introduction essay on hypertension

Hypertension: Introduction, Types, Causes, and Complications

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• Yoshihiro Kokubo MD, PhD, FAHA, FACC, FESC, FESO 4 ,
• Yoshio Iwashima MD, PhD, FAHA 5 &
• Kei Kamide MD, PhD, FAHA 6  

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Hypertension remains one of the most significant causes of mortality worldwide. It is preventable by medication and lifestyle modification. Office blood pressure (BP), out-of-office BP measurement with ambulatory BP monitoring, and self-BP measurement at home are reliable and important data for assessing hypertension. Primary hypertension can be defined as an elevated BP of unknown cause due to cardiovascular risk factors resulting from changes in environmental and lifestyle factors. Another type, secondary hypertension, is caused by various toxicities, iatrogenic disease, and congenital diseases. Complications of hypertension are the clinical outcomes of persistently high BP that result in cardiovascular disease (CVD), atherosclerosis, kidney disease, diabetes mellitus, metabolic syndrome, preeclampsia, erectile dysfunction, and eye disease. Treatment strategies for hypertension consist of lifestyle modifications (which include a diet rich in fruits, vegetables, and low-fat food or fish with a reduced content of saturated and total fat, salt restriction, appropriate body weight, regular exercise, moderate alcohol consumption, and smoking cessation) and drug therapies, although these vary somewhat according to different published hypertension treatment guidelines.

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This study was supported by grants-in-aid from the Ministry of Education, Science, and Culture of Japan (Nos. 25293147 and 26670320), the Ministry of Health, Labor, and Welfare of Japan (H26-Junkankitou [Seisaku]-Ippan-001), the Rice Health Database Maintenance industry, Tojuro Iijima Memorial Food Science, the Intramural Research Fund of the National Cerebral and Cardiovascular Center (22-4-5).

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Department of Preventive Cardiology, National Cerebral and Cardiovascular Center, 5-7-1, Fujishiro-dai, Suita, Osaka, 565-8565, Japan

Yoshihiro Kokubo MD, PhD, FAHA, FACC, FESC, FESO

Divisions of Hypertension and Nephrology, National Cerebral and Cardiovascular Center, 5-7-1, Fujishiro-dai, Suita, Osaka, 565-8565, Japan

Yoshio Iwashima MD, PhD, FAHA

Division of Health Science, Osaka University Graduate School of Medicine, Suita, Osaka, Japan

Kei Kamide MD, PhD, FAHA

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Kokubo, Y., Iwashima, Y., Kamide, K. (2015). Hypertension: Introduction, Types, Causes, and Complications. In: Jagadeesh, G., Balakumar, P., Maung-U, K. (eds) Pathophysiology and Pharmacotherapy of Cardiovascular Disease. Adis, Cham. https://doi.org/10.1007/978-3-319-15961-4_30

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Introduction Hypertension is a multifactor disease characterized by chronic elevation in blood pressure to levels equal to or above 140 mmHg systolic blood pressure (SBP) and above 90 mmHg of diastolic blood pressure (DBP). Considered a worldwide epidemic disease, hypertension is the main risk factor for cardiovascular disease, being epidemiologically closely associated with metabolic diseases such as obesity and diabetes. Hypertension is the main risk factor for cardiovascular diseases, which include stroke, coronary artery disease (CAD), and heart failure (HF) leading to ∼1.8 million deaths worldwide every year, cardiovascular disease leads to ∼17 millions of death per year, and, from this total, it is reported that high blood pressure is estimated to cause more than half of these deaths (over 9 million deaths every year), making it also the main risk factor in the global disease burden. Aging is a major risk factor for developing hypertension. The prevalence of the disease increases with age, with a higher rate in men than women. People who don’t have hypertension at age 55 have 90% chance of developing it later in life. The goal of hypertension treatment is to prevent death and complication by achieving and maintaining the blood pressure at 140/90 mm Hg or lower. Life style modification is the first line of intervention for all patients with hypertension, but pharmacological is the cornerstone for the disease treatment to reduce the high blood pressure and prevent complications such as cardiovascular and renal morbidity and mortality. For many years the right ventricle was grossly undervalued and considered to function mainly as a conduit, while its contractile performance was considered haemodynamically unimportant. Since the early 1950s, however, the relevance of the chamber in the maintenance of normal cardiac physiology was recognized in several cardiovascular disorders. Tricuspid annular plane systolic excursion (TAPSE) has been proposed as a simple and reproducible parameter for quantitative assessment of RV ejection fraction. It provides a simple method for global RV functional assessment and is a strong predictor of prognosis in heart failure. Although the right ventricle can now be imaged and studied in several ways, two-dimensional (2D) guided M-mode echocardiography is an attractive tool due to its simplicity. Studies on RV function among patients with hypertensive heart disease (HHD) are rather few and have focused mainly on the diastolic function of the chamber. Aim of Work This study is aiming to assess the systolic function of the right ventricle in patients with systemic hypertension using tricuspid annular plane systolic excursion (TAPSE). Chapter (1) Systemic Hypertension • Definition of Hypertension The cut-off mark for the definition of hypertension has evolved over time. Hypertension is defined as a systolic blood pressure (SBP) of 140 mm Hg or more, or a diastolic blood pressure (DBP) of 90 mm Hg or more, or taking antihypertensive medication. • Classification of hypertension Hypertension has been classified according to 2013 ESH/ESC guidelines, as shown in Table 1. • Prevalence of Hypertension Hypertension is one of the most significant risk factors for cardiovascular diseases and cerebro-vascular, which ranks as the first and third most frequent causes of death in elderly population all over the world. Blood pressure is a complex genetic trait with heritability estimates of 30–50%, but the intrinsic origin of essential hypertension remains obscure although many environmental factors are known. Available data on the prevalence of hypertension and the temporal trends of BP values are limited comparable data. Overall the prevalence of hypertension appears to be around 30–45% of the general population, with a steep increase with ageing, also a noticeable difference appear to be in the average BP levels across countries, with no systematic trends towards BP changes in the past decade. Stroke mortality is a good candidate, because hypertension is by far the most important cause of this event. A close relationship between prevalence of hypertension and mortality for stroke has been reported. • Path-physiology of hypertension The path-physiology of hypertension is an area of active research, attempting to explain causes of hypertension, which is a chronic disease characterized by elevation of blood pressure. Hypertension can be classified as either essential or secondary. Essential hypertension indicates that no specific medical cause can be found to explain a patient’s condition. About 90-95% of hypertension is essential hypertension. Secondary hypertension indicates that high blood pressure is a result of another underlying condition, such as kidney disease or tumors (adrenal-adenoma or pheochromocytoma). Persistent hypertension is one of the risk factors for strokes, heart attacks, heart failure and arterial aneurysm, and is a leading cause of chronic renal failure. Most mechanisms leading to secondary hypertension are well understood. The path-physiology of essential hypertension remains an area of active research, with many theories and different links to many factors. Cardiac and peripheral resistance are the two determinants of arterial pressure. Hence, for understanding the pathogenesis and treatment of hypertensive disorders, it is useful to understand factors involved in the regulation of normal and elevated arterial blood pressure. Cardiac output (CO) and peripheral vascular resistance (PVR) are the two determinants of arterial blood pressure (ABP), ABP = CO X PVR. Cardiac output is the volume of the blood pumped by the heart in a specific period of time (usually 1 minute), while peripheral vascular resistance is the force in the blood vessels that the left ventricle must overcome to eject blood from the heart. Resistance of blood flow is determined primarily by the diameter of blood vessels and blood viscosity. Increased peripheral vascular resistance results from a narrowing of the arteries and arterioles or and increased in fluid volume in the blood vessels that results from sodium and water retention. Increased peripheral vascular resistance is the most prominent characteristic of hypertension. The aging process is associated with multiple structural and functional alterations in cardiovascular system that can influence blood pressure regulation. Arterial stiffness, especially in the large arteries, is the pathological characteristic that best exemplifies geriatric hypertension. Histological, the changes are apparent in the vascular sub endothelial and media layers, which thickness of the arteries due to the accumulation of collagenous fibers, calcium deposition, and loss of elastic fibers, resulting in narrowing and increased stiffness of blood vessels. It is directly leads to increase in peripheral vascular resistance, a path gnomic characteristic of hypertension in the elderly population. Moreover, with increasing the age, blood vessels also become less responsive to B- adrenergic stimulation, which is necessary for vasodilatation. On the other hand, alpha- adrenergic responsiveness remains unchanged. These changes also contribute to increase peripheral vascular resistance and lead to hypertension. Beyond this structural change in the arteries, the regulation of vascular resistance is also affected by age related changes in the autonomic nervous system. There is an age associated decline in the sensitivity of the arterial baroreceptor. This effects the regulation of vascular resistance in two important ways. First, a larger change in blood pressure is required to stimulate the baroreceptor to invoke the appropriate compensatory response in heart rate. This also contributes to the age related increase in blood pressure variability. Second, the decrease in baroreceptor sensitivity leads to relatively greater activation of sympathetic nervous system outflow for a given level of blood pressure. An age associated increase in sympathetic nervous system activity has been demonstrated by higher plasma epinephrine and nor epinephrine levels. These hormones called catecholamine are vasoconstrictors which they cause the blood pressure to constrict making the diameter smaller. By constricting blood vessels, nor-epinephrine increases peripheral vascular resistance and raises blood pressure. Epinephrine constricts blood vessels and increases the force of cardiac contraction, causing blood pressure to rise. Regulation of peripheral vascular resistance by the vascular endothelium is also changed in relation to age. the cell of which become smaller and less uniformly aligned, this change may result in decrease production of endogenous vasodilating substances (e.g., Nitric Oxide ) and decline in local control of vascular tone. Impaired nitric oxide – mediated vasodilatation is a potential contributor to the age related increase in peripheral vascular resistance. Age related changes in renal function, particularly in renal regulation of sodium balance may also contribute to an increase in blood pressure. Decreased renal blood flow and glomelular filtration rate impair the aging kidney’s ability to excrete a sodium load. These renal changes in the regulation of sodium balance create a tendency for sodium retention. This likely plays a part in the finding that a high proportion of older hypertensive individuals, perhaps as high as two thirds, are characterized as having salt sensitivity. Slat sensitivity is operationally defined as an increase in mean arterial blood pressure, commonly 5 mmHg or more, during a high compared to a low dietary sodium intake. Additionally, aging also alter the Rennin – Angiotensin – Aldosterone – System (RAAS). This affects blood pressure through control of angiotensin II, which has been found to be responsible for sodium and volume retention, vasoconstriction, sympathetic activation, cell growth and proliferation, and possibility atherogenesis. With age, plasma rennin levels decline, and rennin response to sodium depletion, diuretic administration, and upright posture declines as well. • Risk factors for hypertension In most cases, the underlying causes of hypertension remain unknown. These risk factors can be classified as modifiable and non modifiable. Modifiable determinants include factors that can be altered, such as individual and community influences, living and working condition, and socio – cultural factors. On the other hand, non modifiable determinants include those factors that are beyond the control of the individual. A- Non modifiable risk factors: Non modifiable risk factors are inherited characteristics in a particular individual that cannot be changed such as age, sex, race or ethnicity, and heredity. i. Age Age is the most powerful risk factor for developing hypertension. The worldwide increase in the elderly population (age ≤65 years) is associated with concurrent increases in the prevalence of systemic hypertension and morbidity and mortality from vascular complications of hypertensive disease.  Cardiovascular disease becomes increasingly common with advancing age. As a person gets older, the heart undergoes subtle physiologic changes, even in the absence of disease.  The heart muscle of the aged heart may relax less completely between beats, and as a result, the pumping chambers become stiffer and may work less efficiently.  The combination of changes probably reflects stiffening of the blood vessels (reduced arterial compliance) and leads to a large increase in pulse pressure with aging.  Age related hypertension appears to be predominantly systolic rather than diastolic. Both systolic blood pressure and diastolic blood pressure increase with age. Systolic blood pressure rises progressively until the age of 70 or 80 years, whereas diastolic blood pressure increases until the age 50 or 60 years and tends to level off or even decline slightly. ii. Sex The overall incidence of hypertension is higher in men than in women until the age 55 years. After that, women’s risk for hypertension increases sharply. The National Health and Nutrition Examination Survey (NHANES) in USA (2003) showed that, the prevalence of hypertension was higher in women than in men aged 70 years old and above. iii. Heredity Family history of hypertension among first degree relatives (e.g. parents, siblings, and off-spring) is considered a risk factor for developing hypertension. First degree relatives of patients with hypertension have two fold greater risk of hypertension , and the risk increases to four fold when more family member are hypertensive. A family history of hypertension at an early age increases the risk. iv. Race or Ethnicity Prevalence of hypertension is twice as high in African American as in whites. The reason for the increased prevalence of hypertension among blacks is unclear, but the increase has been attributed to lower rennin levels, greater sensitivity to vasopressin, higher salt intake, and greater environmental stress. B. Modifiable risk factors: Modifiable risk factors could be controlled through life style modification or by medical intervention. These risk factors include diabetes mellitus, elevated serum lipids, sleep apnea, and unhealthy lifestyle as physical inactivity, consumption of unhealthy diet, obesity, smoking, excessive alcohol or caffeine intake, and poor stress management. i. Diabetes mellitus Patients with diabetes have 1.5 to 2 time increased risk of having hypertension. WHO reported that, about 60 to 65% of people with diabetes have high blood pressure. Diabetes mellitus accelerates atherosclerosis via numerous metabolic events: chronic hyperglycemia, insulin resistance, and dyslipidemia, which alter the function of multiple cell types, including endothelium, smooth muscle cells, and platelets leading to build up of atheroma in the arterial wall. Insulin resistance is a cardinal defect in type II diabetes in elderly. Insulin resistance and hyper-insulinemia are associated with hypertension. The mechanism of developing hypertension in elderly with insulin resistance may be due to increase the activity of sympathetic nervous system leading to increases in cardiac output and peripheral vascular resistance. Recent evidence suggests that glycemic control may decrease the hypertension risk. Keeping sugar well controlled minimize potential damage to blood vessels, offering strong protection against the development of high blood pressure. ii. Elevated serum lipids Raised blood cholesterol increases the risk of heart disease and stroke. Elevated levels of serum lipids (cholesterol and triglycerides are extremely common and are one of the most important risk factors that can be changed. Lowering raised blood cholesterol reduces the risk of heart disease. The prevalence of raised total cholesterol noticeably increases according to the income level of the country. In low-income countries, around 25 percent of adults have raised total cholesterol, while in high-income countries; over 50 per cent of adults have raised total cholesterol. The major lipid particles, cholesterol and triglycerides, both have important functions in the body. Cholesterol is an essential component of the cell membranes functioning to provide stability while permitting membrane transport. It is a precursor to adrenal steroids, sex hormones, bile and bile acids. Triglycerides are the major source of energy for the body. Both cholesterol and triglycerides are in soluble molecules and are transported in the circulation as lipoproteins. Normal serum cholesterol level is below 200mg/dl. When there is too much cholesterol in the body because of diet and the rate at which the cholesterol is processed, it is slowly build up in the inner lining of the arteries. This can lead to narrowing of the arteries and build up atherosclerosis. Most cholesterol in the blood is carried in two kinds of a protein called (lipoproteins): low-density lipoprotein (LDL), and high density lipoprotein (HDL). Low-density lipoprotein cholesterol, which is “bad” cholesterol causing the build-up of plaque. The optimal level of LDL cholesterol is less than 100 mg/dl. High-density lipoprotein cholesterol is the “good” cholesterol because it tends to carry excess cholesterol back to the liver where it is removed from the body. The HDL level of 60 mg/dl and above is considered protective against cardiovascular disease (CVD). People with a low level of HDL cholesterol (less than 40 mg/dl) have a higher risk of cardiovascular disease. Triglycerides are the most common type of fat in the body. The normal triglycerides level is less than 150 mg/dl. Many people who have CVD or DM have high triglycerides level combined with low HDL cholesterol or high LDL cholesterol seems to speed up atherosclerosis. Epidemiological study conducted in Japan (2004) has shown that, the level of total cholesterol in the blood is a strong predictor of elevated blood pressure. Other studies confirmed that the relation between the incidence of hypertension and high plasma cholesterol levels is gradually attenuated after the age of 65 years. Decreasing fat content in the diet is the first step in reducing cholesterol levels. Several clinical trials have shown the efficiency of lipid lowering agent as statins for reducing cardiovascular risk in patients with elevated serum lipid. iii. Sleep apnea Obstructive sleep apnea (OSA) is the most common category of sleep-disordered breathing. The term “sleep-disordered breathing” is commonly used in the U.S. to describe the full range of breathing problems during sleep in which not enough air reaches the lungs (hypopnea and apnea). Hypertension occurs in more than 50% of individuals with obstructive sleep apnea. Approximately 70% of patients with obstructive sleep apnea are obese. Hypertension related to (OSA) should also be considered in patients with drug–resistant hypertension and in patients with a history of snoring. Despite extensive research, the underlying mechanisms of obstructive sleep apnea induced hypertension are not entirely understood. Evidence indicates that sympathetic activation plays a central role on OSA–induced hypertension. iv. Lifestyle factors Lifestyle changes are important for preventing and treating high blood pressure. Healthy changes include maintaining a normal weight, exercising regularly, quitting smoking, limiting alcohol consumption to no more than one or two drinks a day, reducing sodium (salt) intake, and increasing potassium intake. • Lifestyle factors include: A) Physical inactivity: Lack of physical activity increases the risk of blood vessel disease, heart disease, and stroke. It also makes it easier to put on unwanted pounds. In addition, when you are out of shape, it takes more effort for your heart to pump blood. This increases the force exerted on arteries, which can lead to high blood pressure. Regular exercise and increasing amount of physical activity have been shown to favorably affect positively on blood pressure in people with hypertension, independent of changes in body weight and also prevent hypertension in normo-tensive individuals. An epidemiological study in USA illustrates that regular exercise and physical activity can attenuate systolic and diastolic blood pressure by 11 and 8 mmHg respectively. B) Unhealthy diet: A diet that’s high in calories, fats and sugars and low in essential nutrients contributes directly to poor health as well as to obesity. In addition, there are some problems that can happen from eating too much salt. Some people are “salt sensitive,” meaning a high-salt (sodium) diet raises their high blood pressure. Salt keeps excess fluid in the body that can add to the burden on the heart. While too much salt can be dangerous, healthy food choices can actually lower blood pressure. High dietary sodium intake is associated with an increased incidence of hypertension. At least 40% of elders who eventually develop hypertension are salt sensitive and the excess salt may be the precipitating cause of hypertension in these individuals. Decrease intake of fresh fruits and vegetables has been proposed to be a vascular risk factor. Most of this food are antioxidants and protect the arterial intima from oxidative damage. Diet low in potassium is associated with an increased risk of hypertension. Some clinical trials suggest that increasing dietary potassium by approximately (54 mmol) per day can reduce systolic blood pressure by 2-3 mmHg in hypertensive patients. C) Obesity: The prevalence of obesity is increasing drastically in the recent decade and it has become particularly high in the elderly population. The prevalence of overweight and obesity is commonly assessed by using body mass index (BMI), defined as the weight in kilograms divided by the square of the height in meters (kg/m2). A BMI ≤ 25 kg/m2 is defined as overweight and a BMI ≤ 30 kg/m2 as obese. In the elderly, obesity has been associated not only with increased mortality, but also with elevated risks of hypertension and other CVD. Anyone who is overweight has a risk for developing hypertension 50% more than people with normal weight. D) Smoking: Cigarette smoking is a major risk factor for high blood pressure. Cigarette smokers have twice the chance of developing hypertension and four times the chance of sudden death compared with non smokers. Smoking is one of the leading causes of preventable death in the United States, and it increases the risk of having a heart attack or stroke. With each cigarette you smoke, blood pressure also shoots up by as much as 10 points and stays higher for up to an hour. If you constantly have a cigarette in your hand, that could keep your blood pressure elevated for much of the day. High amounts of secondhand smoke, environmental smoke, and passive smoking can also contribute to high blood pressure; it is best to avoid cigarette smoke as much as possible. The mechanism of hypertension risk associated with smoking is complex. The main mechanism appears to be through the development and progression of atherosclerosis. Cigarette tobacco contains high concentration of oxidants and free radicals (like Nitric oxide), as well as nicotine, a major constituent of cigarettes. These constituents are considered to be absorbed into the systemic circulation, to injure the arterial endothelium and thus promote atherogenesis. Nicotine has been suggested to contribute to atherosclerosis via its effect on changes in the lipid metabolism, endothelial damage and production of growth factors. Smoking also increases insulin resistance enhances sympathetic activity which increases heart rate and blood pressure. E) Alcohol consumption: Heavy and regular use of alcohol can increase blood pressure dramatically. It can also cause heart failure, lead to stroke and produce irregular heartbeats. Too much alcohol can contribute to high triglycerides, cancer and other diseases, obesity, alcoholism, suicide and accidents. The effect of alcohol appears to be depending on the amount consumed. Reducing alcohol gradually in hypertensive patients can lower blood pressure by average of 13 mmHg systole and 15 mmHg diastole. However, the abrupt cessation of alcohol intake in individuals consuming great amounts resulted in a rapid increase in their blood pressure. F) Caffeine consumption: Caffeine can cause a short-lived but dramatic rise in blood pressure. The amount of caffeine in two to three cups of coffee can raise systolic pressure 3 to 14 millimeters of mercury (mm Hg). Diastolic pressure can be increased 4 to 13 mm Hg. However, this transient rise in blood pressure due to caffeine has not been shown to increase risk of hypertension. Caffeine actually increases blood pressure, but the association between habitual consumption of caffeinated beverages and incidence of hypertension is uncertain. However, a recent longitudinal study found a positive association between caffeine consumption and blood pressure. G) Poor stress management: Severe stress can lead to a temporary but dramatic spike in blood pressure. Over time, this might contribute to high blood pressure, although that has never been conclusively proved. In addition, some people cope with stress by overeating, drinking too much, or smoking. A study carried out in Brazil shows that people exposed to high levels of repeated psychological stress develop hypertension to a greater extent than those who do not experience as much stress. Left Ventricular hypertrophy in Hypertension Left ventricular hypertrophy (LVH) is defined as an increase in the mass of the left ventricle, which can be secondary to an increase in wall thickness, an increase in cavity size, or both. LVH as a consequence of hypertension usually presents with an increase in wall thickness, with or without an increase in cavity size. This increase in mass predominantly results from a chronic increase in afterload of the LV caused by the hypertension, although there is also a genetic component. A significant increase in the number and /or size of sarcomeres within each myocardial cell is the pathologic mechanism. Left ventricular wall thickness and/or mass is the best studied marker of hypertensive heart disease. Increased left ventricular wall thickness and mass have continuously been found to be associated with the level of blood pressure and age. However, without increased systolic blood pressure, clinically significant increases in left ventricular mass do not occur with advancing age. Chronic systolic hypertension therefore seems to be the principal cause of left ventricular hypertrophy . LVH serves as an integrated surrogate for cumulated blood pressure load and is best described as being proportional to the area under the lifetime BP curve. This is also supported by the fact that there is a strong association of left ventricular mass and mean 24-hour ambulatory blood pressure. The increase of LV mass with age might reflect the influence that other risk factors exert with time on the development of LVH. The relationship between echocardiographic LV mass and clinical blood pressure is usually weak. Twenty-four-hour blood pressure recordings have shown a much closer correlation between LV mass and average daily blood pressure. Non-haemodynamic factors, such as age, sex, race, body mass index, diabetes, and dietary salt intake, may contribute to determine who among hypertensive patients develop LVH and to what degree LVM is increased. In fact, the coexistence of hypertension with diabetes increases the prevalence of LVH. Moreover, insulin resistance and high insulin levels are associated with the development of LVH in hypertensive patients. Other major cardio-metabolic risk factors, notably hyper-cholesterolaemia and hyper-glycaemia, may also modify the extent of LVM and the prevalence of LVH in the hypertensive population. Genetic factors might also exert a powerful modulation of LV mass; in fact monozygotic twins have more similar LV mass values then di-zygotic twins. • Pathogenesis of Left Ventricular Hypertrophy: Two major triggers for LVH are biomechanical stress and neuro –hormonal factors. LVH is mainly due to pressure or volume overload on the heart. Common causes of pressure overload are systemic hypertension, aortic stenosis, coarctation of the aorta and hypertrophic cardiomyopathy. It is thought that a mechanical signal initiates a cascade of biological events which lead to coordinated cardiac growth. There is then an increased myosin heavy chain synthesis (by about 35%) within hours of pressure overload. This increase is initially predicted by an increase in translational efficiency. Neurohormonal factors that have been implicated in left ventricular hypertrophy include: Angiotensin II, endothelin, calcineurin, metallo proteinases and heterometrimeric G. Angiotensin II – It has been postulated that angiotensin II, via the AT1 receptor, plays a key role in the induction of hypertrophy because it can directly induce the molecular events of early cardiac growth. Cardiac rennin-angiotensin system has been proposed as an important determinant of hypertrophic response. The importance of angiotensin II in the development of LVH in hypertensive subjects is also suggested indirectly by the observation that an ACE inhibitor causes regression of left ventricular hypertrophy, more than other antihypertensive drugs. Endothelin – Some animal studies suggest that endothelin plays a role in the development of left ventricular wall hypertrophy in response to elevated blood pressure. Calcineurin – Calcineurin is a calcium calmodulin–dependent phosphatase. It serves as a master switch for clinical hypertrophy. In animal studies, that transgenic mice that over-express components of the calcineurin signaling pathway, develop a hypertrophic phenotype that can be expressed by pharmacological inhibitors of calcineurin. Metalloproteinase (MMPs) – Matrix metalloproteinase is a family of zinc dependant interstitial enzymes. Their tissue inhibitors (TIMPs) control the breakdown of collagen. The role of MMPs in concentric hypertrophy is not fully understood, but preliminary observations show that they are activated in experimental pressure overload hypertrophy. Studies have also shown that imbalance between MMPs and TIMPs could lead to LVH and diastolic dysfunction. Heterometrimeric G Proteins – Many hormones and neurotransmitters implicated in the initiation and exacerbation of myocardial hypertrophy including angiotensin II and endothelin, bind to cell membrane receptors which couple to a subset of intracellular hetero-metrimeric G proteins – the G (q) class.

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Essay on Hypertension

Students are often asked to write an essay on Hypertension in their schools and colleges. And if you’re also looking for the same, we have created 100-word, 250-word, and 500-word essays on the topic.

Let’s take a look…

100 Words Essay on Hypertension

What is hypertension.

Hypertension is when blood pushes too hard against the walls of your blood vessels. Imagine a garden hose with too much water pressure; it’s similar for your blood vessels. It’s often called high blood pressure and is a common health issue.

Causes of High Blood Pressure

High blood pressure can come from eating too much salt, not exercising, stress, or family history. Sometimes, it happens for no clear reason. It’s important to eat healthy and stay active to prevent it.

Why It’s Serious

If not treated, hypertension can hurt important organs like the heart and kidneys. It can lead to heart attacks, strokes, and other health problems. That’s why checking your blood pressure regularly is crucial.

Treatment and Control

Doctors usually suggest changes in diet and exercise to manage high blood pressure. In some cases, medicine is also needed. Eating less salt, more fruits and vegetables, and regular physical activity can help control it.

250 Words Essay on Hypertension

Hypertension is another name for high blood pressure. It’s a health problem where the force of your blood against your artery walls is too high. Imagine a garden hose with too much water pressure; it’s similar with blood in your body’s pipes.

Causes of Hypertension

Many things can make your blood pressure go up. Eating too much salt, not exercising, being overweight, and stress are common causes. Sometimes, it runs in families, so your parents might have it too.

Why Hypertension is Bad

High blood pressure is sneaky because you can’t feel it, but it can hurt your body. It can make your heart work too hard and weaken your blood vessels. Over time, this can lead to heart problems and strokes, which are very serious.

How to Know If You Have It

Doctors can check your blood pressure with a cuff that squeezes your arm. It’s quick and doesn’t hurt. Numbers tell if your pressure is normal, a bit high, or too high. Regular checks are important.

Keeping Blood Pressure Normal

To keep your blood pressure in check, eat healthy foods like fruits and veggies, stay active, and keep a healthy weight. If your doctor says so, you might need medicine too. Remember, taking care of your blood pressure is taking care of your heart.

500 Words Essay on Hypertension

What is hypertension.

Hypertension is the medical term for high blood pressure. Imagine the water pipes in your house. When the water pressure is too high, pipes can get damaged. Similarly, when blood moves through your body with too much force, it can harm your blood vessels and organs.

There are often no clear causes of hypertension, but many things can play a role. Eating a lot of salty foods, not exercising enough, being overweight, and smoking can increase your risk. Also, if your family members have high blood pressure, you might be more likely to have it too.

Why Is High Blood Pressure Bad?

If your blood pressure is high for too long, it can cause problems. It can make your heart work too hard and become weak. It can also damage your blood vessels, making it hard for blood to reach important parts of your body. This can lead to heart attacks, strokes, or kidney problems.

How Do You Know You Have It?

High blood pressure doesn’t usually make you feel sick, so many people don’t know they have it. That’s why it’s called a “silent killer.” The only way to know for sure is to get your blood pressure checked by a doctor or nurse.

How to Control Hypertension

If you have high blood pressure, your doctor might give you medicine to help control it. But there are also things you can do on your own. Eating healthy foods, staying at a good weight, exercising, and not smoking can all help lower your blood pressure. Cutting back on salt is especially important because salt makes your body hold on to water, which raises blood pressure.

Living with High Blood Pressure

People with high blood pressure can live normal, healthy lives if they take care of themselves. It’s important to follow your doctor’s advice, take your medicine, and make good choices like eating right and staying active. Checking your blood pressure at home and writing down the numbers can help you and your doctor know how well your treatment is working.

Hypertension, or high blood pressure, is a health issue that can lead to serious problems if not managed. It’s often caused by things we can change, like our diet or how much we exercise. By getting regular check-ups, eating well, staying active, and following your doctor’s advice, you can control your blood pressure and live a healthy life. Remember, even though high blood pressure can be dangerous, taking the right steps can help you keep it in check.

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What is Hypertension? Report

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Introduction

History of hypertension, reference list.

Medically, for one to be healthy; as concerns one’s blood pressure, the body’s arteries must maintain a pressure that should not exceed 120 systolic (maximum amount) and 80 diastolic (minimum amounts). If the body fails to maintain such pressures; more so in elevated states, two cases of blood pressure anomalies result namely: pre-hypertension and hypertension.

The former has a blood pressure ranging from 139 systolic to 89 diastolic and in most cases, it is a clear indication of likelihoods of hypertension occurring. The latter has blood pressure ranging from 140 systolic to 90 diastolic; hence, hypertension (Medilexicon International Limited, 2010, Para. 2-3).

This is one of the most chronic and common blood pressure disorders, with many associated health complications. In common life scenarios, it is very hard for individuals to recognize they suffer from the ailment, because it lacks clear symptoms that are detectable physically. In addition, the fact that, it lacks common symptoms; because of the variations that occur among different ailing individuals symptomatically, makes it harder for one to detect that, they are suffering from hypertension.

This fact makes most individuals call it the “silent assassin,” because most individuals discover they are suffering from the ailment when it is in its advanced stages. Two main forms of this ailment exist; essential and secondary, which primarily depend on the causal factors. That is, the former has no proved medical cause whereas, the latter results due to other external factors, which include tumors and kidney failures.

It is important to note that, early detection of the ailment can help in taming side effects that may result from elevated blood pressure however, if the same never happens, its persistent state is the main contributor of most health complications, which include arterial aneurysm, renal failures, and many heart complications (Cunha & Marks, 2010, p.1).

This blood pressure anomaly affects more than seventy five million U.S. inhabitants, a problem that becomes more serious in developing nations, due to lack of proper medication and detection mechanisms. It is important to note that, the condition is more prevalent among the elderly, although it also affects a good percentage of children and adults.

Hypertension is a historical health problem, which has been under study by most concerned medical researchers. The whole hypertension idea dates back to the time when Europeans endeavored to ascertain the blood circulation system. The main issue of concern then was the flow of blood and air in the human body.

As the quest continued, scientist such as Leonardo da Vinci came up with the coronary theory of blood circulation hence, disqualifying early held notions. As times passed and more questions arose as concerned blood pressure, scientist such as Cesalpino and Realdo Colombo advanced the theory of blood circulation and pressure, by bringing in the artery concept, as pertained blood circulation.

By the 19 th century, the entire concept of blood pressure received a lot of support with Claude’s findings on working of vascular nerves. Such discoveries gave a methodology that Richard bright used to link arterial contractions and blood pressure.

By wake of the 20 th century, scientist such as McLeod and Framingham in their quest to understand the factors behind hypertension linked various heart ailments to hypertension hence, making individuals to venture into discovering its causes, treatment and prevention mechanisms. In addition, this formed the main basis of the current understanding of the ailment hence, the current taming strategies adopted in most medical scenarios (Blood Pressure, 2010, p.1 and Hamdy, 2002, p.1)

Blood Pressure. A brief history of Hypertension. Blood Pressure . Web.

Cunha, P. J., & Marks, J. W. (2010). High blood pressure (hypertension) . Medicine Net . Web.

Hamdy, R. C. (2002). Hypertension: a turning point in the history of medicine and mankind . South Medical Journal , 94(11), p.1. Web.

Medilexicon international limited. What is hypertension? What causes hypertension? Medical News Today. Web.

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Hypertension

Suzanne oparil.

1 Vascular Biology and Hypertension Program, Division of Cardiovascular Disease, Department of Medicine, School of Medicine, The University of Alabama at Birmingham (UAB), 1720 2nd Avenue South, Birmingham, Alabama, USA 35294-0007

Maria Czarina Acelajado

2 Athens-Limestone Hospital, Athens, Alabama, United States of America (U.S.A.)

George L. Bakris

3 University of Chicago Medicine, Chicago, Illinois, United States of America (U.S.A.)

Dan R. Berlowitz

4 Center for Healthcare Organization and Implementation Research, Bedford Veteran Affairs Medical Center, Bedford, Massachusetts

5 Schools of Medicine and Public Health, Boston University, Boston, Massachusetts, United States of America (U.S.A.)

Renata Cífková

6 Center for Cardiovascular Prevention, Charles University in Prague, First Faculty of Medicine and Thomayer Hospital, Prague, Czech Republic

Anna F. Dominiczak

7 Institute of Cardiovascular and Medical Science, College of Medical, Veterinary and Life Sciences, University of Glasgow, United Kingdom (U.K.)

Guido Grassi

8 Clinica Medica, University of Milano-Bicocca, Milan, Italy

9 IRCCS Multimedica, Sesto San Giovanni, Milan, Italy

Jens Jordan

10 Institute of Aerospace Medicine, German Aerospace Center (DLR), University of Cologne, Cologne, Germany

Neil R. Poulter

11 Imperial Clinical Trials Unit, School of Public Health, Imperial College London, London, United Kingdom (U.K.)

Anthony Rodgers

12 The George Institute for Global Health, Sydney, New South Wales, Australia

Paul K. Whelton

13 Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine, New Orleans, Louisiana, United States of America (U.S.A.)

Author contributions

Systemic arterial hypertension is the most important modifiable risk factor for all-cause morbidity and mortality worldwide and is associated with increased risk of cardiovascular disease (CVD). Fewer than half of those with hypertension are aware of their condition, and many others are aware but not treated or inadequately treated, although successful treatment of hypertension reduces the global burden of disease and mortality. The aetiology of hypertension involves the complex interplay of environmental and pathophysiological factors that affect multiple systems, as well as genetic predisposition. Evaluation of patients with hypertension includes accurate standardized blood pressure (BP) measurement, assessing patients’ predicted risk of atherosclerotic CVD, evidence of target organ damage, detection of secondary causes of hypertension and presence of comorbidities, including CVD and kidney disease. Lifestyle changes, including dietary modifications and increased physical activity, are effective in lowering BP and preventing hypertension and its CVD sequelae. Pharmacological therapy is very effective in lowering BP and preventing CVD outcomes in most patients; first line antihypertensive medications include angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers, dihydropyridine calcium channel blockers and thiazide diuretics.

INTRODUCTION

Systemic arterial hypertension (hereafter referred to as hypertension) is characterized by persistently high blood pressure (BP) in the systemic arteries. BP is commonly expressed as the ratio of the systolic BP (that is, the pressure that the blood exerts on the arterial walls when the heart contracts) and the diastolic BP (the pressure when the heart relaxes). The BP thresholds that define hypertension depend on the measurement method ( Table 1 ). Several aetiologies can underlie hypertension. The majority (90–95%) of patients have a highly heterogeneous ‘essential’ or primary hypertension with a multifactorial gene-environment aetiology. A positive family history is a frequent occurrence in patients with hypertension, with the heritability (a measure of how much of the variation in a trait is due to variation in genetic factors) estimated between 35% and 50% in the majority of studies 1 , 2 . Genome-wide association studies (GWAS) have identified ~120 loci that are associated with BP regulation and together explain 3.5% of the trait variance 3 , 4 , 5 . These findings are becoming increasingly important as we search for new pathways and new biomarkers to develop more-modern ‘omics’-driven diagnostic and therapeutic modalities for hypertension in the era of precision medicine 6 .

Definitions of hypertension based on the 2013 ESH/ESC guidelines

For the diagnosis of hypertension, systolic BP, diastolic BP or both have to exceed the reported values.

NA, not applicable. Modified from Ref 77 .

Several rare, monogenic forms of hypertension have been described (for example, the Liddle syndrome, glucocorticoid-remediable aldosteronism (a mineralocorticoid excess state) and mutations in PDE3A (which encodes cGMP-inhibited 3’,5’-cyclic phosphodiesterase A)), in which a single gene mutation fully explains the pathogenesis of hypertension and indicates the best treatment modality 7 , 8 , 9 . If hypertension is caused by another condition (for example, primary aldosteronism, pheochromocytoma (a neuroendocrine tumour of the adrenal glands or other neuroendocrine tissues) or renal artery stenosis), it is referred to as secondary hypertension.

Hypertension is the most common preventable risk factor for cardiovascular disease (CVD; including coronary heart disease, heart failure, stroke, myocardial infarction, atrial fibrillation and peripheral artery disease), chronic kidney disease (CKD) and cognitive impairment, and is the leading single contributor to all-cause death and disability worldwide 10 . The relationship between BP and the increased risk of CVD is graded and continuous, starting as low as 115/75 mmHg, well within what is considered to be the normotensive range. Successful prevention and treatment of hypertension are key in reducing disease burden and promoting longevity in the world’s population. In treating hyperteinsion, it is important to consider a person’s predicted atherosclerotic CVD (ASCVD) risk more than the level of BP alone, as persons with high CVD risk derive the greatest benefit from BP lowering treatment 11 .

This Primer will discuss the epidemiology and pathophysiology of primary hypertension, prevention strategies for slowing the progression of BP elevation, management strategies (including optimal BP targets) for lowering BP and preventing CVD outcomes in patients with established hypertension and the effects of antihypertensive treatment on quality of life; finally, we will explore knowledge gaps, future trends and the outlook for hypertension research and treatment over the next decade.

EPIDEMIOLOGY

In pre-industrial societies, BP levels had narrow distributions with mean values that changed little with age and averaged around 115/75 mmHg 12 , a value that probably represents the normal (or ideal) BP for humans. However, in most contemporary societies, systolic BP levels rise steadily and continuously with age in both men and women. This ubiquitous finding could be explained because age is a proxy for the probability and duration of exposure to the numerous environmental factors that increase BP gradually over time, such as excessive sodium consumption, insufficient intake of dietary potassium, overweight and obesity, alcohol intake and physical inactivity. Other factors, such as genetic predisposition or adverse intrauterine environment (such as gestational hypertension or pre-eclampsia), have small but definite associations with high BP levels in adulthood 13 . Even modest rises in mean population BP lead to large increases in the absolute number of people with hypertension 14 .

As economic development progresses, hypertension initially affects those with a high socioeconomic status, but at later stages of economic development, the prevalence of hypertension and its consequences are greatest in those with lower socioeconomic status; this phenomenon is seen both within and between countries. Further, the speed of change prevalence of hypertension since 2000 to 2010 has been much more rapid than in previous epidemiological transitions 15 .

Disease burden

Globally, 3.5 billion adults now have non-optimal systolic BP levels (that is, >110–115 mmHg) and 874 million adults have systolic BP ≥140 mmHg. Thus, approximately one in four adults has hypertension 16 . Between 1990 and 2015 there was a 43% increase in the total global number of healthy life years lost to non-optimal BP, driven by population increase, population aging and a 10% increase in the age-standardized prevalence of hypertension 16 . The Global Burden of Disease study has shown that non-optimal BP continues to be the biggest single risk factor contributing to the global burden of disease and to global all-cause mortality, leading to 9.4 million deaths and 212 million lost healthy life years (8.5% of the global total) each year 10 .

Prospective observational studies have repeatedly demonstrated a strong, continuous positive relationship between BP and CVD, with no evidence of a threshold for risk throughout the usual range of BP observed in clinical practice 17 , 18 , 19 . The relationship between BP and CVD applies to both systolic BP and diastolic BP, but is somewhat more robust for systolic BP in adults 19 . It is noted in both sexes, at all ages throughout adulthood and for all major manifestations of CVD, including stroke (ischaemic and haemorroagic), coronary artery disease, heart failure, peripheral vascular disease and end stage renal disease (although there are variations in the strength of the associations and the slopes of the curves) 17 , 18 , 19 , 20 ( Figure 1 ). The relationship is independent of other CVD risk factors, and level of BP has proven to be a major component of CVD risk in all prediction models 21 . Approximately two-thirds of all adults who have hypertension or receive treatment with BP lowering medication at 30 years of age have a ~40 % higher risk of experiencing a CVD event than their age-matched and sex-matched counterparts with a lower level of BP 18 . In addition, CVD events in individuals with hypertension tend to manifest about five years earlier than in individuals with a lower level of BP 18 .

Relationship of systolic BP to subsequent risk of coronary heart disease mortality in >340,000 US men 35–57 years of age at the beginning of the study followed-up for an average 11.6 years. A | Distribution of the incidence of coronary heart disease mortality, adjusted for age, race, total serum cholesterol level, cigarettes smoked per day, use of medication for diabetes, and income. Individuals with the highest BPs were at greatest risk for CVD mortality. B | Prevalence of coronary heart disease mortality; only a minority of the sample was exposed to the high risk associated with hypertension (≥140 mmHg for systolic BP, as per office BP measurement). However, a much larger number of them, who had BP in the non-hypertensive range, were exposed to the more modest but still important increases in CVD risk. C | Estimation of the percent of excess coronary heart disease deaths occurring in each category of systolic BP, using those with a systolic BP <110 mm Hg as the reference group. About two-thirds of the overall burden of BP-related CHD mortality occurred in men who had a systolic BP ≥140 mmHg (25% of the sample). However, about two-thirds of the remaining disease burden could be attributed to the approximately 20% of adults who had a systolic BP in the high-normal range (systolic BP 130–139 mmHg) 204 . Data from Ref. 19 .

In individuals of 40–69 years of age, a 20 mmHg rise of systolic BP or a 10 mmHg rise of diastolic BP regardless of baseline values is associated with more than a doubling of the risk for stroke or ischaemic heart disease mortality 17 , whereas a systolic BP reduction of 5 mmHg can decrease stroke mortality by 14% and CVD mortality by 9%. At older ages (≥80 years), the corresponding relative risk is slightly lower, but the absolute risk is far greater than earlier in life 17 . For example, a 20 mm Hg difference in systolic BP between 120 and 140 mmHg is associated with an annual difference in absolute risk that is nearly ten times larger at ages 80–89 years than that at ages 50–59 years 17 .

MECHANISMS/PATHOPHYSIOLOGY

Bp regulation.

BP is determined by several parameters of the cardiovascular system, including blood volume and cardiac output (the amount of blood pumped by the heart per minute) as well as the balance of arterial tone that is affected by both intravascular volume and neurohumoral systems (discussed in the following sections). The maintenance of physiological BP levels involves a complex interplay of various elements of an integrated neurohumoral system that includes the renin-angiotensin-aldosterone system (RAAS), the role of natriuretic peptides and the endothelium, the sympathetic nervous system (SNS) and the immune system ( Figure 2 ). Malfunction or disruption of factors involved in BP control in any of these systems can directly or indirectly lead to increases in mean BP, BP variability or both, over time resulting in target organ damage (for example, left ventricular hypertrophy and CKD) and CVD outcomes 22 .

Neurohumoral, immune and organ systems involved in the maintenance of blood pressure. BP: Blood pressure, RAAS: renin-angiotensin-aldosterone system.

The pathophysiological mechanisms responsible for hypertension are complex and act on a genetic background. Primary hypertension involves multiple types of genes; some allelic variants of several genes are associated with an increased risk of developing primary hypertension and are linked in almost all cases to a positive family history ( Box 1 ) This genetic predisposition, along with a host of environmental factors, such as high Na + intake, poor sleep quality or sleep apnoea, excess alcohol intake and high mental stress, contribute to the development of hypertension 22 , 23 , 24 . Finally, the probability of developing hypertension increases with aging, owing to progressive stiffening of the arterial vasculature caused by, among other factors, slowly developing changes in vascular collagen and increases in atherosclerosis 25 , 26 , 27 . Immunological factors can also play a major part, especially on the background of infectious or rheumatological diseases such as rheumatoid arthritis. The mosaic theory of hypertension describes its multifaceted pathophysiology 28 , 29 .

Genetic predisposition to hypertension

A large GWAS of 2.5 million genotyped single nucleotide polymorphisms (SNPs) in >69,000 individuals of European ancestry from 29 studies demonstrated that most SNPs related to BP regulation and CVD risk involved natriuretic peptides 198 . SNPs in genes that encode precursors for ANP and BNP had been previously identified 199 , and two other loci were identified in this study, containing genes involved in natriuretic peptide and NO signalling pathways; both these pathways regulate cyclic guanosine monophosphate, which promotes vasodilation. A 2016 study identified 66 BP–associated loci, which were enriched for cis -regulatory elements in vascular endothelial cells, consistent with a role in BP control through modulation of vascular tone. This information prompted development of a genetic risk score to predict target organ damage 4 .

Gene deletion studies in rodent models have evaluated cardiac ANP and BNP as paracrine regulators of vascular regeneration. Deletion of the genes encoding ANP and BNP exaggerates cardiac fibrosis and increase adverse left ventricular (LV) remodelling 38 , and natriuretic peptide receptor A (NPRA) deficiency leads to increased BP, severe fibrosis and LV dysfunction. Further, deletion of the gene encoding the endothelial guanylyl cyclase-A (GC-A) receptor, a cell surface receptor for natriuretic peptides, leads to diminished vascular regeneration and angiogenesis in response to critical hind limb ischemia, as well as cardiac fibrosis and diastolic dysfunction.

Further, clinical studies have observed an association between certain corin gene polymorphisms and risk of pre-eclampsia and hypertension, particularly among African-American but not Chinese populations 200 .

Sodium homeostasis regulation

Sodium (Na + ) is a crucial regulator of blood volume: high serum Na + concentration promotes fluid (water) retention, thereby increasing blood volume and BP. When dietary Na + increases in normotensive individuals, compensatory haemodynamic changes occur to maintain constant BP. These changes include reduction in renal and peripheral vascular resistance and increased production of nitric oxide (a vasodilator) from the endothelium. However, if the effect of nitric oxide is impaired or absent, an increase in BP occurs. Endothelial dysfunction is a risk factor for the development of salt sensitivity and subsequent hypertension. Salt sensitivity is defined as a marked elevation in BP following a Na + load of ≥5 g and is characterized by an elevation of systolic BP of at least 10 mmHg within a few hours of ingestion. Salt sensitive individuals have underlying endothelial dysfunction due to genetic or environmental influences. In response to a high salt load these individuals generally manifest overproduction of transforming growth factor β (TGF-β), which increases the risk of fibrosis, and oxidative stress, and have limited bioavailable nitric oxide. Chronic high salt ingestion can result in endothelial dysfunction, even in salt-resistant individuals 30 , and also affects the gut microbiota, with resultant changes that contribute to increased salt sensitivity and the development of hypertension 31 . High salt intake also appears to drive autoimmunity by inducing T helper 17 (T H 17) cells 31 . High salt intake in mice has been shown to deplete Lactobacillus murinus in the gut microbiota. Treatment of mice with L. murinus prevented salt-induced exacerbation of salt-sensitive hypertension by modulating T H 17 cells 31 . In line with these findings, a moderate high-salt challenge in a pilot study in humans reduced intestinal survival of Lactobacillus spp., increased the activity of T H 17 cells and increased BP 31 . Thus, the gut microbiota appears to contribute to salt sensitivity of BP and the pathogenesis of hypertension.

Renin-Angiotensin-Aldosterone System

The RAAS has wide-ranging effects on BP regulation, mediating Na + retention, pressure natriuresis (that is, the mechanism whereby increases in renal perfusion pressure (the gradient between renal arterial and venous blood pressure) lead to decreased Na + reabsorption and increased Na + excretion), salt sensitivity, vasoconstriction, endothelial dysfunction and vascular injury, and plays an important part in the pathogenesis of hypertension 22 . The RAAS is present at the cellular level in many organs, but its most crucial role is to help regulate pressure-volume homeostasis in the kidney, where it maintains perfusion in volume depleted states (that is, when there is a reduction in extracellular fluid volume as a result of sodium and fluid loss) and is suppressed in volume expanded (fluid overload) conditions. Renin and its precursor pro-renin are synthesized and stored in the juxtaglomerular cells of the kidney and are released in response to various stimuli ( Figure 3 ). The main function of renin is to cleave angiotensinogen to form angiotensin I. Angiotensin-converting enzyme (ACE) cleaves angiotensin I to form angiotensin II, which is at the center of the pathogenetic role of the RAAS in hypertension ( Figure 3 ) 32 ..

Decreased renal afferent perfusion pressure, reduced Na + delivery to the macula densa (an area lining the wall of the distal convoluted tubule in correspondence of the glomerulus), activation of renal sympathetic nerves (via β 1 adrenergic receptor stimulation) and a variety of vasodilators, including prostaglandin E2, stimulate the release of renin. Angiotensin II activates the AT1 receptor, triggering smooth muscle cell contraction, systemic vasoconstriction, increased renovascular resistance and decreased renal medullary blood flow, a mediator of salt sensitivity. Stimulation of the AT2 receptor has opposite effects, resulting in vasodilation, natriuresis and anti-proliferative actions. Cross-transplantation studies using wild-type mice and mice lacking the AT1 receptor have shown that both systemic and renal actions of angiotensin II are relevant to physiologic BP regulation, but that the detrimental effects of angiotensin II in hypertension are mediated mainly via the kidney 205 , 206 . ACE inhibitors and AT1 receptor antagonists have been shown to increase Ang-(1–7) levels in plasma and urine of normotensive animals and enhance renal ACE2 activity 33 .. Studies in rodents and humans with non-diabetic kidney disease suggest that upregulation of ACE2 may delay progression of kidney disease 207 .

Angiotensin II enhances Na + reabsorption in the proximal tubule by increasing the activity of the sodium-hydrogen exchanger (NHE3), sodium-bicarbonate exchanger and sodium-potassium ATPase, and by inducing aldosterone synthesis and release from the adrenal glomerulosa 22 . Angiotensin II is also associated with endothelial dysfunction and has pro-fibrotic and pro-inflammatory effects, mediated in large part by increased oxidative stress, resulting in renal, cardiac and vascular injury. Angiotensin II is tightly linked to target organ damage in hypertension via these mechanisms 22 ..

Angiotensin-converting enzyme 2 (ACE2) has emerged as an important modulator in the pathophysiology of hypertension, CVD and renal disease, owing to its role in metabolizing angiotensin II into angiotensin-(1–7) 33 . Ang-(1–7) induces systemic and regional vasodilation, diuresis and natriuresis, and exerts antiproliferative and antigrowth effects on vascular smooth muscle cells, cardiac myocytes and fibroblasts as well as glomerular and proximal tubular cells 33 . Ang-(1–7) also has cardiorenal protective effects that are mediated by the proto-oncogene Mas receptor through signalling pathways that include mitogen-activated protein kinases (MAPK), PI3K-AKT, NADPH oxidase, TGF-β1, the EGF receptor, and NF-κB activity 33 , 34 , 35 .

Aldosterone plays a crucial part in hypertension: by binding to the mineralocorticoid receptor, it induces non-genomic effects (that is, without directly modifying gene expression) that include activation of the amiloride-sensitive sodium channel, commonly known as the epithelial sodium channel (ENaC) and result in the stimulation of renal Na + reabsorption in the cortical collecting duct 36 . Aldosterone also has many non-epithelial effects that contribute to endothelial dysfunction, vasoconstriction and hypertension 36 , 37 . These include vascular smooth muscle cell proliferation, vascular extracellular matrix deposition, vascular remodeling, fibrosis, and increased oxidative stress 36 , 37 .

Natriuretic Peptides

Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) play an important part in salt sensitivity and hypertension. They have important natriuretic and vasodilator properties that allow maintenance of Na + balance and BP during Na + loading 38 , 39 . Upon administration of a Na + load, atrial and ventricular stretch leads to release of ANP and BNP, respectively, which leads to systemic vasodilation and decreased plasma volume (owing to fluid shifts from the intravascular to the interstitial compartment) and results in BP lowering 40 . Natriuretic peptides increase glomerular filtration rate via an increase in efferent arteriolar tone in volume-expanded states and inhibit renal Na + reabsorption through both direct and indirect effects. Direct effects include decreased activity of Na + -K + -ATPase and the sodium-glucose co-transporter in the proximal tubule and inhibition of the epithelial sodium channel in the distal nephron. Indirect effects include inhibition of renin and aldosterone release 39 .

Natriuretic peptide deficiency promotes hypertension. Corin is a serine protease that is largely expressed in the heart and converts the ANP and BNP precursors pro-ANP and pro-BNP to their active forms. Corin deficiency has been associated with volume overload, heart failure and salt-sensitive hypertension 41 . Natriuretic peptide deficiency also predisposes to insulin resistance and type 2 diabetes mellitus. Obesity is associated with natriuretic peptide deficiency, probably through upregulation of the natriuretic peptide scavenger receptor NPR-C in adipose tissue 42 . Natriuretic peptides have therapeutic potential for the metabolic syndrome; the metabolic syndrome is a cluster of conditions (including high BP, high fasting glucose levels, abdominal obesity, high triglycerides and microalbuminuria) that occur together, increasing the risk of CVD and diabetes mellitus 42 .

The Endothelium

The endothelium is a major regulator of vascular tone and major contributor to salt sensitivity through NO. Endothelial cells produce a host of vasoactive substances, of which NO is the most important in BP regulation 43 , 44 . NO is continuously released by endothelial cells in response to flow-induced shear stress, leading to vascular smooth muscle relaxation through activation of guanylate cyclase and generation of intracellular cyclic guanosine monophosphate 45 . Interruption of NO production via inhibition of constitutively expressed endothelial NO synthase (eNOS) causes BP elevation and development of hypertension in animals and humans 46 . Studies to evaluate NO activity in humans have demonstrated decreased whole-body production of NO in patients with hypertension compared with normotensive controls 46 , 47 .

Endothelial cells also secrete a variety of other vasoregulatory substances, including vasodilators such as prostacyclin and endothelium-derived hyperpolarizing factors, and vasoconstrictors such as endothelin 1 (ET-1), locally generated angiotensin II and the prostanoids thromboxane A2 and prostaglandin A2. ET-1 is a potent vasoconstrictor that activates ET-A receptors in vascular smooth muscle 48 . Other vasodilating substances, secreted by a variety of cells types, such as calcitonin gene related peptide, adrenomedullin and substance P act primarily through increases in NO release from endothelial cells 49 , 50 . The glucose-regulating gut hormone glucagon-like peptide-1 (GLP-1) also has vasodilating properties 51 . The balance between these factors, along with NO and ET-1, determines the final effect of the endothelium on vascular tone 52 , 48 , 53 , 51 . Circulating ET-1 levels are not consistently increased in hypertension, but there is a trend toward increased sensitivity to the vasoconstrictor and hypertensive effects of ET-1 in individuals with hypertension 53 . ET-A receptor antagonists attenuate or abolish hypertension in a variety of experimental models and are effective in lowering BP in humans 48 , 53 .

Endothelial dysfunction plays a seminal part in the pathogenesis of hypertension. Normotensive offspring of parents with hypertension often have impaired endothelium-dependent vasodilation, which implies a genetic component in the development of endothelial dysfunction 47 . Endothelial dysfunction in the setting of chronic hypertension is related to a combination of direct pressure-induced injury and increased oxidative stress. Several enzyme systems, including NADPH oxidase, xanthine oxidase and cyclooxygenase, as well as decreased activity of superoxide dismutase generate reactive oxygen species 47 , 54 . Excess superoxide anions bind to NO, decreasing NO bioavailability and generating the pro-inflammatory oxidant, peroxynitrite. Decreased NO bioavailability is the central factor that links oxidative stress to endothelial dysfunction and hypertension 47 . Salt-sensitive individuals may be very sensitive to the hemodynamic stress of increased blood volume, leading to overproduction of TGF-beta, oxidative stress, and limiting bioavailable NO 30 . Angiotensin II, along with other factors, including cyclic vascular stretch as a result of BP changes, endothelin-1 (ET-1), uric acid, systemic inflammation, norepinephrine, free fatty acids, and tobacco smoking, enhances NADPH oxidase activity and plays a central part in the generation of oxidative stress in hypertension 52 .

Sympathetic Nervous System

Baroreceptors, mechanoreceptors that sense pressure changes of the circulatory system, are housed in various locations in the arterial tree, a key place being the carotid sinus, a dilated area at the base of the internal carotid artery just superior to bifurcation of the common carotid artery. When this artery is stretched by elevated BP, nerve bundles projecting from the baroreceptors in the carotid sinus send messages to the brain to reduce sympathetic outflow of nerve impulses or nerve traffic and, thereby, BP 55 , 56 , 57 . The SNS is generally more activated in persons with hypertension than in normotensive individuals. 58 , 59 SNS activity is also greater in individual with obesity, in men than in women, in younger than in older persons, and in those with advanced kidney disease. 60 , 61 Many patients with hypertension are in a state of autonomic imbalance with increased sympathetic and decreased parasympathetic activity 59 , 62 . SNS hyperactivity is relevant to both the generation and maintenance of hypertension. Studies in humans have also identified markers (such as increased catecholamine spillover and sural nerve activity assessed by microneurography) of sympathetic overactivity in normotensive individuals with a family history of hypertension 63 . Among patients with hypertension, increasing severity of hypertension is associated with increasing levels of sympathetic activity measured by microneurography 64 , 65 . Plasma catecholamine levels, microneurographic recordings and systemic catecholamine spillover (the amount of catecholamines released from sympathetic nerves innervating blood vessels that enter the bloodstream) studies have given evidence of increased sympathetic activity in patients with hypertension who are obese, in those with the metabolic syndrome, and in those whose hypertension is complicated by heart failure or kidney disease 65 .

The importance of the SNS in the pathogenesis of hypertension has been defined in a variety of experimental models. Models of obesity-related hypertension demonstrate that increased renal sympathetic nerve activity and its attendant increase in renal sodium reabsorption are key factors in the maintenance of sustained hypertension 62 . In another animal model, rats that received daily infusions of phenylephrine for 8 weeks developed hypertension during the infusions; their BP normalized under a low salt diet after discontinuation of phenylephrine, but once re-challenged with a high salt diet, the animals became hypertensive again 30 . The degree of BP elevation on the high salt diet was directly related to the degree of renal tubulo-interstitial fibrosis and decrease in glomerular filtration rate, suggesting that catecholamine-induced hypertension causes renal interstitial injury and a salt-sensitive phenotype that persists even after sympathetic overactivity is no longer present. In addition, enhanced SNS activity results in alpha-1 adrenergic receptor mediated endothelial dysfunction, vasoconstriction, vascular smooth muscle proliferation and increased arterial stiffness, which contribute to the development and maintenance of hypertension 66 . Finally, there is evidence that sympathetic overactivity enhances salt-sensitivity owing to a reduction in activity of the WNK lysine deficient protein kinase 4 ( WNK4 ) gene, which encodes a serine/threonine kinase that inhibits the thiazide-sensitive-Na-Cl co-transporter, resulting in increased distal tubular Na + retention 67 . These mechanisms have been reviewed recently 66 .

Inflammation and the immune system

Inflammation makes an important contribution to the genesis of hypertension and related target organ damage. Inflammation is associated with increased vascular permeability and release of potent mediators, such as reactive oxygen species, NO, cytokines and metalloproteinases. Cytokines mediate the formation of neo-intima (a new or thickened layer of arterial intima), thereby decreasing the lumen diameter of resistance vessels (small arteries and arterioles highly innervated by autonomic nerves and the primary vessels involved in the regulation of BP), and promoting vascular fibrosis, leading to increased vascular resistance and stiffness. Cytokines also affect renal tubular function by increasing local synthesis of angiotensinogen and angiotensin II, as well as promoting sodium and volume retention in hypertension 68 . Matrix metalloproteinases stimulate the degradation of the extracellular matrix, allowing infiltration of immune cells through the vessel wall into the interstitium of the affected organs, promoting apoptosis and enhancing collagen synthesis and matrix deposition, leading to target organ damage 68 .

While animal data are clear about the relationship between inflammation and hypertension, the data in humans are limited. There are associations between C-reactive protein, TNF-alpha and various interleukins and hypertension, but no direct link 68 . GWASs have identified a single nucleotide polymorphism of SH2B3 (SNP rs3184504), which results in an amino acid substitution in SH2B adapter protein 3 (a protein involved in T cell receptor activation and signalling), that is associated with many autoimmune and cardiovascular disorders, including hypertension 69 . Further, drugs that are used to treat inflammation, such as non-steroidal anti-inflammatory drugs and cyclosporine, raise rather than lower BP in hypertensive individuals, highlighting the complex nature of the relationship between inflammation and hypertension 69 .

Both innate and adaptive immune responses participate in the generation of reactive oxygen species and inflammatory changes in the kidneys, blood vessels and brain in hypertension 68 , 70 . Innate immune responses, especially those mediated by macrophages, have been linked to hypertension induced by angiotensin II, aldosterone and NO antagonism 68 , 70 . Reductions in macrophage infiltration of the kidney or the peri-adventitial space of the aorta and medium sized arteries lead to reductions in BP and salt-sensitivity 68 . Adaptive immune responses via T cells have also been linked to the genesis of hypertension and its target organ damage. T cells express AT1 receptors and mediate angiotensin II-dependent hypertension, 70 and it has been shown that depletion of mature lymphocytes ameliorated hypertension and kidney injury resulting from a high-salt diet in the Dahl SS rat 71 . Thus, a balance between proinflammatory T cell reactivity and inflammatory suppression induced by T regulatory cells determines the development of hypertension, as demonstrated by the amelioration of hypertension with the adoptive transfer of T regulatory cells in several animal models of hypertension 68 – 70 . Abnormalities in both pro-inflammatory T cells and regulatory T cells are implicated in hypertension-induced target organ damage, as they regulate the inflammatory processes in the kidney and vasculature that underlie hypertension-induced kidney disease 68 , 70 , 71 .

DIAGNOSIS, SCREENING AND PREVENTION

Diagnosis and screening.

Essential or primary hypertension is usually asymptomatic; thus, in clinical practice all adults should have their BP measured at regular office visits. Hypertension is most commonly diagnosed based on repeated BP measurements in a clinical office setting. Accurate measurement and recording of BP is essential to categorize the level of BP, ascertain BP-related CVD risk and guide management. Since 2010, methods to measure out-of-office BP have been increasingly introduced to guide diagnosis and treatment of hypertension 72 , 73 . Table 1 These include home BP monitoring (HBPM) and ambulatory BP monitoring (ABPM). HBPM refers to the measurement of BP at regular intervals by an individual at their home or elsewhere outside the clinic setting. ABPM consists of measuring and recording the BP at regular intervals (usually every 20–30 minutes), typically for the 24-hour period and while individuals go about their daily activities. The ability to measure out-of-office BP has enabled the identification of distinct BP phenotypes, including white coat or isolated clinic hypertension and masked or isolated ambulatory hypertension 74 , 75 . White coat hypertension is characterised by elevated office BP but normal ABPM or HBPM readings. By contrast, masked hypertension is characterised by normal office readings but elevated out –of-office readings ( ABPM and HBPM ) 74 , 75 .

The evaluation of a patient with hypertension requires more than the diagnosis of elevated BP. It should also include assessment of the CVD risk, target organ damage, and concomitant clinical conditions that may affect the BP or related target organ damage as well as recognition of features suggestive of secondary hypertension. Some of these investigations are routine tests necessary in all patients, but others only in specific patient groups identified by history, clinical examination, and routine tests. In rare inherited forms of hypertension, a single gene mutation explains the pathogenesis of hypertension 7 , 8 , 9 . ( Figure 4 ) A small proportion of patients have a potentially reversible cause of hypertension, and a correct diagnosis might lead to a cure or a substantial improvement in BP control with a reduction of CVD risk. It is therefore appropriate to implement a simple screening for secondary hypertension in all patients. The screening is based on clinical history, physical examination and routine laboratory investigations ( Box 2 and 3 ). Secondary hypertension should also be considered in cases of a sudden worsening of hypertension, poor BP response to drug treatment or severe target organ damage, which is out of proportion to the duration and severity of hypertension. In these cases, specific diagnostic tests are indicated ( Table 2 ).

Some inherited diseases can affect the renal-angiotensin-aldosterone system pathways and, therefore, the blood pressure; hypertensive disorders are listed in red boxes and hypotensive disorders in green boxes. MR, mineralocorticoid receptor; GRA, glucocorticoid-remediable aldosteronism; PHA1, pseudohypoaldosteronism, type-1; AME, apparent mineralocorticoid excess; SLC12A1, solute carrier family 12 member 1; SLC12A3, solute carrier family 12 member 3; CLCNKB, chloride channel protein ClC-Kb; KCNJ, inward rectifier potassium channel; ECaC, epithelial calcium channel; ENaC; epithelial Na channel; WNK1, Serine/threonine-protein kinase WNK1; HSD11B1, corticosteroid 11-beta-dehydrogenase isozyme 1; CYP21A2, steroid 21-hydroxylase; CYP17A1, steroid 17-alpha-hydroxylase/17,20 lyase; CYP11B1, cytochrome P450 11B1, mitochondrial. Modified from Ref 7

Table 2 –

Diagnostics of secondary hypertension

CT, computed tomography; GFR, glomerular filtration rate; MRI, magnetic resonance imaging; RAA, renin–angiotensin–aldosterone

Modified from Ref 77 .

Box 2 –

Physical examination for secondary hypertension, organ damage and obesity.

BMI, body mass index

Box 3 –

Laboratory investigations in the diagnosis of hypertension.

The medical history has to address the time of the first diagnosis of hypertension, current and past BP measurements and antihypertensive medications. A history of pregnancy-related hypertension is an important factor in the assessment of women with hypertension. Hypertension results in an increased risk of CVD complications, and chronic kidney disease (CKD). Thus, a careful medical history should be taken in all patients to allow for assessment of global CVD risk, with special emphasis on current and past smoking habits and evidence of dyslipidaemia and diabetes mellitus. CVD risk should be estimated using an established calculator (e.g. http://ASCVD-Risk-Estimator/ ). Adults at high risk for CVD have a high probability to benefit from antihypertensive drug therapy in addition to lifestyle change 76 .

The physical examination aims to establish the diagnosis of hypertension and screen for target organ damage and secondary causes ( box 2 ). The patient should sit quietly for 5 minutes before a BP reading is taken and BP cuff should be at heart level. An average of 2 to 3 BP measurements obtained at 2 to 3 separate occasions provides an accurate basis for estimation of BP 77 , 78 . At least once, BP should be measured on both arms, and differences in SBP > 20 mmHg and/or in DBP >10mmHg should initiate investigations of vascular abnormalities 77 . Careful attention should be paid to choosing appropriately sized cuff, particularly for the increasing number of patients with obesity. Further, BP should be measured in both sitting and standing positions to rule out orthostatic hypotension (a sudden drop of the BP when a person stands up from a lying or sitting position). This is particularly important in elderly individuals.

All patients should undergo auscultation of the carotid arteries, heart and renal arteries. Detection of murmurs (sounds audible via the stethoscope) should lead to further investigations: carotid ultrasound, echocardiography and renal ultrasound, respectively. An irregular pulse frequently indicates atrial fibrillation, which should be confirmed by an electrocardiogram (EKG). Laboratory investigations are used to detect additional risk factors, to confirm or exclude secondary hypertension, to detect clinical or subclinical target organ damage and to estimate global CVD risk ( box 3 ).

Despite overwhelming evidence that hypertension is a major treatable CVD risk factor, studies across the world show that a large proportion of individuals with hypertension are either unaware of their high BP or aware but not treated or inadequately treated 79 , 15 . Thus, there is a strong indication to screen middle-aged or younger persons in order to detect and treat more patients with hypertension. The most serious attempt by a healthcare system to improve the diagnostic aspects of hypertension has been done in the UK, based on pay-for-performance principle, that is, to give incentives to general practitioners (primary care physicians) for the appropriate diagnosis and treatment of chronic diseases, including hypertension. Early reports 80 , 81 showed that this initiative was associated with an increased rate of BP monitoring and better BP control, but a later report suggested that this was not a sustained improvement 82 . It is possible that the initiative championed by the International Society of Hypertension and many national societies, which targeted entire populations by screening for hypertension in public places over the entire month of May 2017, might have better and more sustained results 83 .

The association between BP and risk of CVD highlights the importance of treating hypertension, especially when severe. Further, it also underscores the importance of strategies to reduce BP-related CVD risk in those who have a higher than normal level of BP (average systolic BP 120–129 mmHg) but below the hypertension threshold. Reducing BP in adults with a high normal BP (referred to as elevated BP in the 2017 US guidelines) provides the potential to directly reduce CVD risk and to prevent or at least slow the age-related tendency for individuals to develop hypertension.

In most countries there is a strong tendency for BP, especially systolic BP, and the prevalence of hypertension to increase progressively from childhood until late in life 79 . However, studies in isolated societies that have limited contact with the outside world 84 , 85 indicate that high BP is not an inevitable consequence of aging and that the rise in BP associated with local migration by members of isolated societies is related to changes in diet, decreased physical activity and consumption of alcohol 84 , 86 , 87 . These reports underscore the logic of efforts to prevent high BP in settings where an age-related increase in BP is common.

Lifestyle changes

A variety of nonpharmacological interventions have been shown to be effective in lowering BP and preventing hypertension. The most effective interventions are weight loss 88 , 89 , 90 , reduced Na + intake 88 , 89 , 90 , 91 , increased potassium intake 92 , 93 , increased physical activity 94 , reduced consumption of alcohol 95 , 96 and diets like the Dietary Approaches to Stop Hypertension (DASH) diet 97 that combine several elements which favorably affect BP 98 , 99 ( table 3 ). The DASH diet is especially successful when combined with other effective BP lowering interventions such as a reduced intake of dietary sodium 91 . Lifestyle change is the best way for the individual to implement these interventions. Even small improvements in an individual’s lifestyle can be valuable. Government agency and professional society websites provide helpful tips for lifestyle change and monitoring of BP. Careful monitoring of BP is essential because the beneficial effects of lifestyle change are predicated on maintenance of the intervention 100 .

Dietary Approaches to Stop Hypertension (DASH) eating plan

Two complementary strategies aimed at achieving a small population-wide reduction in BP or a larger reduction in those who are at higher risk to develop hypertension can be employed to implement hypertension prevention interventions 98 , 99 , 101 . Modeling studies suggest that a downward shift of as little as 2 mmHg in the population distribution of diastolic BP would result in a 17% reduction in the incidence of hypertension, a 14% reduction in the risk of stroke and transient ischemic attacks, and a 6% reduction in the risk of coronary heart disease 102 . Public health interventions focused on dietary improvements and increases in physical activity that are known to lower BP provide the basis for the population-wide strategy. Diet in the general population can be favorably influenced by means of public health education campaigns, food product labeling, and collaborations with food manufacturers to reduce the calorie and sodium content of their products, as well as with fast food companies and restaurants to reduce portion size and to promote healthier food preparation and promotion practices. Physical activity can be enhanced by making it easier for members of the community to engage in exercise on a routine basis.

Pharmacological interventions

Low-dose pharmacological therapy has also been shown to be effective in lowering BP and preventing hypertension in three randomized controlled trials conducted in adults with high normal BP 103 , 104 , 105 . The Brazilian multi-center PREVER-Prevention Trial compared treatment with the low-dose long-acting thiazide-like diuretic chlorthalidone in combination with the potassium sparing agent amiloride with treatment with placebo 105 . Treatment with the low-dose chlorthalidone and amiloride combination resulted in both a decrement in BP and prevention of hypertension and a reduction in left ventricular mass. A drug intervention is easier to implement and maintain than a lifestyle change intervention but there is a natural reluctance to recommend a lifetime of pharmaceutical therapy for prevention of hypertension. Consideration of low-dose pharmacotherapy should be restricted to those who are at high risk of developing hypertension despite energetic efforts to lower BP by means of one or more nonpharmacological interventions 105 .

BP treatment thresholds and targets

Until 2015, most guidelines recommended a target BP < 140/90 mmHg for most patients and < 150/90 mmHg for elderly patients over 60 or 80 years of age ( Table 4 ) 77 , 106 . However, after the publication of the Systolic blood PRessure Intervention Trial (SPRINT) 107 , target systolic BP values have been frequently debated. SPRINT was a randomized, open-label controlled trial that enrolled 9361 participants without diabetes mellitus but with increased CVD risk. Patients with a history of stroke were excluded. Participants were randomized to a standard systolic BP target < 140 mmHg or intensive systolic BP target < 120 mmHg. Intensive BP treatment in SPRINT resulted in a significantly greater (25%) reduction in the primary endpoint (first occurrence of myocardial infarction, acute coronary syndrome, stroke, heart failure or death from cardiovascular causes), compared with standard treatment. Office BP measurement in SPRINT was performed with an automated device timed to start measurement after 5 minutes of rest in an effort to standardize measurements in the various clinics and minimize the white coat effect. Because large differences had been observed between automated office BP measurement and conventional auscultatory measurements (with the automated technique showing lower values) 108 , some groups have questioned the applicability of the SPRINT intensive systolic BP target of < 120 mmHg to ordinary office practice 109 . Both the appropriate method(s) of measuring office BP (automated versus manual; unattended versus attended) and the appropriate BP targets for antihypertensive treatment are currently topics of vigorous debate. In summary, newer guidelines published after the SPRINT trial generally have more aggressive goals, at least for individuals < 65 years of age ( Table 4 ).

Blood pressure targets recommended by various guidelines

The 2013 ASH/ISH guidelines were written to provide information for practitioners in low-income and middle-income countries as well as in developed countries.

Patient’s global CVD risk and comorbidities should be considered in determining the need for pharmacologic antihypertensive treatment. The 2017 US ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation and Management of High Blood Pressure in Adults 110 recommend the use of antihypertensive medication in patients with pre-existing CVD and those without a CVD event but an estimated 10-year atherosclerotic cardiovascular disease (ASCVD) risk of 10% or higher at BP levels ≥ 130/80 mmHg. In individuals without CVD and with 10-year ASCVD risk < 10%, antihypertensive medication should be initiated at BP ≥ 140/90 mmHg. ( Figure 5 ).

Reproduced from ref 110 .

Non-Pharmacological Management

Lifestyle advice is recommended for all patients with hypertension. The most effective interventions are the same as for prevention of hypertension. Targeted dietary approaches can reduce the systolic BP in individuals with hypertension. For example, reducing sodium intake (ideally to <2.3 g per day, or <1.5 g per day in those most susceptible to the effects of sodium on BP, but reduction by at least 1.0 g per day is desirable) can lower the systolic BP by 2–4 mmHg (Ref 110 , 111 , 112 ). A similar reduction can be expected with increases in potassium intake to 3.5– 5.0 g per day 92 .

Reduced salt intake

For metabolic balance, the amount of salt consumed must be equal to that lost. Thus, under normal living conditions and physical activity levels, an intake of 5 g salt/day is considered sufficient, in line with the WHO recommendation (< 5 g per day) 113 . By contrast, the currently estimated dietary intake of salt is about 9–12 g per day in most countries. The current recommendations of the American Heart Association 114 and American Society of Hypertension 115 are stricter than the European guidelines, recommending lowering salt intake to 3.8 g per day, whereas the 2013 ESH/ESC guidelines recommend 5–6 g of salt per day 77 .

Randomized controlled trials carried out in persons with hypertension have consistently shown that reduced sodium intake is associated with reduction of BP 116 . The most convincing evidence is provided by the Dietary Approaches to Stop Hypertension (DASH-sodium) trial 91 , in which the effects of three different sodium intakes were tested separately in combination with two diets: the DASH diet, rich in fruit, vegetables, low-fat dairy products and reduced in saturated fat and cholesterol, and a control diet consisting of what many people in the United States typically eat. Reduction of sodium intake by ~0.9 g per day induced a greater BP reduction when the starting sodium intake was <2.3 g per day, which corresponds to about 6 g of salt per day; thus it is slightly more than the currently recommended < 1,500 mg/day of sodium by the 2017 US hypertension guidelines. Of note, sodium reduction reduced BP in non-hypertensive individuals on both diets. Reduced sodium intake can also prevent hypertension (relative risk reduction of about 20% with or without concomitant weight loss) 90 , improve hypertension control 117 and thus, possibly, reduce need for antihypertensive medication 100 . In the Intersalt study 118 , lower sodium intake was associated with a blunted age-related rise in systolic BP.

There is strong evidence to support population-wide recommendations to lower salt intake 119 , 120 . As more than 75% of dietary salt comes from processed foods (in western countries), any population strategy to reduce salt intake must involve food manufacturers and restaurants, in order to progressively reduce salt added to foods. So far, only three countries (Japan, Finland and the United Kingdom) have successfully reduced population salt intake 121 .

Increased potassium intake

Healthy individuals with normal kidney function usually have a potassium intake of 4.7 g/day; a higher intake is not associated with increased risk because potassium is readily excreted in persons who do not have CKD. Increased potassium intake is associated with reduced BP in individuals with low as well as high baseline potassium intake 91 , 92 . Of note, potassium reduces BP to a greater extent in blacks than in whites 122 . The effect of potassium on BP is dependent on salt intake. There is a greater BP reduction with increased potassium intake in the context of lower salt intake 123 . Thus, the best strategy is to increase potassium intake and reduce sodium intake at the same time. The preferred strategy to increase potassium intake is to increase consumption of fruits and vegetables that are rich in potassium rather than using supplements 115 . In individuals with impaired urinary potassium excretion, a potassium intake <4.7 g per day is recommended 124 .

Moderate alcohol consumption

Keeping alcohol intake ≤2 standard drinks (~3.5 alcohol units) per day for men and ≤1 standard drink (~1.75 alcohol units) per day for women can also contribute to a 2–4 mmHg BP reduction. 95 , 96

Physical activity

Regular physical activity reduces BP in individuals with hypertension. Endurance training reduces BP more in persons with hypertension than in individuals with normal BP. A narrative review of 27 randomized clinical trials in individuals with hypertension showed that regular medium-intensity to high-intensity aerobic activity reduced BP by a mean of 11/5 mmHg 125 . Sessions lasting 40–60 minutes performed at least three times a week had the greatest effect on BP. Three randomized controlled trials of isometric exercise (strength training) showed a BP reduction of similar magnitude to that induced by aerobic exercise in individuals with hypertension 125 . A meta-analysis of 64 controlled studies of the efficacy of dynamic resistance training as stand-alone antihypertensive therapy showed BP reductions comparable with or greater than those with aerobic exercise training 126 . Greater BP reductions occurred in individuals with higher resting BP (approx. 6/5 mmHg for individuals with hypertension and 3/3 mmHg for individuals with pre-hypertension) and in non-white individuals 126 .

Weight Loss

Excess adiposity generally raises BP in susceptible individuals, and patients with hypertension who also have obesity require more antihypertensive medications to control their BP and are more likely to be treatment resistant 127 . In a recent meta-analysis, any reduction in body weight lowered systolic BP by on average 2.69 mmHg and in diastolic BP by on average 1.34 mmHg (Ref 128 ). However, the response varies substantially between individuals. Lifestyle interventions, including hypocaloric diets and physical exercise, are commonly recommended for patients with obesity and hypertension, yet average weight loss is modest and most patients regain weight 129 ( box 4 ).

Hypertension and obesity

Weight loss is recommended for individuals with obesity, and may be particularly important if these patients also have hypertension. Medications have been developed for the treatment of obesity, but their approval status differs between the United States and Europe: some drugs are only approved in the United States (for example, lorcaserin and topiramate/phentermine), whereas others are approved in Europe only. BP reductions in patients with hypertension have been reported for some weight loss medications 201 , but their specific pharmacological actions may attenuate the positive influences of weight loss on BP and CVD outcomes 133 . Bariatric surgery is very effective in reducing body weight, and the risk for arterial hypertension is substantially reduced up to five years following bariatric surgery 202 . However, large and sustained body weight reductions are needed to substantially reduce BP following bariatric surgery 203 and there are no large clinical trials specifically testing the effects of weight loss medications or bariatric surgery on hypertension control.

Antihypertensive Pharmacotherapy

Antihypertensive pharmacotherapy has evolved over several decades driven by development of various antihypertensive medication classes and large-scale outcomes trials proving their benefits on CVD morbidity and mortality 130 . Clinicians are now faced with a plethora of antihypertensive medications of different drug classes and a variety of fixed dose combinations. Typically, antihypertensive pharmacotherapy begins with first-line antihypertensive medications either in monotherapy or in combination 131 . Combination therapy may be preferable in patients with higher levels of pretreatment BP. First-line antihypertensive medications include ACE inhibitors, angiotensin II receptor blockers (also known as sartans), dihydropyridine calcium channel blockers, and thiazide diuretics 106 . Beta-blockers are also indicated in patients with heart failure and reduced left ventricular ejection fraction or post myocardial infarction, and some guidelines recommend beta-blockers as first line antihypertensive medications 77 , 132 . The choice should be based on individual efficacy and tolerability. Ethnicity affects the response to antihypertensive medications, and it has been suggested that calcium channel blockers and diuretics may be the first choice in blacks 106 , 133 , 134 . Further, in specific clinical situations, for example hypertension in pregnant women, other medications such as alpha-methyldopa (an agonist of alpha adrenoreceptors in the central nervous system that inhibits the sympathetic nervous system) or labetalol (a beta adrenoreceptor blocker) are preferable, whereas some first line antihypertensives, for example ACE inhibitors and angiotensin II receptor blockers, are contraindicated because of increased risk for renal teratogenicity. Divided dosing of antihypertensive drugs tends to decrease adherence and should be avoided when possible 135 .

BP cannot be controlled with monotherapy in many patients, particularly those with severe hypertension. When combining antihypertensive medications, it is important to consider whether the drugs have additive effects on BP or adverse effects, and whether the patient has comorbidities that mandate particular drug choices 77 . ACE inhibitors or angiotensin II receptor blockers, thiazide diuretics and dihydropyridine calcium channel blockers are additive in lowering BP and can be combined as double or triple combination therapies. By contrast, combining ACE inhibitors and angiotensin II receptor blockers adds little BP lowering while increasing the risk for renal dysfunction and hyperkalemia (high blood potassium levels, which can lead to cardiac arrhythmias). Similarly, combining RAAS inhibitors with beta-adrenoreceptor blockers adds little BP reduction, but this combination is indicated in patients following acute myocardial infarction or heart failure with reduced left ventricular ejection fraction for reasons beyond BP reduction.

Angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers.

Among medications that inhibit components of the RAAS, ACE inhibitors and angiotensin II receptor blockers are considered first line antihypertensives, whereas other antihypertensive medications targeting RAAS, including direct renin inhibitors and mineralocorticoid receptor antagonists, are usually considered reserve medications because there is less clinical trial evidence supporting their use as first line antihypertensive therapy. ACE inhibitors and angiotensin II receptor blockers have been tested extensively in large-scale hypertension trials 136 . In patients with heart failure with reduced left ventricular ejection fraction or with diabetic nephropathy, both drug classes improved outcomes, making them particularly good choices in these populations. Both classes appear to be comparable in reducing CVD risk 137 . and also tend to improve glucose metabolism and, therefore, could be preferable in younger patients and in patients with conditions predisposing to type 2 diabetes mellitus, including obesity and the metabolic syndrome 138 . ACE inhibitors are generally well tolerated, but reductions in kidney function, hyperkalemia, cough, and – less commonly – angioedema (swelling caused by fluid accumulation) could occur with their use. The risk for angioedema, which can be life threatening, is substantially increased in blacks 139 and modestly increased in patients treated with dipeptidyl peptidase-IV inhibitors (used in the treatment of diabetes, examples of which include sitagliptin, vildagliptin, saxagliptin, and linagliptin) 140 . ACE inhibitors that can be dosed once daily are preferred. Angiotensin II receptor blockers can also elicit hyperkalemia and worsening of kidney function, but are not likely to cause cough or angioedema 137 .

Dihydropyridine calcium channel blockers.

Dihydropyridine calcium channel blockers elicit vasodilation by blocking vascular smooth muscle L-type calcium channels. They are effective antihypertensive drugs with extensive experience in large clinical trials 136 . A practical advantage of this drug class is that it can be combined with all other first-line antihypertensives. Peripheral edema, which is explained by peripheral arterial vasodilation rather than worsening heart failure or kidney dysfunction, is a common side effect, particularly in individuals with obesity. Non-dihydropyridine calcium channel blockers, especially verapamil, also inhibit cardiac calcium channels, which can reduce heart rate and cardiac contractility 141 . Calcium channel blockers can induce or worsen constipation, especially in institutionalized older persons 142 . All calcium channel blockers modestly inhibit the drug metabolizing enzyme cytochrome P450 3A4, and, therefore, could elicit important drug-interactions 143 .

Thiazide-type and thiazide-like diuretics.

Thiazide-type diuretics (for example, hydrochlorothiazide) have a benzothiadiazine ring, whereas thiazide-like diuretics (for example, chlorthalidone, metolazone and indapamide) lack the benzothiadiazine structure. Both subclasses of thiazide diuretics inhibit Na + and CI - co-transporters in renal tubules, thereby promoting natriuresis, and have been an important component of pharmacological hypertension management ever since the first trials showing morbidity benefits of antihypertensive therapy 144 . Over the years, diuretic doses have been substantially reduced to attain better risk-benefit profiles. Thiazide-type and thiazide-like diuretics can worsen glucose metabolism increasing the risk for new onset diabetes mellitus, but whether or not this metabolic action translates into long-term increases in CVD risk has been called into question 145 . Hydrochlorothiazide, the most commonly prescribed thiazide-type diuretic worldwide, may be less effective in mitigating CVD risk compared to chlorthalidone or indapamide 146 , 147 . Drug-related electrolyte disturbances, including hypokalemia and hyponatremia (low blood potassium and sodium levels, respectively), are particularly important adverse effects; hypokalemia can lead to cardiac arrhythmias and muscle weakness, and hyponatremia can cause confusion, seizures and coma. The risk for hypokalemia is reduced when thiazide-type and thiazide-like diuretics are combined with potassium supplements or potassium-sparing agents, such as ACE inhibitors, angiotensin receptor blockers, or potassium-sparing diuretics. Hyponatremia is a potentially life threatening adverse effect, particularly in elderly persons.

Beta-adrenoreceptor blockers.

Beta-adrenoreceptor blockers lower BP reducing cardiac output, heart rate, renin release and adrenergic control nervous system effects 148 . They improve outcomes following acute myocardial infarction and in patients with heart failure with reduced left ventricular ejection fraction, but, in the absence of these comorbidities, beta-adrenoreceptor blockers are inferior to other first line antihypertensives in reducing CVD morbidity and mortality 149 . This effect has been attributed to lesser reductions in aortic BP 150 and adverse effects on body weight 151 and glucose metabolism with beta-adrenoreceptor blockade. Some of these disadvantages might be mitigated with newer vasodilator beta-adrenoreceptor blockers, such as nebivolol and carvedilol 152 . However, there are no large-scale antihypertensive trials demonstrating that this difference translates into better clinical outcomes. Beta-adrenoreceptor blockers may promote bronchial obstruction is patients with asthma and should not be combined with non-dihydropyridine calcium channel blockers such as verapamil that lower sinus node rate or atrioventricular conduction.

Newer pharmacological agents

Overall, the interest of the pharmaceutical industry in developing new antihypertensive medications has been limited in recent years. Moreover, most antihypertensive drugs are out of patent and, therefore, available as relatively inexpensive generics. Further, some of the currently approved drugs, such as angiotensin II receptor blockers, have placebo-like tolerability. Newer pharmacological agents approved for other indications, including combined angiotensin II receptor and neprilysin inhibitors 153 (for heart failure), soluble guanylyl cyclase modulating drugs 154 (for erectile dysfunction), and sodium-glucose cotransporter 2 (SGLT2) inhibitors 155 (for type 2 diabetes mellitus) may also be useful in treating hypertension. Other pharmacological agents, such as newer mineralocorticoid receptor antagonists, aldosterone synthase inhibitors, activators of the angiotensin-converting enzyme 2/ angiotensin (1–7)/ MAS receptor axis, and natriuretic peptide receptor agonists, are in various stages of preclinical or clinical development 156 , often for indications other than hypertension. Drugs addressing novel pressor mechanisms could be useful in patients with treatment resistant hypertension, particularly those not responding to or not tolerating mineralocorticoid receptor antagonists. Moreover, drugs with actions in addition to BP reduction could prove clinically useful. For example, combined angiotensin II receptor blockade and neprilysin inhibition has been shown to ameliorate insulin resistance in patients with obesity and hypertension 157 and decrease the progression to type 2 diabetes mellitus in patients with heart failure 158 .

Treatment Resistant Hypertension

Treatment resistant hypertension is commonly diagnosed when office BP is >140/90 mmHg despite treatment with three or more properly dosed antihypertensive drugs including a diuretic and secondary hypertension has been ruled out 159 . Poor treatment adherence is a common cause of apparent treatment resistant hypertension. The true prevalence of treatment resistant hypertension is unknown, but an estimated 12.8% of all individuals with hypertension in the United States and 15.3 % of those treated with antihypertensives fulfill the criteria for treatment resistant hypertension 160 . Adding a fourth or fifth drug could lead to satisfactory BP control in these patients. The PATHWAY trial rotated patients with treatment resistant hypertension through different add on drugs or placebo in a randomized fashion 161 . All patients received a standardized antihypertensive regimen comprising three drugs, including a diuretic. Compared with alpha-adrenoreceptor or beta-adrenoreceptor blockade, the mineralocorticoid receptor antagonist spironolactone was the most effective fourth antihypertensive drug. In another study in patients whose BP was uncontrolled despite receiving three drugs, sequential addition of a mineralocorticoid receptor antagonist followed by a loop diuretic (which acts at the ascending limb of the loop of Henle in the kidney) was more effective than adding an ACE inhibitor followed by a beta-adrenoreceptor blocker 162 . Overall, mineralocorticoid receptor antagonism is a reasonable choice in patients with difficult to control hypertension. Given the risk of inducing hyperkalemia 163 , serum potassium concentrations should be monitored.

Device-based Treatments

Device-based treatments have been primarily developed for patients with severe resistant hypertension whose BP cannot be controlled with antihypertensive drugs 156 . Catheter-based renal nerve ablation 164 , 165 , electrical carotid sinus stimulation 166 , 167 , modulation of baroreflex transduction with a dedicated carotid stent 168 , carotid body denervation 169 , and deep brain stimulation 170 are thought to lower BP through SNS inhibition. Creation of a defined arteriovenous stent with a coupler device lowers BP by reducing peripheral vascular resistance 171 . These treatments are in various stages of clinical development, with the most extensive data available on renal nerve ablation and electrical carotid sinus stimulation. None has yet been proven efficacious in lowering BP in randomized sham-controlled clinical trials 164 , 161 , 167 , because either the primary endpoint was not achieved or no trials have been conducted. Finally, trials with hard clinical endpoints do not exist.

QUALITY OF LIFE

Health-related quality of life (HRQoL) is a multi-dimensional concept that includes domains related to physical, mental, emotional, and social functioning; studies demonstrate that each additional disease, as well as the severity of these diseases, is associated with declines in HRQOL 172 . Population-based studies have consistently shown that being diagnosed with hypertension is associated with worsening of HRQoL even after adjusting for other comorbidities 173 , 174 . Altered HRQoL in persons with hypertension has been attributed to a variety of factors, including the diagnosis, treatment, and effects of alterations (both elevations and reductions) in BP 173 .

Labeling someone as having hypertension can result in worsening of self-perceived health status 175 . This was well-demonstrated in a classic study of otherwise healthy Canadian steelworkers identified as having hypertension as part of a screening program. In the year following diagnosis, absenteeism from work owing to illness more than tripled in those made newly aware of their hypertension, whereas it increased only slightly in those previously aware of their hypertension 176 . This finding could not be explained by hypertension treatment or BP level and was believed to be a direct consequence of people adopting a “sick role.” These findings have been replicated in studies carried out in diverse settings and using different measures of physical and mental health 175 .

Antihypertensive medication use is associated with a variety of symptoms that could lower HRQoL 177 . Observational studies showed an association between the number of antihypertensive medications prescribed and worsening of the HRQoL 178 . Some classes of antihypertensive medications, (for example, ACE inhibitors) are better tolerated than others (for example, beta blockers and centrally acting agents, such as alpha-methyldopa) and result in significantly better scores on measures of general well-being 179 . Further, small differences in HRQoL have even been reported among medications of the same class, e.g., enalapril vs. captopril 180 . However, clinical trials with newer antihypertensive agents have generally indicated that they are extremely well-tolerated and can enhance the effects of non-pharmacological treatment on HRQoL 177 , 181 . In the Treatment of Mild Hypertension Study (TOMHS), combining lifestyle modifications with any of five different antihypertensive medication classes resulted in greater improvements in HRQoL than lifestyle modifications plus placebo 181 .

Treatment-related reductions in BP could have a negative effect on HRQoL, particularly in older and more frail patients at high risk of hypotension. Clinical trials performed in the 1990s that evaluated patients with very high baseline BP, for example, the Systolic Hypertension in the Elderly Program Trial (SHEP) and the Systolic Hypertension in Europe Trial (Syst-Eur), generally found minimal effects of BP reductions on HRQoL 182 , 183 . Two more recent clinical trials have targeted lower BPs (intensive systolic BP target < 120 mmHg versus standard systolic BP target < 140 mmHg ), it had been postulated that this lower BP might be expected to cause cerebral hypoperfusion, resulting in falls, dizziness, and cognitive impairment 184 , 185 , 107 . In a substudy of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) study, HRQoL was evaluated in 1,028 participants randomized to either intensive or standard therapy. No differences in mental function were noted between treatment groups, but intensive therapy was associated with a small, not clinically significant, decrease in physical function 185 . In the Systolic Blood Pressure Intervention Trial (SPRINT), targeting systolic BP <120 mmHg required 1 additional antihypertensive medication compared to standard treatment to target systolic BP < 140 mmHg and was generally safe and well tolerated 107 , 186 . Compared to standard treatment, intensive treatment did not affect the perceived HRQOL of SPRINT participants, measured by patient reported outcomes of physical and mental health, self-reported satisfaction with care and medication adherence, even when stratifying on age and comorbidities 186 . Almost 90% of participants in both treatment groups reported satisfaction with their BP care, and more than 1/3 described improvement in satisfaction over baseline levels.

Quality of life concerns remain an important aspect of hypertension management. SPRINT has demonstrated that with careful clinical management, lower BP can be targeted without concern of worsening physical and mental function. Clinicians must seek the optimal balance of reducing CVD morbidity and mortality while maximizing well-being for each individual patient.

Although there is regional variability in the outlook for hypertension over the next 5 to 10 years, It is clear overall that the prevalence of hypertension and, therefore, the associated global burden attributable to hypertension, will increase 187 . Global population growth and aging will largely contribute to this increase – 1.5 billion people are expected to be affected by 2025 (Ref. 188 ) – which will be focused in low and middle income countries 187 . However, these adverse trends in disease burden will be variably offset by improvements in prevention, awareness and treatment. The size of improvements in each of these 3 areas will vary from non-existent (-hypertension prevention could even worsen in some parts of the world, as exposure to factors that promote raised BP increases) to substantially large and important elsewhere in the world.

Overall, prevention will probably contribute least to any improvement in BP-associated disease burden. This is because 80% of the world is in the process of developing, which hitherto has inevitably been associated with increased exposure to the main environmental determinants of raised BP such as excess intake of calories, alcohol and salt. Food and drink industries, governments and education systems would be required to cooperate in order to reverse this pattern

Implementation of preventive strategies has largely been limited to high income countries. Despite reasonably compelling evidence to the contrary 111 , recommendations that the general population should restrict salt intake have been questioned on the basis of largely suboptimal observational data 189 . Such confusion worsens an already very difficult public health challenge. Data show that only approximately half of people with hypertension are aware of their condition 190 , and the Lancet Commission on hypertension identified improving awareness of hypertension is a critical action needed to improve the current disease burden 191 , 192 . The global BP awareness campaign promoted by the International Society of Hypertension whereby World Hypertension Day was extended to become May Measurement Month (MMM) in 2017 could contribute substantially to improving rates of routine BP screening around the world 83 . Over 1.20 million adults (≥18 years) from >100 countries were screened as part of MMM and the ensuing data allied to health-economic analyses will be used to persuade policy makers in each country that enhanced local BP screening and treatment facilities are wise financial investments.

Improving the efficacy of drug treatment also holds great promise for reducing hypertension-associated disease burden. Rather than focusing on rare secondary causes of hypertension or the optimal management of treatment resistant hypertension 193 , the greatest effect could be achieved by the delivery and distribution of affordable, effective single-pill combinations of 2 or 3 drugs to low-income and middle income countries where the burden of hypertension is considerable and where any such therapies are currently either largely unavailable or unaffordable . 194 . Unfortunately, optimal combinations of 2 antihypertensive agents have not been identified for the majority of the world’s hypertensive population: no such data are available for black, south Asian or east Asian patients 195 . However, the first in a series of trials in these ethnic groups is underway in Sub-Saharan Africa.

Meanwhile, single-pill formulations of the drug combinations most commonly recommended in current guidelines (calcium channel blocker plus a diuretic, calcium channel blocker plus a RAAS-blocker or diuretic plus a RAAS-blocker) are readily available and have low production costs. In addition, a 3-drug combination of a calcium channel blocker, a diuretic and a RAAS-blocker 132 should also be produced for more severe hypertension, with low dose spironolactone available as a fourth-line agent 161 . Hence, 1 or 2 tablets will be able to control BPs of all but a small proportion of patients with hypertension.

These formulations should be made available and affordable in all countries of the world. 191 Additional local obstacles to the distribution and delivery of these agents to patients with hypertension within each country will also have to be overcome – among which the lack of effective screening programmes is crucial 191 .

Antihypertensive medications are prescribed by different health professionals in different countries. However, even in high income countries, much of the “routine” uncomplicated hypertension management could, and probably should be carried out by nurse practitioners or other non-physician health workers. In more remote parts of the world, the use of e-healthcare techniques 196 should be increasingly used to facilitate task-shifting or task sharing by non-physician health-workers where doctors are unavailable 197 .

In summary, although there are many interesting unanswered scientific research questions in the field of hypertension ( Box 5 ), perhaps the most pressing need to reduce the diseas burden is to evaluate the best way(s), at a local level, to screen routinely for raised BP and then to deliver the best, most affordable, evidence-based combination of antihypertensive agents. Meanwhile, efforts to drive public health policy towards encouraging more healthy diets and lifestyles from a BP and CVD viewpoint should be encouraged and basic scientific research that might allow precision medicine to be applied to patients with hypertension must also continue.

Outstanding Research Questions:

Measurement issues.

• Is hypertension management improved by basing treatment strategies on serial unattended office BP measurements, out of office (home or ambulatory) BP measurements or central BP measurements?
• How should BP be measured in patients with atrial fibrillation?

Treatment Issues

• Should salt restriction at the population level continue to be recommended at current targets?
• To what extent should age, estimated CVD risk and concomitant conditions influence treatment thresholds?
• Should white-coat hypertension be treated?
• If management strategy is to be influenced by central or out of office BP levels, what treatment thresholds and targets should be used?
• Should reducing 24-hour and longer-term BP variability be a consideration in the selection of drug treatment for optimal CVD protection?
• What combinations of antihypertensive agents give optimal CVD protection, stratified by age and ethnicity?
• What is the optimal BP treatment target stratified by age, CVD risk and concomitant disease status?
• What is the optimal management of treatment resistant hypertension that is resistant to 4 agents including spironolactone?
• If treatment thresholds are to be driven by estimated CVD risk, at what level should antihypertensive drug treatment be initiated and what other CVD protective agents should be considered?
• Is initiating drug therapy with 2 hypertensive agents more effective than initiating with monotherapy for optimal CVD prevention?

Acknowledgments

P.K.W. was supported by P20GM109036 (Tulane COBRE for Clinical and Translational Research in Cardiometabolic Diseases) from the National Institute of General Medical Sciences.

Competing interests

G.B. served as Consultant for Janssen, Bayer, AbbVie, Vascular Dynamics, Relypsa and Merck; served/serves as Principal Investigator for FIDELIO trial (Bayer), Steering Committee member (CREDENCE)-Janssen, SONAR-AbbVie, and CALM-2-Vascular Dynamics. J.J. served as consultant for Novartis, Novo-Nordisc, Boehringer-Ingelheim, Sanofi, Orexigen, Riemser, Theravance, Vivus; and is cofounder of Eternygen GmbH. S.O. (in the previous 24 months) has received research grant support or reimbursement for travel to meetings or other, non-financial support from Actelion Clinical Research/George Clinical; AstraZeneca AB; Bayer; Lundbeck; Novartis; Novo Nordisk; Rox Medical; has consulted for Actelion/George Clinical, Lundbeck, Novo Nordisk and ROX Medical; served as Director/Principal Investigator, SPRINT University of Alabama at Birmingham (UAB) Clinical Center Network (CCN); and sub-investigator UAB CCN clinical site; for which Takeda and Arbor Pharmaceuticals donated 5% of medication used. N.R.P. served as advisory board member (ad hoc) for Pfizer, Takeda, MSD, Servier, and Medtronic (companies producing blood pressure lowering agents/devices); received speaker honoraria from Servier, AstraZeneca, Napi Labs, and Menarini; received research funding from Servier, Pfizer and Menarini; and is the President of the International Society of Hypertension. George Health Enterprises, the social enterprise arm of The George Institute for Global Health, has applied for a patent in the area of low-dose combinations on which A.R. is listed as an inventor; and has received investment to develop fixed-dose combinations containing aspirin, statin and BP lowering drugs. AR is an investigator on grants for several trials of blood pressure lowering interventions. G.G. has received lectures fees from Merck and Astra Zeneca. M.C.A., R.C., A.F.D., D.R.B. and P.K.W. declare no competing interests.

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Hypertension Essay

Introduction, analysis of underpinning care planning, patient presentation and condition, reflect on the nursing assessment of the patient, adpie (assessment, diagnosis, planning, implementation, and evaluation), priorities of care, recommendations for future practice, conclusions.

Nursing is an emerging sector, which is related with the well being of population. The skills, knowledge, and experience in nursing field are the prime aspects that help in managing the overall care procedures for the patients. Care management is important for an individual patient to improve their condition and well being (Barrett et al. 2012). To analyse the importance, here I stated about my personal care experience with a hypertension patient. Hypertension is the situation that elevates the blood pressure and can extend to damage multiple organs (Alexander 2017). My hypertension patient is suffering from chest pain, severe dizziness, breathing trouble, and lethargy. Hypertension is one of the most common and acute disease, which needs immense clinical care settings including emergency departments, acute care medical clinics, and urgent care centres. Hypertension is often identified from associated symptoms such as end-organ injuries, which cannot be managed without immediate treatment and medications (McNaughton et al. 2013). Schmieder (2010) depicted, “end organ damage in hypertension can be detected early, reflects accurately the hypertensive patient’s overall cardiovascular risk, and should be prevented and treated with antihypertensive treatment” (p.866).

Rosendaal et al. (2016) noted that hypertension care, acute care, follow-up care, intervention, and reference for treatment along with others need financial assistance in those countries, wherein free healthcare provision is lacking. Doctors’ visits and prescription medication are some of the prime concerns during the treatment of hypertension, which is relatively cost-effective for a health insurance holder (High Blood Pressure Treatment Cost 2017). The roles of nurses in hypertension treatment and management include several aspects such as diagnostics and medication management. This also includes detection, referral, follow up, coordination of care, patient education, counselling, performance measurement, and quality improvement along with population health management (Himmelfarb et al. 2016). McCormac & Krause (2012) asserted that the patient-centred care facilities, as well as, the multidisciplinary care team can be effective for hypertension care management. The awareness regarding the hypertension and effective screening both are important for the treatment and disease management procedure (Himmelfarb et al. 2016). Considering these contexts, the study focuses on providing an in-depth care for my patient from his admission to the treatment process twice in a month. Therefore, I will choose Roper, Logan and Tierney’s (RLT) model for effective care setting for the patient with hypertension.

Besides, socio-cultural factors have the significant impact on culture, as well as, the society of an individual patient. Culture and socio-cultural beliefs distinctively affects the values and interdependence of the individuals. Furthermore, the culture and socio-cultural beliefs of individual nurses are significantly affecting the perception of care practice. Additionally, it also affects the patient outcomes. Hence, it can be stated that culture and socio-cultural beliefs influences the nursing environment as well. The environmental factor of RLT model can represent the theory as a ‘green’ version. From the environmental aspects, this model can be stated as ‘green’ model, as it has a significant impact on daily living of the individuals. The model considers positive ‘green’ environmental impact on the patients’ standard living in an effective way. Politico-economic factor is related with government, politics, and economies that also have a critical affect the living pattern of individuals. These activities can be significantly utilise within the nursing practice without any kind of hesitation, but most often the nurses are uncomfortable in delivering the care provisions as per the patient’s preferences and activities of their daily living. This situation can occur due to the rigidness of individual’s practice or lack of awareness regarding multicultural nursing aspects. It has been evident that the RLT model also represented the similar aspect regarding the significant impact over the patients. The conjunction of these stated factors with the daily life of the patients can also be affects the treatment criteria (Roper-Logan-Tierney Model of Living 2016).

Gibbs Model of Reflection

• Care provider nurse should deliver Aspirin (300 mg) for oral intake soon after identification of chest pain
• Nitroglycerine tablet or spray can be used as the second step
• If the patient suffers from the breathing trouble, he need to take concentrated oxygen, which I can prescribe him
• To avoid the chances of respiratory depression and sedation, the patient should be given intravenous Morphine (Resuscitation Council 2017)

1. Alexander, MR 2017, Hypertension Clinical Presentation, viewed 25 November 2017, <https://emedicine.medscape.com/article/241381-clinical>

2. American College of Emergency Physicians 2016, Quality of Care and the Outcomes Management Movement, viewed 15 December 2017, <https://www.acep.org/Clinical—Practice-Management/Quality-of-Care-and-the-Outcomes-Management-Movement/#sm.0001xdrzdxzyhczhw5q20vacffxn6>

3. Barrett, D, Wilson, B & Woollands, A 2012, Care planning: a guide for nurses, Pearson Education, Harlow.

4. Brown, SJ 2013, Evidence-based nursing: the research-practice connection, Jones & Bartlett Publishers, US.

5. Busko, M. 2017. Age at Onset of Hypertension should Influence Management, viewed 25 November 2017, <https://www.medscape.com/viewarticle/877094>

6. Eldh, AC, Almost, J, DeCorby-Watson, K, Gifford, W, Harvey, G, Hasson, H, Kenny, D, Moodie, S, Wallin, L & Yost, J 2017, ‘Clinical interventions, implementation interventions, and the potential greyness in between -a discussion paper’, BMC Health Serv Res., vol. 17, pp. 16-19.

7. Good, VS & Kirkwood, PL 2017, Advanced critical care nursing – e-book, Elsevier Health Sciences, Amsterdam.

8. Grzeskowiak, M. 2015, Protecting the Airway, Protecting the Patient, viewed 15 December 2017, <http://www.rtmagazine.com/2015/02/protecting-airway-protecting-patient/>

9. Hamrahian, A. M. 2017, Pathophysiology of Hypertension, viewed 25 November 2017, <https://emedicine.medscape.com/article/1937383-overview>

10. Himmelfarb, CRD, Commodore-Mensah, Y & Hill, MN 2016, ‘Expanding the role of nurses to improve hypertension care and control globally’, Annals of Global Health, vol. 82, iss. 2, pp. 243-253.

11. High Blood Pressure Treatment Cost 2017, Cost Helper Health, viewed 26 December 2017, <http://health.costhelper.com/treating-high-blood-pressure-cost.html>

12. Ilic, D. 2009, ‘Assessing competency in evidence based practice: strengths and limitations of current tools in practice’, BMC Med Educ., vol. 9, p. 53.

13. Kennard, L & O’Shaughnessy, K. M. 2016, ‘Treating hypertension in patients with medical comorbidities’, BMJ, vol. 352, p. i101.

14. Mayo Foundation for Medical Education and Research 2017, Causes, viewed 25 November 2017 <https://www.mayoclinic.org/diseases-conditions/high-blood-pressure/basics/causes/con-20019580>

15. Mayo Foundation for Medical Education and Research 2017a, Risk Factors, viewed 25 November 2017 <https://www.mayoclinic.org/diseases-conditions/high-blood-pressure/basics/risk-factors/con-20019580>

16. Mayo Foundation for Medical Education and Research 2017b, Complications, viewed 25 November 2017 <https://www.mayoclinic.org/diseases-conditions/high-blood-pressure/basics/complications/con-20019580>

17. McCormac, T & Krause, T 2012, ‘Management of hypertension in adults in primary care: NICE guideline’, Br J Gen Pract., vol. 62, iss. 596, pp. 163-164.

18. McNaughton, CD, Self, WH, Levy, PD & Barrett TW 2013, ‘High-Risk patients with hypertension: clinical management options’, Clin Med Rev Vasc Health., vol. 2012, iss. 4, pp. 65–71.

19. Medeiros, ACT, Nóbrega, MML, Rodrigues, RAP & Fernandes, MDGM 2013, ‘Nursing diagnoses for the elderly using the International Classification for Nursing Practice and the activities of living model’, Rev. Latino-Am. Enfermagem, vol. 21, iss. 2, pp. 523-530.

20. NurseTheory 2017, ADPIE – Nursing Process Steps, viewed 23 December 2017 <https://www.nursetheory.com/adpie/>

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22. Omole, FS, Sow, CM, Babalola, D & Strothers, H 2011, ‘Interacting with patients’ family members during the office visit’, Am Fam Physician, vol. 84, iss. 7, pp. 780-784.

23. Oncology Nursing Society 2016, Supportive Care/Support Interventions, viewed 25 November 2017, <https://www.ons.org/intervention/supportive-caresupport-interventions>

24. Peate, I & Dutton, H 2014, Acute nursing care: recognising and responding to medical emergencies, Routledge, UK.

25. Roper-Logan-Tierney Model of Living 2016, Nursing Theory, viewed 26 December 2017, <http://www.nursing-theory.org/theories-and-models/roper-model-for-nursing-based-on-a-model-of-living.php>

26. Resuscitation Council 2017. Guidelines and Guidance, viewed 25 November 2017, <https://www.resus.org.uk/resuscitation-guidelines/abcde-approach/>

27. Rossaint, R, Bouillon, B, Cerny, V, Coats, TJ, Duranteau, J, Fernández-Mondéjar, E, Hunt, BJ, Komadina, R, Nardi, G, Neugebauer, E, Ozier, Y, Riddez, L, Schultz, A, Stahel, PF, Vincent, JL & Spahn, DR 2010, ‘Management of bleeding following major trauma: an updated European guideline’, Crit Care, vol. 14, iss. 2, pp. 52-54.

28. Rosendaal, NTA, Hendriks, ME, Verhagen, MD, Bolarinwa, OA, Sanya, EO, Kolo, PM, Adenusi, P, Agbede, K, Eck, D, Tan, SS, Akande, TM, Redekop, W, Schultsz, C. & Gomez, GB 2016, ‘Costs and cost-effectiveness of hypertension screening and treatment in adults with hypertension in rural Nigeria in the context of a health insurance program’, PLoS One., vol. 11, iss. 6, p. e0157925.

29. Schmieder, RE, 2010. ‘End organ damage in hypertension’, Dtsch Arztebl Int., vol. 107, iss. 49, pp. 866-873.

30. Thim, T, Krarup, NHV, Grove, EL, Rohde, CV & Løfgren, B 2012, ‘Initial Assessment and Treatment with the Airway, Breathing, Circulation, Disability, Exposure (ABCDE) Approach’, Int J Gen Med., vol. 5, pp. 117-121.

• AACN Synergy Model
• Advanced Practice Nurse (ADN)
• American Nurses’ Association (ANA)
• Communication

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Hypertension Essay Samples

Type of paper: Essay

Topic: Hypertension , Health , Blood , Diabetes , Medicine , Nursing , Stress , Pressure

Words: 1100

Published: 10/31/2021

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Many people suffer from hypertension unawares because, it is a public health problem with no apparent symptoms. Also known as high blood pressure, hypertension is an enduring medical ailment whereby the blood pressure in the arteries is raised. When the blood flows through the arteries, it pushes against the artery walls with a lot of pressure causing a rise in the blood pressure. Hypertension can either be primary or secondary hypertension whereby primary hypertension has no fundamental causes while secondary hypertension has discernible causes. Hypertension is more predominant in men than in women and in people over the age of 65 years. The underlying causes of hypertension are unidentified, but primary hypertension is linked to environmental factors and gene interactions. However, the generic cause of hypertension is still unclear, but genes with effects on blood pressure are said to cause hypertension. According to Casey, environmental factors are said to influence and individuals blood pressure (2011). For instance, environmental factors such as high salt intake, stress, depression, obesity and lack of physical exercises. Other possible causes of hypertension are vitamin D deficiency, too much of caffeine consumption, and insulin resistance. Secondary hypertension is caused by specific health conditions, for instance, kidney disease, hyperthyroidism, acromegaly, Cushing’s syndrome, pheochromocytoma, and Conn’s syndrome. Secondary hypertension can also be caused by pregnancy, excessive consumption of liquor, obesity, and the intake of herbal and illegal drugs. Smoking, aging, kidney disease, and living a sedentary life are also associated with hypertension. Hypertension is a public health condition that is rarely accompanied by symptoms, and can only be diagnosed through screening. In addition, hypertension can also be identified when a patient seeks medical help for other health conditions. Chummun notes that, many people are unaware of the condition and can live with it for many years before it is diagnosed due to lack of symptoms (2011). Hypertension is characterized by instances of persistent high blood pressure. In addition, patients with hypertension experience constant headaches, vertigo, fainting episodes, and tinnitus. Other symptoms include nausea, chest pains, vision problems, irregular heartbeats, and breathing problems. It is important for people who notice these symptoms to seek medical advice, before the problem advances. Hypertension is a serious condition if not treated because it puts the patients at a high risk of suffering from a heart disease and other chronic illnesses. Therefore, it is essential for patients to check their blood levels regularly. The preeminent way to treat hypertension is to help the patient lower the increased blood pressure. The blood pressure ought to be below 140/90 and even less than that for patients with chronic kidney failures, and diabetes. Therefore, treating hypertension is a way of reducing the development of other hypertension-related diseases, for instance, heart failure, and stroke. Hypertension can either be treated medically or by changing an individual’s lifestyle. In addition, a patient can use the two combined for better results. Several drugs can be used for the treatment of hypertension, for instance, ARB drugs, AC inhibitors, calcium channel blockers, diuretics, beta-blockers, and peripheral vasodilators. These drugs can be used alone or combined depending on the patients conditions. Apart from the drugs, it is essential for hypertension patient to change their sedentary lifestyle and indulge in physical exercise. Physical activities help the patients to burn the unused fats in the body in addition to helping the heart pump regularly. Moreover, hypertension patients are required to practice healthy eating by avoiding foods rich in fats. Additionally, they are also advised to consume foods rich in nitrates, for instance, beetroots, lettuce, cabbage, radishes, fennel, just to mention but a few. Hypertension is a health condition that can be prevented when people learn to live a healthy life with regular exercises. It is important to reduce stress, avoid regular and excessive intake of alcohol, reduce the salt intake, and regularly exercise for a life free from hypertension. Diabetes is a type of metabolic condition that is characterized by inadequate insulin and high blood sugar. It is considered to be an enduring illness that causes high blood sugar levels if not monitored well. There is type 1 diabetes, type 2 diabetes, and gestational diabetes that affects pregnant women mostly. The most common symptoms for diabetes are intense thirst and hunger, frequent urination, fatigue, strange weight loss or gain, numbness, and bruises and cuts that fail to heal. There is no underlying cause of the types of diabetes because the reasons differ dependent on the type of diabetes and the person suffering from the condition. Diabetes is a treatable disease, but diabetes type one has no cure and last for a lifetime. Likewise, type 2 diabetes lasts for a lifetime but it is manageable and treatable through regular exercises, eating healthily, and avoiding unnecessary weight loss and gain. The best treatment for type 1 diabetes is the daily use of insulin injections combined with exercise and a special diet. Alternatively, type 2 diabetes is treated with a special diet, tablets, exercises and at times insulin injections. Hyperlipidemia is a condition involving irregular raised levels of lipids in the blood. This condition can either be primary which is caused by genetic abnormalities or secondary, which is caused by an underlying illness that alters plasma lipids, and idiopathic which has no known cause. Hyperlipidemia has no symptoms and is mainly caused by an individual’s lifestyle or untreatable severe medical conditions. The condition is also genetic and needs a blood test for diagnosis because it has no symptoms. Hyperlipidemia is treatable depending on an individual’s lipid levels and general health. There are medications that lower the lipid levels in the body for instance statin drugs, fibrates, and niacin. However making a change in one’s lifestyle is necessary for the treatment of hyperlipidemia, for example, low cholesterol intake and regular physical exercises. Thyroid disease is a condition that impairs the thyroid functions. There are different types of thyroid disorders, hyperthyroidism, Hashimoto’s thyroiditis, and hypothyroidism. The disease is caused by the overproduction of thyroid hormones that causes inflammation in the thyroid. Thyroid disease is treatable with medications, surgery, or radioiodine therapy.

Casey, G. (2011). Blood and hypertension: the damage of too much pressure. Kai Tiaki Nursing New Zealand, 17(8), 26-31. Chummun, H. (2011). The management of hypertension: the impact of nurse-led clinics. Nurse Prescribing, 9(2), 68-74.

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