormal cardiovascular development

The normal cardiovascular system develops so that elasticity of the great arteries is matched to the resistance in the periphery to optimize large vessel pressure waves. In this way, myocardial oxygen consumption is minimized and coronary flow maximized. Elevated blood pressure later in life could arise from abnormal development of aortic elasticity or reduced development of the micro vascular network. This has been postulated as the sequence of events in low birth weight infants who have an increased risk of hypertension developing in adulthood.

3. Renin-angiotensin system activity

Renin, a proteolytic enzyme, is secreted by the juxtaglomerular cells surrounding afferent arterioles in response to a number of stimuli, including reduced renal perfusion pressure, diminished intravascular volume, circulating catecholamine’s, increased sympathetic nervous system activity, increased arteriolar stretch, and hypokalemia. Plasma renin levels are classified in relation to dietary sodium intake or urinary sodium excretion.

4. Defect in natriuresis

Normal individuals increase their renal sodium excretion in response to elevations in arterial pressure and to a sodium or volume load. Hypertensive patients, particularly when their blood pressure is controlled, exhibit a diminished ability to excrete a sodium load. This defect may result in increased plasma volume and hypertension. During chronic hypertension, a sodium load is usually handled normally.

5. Intracellular sodium and calcium

Intracellular Na+ is elevated in blood cells and other tissues in primary (essential) hypertension. This may result from abnormalities in Na+-K+ exchange and other Na+ transport mechanisms. An increase in intracellular Na+ may lead to increased intracellular Ca2+ concentrations as a result of facilitated exchange and might explain the increase in vascular smooth muscle tone that is characteristic of established hypertension.

6.Exacerbating factors

A number of conditions elevate blood pressure, especially in predisposed individuals. Obesity is associated with an increase in intravascular volume and an elevated cardiac output. Weight reduction lowers blood pressure modestly. The relationship between sodium intake and hypertension remains controversial, and some not all persons with hypertension respond to high salt intake with substantial increases in blood pressure. Patients with high normal or elevated blood pressures should consume no more than 100 mmol/d of salt (2.4 g of sodium, 6 g of sodium chloride daily).

Excessive use of alcohol also raises blood pressure, perhaps by increasing plasma catecholamines. Hypertension can be difficult to control in patients who consume more than 40 g of ethanol (two drinks) daily or drink in "binges". Cigarette smoking raises blood pressure, again by increasing plasma norepinephrine. Aerobic exercise lowers blood pressure in previously sedentary individuals, but increasingly strenuous exercise in already active subjects has less effect. Polycythemia, whether primary or due to diminished plasma volume, increases blood viscosity and may raise blood pressure. Nonsteroidal anti-inflammatory drugs (NSAIDs) produce increases in blood pressure averaging 5 mm Hg and are best avoided in patients with borderline or elevated blood pressures. Low potassium intake is associated with higher blood pressure in some patients; an intake of 9 mmol/d is recommended.

B. SECONDARY HYPERTENSION

In particular, patients in whom hypertension develops at an early age, those who first exhibit hypertension when over age 50 years, or those previously well controlled who become refractory to treatment are more likely to have secondary hypertension. Causes include renal disease, genetic causes, renal vascular hypertension, primary hyperaldosteronism, Cushing's syndrome, pheochromocytoma, coarctation of the aorta (uncommon), hypertension associated with pregnancy, estrogen use, as well as other causes (eg, hypercalcemia and medications).

1. Renal disease

Renal parenchymal disease is the most common cause of secondary hypertension. Hypertension may result from diabetic and inflammatory glomerular diseases, tubular interstitial disease, and polycystic kidneys. Most cases are related to increased intravascular volume or increased activity of the renin-angiotensin-aldosterone system.

2. Genetic causes

Hypertension can be caused by mutations in single genes, inherited on a Mendelian basis. Although rare, these conditions provide important insight into blood pressure regulation and possibly, the genetic basis of essential hypertension. Glucocorticoid remediable aldosteronism is an autosomal dominant cause of early-onset hypertension with normal or high aldosterone and low renin levels. It is caused by the formation of a chimeric gene encoding both the enzyme responsible for the synthesis of aldosterone (transcriptionally regulated by AII) and an enzyme responsible for synthesis of cortisol (transcriptionally regulated by ACTH).

As a consequence, aldosterone synthesis becomes driven by ACTH, which can be suppressed by exogenous cortisol. In the syndrome of apparent mineralocorticoid excess, early-onset hypertension with hypokalemic metabolic alkalosis is inherited on an autosomal recessive basis.

3. Renal vascular hypertension

Renal artery stenosis is present in 1-2% of hypertensive patients. Its cause in younger individuals is fibromuscular hyperplasia, particularly in women under 50 years of age. The remainder of renal vascular disease is due to atherosclerotic stenosis of the proximal renal arteries. The mechanism of hypertension is excessive renin release due to reduction in renal blood flow and perfusion pressure. Renal vascular hypertension may occur when a single branch of the renal artery is stenotic, but in as many as 25% of patients both arteries are obstructed.

4. Primary hyperaldosteronism

Primary hyperaldosteronism occurs because of excessive secretion of aldosterone by the adrenal cortex. In the past, the diagnosis was often suspected when hypokalemia prior to diuretic therapy associated with excessive urinary potassium excretion (usually > 40 mEq/L on a spot specimen) and suppressed levels of plasma renin activity presented in hypertensive patients. Currently, the best screening test for primary hyperaldosteronism involves determinations of plasma aldosterone concentration (normal: 1-16 ng/dL) and plasma renin activity (normal: 1-2.5 ng/mL/h) and calculation of the plasma aldosterone/renin ratio (normal: < 25). Medications that alter renin and aldosterone levels, including ACE inhibitors, angiotensin receptor blockers (ARBs), and diuretics (especially spironolactone), should be discontinued at least a week before sampling. Patients with aldosterone/renin ratios of ≥ 25 require further evaluation for primary hyperaldosteronism.

5. Cushing's syndrome

Less commonly, hypertension presents in patients with Cushing's syndrome (glucocorticoid excess). However, among those with spontaneous Cushing's syndrome, hypertension occurs in about 75-85% of patients. It may be related to salt and water retention from the mineralocorticoid effects of the excess glucocorticoid. Alternatively, it may be due to increased secretion of angiotensinogen. While plasma renin activity and concentrations are generally normal or suppressed in Cushing's syndrome, angiotensinogen levels are elevated to approximately twice normal because of a direct effect of glucocorticoids on its hepatic synthesis, and angiotensin II levels are increased by about 40%. Administration of the angiotensin II antagonist saralasin to patients with Cushing's syndrome causes a prompt 8 to 10 mmHg drop in systolic and diastolic blood pressure. In addition, glucocorticoids exert permissive effects on vascular tone by a variety of mechanisms.

6. Pheochromocytoma

In about 50% of patients with pheochromocytoma, hypertension is sustained but the blood pressure shows marked fluctuations, with peak pressures during symptomatic paroxysms. During a hypertensive episode, the systolic blood pressure can rise to as high as 300 mm Hg. The blood pressure elevation caused by the catecholamine excess results from two mechanisms: α-receptor-mediated vasoconstriction of arterioles, leading to an increase in peripheral resistance, and β1-receptor-mediated increases in cardiac output and in renin release, leading to increased circulating levels of angiotensin II. The increased total peripheral vascular resistance is probably primarily responsible for the maintenance of high arterial pressures. Chronic vasoconstriction of the arterial and venous beds leads to a reduction in plasma volume and predisposes to postural hypotension.

7. Coarctation of the aorta

This is uncommon cause ofhypertension.

8. Hypertension associated with pregnancy

Hypertension occurring during pregnancy, including preeclampsia and eclampsia, is one of the most common causes of maternal and fetal morbidity and mortality.

9. Estrogen use

A small increase in blood pressure occurs in most women taking oral contraceptives, but considerable increases are noted occasionally. This is caused by volume expansiondue to increased activity of the renin-angiotensin-aldosterone system. The primary abnormality is an increase in the hepatic synthesis of renin substrate. Five percent of women taking oral contraceptives chronically exhibit a rise in blood pressure above 140/90 mm Hg, twice the expected prevalence. Contraceptive-related hypertension is more common in women over 35 years of age, in those who have taken contraceptives for more than 5 years, and in obese individuals. It is less common in those taking low-dose estrogen tablets. In most, hypertension is reversible by discontinuing the contraceptive, but it may take several weeks. Postmenopausal estrogen does not generally cause hypertension, but rather maintains endothelium-mediated vasodilatation.

10. Other causes of secondary hypertension

Hypertension has also been associated with hypercalcemia due to any cause: acromegaly, hyperthyroidism, hypothyroidism, and a variety of neurologic disorders causing increased intracranial pressure. A number of other medications may cause or exacerbate hypertension - most importantly cyclosporine. (Reference: Hypertension Etiology & Classification http://www.health.am/hypertension/hypertension-etiology classification/#xzz2an8SF54d).

1.4 PATHOPHYSIOLOGY:

Clinical Presentation and Diagnosis:

1.4.1 Measurement of Blood Pressure:

Because hypertension is usually an asymptomatic disease, it is usually detected during routine screening. The diagnosis of hypertension is made only after the average of two or more measurements, taken on separate occasions, determines the patient to be hypertensive based on the data in (Table 4). Accurate and consistent technique in measuring BP is paramount, as many therapy decisions will be based on these results. (Table 6) describes the appropriate technique for the accurate measurement of BP.

Patient self-monitoring and ambulatory BP monitoring can both serve as important tools to assess BP outside the clinical setting, though self-monitoring may not be as reliable. These techniques may be particularly helpful in the assessment of BP in smoking patients and patients with “white-coat hypertension.” Ambulatory BP monitoring devices are worn for 24-hour periods with measurements taken either at regular or random intervals throughout the entire day. Studies have suggested that readings from ambulatory monitoring may correlate better with target organ damage than measurements taken in the­­­ physician's office. Though limited, Medicare reimbursement is available in defined situations for the use of ambulatory BP monitoring (Table 7).

Table 4. Classification of Blood Pressure for Adults:

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Table 5. Cardiovascular Risk Factors and Target Organ Damage:

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Table 6. Appropriate Blood Pressure Measurement Techniques

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Table 7. Clinical Situations in Which Ambulatory Blood Pressure Monitoring May Be Helpful

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1.4.2 Evaluation of the Hypertensive Patient :

Evaluation of the patient newly diagnosed with hypertension has three purposes: (a) to assess the patient's lifestyle and cardiovascular risk factors and other significant diagnoses that will affect pharmacotherapy recommendations (Table 5), (b) to assess for secondary correctable causes of elevated BP (Table 9) and (c) to assess for preexisting target organ damage (Table 5) or cardiovascular or cerebrovascular disease. The initial evaluation visit of the hypertensive patient (Table 9) should include an interview for individual and family history issues, an appropriate physical examination to assess for target organ damage from preexisting hypertension as well as secondary causes of hypertension (Table 8), and appropriate laboratory testing to assess for secondary causes of hypertension as well as to control aspects of comorbid conditions (e.g., diabetes, hyperlipidemia, and chronic kidney disease).

Table 8. Identifiable Causes and Diagnostic Tests/Clinical Findings for Secondary Hypertension

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Table 9. Evaluation of Hypertensive Patients

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In addition to the basic laboratory testing recommended in (Table 9) during the initial assessment of the patient with hypertension, special consideration should be given to the assessment of renal function and newer emerging risk factors that may help in the further risk stratification of high-risk patients for CVD. Decreases in glomerular filtration rate (GFR) or the presence of albuminuria, including micro albuminuria, have been shown to increase cardiovascular risk. Other risk factors that may provide improved cardiovascular risk assessment of patients in the future include elevated heart rate, high-sensitive C-reactive protein (hs-CRP), and homocysteine, hs-CRP levels, a marker of inflammation, have been suggested to predict independent higher risk for cardiovascular events, especially in women. However, recent evidence has suggested that the ability of hs-CRP to independently predict cardiovascular risk may not be as significant as originally thought.

Secondary Causes of Hypertension:

The initial laboratory tests and physical examination, in addition to patient age and BP severity, often provide clues suggestive of secondary causes of hypertension. Further consideration and possible work up for secondary hypertension is advised for patients who respond poorly to drug therapy, haveincreasing BPs after periods of good control, or have a sudden onset of hypertension. (Table 8)describes secondary causes of hypertension and corresponding diagnostic tests and clinical findings.

1.5 TREATMENT:

The treatment of hypertension requires a multimodal approach that encompasses the use of non-pharmacologic treatments such as weight reduction through appropriate physical activity and dietary habits, dietary sodium reduction, and moderation of alcohol consumption as well as individualized pharmacotherapy.

1.5.1 Non pharmacologic Therapy:

Appropriate lifestyle modifications are important therapies in both the prevention and treatment of hypertension. The Dietary Approaches to Stop Hypertension (DASH) trial showed that eating a diet rich in fruits, vegetables, low-fat dairy products, potassium, and calcium with decreased dietary cholesterol and potassium can significantly improve BP. This dietary modification was as effective as drug therapy with one agent in some patients. Patients with hypertension should take part in regular aerobic physical activity, after consultation with their physicians, 30 minutes a day on most days of the week. 60 to 90 minutes per week of walking has been shown to decrease cardiovascular mortality by approximately 50%. Alcohol intake should be no more than two drinks (24 oz of beer, 10 oz of wine, or 3 oz of 80-proof liquor) per day in most men and one drink per day in women and lighter-weight people. The lifestyle modifications recommended by JNC-VII (Table 10) not only help to lower BP, but also increase the effectiveness of pharmacotherapy regimens.

1.5.2 Pharmacotherapy:

The pharmacotherapy of hypertension comprises nine classes of medications: diuretics, aldosterone receptor blockers, β-blockers, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II antagonists, calcium channel blockers, α1-blockers, central α2 agonists and other centrally acting drugs, and direct vasodilators (Tables 11 and 12). Therapy selection should be tailored to the patient, taking into consideration such issues as safety, cost, adverse event profile, and presence of compelling indications for certain drug classes and risk factors for CVD, as well as clinical evidence of decreased morbidity and mortality secondary to their use. Common adverse effects and special precautions for antihypertensive drugs are given in (Table 10). Drug interactions are listed in (Table 14).

SBP is now the recommended treatment focus for most patients, as it has been shown that if SBP is controlled, DBP will usually be controlled as well. The JNC-VII guidelines also recommend thiazide diuretics as first-line therapy in patients with uncomplicated hypertension, and as the second agent to be added to other classes used for compelling indications if further BP reduction is required. For patients whose BP is more than 20/10 mm Hg above their goal, JNC-VII now recommends that therapy be initiated with two agents.

Uncomplicated Hypertension:

For patients without compelling indications that require specified antihypertensive therapies (Table 15), JNC-VII recommends that thiazide-type diuretics be considered as the initial agent in most patients with stage 1 hypertension, and a two-drug combination that includes a thiazide-type diuretic in most patients with stage 2 hypertension. Recent data from the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), as well as older data from the Systolic Hypertension in the Elderly Program (SHEP) trial, confirm the ability of thiazide diuretics to consistently reduce cardiovascular morbidity and mortality.

Table 10. Lifestyle Modifications to Manage Hypertension

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Table 11. Oral Antihypertensive Drugs

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