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Hypertension
SpecialtyFamily medicine, hypertensiology Edit this on Wikidata

Hypertension (HTN or HT) or high blood pressure, sometimes called arterial hypertension, is a chronic medical condition in which the blood pressure in the arteries is elevated. Blood pressure is defined by two measurements, systolic and diastolic, which depend on whether the heart muscle is contracting (systole) or relaxed between beats (diastole). These two numbers are the maximum and minimum pressure, respectively. Normal blood pressure at rest is within the range of 100–140 mmHg systolic (top reading) and 60–90 mmHg diastolic (bottom reading). High blood pressure is said to be present if it is often at or above 140/90 mmHg.

Hypertension may lead to hypertensive heart disease, coronary artery disease,[1] stroke, aortic aneurysm, peripheral arterial disease and chronic kidney disease.

Hypertension may be classified by cause as either primary (essential) hypertension or secondary hypertension; about 90–95% of cases are categorized as primary hypertension which means high blood pressure of no known cause.[2] The remaining 5–10% of cases are categorized as secondary hypertension and have an identifiable cause. Hypertension may also be classified as combined systolic-diastolic, isolated systolic, or isolated diastolic.

Dietary and lifestyle changes can improve blood pressure and decrease cardiovascular risk. When such changes are not sufficient, or the person will not or cannot make the needed changes, medication is used. The treatment of moderately high arterial blood pressure (defined as >160/100 mmHg) with medications is associated with an improved life expectancy.[3][4] The benefits of treatment of blood pressure that is between 140/90 mmHg and 160/100 mmHg are less clear, with some reviews finding no benefit[3][4] and other reviews finding benefit.[5]

Signs and symptoms

Hypertension is rarely accompanied by any symptoms, and its identification is usually through screening, or when seeking healthcare for an unrelated problem. A proportion of people with high blood pressure report headaches (particularly at the back of the head and in the morning), as well as lightheadedness, vertigo, tinnitus (buzzing or hissing in the ears), altered vision or fainting episodes.[6] These symptoms, however, might be related to associated anxiety rather than the high blood pressure itself.[7]

On physical examination, hypertension may be suspected on the basis of the presence of hypertensive retinopathy detected by examination of the optic fundus found in the back of the eye using ophthalmoscopy.[8] Classically, the severity of the hypertensive retinopathy changes is graded from grade I–IV, although the milder types may be difficult to distinguish from each other.[8] Ophthalmoscopy findings may also give some indication as to how long a person has been hypertensive.[6]

Secondary hypertension

Some additional signs and symptoms may suggest secondary hypertension, i.e. hypertension due to an identifiable cause. The following diseases cause hypertension and have characteristic symptoms and signs:

Hypertensive crisis

Severely elevated blood pressure (equal to or greater than a systolic 180 or diastolic of 110—sometimes termed malignant or accelerated hypertension) is referred to as a "hypertensive crisis", as blood pressure at this level confers a high risk of complications. People with blood pressures in this range may have no symptoms, but are more likely to report headaches (22% of cases)[10] and dizziness than the general population.[6] Other symptoms accompanying a hypertensive crisis may include visual deterioration or breathlessness due to heart failure or a general feeling of malaise due to renal failure.[9] Most people with a hypertensive crisis are known to have elevated blood pressure, but additional triggers may have led to a sudden rise.[11]

A "hypertensive emergency", previously "malignant hypertension", is diagnosed when there is evidence of direct damage to one or more organs as a result of severely elevated blood pressure greater than 180 systolic or 120 diastolic.[12] This may include hypertensive encephalopathy, caused by brain swelling and dysfunction, and characterized by headaches and an altered level of consciousness (confusion or drowsiness). Retinal papilloedema and/or fundal hemorrhages and exudates are another sign of target organ damage. Chest pain may indicate heart muscle damage (which may progress to myocardial infarction) or sometimes aortic dissection, the tearing of the inner wall of the aorta. Breathlessness, cough, and the expectoration of blood-stained sputum are characteristic signs of pulmonary edema, the swelling of lung tissue due to left ventricular failure an inability of the left ventricle of the heart to adequately pump blood from the lungs into the arterial system.[11] Rapid deterioration of kidney function (acute kidney injury) and microangiopathic hemolytic anemia (destruction of blood cells) may also occur.[11] In these situations, rapid reduction of the blood pressure is mandated to stop ongoing organ damage.[11] In contrast there is no evidence that blood pressure needs to be lowered rapidly in hypertensive urgencies where there is no evidence of target organ damage and over aggressive reduction of blood pressure is not without risks.[9] Use of oral medications to lower the BP gradually over 24 to 48h is advocated in hypertensive urgencies.[11]

Pregnancy

Hypertension occurs in approximately 8–10% of pregnancies.[9] Two blood pressure measurements six hours apart of greater than 140/90 mm Hg is considered diagnostic of hypertension in pregnancy.[13] Most women with hypertension in pregnancy have pre-existing primary hypertension, but high blood pressure in pregnancy may be the first sign of pre-eclampsia, a serious condition of the second half of pregnancy and puerperium.[9] Pre-eclampsia is characterised by increased blood pressure and the presence of protein in the urine.[9] It occurs in about 5% of pregnancies and is responsible for approximately 16% of all maternal deaths globally.[9] Pre-eclampsia also doubles the risk of perinatal mortality.[9] Usually there are no symptoms in pre-eclampsia and it is detected by routine screening. When symptoms of pre-eclampsia occur the most common are headache, visual disturbance (often "flashing lights"), vomiting, epigastric pain, and edema. Pre-eclampsia can occasionally progress to a life-threatening condition called eclampsia, which is a hypertensive emergency and has several serious complications including vision loss, cerebral edema, seizures or convulsions, renal failure, pulmonary edema, and disseminated intravascular coagulation (a blood clotting disorder).[9][14]

Children

Failure to thrive, seizures, irritability, lack of energy, and difficulty breathing[15] can be associated with hypertension in neonates and young infants. In older infants and children, hypertension can cause headache, unexplained irritability, fatigue, failure to thrive, blurred vision, nosebleeds, and facial paralysis.[15][16]

Cause

Primary hypertension

Primary (essential) hypertension is the most common form of hypertension, accounting for 90–95% of all cases of hypertension.[2] In almost all contemporary societies, blood pressure rises with aging and the risk of becoming hypertensive in later life is considerable.[17] Hypertension results from a complex interaction of genes and environmental factors. Numerous common genetic variants with small effects on blood pressure have been identified[18] as well as some rare genetic variants with large effects on blood pressure[19] but the genetic basis of hypertension is still poorly understood. Several environmental factors influence blood pressure. Lifestyle factors that lower blood pressure include reduced dietary salt intake,[20][21] increased consumption of fruit and low fat products (Dietary Approaches to Stop Hypertension (DASH diet)), exercise,[22] weight loss[23] and reduced alcohol intake.[24] Stress appears to play a minor role[7] with specific relaxation techniques not supported by the evidence.[25][26] The possible role of other factors such as caffeine consumption,[27] and vitamin D deficiency[28] are less clear cut. Insulin resistance, which is common in obesity and is a component of syndrome X (or the metabolic syndrome), is also thought to contribute to hypertension.[29]

Recent studies have also implicated events in early life (for example low birth weight, maternal smoking and lack of breast feeding) as risk factors for adult essential hypertension,[30] although the mechanisms linking these exposures to adult hypertension remain obscure.[30] Hypertension has also been associated with depression.[31]

Secondary hypertension

Secondary hypertension results from an identifiable cause. Renal disease is the most common secondary cause of hypertension.[9] Hypertension can also be caused by endocrine conditions, such as Cushing's syndrome, hyperthyroidism, hypothyroidism, acromegaly, Conn's syndrome or hyperaldosteronism, hyperparathyroidism and pheochromocytoma.[9][32] Other causes of secondary hypertension include obesity, sleep apnea, pregnancy, coarctation of the aorta, excessive liquorice consumption and certain prescription medicines, herbal remedies and illegal drugs.[9][33]

Pathophysiology

Determinants of mean arterial pressure
Illustration depicting the effects of high blood pressure

In most people with established essential (primary) hypertension, increased resistance to blood flow (total peripheral resistance) accounts for the high pressure while cardiac output remains normal.[34] There is evidence that some younger people with prehypertension or 'borderline hypertension' have high cardiac output, an elevated heart rate and normal peripheral resistance, termed hyperkinetic borderline hypertension.[35] These individuals develop the typical features of established essential hypertension in later life as their cardiac output falls and peripheral resistance rises with age.[35] Whether this pattern is typical of all people who ultimately develop hypertension is disputed.[36] The increased peripheral resistance in established hypertension is mainly attributable to structural narrowing of small arteries and arterioles,[37] although a reduction in the number or density of capillaries may also contribute.[38] Hypertension is also associated with decreased peripheral venous compliance[39] which may increase venous return, increase cardiac preload and, ultimately, cause diastolic dysfunction. Whether increased active vasoconstriction plays a role in established essential hypertension is unclear.[40]

Pulse pressure (the difference between systolic and diastolic blood pressure) is frequently increased in older people with hypertension. This can mean that systolic pressure is abnormally high, but diastolic pressure may be normal or low — a condition termed isolated systolic hypertension.[41] The high pulse pressure in elderly people with hypertension or isolated systolic hypertension is explained by increased arterial stiffness, which typically accompanies aging and may be exacerbated by high blood pressure.[42]

Many mechanisms have been proposed to account for the rise in peripheral resistance in hypertension. Most evidence implicates either disturbances in renal salt and water handling (particularly abnormalities in the intrarenal renin-angiotensin system)[43] and/or abnormalities of the sympathetic nervous system.[44] These mechanisms are not mutually exclusive and it is likely that both contribute to some extent in most cases of essential hypertension. It has also been suggested that endothelial dysfunction and vascular inflammation may also contribute to increased peripheral resistance and vascular damage in hypertension.[45][46] Interleukin 17 has garnered interest for its role in increasing the production of several other immune system chemical signals thought to be involved in hypertension such as tumor necrosis factor alpha, interleukin 1, interleukin 6, and interleukin 8.[47]

Diagnosis

Typical tests performed
System Tests
Renal Microscopic urinalysis, proteinuria, BUN and/or creatinine
Endocrine Serum sodium, potassium, calcium, TSH
Metabolic Fasting blood glucose, HDL, LDL, and total cholesterol, triglycerides
Other Hematocrit, electrocardiogram, and chest radiograph
Sources: Harrison's principles of internal medicine[48] others[49][50][51][52][53]

Hypertension is diagnosed on the basis of a persistent high blood pressure. Traditionally, the National Institute of Clinical Excellence recommends three separate sphygmomanometer measurements at one monthly intervals.[54][55] The American Heart Association recommends at least three measurements on at least two separate health care visits.[56] An exception to this is those with very high blood pressure readings especially when there is poor organ function.[55] Initial assessment of the hypertensive people should include a complete history and physical examination. With the availability of 24-hour ambulatory blood pressure monitors and home blood pressure machines, the importance of not wrongly diagnosing those who have white coat hypertension has led to a change in protocols. In the United Kingdom, current best practice is to follow up a single raised clinic reading with ambulatory measurement, or less ideally with home blood pressure monitoring over the course of 7 days.[55] Pseudohypertension in the elderly or noncompressibility artery syndrome may also require consideration. This condition is believed to be due to calcification of the arteries resulting in abnormally high blood pressure readings with a blood pressure cuff while intra arterial measurements of blood pressure are normal.[57] Orthostatic hypertension is when blood pressure increases upon standing.[58]

Once the diagnosis of hypertension has been made, physicians will attempt to identify the underlying cause based on risk factors and other symptoms, if present. Secondary hypertension is more common in preadolescent children, with most cases caused by renal disease. Primary or essential hypertension is more common in adolescents and has multiple risk factors, including obesity and a family history of hypertension.[59] Laboratory tests can also be performed to identify possible causes of secondary hypertension, and to determine whether hypertension has caused damage to the heart, eyes, and kidneys. Additional tests for diabetes and high cholesterol levels are usually performed because these conditions are additional risk factors for the development of heart disease and may require treatment.[2]

Serum creatinine is measured to assess for the presence of kidney disease, which can be either the cause or the result of hypertension. Serum creatinine alone may overestimate glomerular filtration rate and recent guidelines advocate the use of predictive equations such as the Modification of Diet in Renal Disease (MDRD) formula to estimate glomerular filtration rate (eGFR).[60] eGFR can also provide a baseline measurement of kidney function that can be used to monitor for side effects of certain antihypertensive drugs on kidney function. Additionally, testing of urine samples for protein is used as a secondary indicator of kidney disease. Electrocardiogram (EKG/ECG) testing is done to check for evidence that the heart is under strain from high blood pressure. It may also show whether there is thickening of the heart muscle (left ventricular hypertrophy) or whether the heart has experienced a prior minor disturbance such as a silent heart attack. A chest X-ray or an echocardiogram may also be performed to look for signs of heart enlargement or damage to the heart.[9]

Adults

Classification (JNC7)[60] Systolic pressure Diastolic pressure
mmHg kPa mmHg kPa
Normal 90–119 12–15.9 60–79 8.0–10.5
High normal[61] or prehypertension 120–139 16.0–18.5 80–89 10.7–11.9
Stage 1 hypertension 140–159 18.7–21.2 90–99 12.0–13.2
Stage 2 hypertension ≥160 ≥21.3 ≥100 ≥13.3
Isolated systolic
hypertension
≥140 ≥18.7 <90 <12.0

In people aged 18 years or older hypertension is defined as a systolic and/or a diastolic blood pressure measurement consistently higher than an accepted normal value (currently 139 mmHg systolic, 89 mmHg diastolic: see table —Classification (JNC7)). Lower thresholds are used (135 mmHg systolic or 85 mmHg diastolic) if measurements are derived from 24-hour ambulatory or home monitoring.[55] Recent international hypertension guidelines have also created categories below the hypertensive range to indicate a continuum of risk with higher blood pressures in the normal range. JNC7 (2003)[60] uses the term prehypertension for blood pressure in the range 120-139 mmHg systolic and/or 80-89 mmHg diastolic, while ESH-ESC Guidelines (2007)[62] and BHS IV (2004)[63] use optimal, normal and high normal categories to subdivide pressures below 140 mmHg systolic and 90 mmHg diastolic. Hypertension is also sub-classified: JNC7 distinguishes hypertension stage I, hypertension stage II, and isolated systolic hypertension. Isolated systolic hypertension refers to elevated systolic pressure with normal diastolic pressure and is common in the elderly.[60] The ESH-ESC Guidelines (2007)[62] and BHS IV (2004),[63] additionally define a third stage (stage III hypertension) for people with systolic blood pressure exceeding 179 mmHg or a diastolic pressure over 109 mmHg. Hypertension is classified as "resistant" if medications do not reduce blood pressure to normal levels.[60]

Children

Hypertension in neonates is rare, occurring in around 0.2 to 3% of neonates, and blood pressure is not measured routinely in the healthy newborn.[16] Hypertension is more common in high risk newborns. A variety of factors, such as gestational age, postconceptional age and birth weight needs to be taken into account when deciding if a blood pressure is normal in a neonate.[16]

Hypertension defined as elevated blood pressure over several visits affects 1% to 5% of children and adolescents and is associated with long term risks of ill-health.[64] Blood pressure rises with age in childhood and, in children, hypertension is defined as an average systolic or diastolic blood pressure on three or more occasions equal or higher than the 95th percentile appropriate for the sex, age and height of the child. High blood pressure must be confirmed on repeated visits however before characterizing a child as having hypertension.[64] Prehypertension in children has been defined as average systolic or diastolic blood pressure that is greater than or equal to the 90th percentile, but less than the 95th percentile.[64] In adolescents, it has been proposed that hypertension and pre-hypertension are diagnosed and classified using the same criteria as in adults.[64]

The value of routine screening for hypertension in children over the age of 3 years is debated.[65][66] In 2004 the National High Blood Pressure Education Program recommended that children aged 3 years and older have blood pressure measurement at least once at every health care visit[64] and the National Heart, Lung, and Blood Institute and American Academy of Pediatrics made a similar recommendation.[67] However the American Academy of Family Physicians[68] support the view of the U.S. preventive Services Task Force that evidence is insufficient to determine the balance of benefits and harms of screening for hypertension in children and adolescents who do not have symptoms.[69]

Prevention

Much of the disease burden of high blood pressure is experienced by people who are not labelled as hypertensive.[63] Consequently, population strategies are required to reduce the consequences of high blood pressure and reduce the need for antihypertensive drug therapy. Lifestyle changes are recommended to lower blood pressure, before starting drug therapy. The 2004 British Hypertension Society guidelines[63] proposed the following lifestyle changes consistent with those outlined by the US National High BP Education Program in 2002[70] for the primary prevention of hypertension:

  • maintain normal body weight for adults (e.g. body mass index 20–25 kg/m2)
  • reduce dietary sodium intake to <100 mmol/ day (<6 g of sodium chloride or <2.4 g of sodium per day)
  • engage in regular aerobic physical activity such as brisk walking (≥30 min per day, most days of the week)
  • limit alcohol consumption to no more than 3 units/day in men and no more than 2 units/day in women
  • consume a diet rich in fruit and vegetables (e.g. at least five portions per day);

Effective lifestyle modification may lower blood pressure as much as an individual antihypertensive drug. Combinations of two or more lifestyle modifications can achieve even better results.[63]

Management

Lifestyle modifications

The first line of treatment for hypertension is identical to the recommended preventive lifestyle changes[71] and includes dietary changes,[72] physical exercise, and weight loss. These have all been shown to significantly reduce blood pressure in people with hypertension.[73] Their potential effectiveness is similar to and at times exceeds a single medication.[61] If hypertension is high enough to justify immediate use of medications, lifestyle changes are still recommended in conjunction with medication.

Dietary change, such as a low sodium diet and a vegetarian diet are beneficial. A long term (more than 4 weeks) low sodium diet is effective in reducing blood pressure, both in people with hypertension and in people with normal blood pressure.[74] Also, the DASH diet, a diet rich in nuts, whole grains, fish, poultry, fruit and vegetables lowers blood pressure. A major feature of the plan is limiting intake of sodium, although the diet is also rich in potassium, magnesium, calcium, as well as protein.[75] A vegetarian diet is associated with a lower blood pressure and switching to such a diet may be useful for reducing high blood pressure.[76] A diet high in potassium lowers blood pressure in those with high blood pressure and may improve outcomes in those with normal kidney function.[77]

Some programs aimed to reduce psychological stress such as biofeedback or transcendental meditation may be reasonable add-ons to other treatment to reduce hypertension.[78] However several techniques, namely yoga, relaxation and other forms of meditation do not appear to reduce blood pressure,[79] and there are major methodological limitations with many studies of stress reduction techniques. [80] There is no clear evidence that the modest reduction in blood pressure with stress reduction techniques results in prevention of cardiovascular disease.[79][80]

Several exercise regimes—including isometric resistance exercise, aerobic exercise, resistance exercise, and device-guided breathing—may be useful in reducing blood pressure.[79]

Medications

Several classes of medications, collectively referred to as antihypertensive drugs, are available for treating hypertension. Use should take into account the person's cardiovascular risk (including risk of myocardial infarction and stroke) as well as blood pressure readings, in order to gain a more accurate picture of the person's risks.[81] Benefit of medications is related to a person's cardiac disease risk.[82] Evidence for medications in those with mild hypertension (between 140/90 mmHg and 160/100 mmHg) and no other health problems is less clear with some reviews finding no benefit[3][4] and other reviews finding benefit.[83] Medications are not recommended for people with prehypertension or high normal blood pressure.[61]

If drug treatment is initiated the Joint National Committee on High Blood Pressure (JNC-7)[60] recommended that the physician not only monitor for response to treatment but should also seek any side effects resulting from the medication. Reduction of the blood pressure by 5 mmHg can decrease the risk of stroke by 34%, of ischaemic heart disease by 21%, and reduce the likelihood of dementia, heart failure, and mortality from cardiovascular disease.[84] For most people, recommendations are to reduce blood pressure to less than or equal to somewhere between 140/90 mmHg to 160/100 mmHg.[81][85] Attempting to achieve lower levels have not been shown to improve outcomes[85] while there is evidence that it increases side effects.[86] In those with diabetes or kidney disease some recommend levels below 120/80 mmHg;[81][87] however, evidence does not support these lower levels.[85][88] If the blood pressure goal is not met, a change in treatment should be made as therapeutic inertia is a clear impediment to blood pressure control.[89]

The best first line medication is disputed.[90] The Cochrane collaboration, World Health Organization and the United States guidelines supports low dose thiazide-based diuretic as first line treatment.[73][90][91][92] The UK guidelines emphasise calcium channel blockers (CCB) in preference for people over the age of 55 years or if of African or Caribbean family origin, with angiotensin converting enzyme inhibitors (ACE-I) used first line for younger people.[93] In Japan starting with any one of six classes of medications including: CCB, ACEI/ARB, thiazide diuretics, beta-blockers, and alpha-blockers is deemed reasonable, while in Canada and Europe all of these but alpha-blockers are recommended as options.[61][90] When compared to placebo and other anti-hypertensive drugs as first-line therapy for hypertension, beta-blockers have greater benefit in stroke reduction, but no difference on coronary heart disease or all-cause mortality.[94] However, three-quarters of active beta-blocker treatment in the randomised controlled trials included in the review were with atenolol and none with the newer vasodilating beta-blockers.[95]

Drug combinations

The majority of people require more than one drug to control their hypertension. In those with a systolic blood pressure greater than 160 mmHg or a diastolic blood pressure greater than 100 mmHg the American Heart Association recommends starting both a thiazide and an ACEI, ARB or CCB.[73] An ACEI and CCB combination can be used as well.[73]

Unacceptable combinations are non-dihydropyridine calcium blockers (such as verapamil or diltiazem) and beta-blockers, dual renin–angiotensin system blockade (e.g. angiotensin converting enzyme inhibitor + angiotensin receptor blocker), renin–angiotensin system blockers and beta-blockers, beta-blockers and centrally acting medications.[96] Combinations of an ACE-inhibitor or angiotensin II–receptor antagonist, a diuretic and an NSAID (including selective COX-2 inhibitors and non-prescribed drugs such as ibuprofen) should be avoided whenever possible due to a high documented risk of acute renal failure. The combination is known colloquially as a "triple whammy" in the Australian health industry.[71] Tablets containing fixed combinations of two classes of drugs are available and while convenient for the people, may be best reserved for those who have been established on the individual components.[97]

Elderly

Treating moderate to severe hypertension decreases death rates and cardiovascular morbidity and mortality in people aged 60 and older.[98] There are limited studies of people over 80 years old but a recent review concluded that antihypertensive treatment reduced cardiovascular deaths and disease, but did not significantly reduce total death rates.[98] The recommended BP goal is advised as <150/90 mm Hg with thiazide diuretic, CCB, ACEI, or ARB being the first line medication in the United States,[99] and in the revised UK guidelines calcium-channel blockers are advocated as first line with targets of clinic readings <150/90, or <145/85 on ambulatory or home blood pressure monitoring.[93]

Resistant hypertension

Resistant hypertension is defined as hypertension that remains above goal blood pressure in spite of using, at once, three antihypertensive medications belonging to different drug classes. Guidelines for treating resistant hypertension have been published in the UK[100] and US.[101] It has been proposed that a proportion of resistant hypertension may be the result of chronic high activity of the autonomic nervous system; this concept is known as "neurogenic hypertension".[102] Low adherence to treatment is an important cause of resistant hypertension.[103]

Epidemiology

Disability-adjusted life year for hypertensive heart disease per 100,000 inhabitants in 2004.[104] Template:Multicol
  no data
  <110
  110-220
  220-330
  330-440
  440-550
  550-660
Template:Multicol-break
  660-770
  770-880
  880-990
  990-1100
  1100-1600
  >1600
Template:Multicol-end

Adults

Worldwide as of 2000, nearly one billion people or ~26% of the adult population had hypertension.[105] It was common in both developed (333 million) and undeveloped (639 million) countries.[105] However rates vary markedly in different regions with rates as low as 3.4% (men) and 6.8% (women) in rural India and as high as 68.9% (men) and 72.5% (women) in Poland.[106] In Europe hypertension occurs in about 30-45% of people as of 2013.[61]

In the United States in 1995 it was estimated that 43 million adults had hypertension or were taking antihypertensive medication, almost 24% of the population.[107] As of 2006 hypertension affects 76 million people in the United States had hypertension, 34% of the population.[108] The prevalence of hypertension in the United States is increasing and reached 29% in 2004.[109][110]

Hypertension is more common in blacks than in whites and Mexican Americans. African American adults have among the highest rates of hypertension in the world at 44%.[108] The incidence increases with age, and is greater in the southeastern United States.[2][111] Hypertension is more common in men than women, though menopause decreases this difference. It is also more common in those of low socioeconomic status.[2]

Children

Rates of high blood pressure in children and adolescents have increased in the last 20 years in the United States.[112] Childhood hypertension, particularly in preadolescents, is more often secondary to an underlying disorder than in adults. Kidney disease is the most common secondary cause of hypertension in children and adolescents. Nevertheless, primary or essential hypertension accounts for most cases.[113]

Complications

Diagram illustrating the main complications of persistent high blood pressure

Hypertension is the most important preventable risk factor for premature death worldwide.[114]

It increases the risk of the following diseases:

History

Image of veins from Harvey's Exercitatio Anatomica de Motu Cordis et Sanguinis in Animalibus

Modern understanding of the cardiovascular system began with the work of physician William Harvey (1578–1657), who described the circulation of blood in his book "De motu cordis". The English clergyman Stephen Hales made the first published measurement of blood pressure in 1733.[117][118] Descriptions of hypertension as a disease came among others from Thomas Young in 1808 and especially Richard Bright in 1836.[117] The first report of elevated blood pressure in a person without evidence of kidney disease was made by Frederick Akbar Mahomed (1849–1884).[119] However hypertension as a clinical entity came into being in 1896 with the invention of the cuff-based sphygmomanometer by Scipione Riva-Rocci in 1896.[120] This allowed the measurement of blood pressure in the clinic. In 1905, Nikolai Korotkoff improved the technique by describing the Korotkoff sounds that are heard when the artery is ausculated with a stethoscope while the sphygmomanometer cuff is deflated.[118]

Historically the treatment for what was called the "hard pulse disease" consisted in reducing the quantity of blood by bloodletting or the application of leeches.[117] This was advocated by The Yellow Emperor of China, Cornelius Celsus, Galen, and Hippocrates.[117]

In the Islamic Golden Age, the symptoms similar to symptoms of patients with hypertensive crisis are discussed in medieval Persian medical texts in the chapter of "fullness disease".[121] This symptoms include headache, heaviness in the head, sluggish movements, general redness and warm to touch feel of the body, prominent, distended and tense vessels, fullness of the pulse, distension of the skin, coloured and dense urine, loss of appetite, weak eyesight, impairment of thinking, yawning, drowsiness, vascular rupture, and hemorrhagic stroke.[122] This disease was supposed that is result from the excessive amount of blood within the blood vessels. The therapeutic approach for the treatment of this disease included changes in lifestyle (staying away from anger and sexual intercourse) and dietary program for patients (avoiding the consumption of wine, meat, and pastries, reducing the volume of food in a meal, maintaining a low-energy diet and the dietary usage of spinach and vinegar)[123].

In the 19th and 20th centuries, before effective pharmacological treatment for hypertension became possible, three treatment modalities were used, all with numerous side-effects: strict sodium restriction (for example the rice diet[117]), sympathectomy (surgical ablation of parts of the sympathetic nervous system), and pyrogen therapy (injection of substances that caused a fever, indirectly reducing blood pressure).[117][124] The first chemical for hypertension, sodium thiocyanate, was used in 1900 but had many side effects and was unpopular.[117] Several other agents were developed after the Second World War, the most popular and reasonably effective of which were tetramethylammonium chloride and its derivative hexamethonium, hydralazine and reserpine (derived from the medicinal plant Rauwolfia serpentina). A major breakthrough was achieved with the discovery of the first well-tolerated orally available agents. The first was chlorothiazide, the first thiazide diuretic and developed from the antibiotic sulfanilamide, which became available in 1958.[117][125] Subsequently beta blockers, calcium channel blockers, angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers and renin inhibitors were developed as antihypertensive agents.

Society and culture

Awareness

Graph showing, prevalence of awareness, treatment and control of hypertension compared between the four studies of NHANES[109]

The World Health Organization has identified hypertension, or high blood pressure, as the leading cause of cardiovascular mortality. The World Hypertension League (WHL), an umbrella organization of 85 national hypertension societies and leagues, recognized that more than 50% of the hypertensive population worldwide are unaware of their condition.[126] To address this problem, the WHL initiated a global awareness campaign on hypertension in 2005 and dedicated May 17 of each year as World Hypertension Day (WHD). Over the past three years, more national societies have been engaging in WHD and have been innovative in their activities to get the message to the public. In 2007, there was record participation from 47 member countries of the WHL. During the week of WHD, all these countries – in partnership with their local governments, professional societies, nongovernmental organizations and private industries – promoted hypertension awareness among the public through several media and public rallies. Using mass media such as Internet and television, the message reached more than 250 million people. As the momentum picks up year after year, the WHL is confident that almost all the estimated 1.5 billion people affected by elevated blood pressure can be reached.[127]

Wirtschaft

High blood pressure is the most common chronic medical problem prompting visits to primary health care providers in USA. The American Heart Association estimated the direct and indirect costs of high blood pressure in 2010 as $76.6 billion.[108] In the US 80% of people with hypertension are aware of their condition, 71% take some antihypertensive medication, but only 48% of people aware that they have hypertension adequately control it.[108] Adequate management of hypertension can be hampered by inadequacies in the diagnosis, treatment, and/or control of high blood pressure.[128] Health care providers face many obstacles to achieving blood pressure control, including resistance to taking multiple medications to reach blood pressure goals. People also face the challenges of adhering to medicine schedules and making lifestyle changes. Nonetheless, the achievement of blood pressure goals is possible, and most importantly, lowering blood pressure significantly reduces the risk of death due to heart disease and stroke, the development of other debilitating conditions, and the cost associated with advanced medical care.[129][130]

Forschung

Selective radiofrequency ablation of the nerves supplying the kidneys, which employs a catheter-based device to cause thermal injury to the nerves surrounding the renal artery, has been proposed to lower blood pressure.[131] So far, major side effects have been relatively infrequent, although cases of renal artery dissection, femoral artery pseudoaneurysm, excessive decreases in blood pressure and heart rate have been reported.[131] It has been suggested that renal nerve ablation may have a role in the management of resistant hypertension;[131] however, in 2014 a prospective, single-blind, randomized, sham-controlled clinical trial failed to confirm a beneficial effect.[132] A 2014 consensus statement from The Joint UK Societies did not recommend the use of renal denervation for treatment of resistant hypertension,[133] but supported continuing research activity in this field.

References

  1. ^ Lewington, S; Clarke, R; Qizilbash, N; Peto, R; Collins, R; Prospective Studies, Collaboration (14 December 2002). "Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies". Lancet. 360 (9349): 1903–13. doi:10.1016/s0140-6736(02)11911-8. PMID 12493255.
  2. ^ a b c d e Carretero OA, Oparil S; Oparil (January 2000). "Essential hypertension. Part I: definition and etiology". Circulation. 101 (3): 329–35. doi:10.1161/01.CIR.101.3.329. PMID 10645931.
  3. ^ a b c Diao, D; Wright, JM; Cundiff, DK; Gueyffier, F (15 August 2012). "Pharmacotherapy for mild hypertension". The Cochrane database of systematic reviews. 8: CD006742. PMID 22895954.
  4. ^ a b c Arguedas, JA; Leiva, V; Wright, JM (30 October 2013). "Blood pressure targets for hypertension in people with diabetes mellitus". The Cochrane database of systematic reviews. 10: CD008277. doi:10.1002/14651858.cd008277.pub2. PMID 24170669.
  5. ^ Sundström, Johan; Arima, Hisatomi; Jackson, Rod; Turnbull, Fiona; Rahimi, Kazem; Chalmers, John; Woodward, Mark; Neal, Bruce (23 December 2014). "Effects of Blood Pressure Reduction in Mild Hypertension". Annals of Internal Medicine. doi:10.7326/M14-0773.
  6. ^ a b c Fisher ND, Williams GH (2005). "Hypertensive vascular disease". In Kasper DL, Braunwald E, Fauci AS; et al. (eds.). Harrison's Principles of Internal Medicine (16th ed.). New York, NY: McGraw-Hill. pp. 1463–81. ISBN 0-07-139140-1. {{cite book}}: Explicit use of et al. in: |editor= (help)CS1 maint: multiple names: editors list (link)
  7. ^ a b Marshall, IJ; Wolfe, CD; McKevitt, C (9 July 2012). "Lay perspectives on hypertension and drug adherence: systematic review of qualitative research". BMJ (Clinical research ed.). 345: e3953. doi:10.1136/bmj.e3953. PMC 3392078. PMID 22777025.
  8. ^ a b Wong T, Mitchell P; Mitchell (February 2007). "The eye in hypertension". Lancet. 369 (9559): 425–35. doi:10.1016/S0140-6736(07)60198-6. PMID 17276782.
  9. ^ a b c d e f g h i j k l m n o p q r s t u v O'Brien, Eoin; Beevers, D. G.; Lip, Gregory Y. H. (2007). ABC of hypertension. London: BMJ Books. ISBN 1-4051-3061-X.{{cite book}}: CS1 maint: multiple names: authors list (link)
  10. ^ Papadopoulos DP, Mourouzis I, Thomopoulos C, Makris T, Papademetriou V; Mourouzis; Thomopoulos; Makris; Papademetriou (December 2010). "Hypertension crisis". Blood Press. 19 (6): 328–36. doi:10.3109/08037051.2010.488052. PMID 20504242.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  11. ^ a b c d e Marik PE, Varon J; Varon (June 2007). "Hypertensive crises: challenges and management". Chest. 131 (6): 1949–62. doi:10.1378/chest.06-2490. PMID 17565029.
  12. ^ Chobanian, AV; Bakris, GL; Black, HR; Cushman, WC; Green, LA; Izzo JL, Jr; Jones, DW; Materson, BJ; Oparil, S; Wright JT, Jr; Roccella, EJ; Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. National Heart, Lung, and Blood, Institute; National High Blood Pressure Education Program Coordinating, Committee (December 2003). "Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure". Hypertension. 42 (6): 1206–52. doi:10.1161/01.hyp.0000107251.49515.c2. PMID 14656957.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  13. ^ Harrison's principles of internal medicine (18th ed.). New York: McGraw-Hill. 2011. pp. 55–61. ISBN 9780071748896.
  14. ^ Gibson, Paul (30 July 2009). "Hypertension and Pregnancy". eMedicine Obstetrics and Gynecology. Medscape. Retrieved 16 June 2009.
  15. ^ a b Rodriguez-Cruz, Edwin; Ettinger, Leigh M (6 April 2010). "Hypertension". eMedicine Pediatrics: Cardiac Disease and Critical Care Medicine. Medscape. Retrieved 16 June 2009.
  16. ^ a b c Dionne JM, Abitbol CL, Flynn JT; Abitbol; Flynn (January 2012). "Hypertension in infancy: diagnosis, management and outcome". Pediatr. Nephrol. 27 (1): 17–32. doi:10.1007/s00467-010-1755-z. PMID 21258818.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  17. ^ Vasan, RS; Beiser, A; Seshadri, S; Larson, MG; Kannel, WB; D'Agostino, RB; Levy, D (27 February 2002). "Residual lifetime risk for developing hypertension in middle-aged women and men: The Framingham Heart Study". JAMA: the Journal of the American Medical Association. 287 (8): 1003–10. doi:10.1001/jama.287.8.1003. PMID 11866648.
  18. ^ Ehret GB; Munroe PB; Rice KM; et al. (October 2011). "Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk". Nature. 478 (7367): 103–9. doi:10.1038/nature10405. PMC 3340926. PMID 21909115. {{cite journal}}: |first10= missing |last10= (help); |first11= missing |last11= (help); Unknown parameter |author-separator= ignored (help)
  19. ^ Lifton, RP; Gharavi, AG, Geller, DS (23 February 2001). "Molecular mechanisms of human hypertension". Cell. 104 (4): 545–56. doi:10.1016/S0092-8674(01)00241-0. PMID 11239411.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  20. ^ He, FJ; MacGregor, GA (June 2009). "A comprehensive review on salt and health and current experience of worldwide salt reduction programmes". Journal of Human Hypertension. 23 (6): 363–84. doi:10.1038/jhh.2008.144. PMID 19110538.
  21. ^ He, FJ; Li, J; Macgregor, GA (3 April 2013). "Effect of longer term modest salt reduction on blood pressure: Cochrane systematic review and meta-analysis of randomised trials". BMJ (Clinical research ed.). 346: f1325. doi:10.1136/bmj.f1325. PMID 23558162.
  22. ^ Dickinson HO; Mason JM; Nicolson DJ; et al. (February 2006). "Lifestyle interventions to reduce raised blood pressure: a systematic review of randomized controlled trials". J. Hypertens. 24 (2): 215–33. doi:10.1097/01.hjh.0000199800.72563.26. PMID 16508562. {{cite journal}}: Unknown parameter |author-separator= ignored (help)
  23. ^ Haslam DW, James WP; James (2005). "Obesity". Lancet. 366 (9492): 1197–209. doi:10.1016/S0140-6736(05)67483-1. PMID 16198769.
  24. ^ Whelton PK; He J; Appel LJ; Cutler JA; Havas S; Kotchen TA; et al. (2002). "Primary prevention of hypertension: Clinical and public health advisory from The National High Blood Pressure Education Program". JAMA. 288 (15): 1882–8. doi:10.1001/jama.288.15.1882. PMID 12377087. {{cite journal}}: |first10= missing |last10= (help); |first11= missing |last11= (help); Unknown parameter |author-separator= ignored (help)
  25. ^ Dickinson, HO; Mason, JM; Nicolson, DJ; Campbell, F; Beyer, FR; Cook, JV; Williams, B; Ford, GA (February 2006). "Lifestyle interventions to reduce raised blood pressure: a systematic review of randomized controlled trials". Journal of hypertension. 24 (2): 215–33. doi:10.1097/01.hjh.0000199800.72563.26. PMID 16508562.
  26. ^ Ospina MB; Bond K; Karkhaneh M; et al. (June 2007). "Meditation practices for health: state of the research". Evid Rep Technol Assess (Full Rep) (155): 1–263. PMID 17764203. {{cite journal}}: Unknown parameter |author-separator= ignored (help)
  27. ^ Mesas, AE; Leon-Muñoz, LM; Rodriguez-Artalejo, F; Lopez-Garcia, E (October 2011). "The effect of coffee on blood pressure and cardiovascular disease in hypertensive individuals: a systematic review and meta-analysis". The American journal of clinical nutrition. 94 (4): 1113–26. doi:10.3945/ajcn.111.016667. PMID 21880846.
  28. ^ Vaidya A, Forman JP; Forman (November 2010). "Vitamin D and hypertension: current evidence and future directions". Hypertension. 56 (5): 774–9. doi:10.1161/HYPERTENSIONAHA.109.140160. PMID 20937970.
  29. ^ Sorof J, Daniels S; Daniels (October 2002). "Obesity hypertension in children: a problem of epidemic proportions". Hypertension. 40 (4): 441–447. doi:10.1161/01.HYP.0000032940.33466.12. PMID 12364344. Retrieved 3 June 2009.
  30. ^ a b Lawlor, DA; Smith, GD (May 2005). "Early life determinants of adult blood pressure". Current Opinion in Nephrology and Hypertension. 14 (3): 259–64. doi:10.1097/01.mnh.0000165893.13620.2b. PMID 15821420.
  31. ^ Meng, L; Chen, D; Yang, Y; Zheng, Y; Hui, R (May 2012). "Depression increases the risk of hypertension incidence: a meta-analysis of prospective cohort studies". Journal of hypertension. 30 (5): 842–51. doi:10.1097/hjh.0b013e32835080b7. PMID 22343537.
  32. ^ Dluhy RG, Williams GH eds (1998). "Endocrine hypertension". In Wilson JD, Foster DW, Kronenberg HM (ed.). Williams textbook of endocrinology (9th ed.). Philadelphia ; Montreal: W.B. Saunders. pp. 729–49. ISBN 0721661521. {{cite book}}: |author= has generic name (help)CS1 maint: multiple names: editors list (link)
  33. ^ Grossman E, Messerli FH; Messerli (January 2012). "Drug-induced Hypertension: An Unappreciated Cause of Secondary Hypertension". Am. J. Med. 125 (1): 14–22. doi:10.1016/j.amjmed.2011.05.024. PMID 22195528.
  34. ^ Conway J (April 1984). "Hemodynamic aspects of essential hypertension in humans". Physiol. Rev. 64 (2): 617–60. PMID 6369352.
  35. ^ a b Palatini P, Julius S; Julius (June 2009). "The role of cardiac autonomic function in hypertension and cardiovascular disease". Curr. Hypertens. Rep. 11 (3): 199–205. doi:10.1007/s11906-009-0035-4. PMID 19442329.
  36. ^ Andersson OK, Lingman M, Himmelmann A, Sivertsson R, Widgren BR; Lingman; Himmelmann; Sivertsson; Widgren (2004). "Prediction of future hypertension by casual blood pressure or invasive hemodynamics? A 30-year follow-up study". Blood Press. 13 (6): 350–4. doi:10.1080/08037050410004819. PMID 15771219.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  37. ^ Folkow B (April 1982). "Physiological aspects of primary hypertension". Physiol. Rev. 62 (2): 347–504. PMID 6461865.
  38. ^ Struijker Boudier HA, le Noble JL, Messing MW, Huijberts MS, le Noble FA, van Essen H; Le Noble; Messing; Huijberts; Le Noble; Van Essen (December 1992). "The microcirculation and hypertension". J Hypertens Suppl. 10 (7): S147–56. doi:10.1097/00004872-199212000-00016. PMID 1291649.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  39. ^ Safar ME, London GM; London (August 1987). "Arterial and venous compliance in sustained essential hypertension". Hypertension. 10 (2): 133–9. doi:10.1161/01.HYP.10.2.133. PMID 3301662.
  40. ^ Schiffrin EL (February 1992). "Reactivity of small blood vessels in hypertension: relation with structural changes. State of the art lecture". Hypertension. 19 (2 Suppl): II1–9. doi:10.1161/01.HYP.19.2_Suppl.II1-a. PMID 1735561.
  41. ^ Chobanian AV (August 2007). "Clinical practice. Isolated systolic hypertension in the elderly". N. Engl. J. Med. 357 (8): 789–96. doi:10.1056/NEJMcp071137. PMID 17715411.
  42. ^ Zieman SJ, Melenovsky V, Kass DA; Melenovsky; Kass (May 2005). "Mechanisms, pathophysiology, and therapy of arterial stiffness". Arterioscler. Thromb. Vasc. Biol. 25 (5): 932–43. doi:10.1161/01.ATV.0000160548.78317.29. PMID 15731494.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  43. ^ Navar LG (December 2010). "Counterpoint: Activation of the intrarenal renin-angiotensin system is the dominant contributor to systemic hypertension". J. Appl. Physiol. 109 (6): 1998–2000, discussion 2015. doi:10.1152/japplphysiol.00182.2010a. PMC 3006411. PMID 21148349.
  44. ^ Esler M, Lambert E, Schlaich M; Lambert; Schlaich (December 2010). "Point: Chronic activation of the sympathetic nervous system is the dominant contributor to systemic hypertension". J. Appl. Physiol. 109 (6): 1996–8, discussion 2016. doi:10.1152/japplphysiol.00182.2010. PMID 20185633.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  45. ^ Versari D, Daghini E, Virdis A, Ghiadoni L, Taddei S; Daghini; Virdis; Ghiadoni; Taddei (June 2009). "Endothelium-dependent contractions and endothelial dysfunction in human hypertension". Br. J. Pharmacol. 157 (4): 527–36. doi:10.1111/j.1476-5381.2009.00240.x. PMC 2707964. PMID 19630832.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  46. ^ Marchesi C, Paradis P, Schiffrin EL; Paradis; Schiffrin (July 2008). "Role of the renin-angiotensin system in vascular inflammation". Trends Pharmacol. Sci. 29 (7): 367–74. doi:10.1016/j.tips.2008.05.003. PMID 18579222.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  47. ^ Gooch JL, Sharma AC; Sharma (July 2014). "Targeting the immune system to treat hypertension: where are we?". Curr Opin Nephrol Hypertens. 23 (5): 000–000. doi:10.1097/MNH.0000000000000052. PMID 25036747.
  48. ^ Loscalzo, Joseph; Fauci, Anthony S.; Braunwald, Eugene; Dennis L. Kasper; Hauser, Stephen L; Longo, Dan L. (2008). Harrison's principles of internal medicine. McGraw-Hill Medical. ISBN 0-07-147691-1.{{cite book}}: CS1 maint: multiple names: authors list (link)
  49. ^ Padwal RS; Hemmelgarn BR; Khan NA; et al. (May 2009). "The 2009 Canadian Hypertension Education Program recommendations for the management of hypertension: Part 1 – blood pressure measurement, diagnosis and assessment of risk". Canadian Journal of Cardiology. 25 (5): 279–86. doi:10.1016/S0828-282X(09)70491-X. PMC 2707176. PMID 19417858. {{cite journal}}: |first11= missing |last11= (help); Unknown parameter |author-separator= ignored (help)
  50. ^ Padwal RJ; Hemmelgarn BR; Khan NA; et al. (June 2008). "The 2008 Canadian Hypertension Education Program recommendations for the management of hypertension: Part 1 – blood pressure measurement, diagnosis and assessment of risk". Canadian Journal of Cardiology. 24 (6): 455–63. doi:10.1016/S0828-282X(08)70619-6. PMC 2643189. PMID 18548142. {{cite journal}}: |first10= missing |last10= (help); |first11= missing |last11= (help); Unknown parameter |author-separator= ignored (help)
  51. ^ Padwal RS; Hemmelgarn BR; McAlister FA; et al. (May 2007). "The 2007 Canadian Hypertension Education Program recommendations for the management of hypertension: Part 1 – blood pressure measurement, diagnosis and assessment of risk". Canadian Journal of Cardiology. 23 (7): 529–38. doi:10.1016/S0828-282X(07)70797-3. PMC 2650756. PMID 17534459. {{cite journal}}: |first10= missing |last10= (help); |first11= missing |last11= (help); Unknown parameter |author-separator= ignored (help)
  52. ^ Hemmelgarn BR; McAlister FA; Grover S; et al. (May 2006). "The 2006 Canadian Hypertension Education Program recommendations for the management of hypertension: Part I – Blood pressure measurement, diagnosis and assessment of risk". Canadian Journal of Cardiology. 22 (7): 573–81. doi:10.1016/S0828-282X(06)70279-3. PMC 2560864. PMID 16755312. {{cite journal}}: |first10= missing |last10= (help); |first11= missing |last11= (help); Unknown parameter |author-separator= ignored (help)
  53. ^ Hemmelgarn BR; McAllister FA; Myers MG; et al. (June 2005). "The 2005 Canadian Hypertension Education Program recommendations for the management of hypertension: part 1- blood pressure measurement, diagnosis and assessment of risk". Canadian Journal of Cardiology. 21 (8): 645–56. PMID 16003448. {{cite journal}}: |first10= missing |last10= (help); |first11= missing |last11= (help); Unknown parameter |author-separator= ignored (help)
  54. ^ North of England Hypertension Guideline Development Group (1 August 2004). "Frequency of measurements". Essential hypertension (NICE CG18) (PDF). National Institute for Health and Clinical Excellence. p. 53. Retrieved 22 December 2011.
  55. ^ a b c d National Clinical Guideline Centre (August 2011). "7 Diagnosis of Hypertension, 7.5 Link from evidence to recommendations". Hypertension (NICE CG 127) (PDF). National Institute for Health and Clinical Excellence. p. 102. Retrieved 22 December 2011. Cite error: The named reference "NICE127 full" was defined multiple times with different content (see the help page).
  56. ^ Aronow, WS; Fleg, JL; Pepine, CJ; Artinian, NT; Bakris, G; Brown, AS; Ferdinand, KC; Ann Forciea, M; Frishman, WH; Jaigobin, C; Kostis, JB; Mancia, G; Oparil, S; Ortiz, E; Reisin, E; Rich, MW; Schocken, DD; Weber, MA; Wesley, DJ; Harrington, RA; Bates, ER; Bhatt, DL; Bridges, CR; Eisenberg, MJ; Ferrari, VA; Fisher, JD; Gardner, TJ; Gentile, F; Gilson, MF; Hlatky, MA; Jacobs, AK; Kaul, S; Moliterno, DJ; Mukherjee, D; Rosenson, RS; Stein, JH; Weitz, HH; Wesley, DJ (July–August 2011). "ACCF/AHA 2011 expert consensus document on hypertension in the elderly: a report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents developed in collaboration with the American Academy of Neurology, American Geriatrics Society, American Society for Preventive Cardiology, American Society of Hypertension, American Society of Nephrology, Association of Black Cardiologists, and European Society of Hypertension". Journal of the American Society of Hypertension : JASH. 5 (4): 259–352. doi:10.1016/j.jash.2011.06.001. PMID 21771565.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  57. ^ Franklin, SS; Wilkinson, IB; McEniery, CM (February 2012). "Unusual hypertensive phenotypes: what is their significance?". Hypertension. 59 (2): 173–8. doi:10.1161/HYPERTENSIONAHA.111.182956. PMID 22184330.
  58. ^ Kario, K (June 2009). "Orthostatic hypertension: a measure of blood pressure variation for predicting cardiovascular risk". Circulation journal : official journal of the Japanese Circulation Society. 73 (6): 1002–7. PMID 19430163.
  59. ^ Luma GB, Spiotta RT; Spiotta (May 2006). "Hypertension in children and adolescents". Am Fam Physician. 73 (9): 1558–68. PMID 16719248.
  60. ^ a b c d e f g h Chobanian AV; Bakris GL; Black HR; Cushman WC; Green LA; Izzo Jr. JL; Jones DW; Materson BJ; Oparil S; Wright Jr. JT; Roccella EJ; et al. (December 2003). "Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure". Hypertension. 42 (6). Joint National Committee On Prevention: 1206–52. doi:10.1161/01.HYP.0000107251.49515.c2. PMID 14656957. {{cite journal}}: Unknown parameter |author-separator= ignored (help)
  61. ^ a b c d e Giuseppe, Mancia; Fagard, R; Narkiewicz, K; Redon, J; Zanchetti, A; Bohm, M; Christiaens, T; Cifkova, R; De Backer, G; Dominiczak, A; Galderisi, M; Grobbee, DE; Jaarsma, T; Kirchhof, P; Kjeldsen, SE; Laurent, S; Manolis, AJ; Nilsson, PM; Ruilope, LM; Schmieder, RE; Sirnes, PA; Sleight, P; Viigimaa, M; Waeber, B; Zannad, F; Redon, J; Dominiczak, A; Narkiewicz, K; Nilsson, PM; et al. (July 2013). "2013 ESH/ESC Guidelines for the management of arterial hypertension: The Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC)". European heart journal. 34 (28): 2159–219. doi:10.1093/eurheartj/eht151. PMID 23771844.
  62. ^ a b Mancia G; De Backer G; Dominiczak A; et al. (September 2007). "2007 ESH-ESC Practice Guidelines for the Management of Arterial Hypertension: ESH-ESC Task Force on the Management of Arterial Hypertension". J. Hypertens. 25 (9): 1751–62. doi:10.1097/HJH.0b013e3282f0580f. PMID 17762635. {{cite journal}}: |first10= missing |last10= (help); |first11= missing |last11= (help); Unknown parameter |author-separator= ignored (help)
  63. ^ a b c d e Williams, B; Poulter, NR, Brown, MJ, Davis, M, McInnes, GT, Potter, JF, Sever, PS, McG Thom, S, British Hypertension, Society (March 2004). "Guidelines for management of hypertension: report of the fourth working party of the British Hypertension Society, 2004-BHS IV". Journal of Human Hypertension. 18 (3): 139–85. doi:10.1038/sj.jhh.1001683. PMID 14973512.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  64. ^ a b c d e National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents (August 2004). "The fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents". Pediatrics. 114 (2 Suppl 4th Report): 555–76. doi:10.1542/peds.114.2.S2.555. PMID 15286277.
  65. ^ Chiolero, A; Bovet, P; Paradis, G (1 March 2013). "Screening for elevated blood pressure in children and adolescents: a critical appraisal". JAMA pediatrics. 167 (3): 266–73. doi:10.1001/jamapediatrics.2013.438. PMID 23303490.
  66. ^ Daniels, SR.; Gidding, SS. (March 2013). "Blood pressure screening in children and adolescents: is the glass half empty or more than half full?". JAMA Pediatr. 167 (3): 302–4. doi:10.1001/jamapediatrics.2013.439. PMID 23303514.
  67. ^ Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents; National Heart, Lung, and Blood Institute (December 2011). "Expert panel on integrated guidelines for cardiovascular health and risk reduction in children and adolescents: summary report". Pediatrics. 128 Suppl 5: S213–56. doi:10.1542/peds.2009-2107C. PMID 22084329. {{cite journal}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)CS1 maint: multiple names: authors list (link)
  68. ^ http://www.aafp.org/patient-care/clinical-recommendations/all/hypertension.html
  69. ^ Moyer, VA.; U.S. Preventive Services Task Force (October 2013). "Screening for Primary Hypertension in Children and Adolescents: U.S. Preventive Services Task Force Recommendation Statement*". Annals of Internal Medicine. 159 (9): 613–9. doi:10.7326/0003-4819-159-9-201311050-00725. PMID 24097285.
  70. ^ Whelton PK; et al. (2002). "Primary prevention of hypertension. Clinical and public health advisory from the National High Blood Pressure Education Program". JAMA. 288 (15): 1882–1888. doi:10.1001/jama.288.15.1882. PMID 12377087. {{cite journal}}: |first10= missing |last10= (help); |first11= missing |last11= (help); Unknown parameter |author-separator= ignored (help)
  71. ^ a b "NPS Prescribing Practice Review 52: Treating hypertension". NPS Medicines Wise. 1 September 2010. Retrieved 5 November 2010.
  72. ^ Siebenhofer, A; Jeitler, K; Berghold, A; Waltering, A; Hemkens, LG; Semlitsch, T; Pachler, C; Strametz, R; Horvath, K (7 September 2011). Siebenhofer, Andrea (ed.). "Long-term effects of weight-reducing diets in hypertensive patients". Cochrane Database of Systematic Reviews. 9 (9): CD008274. doi:10.1002/14651858.CD008274.pub2. PMID 21901719.
  73. ^ a b c d Go, AS; Bauman, M; King, SM; Fonarow, GC; Lawrence, W; Williams, KA; Sanchez, E (15 November 2013). "An Effective Approach to High Blood Pressure Control: A Science Advisory From the American Heart Association, the American College of Cardiology, and the Centers for Disease Control and Prevention". Hypertension. 63 (4): 878. doi:10.1161/HYP.0000000000000003. PMID 24243703.
  74. ^ He, FJ; MacGregor, GA (2004). MacGregor, Graham A (ed.). "Effect of longer-term modest salt reduction on blood pressure". Cochrane Database of Systematic Reviews (3): CD004937. doi:10.1002/14651858.CD004937. PMID 15266549.
  75. ^ "Your Guide To Lowering Your Blood Pressure With DASH" (PDF). Retrieved 8 June 2009.
  76. ^ Yokoyama, Yoko; Nishimura, Kunihiro; Barnard, Neal D.; Takegami, Misa; Watanabe, Makoto; Sekikawa, Akira; Okamura, Tomonori; Miyamoto, Yoshihiro (2014). "Vegetarian Diets and Blood Pressure". JAMA Internal Medicine. 174 (4): 577. doi:10.1001/jamainternmed.2013.14547. ISSN 2168-6106.
  77. ^ Aburto, NJ; Hanson, S; Gutierrez, H; Hooper, L; Elliott, P; Cappuccio, FP (3 April 2013). "Effect of increased potassium intake on cardiovascular risk factors and disease: systematic review and meta-analyses". BMJ (Clinical research ed.). 346: f1378. doi:10.1136/bmj.f1378. PMID 23558164.
  78. ^ https://www.ncbi.nlm.nih.gov/pubmed/22855971
  79. ^ a b c Brook, RD; Appel, LJ; Rubenfire, M; Ogedegbe, G; Bisognano, JD; Elliott, WJ; Fuchs, FD; Hughes, JW; Lackland, DT; Staffileno, BA; Townsend, RR; Rajagopalan, S; American Heart Association Professional Education Committee of the Council for High Blood Pressure Research, Council on Cardiovascular and Stroke Nursing, Council on Epidemiology and Prevention, and Council on Nutrition, Physical, Activity (June 2013). "Beyond medications and diet: alternative approaches to lowering blood pressure: a scientific statement from the american heart association". Hypertension. 61 (6): 1360–83. doi:10.1161/HYP.0b013e318293645f. PMID 23608661.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  80. ^ a b Nagele, Eva; Jeitler, Klaus; Horvath, Karl; Semlitsch, Thomas; Posch, Nicole; Herrmann, Kirsten H.; Grouven, Ulrich; Hermanns, Tatjana; Hemkens, Lars G.; Siebenhofer, Andrea (2014). "Clinical effectiveness of stress-reduction techniques in patients with hypertension". Journal of Hypertension. 32 (10): 1936–1944. doi:10.1097/HJH.0000000000000298. ISSN 0263-6352.
  81. ^ a b c Nelson, Mark. "Drug treatment of elevated blood pressure". Australian Prescriber (33): 108–112. Retrieved 11 August 2010.
  82. ^ Blood Pressure Lowering Treatment Trialists', Collaboration; Sundström, J; Arima, H; Woodward, M; Jackson, R; Karmali, K; Lloyd-Jones, D; Baigent, C; Emberson, J; Rahimi, K; MacMahon, S; Patel, A; Perkovic, V; Turnbull, F; Neal, B (16 August 2014). "Blood pressure-lowering treatment based on cardiovascular risk: a meta-analysis of individual patient data". Lancet. 384 (9943): 591–8. doi:10.1016/s0140-6736(14)61212-5. PMID 25131978.
  83. ^ Sundström, Johan; Arima, Hisatomi; Jackson, Rod; Turnbull, Fiona; Rahimi, Kazem; Chalmers, John; Woodward, Mark; Neal, Bruce (23 December 2014). "Effects of Blood Pressure Reduction in Mild Hypertension". Annals of Internal Medicine. doi:10.7326/M14-0773.
  84. ^ Law M, Wald N, Morris J; Wald; Morris (2003). "Lowering blood pressure to prevent myocardial infarction and stroke: a new preventive strategy" (PDF). Health Technol Assess. 7 (31): 1–94. doi:10.3310/hta7310. PMID 14604498.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  85. ^ a b c Arguedas, JA; Perez, MI; Wright, JM (8 July 2009). Arguedas, Jose Agustin (ed.). "Treatment blood pressure targets for hypertension". Cochrane Database of Systematic Reviews (3): CD004349. doi:10.1002/14651858.CD004349.pub2. PMID 19588353.
  86. ^ "Treating blood pressure between 140/90 and 160/95 mmHg: no proven benefit". Prescrire Int. 148 (23): 106. . 2014 Apr. PMID 24860904. {{cite journal}}: Check date values in: |date= (help)
  87. ^ Shaw, Gina (7 March 2009). "Prehypertension: Early-stage High Blood Pressure". WebMD. Retrieved 3 July 2009.
  88. ^ Arguedas, JA; Leiva, V; Wright, JM (30 October 2013). "Blood pressure targets for hypertension in people with diabetes mellitus". The Cochrane database of systematic reviews. 10: CD008277. doi:10.1002/14651858.cd008277.pub2. PMID 24170669.
  89. ^ Eni C. Okonofua; Kit N. Simpson; Ammar Jesri; Shakaib U. Rehman; Valerie L. Durkalski; Brent M. Egan (23 January 2006). "Therapeutic Inertia Is an Impediment to Achieving the Healthy People 2010 Blood Pressure Control Goals". Hypertension. 47 (2006, 47:345): 345–51. doi:10.1161/01.HYP.0000200702.76436.4b. PMID 16432045. Retrieved 22 November 2009.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  90. ^ a b c Klarenbach, SW; McAlister, FA, Johansen, H, Tu, K, Hazel, M, Walker, R, Zarnke, KB, Campbell, NR, Canadian Hypertension Education, Program (May 2010). "Identification of factors driving differences in cost effectiveness of first-line pharmacological therapy for uncomplicated hypertension". The Canadian journal of cardiology. 26 (5): e158–63. doi:10.1016/S0828-282X(10)70383-4. PMC 2886561. PMID 20485695.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  91. ^ Wright JM, Musini VM; Musini (2009). Wright, James M (ed.). "First-line drugs for hypertension". Cochrane Database of Systematic Reviews (3): CD001841. doi:10.1002/14651858.CD001841.pub2. PMID 19588327.
  92. ^ James, PA.; Oparil, S.; Carter, BL.; Cushman, WC.; Dennison-Himmelfarb, C.; Handler, J.; Lackland, DT.; Lefevre, ML.; et al. (December 2013). "2014 Evidence-Based Guideline for the Management of High Blood Pressure in Adults: Report From the Panel Members Appointed to the Eighth Joint National Committee (JNC 8)". JAMA. 311 (5): 507–20. doi:10.1001/jama.2013.284427. PMID 24352797.
  93. ^ a b National Institute Clinical Excellence (August 2011). "1.5 Initiating and monitoring antihypertensive drug treatment, including blood pressure targets". GC127 Hypertension: Clinical management of primary hypertension in adults. Retrieved 23 December 2011.
  94. ^ Wiysonge, CS; Bradley, HA; Volmink, J; Mayosi, BM; Mbewu, A; Opie, LH (14 November 2012). "Beta-blockers for hypertension". The Cochrane database of systematic reviews. 11: CD002003. doi:10.1002/14651858.CD002003.pub4. PMID 23152211.
  95. ^ Opie, LH; Wiysonge, CS (26 February 2014). "β-Blocker therapy for patients with hypertension--reply". JAMA : the journal of the American Medical Association. 311 (8): 862–3. doi:10.1001/jama.2014.336. PMID 24570254.
  96. ^ Sever PS, Messerli FH; Messerli (October 2011). "Hypertension management 2011: optimal combination therapy". Eur. Heart J. 32 (20): 2499–506. doi:10.1093/eurheartj/ehr177. PMID 21697169.
  97. ^ "2.5.5.1 Angiotensin-converting enzyme inhibitors". British National Formulary. Vol. No. 62. September 2011. {{cite book}}: |volume= has extra text (help); External link in |chapterurl= (help); Unknown parameter |chapterurl= ignored (|chapter-url= suggested) (help)
  98. ^ a b Musini VM, Tejani AM, Bassett K, Wright JM; Tejani; Bassett; Wright (2009). Musini, Vijaya M (ed.). "Pharmacotherapy for hypertension in the elderly". Cochrane Database of Systematic Reviews (4): CD000028. doi:10.1002/14651858.CD000028.pub2. PMID 19821263.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  99. ^ James, Paul A.; Oparil, Suzanne; Carter, Barry L.; Cushman, William C.; Dennison-Himmelfarb, Cheryl; Handler, Joel; Lackland, Daniel T.; LeFevre, Michael L.; MacKenzie, Thomas D.; Ogedegbe, Olugbenga; Smith, Sidney C.; Svetkey, Laura P.; Taler, Sandra J.; Townsend, Raymond R.; Wright, Jackson T.; Narva, Andrew S.; Ortiz, Eduardo (18 December 2013). "2014 Evidence-Based Guideline for the Management of High Blood Pressure in Adults". JAMA. 311 (5): 507–20. doi:10.1001/jama.2013.284427. PMID 24352797.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  100. ^ "CG34 Hypertension - quick reference guide" (PDF). National Institute for Health and Clinical Excellence. 28 June 2006. Retrieved 4 March 2009.
  101. ^ Calhoun DA; Jones D; Textor S; et al. (June 2008). "Resistant hypertension: diagnosis, evaluation, and treatment. A scientific statement from the American Heart Association Professional Education Committee of the Council for High Blood Pressure Research". Hypertension. 51 (6): 1403–19. doi:10.1161/HYPERTENSIONAHA.108.189141. PMID 18391085. {{cite journal}}: |first10= missing |last10= (help); |first11= missing |last11= (help); Unknown parameter |author-separator= ignored (help)
  102. ^ Zubcevic J, Waki H, Raizada MK, Paton JF; Waki; Raizada; Paton (June 2011). "Autonomic-immune-vascular interaction: an emerging concept for neurogenic hypertension". Hypertension. 57 (6): 1026–33. doi:10.1161/HYPERTENSIONAHA.111.169748. PMC 3105900. PMID 21536990.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  103. ^ Santschi, V; Chiolero, A; Burnier, M (November 2009). "Electronic monitors of drug adherence: tools to make rational therapeutic decisions". Journal of hypertension. 27 (11): 2294–5, author reply 2295. doi:10.1097/hjh.0b013e328332a501. PMID 20724871.
  104. ^ "WHO Disease and injury country estimates". World Health Organization. 2009. Retrieved 11 November 2009.
  105. ^ a b Kearney PM, Whelton M, Reynolds K, Muntner P, Whelton PK, He J; Whelton; Reynolds; Muntner; Whelton; He (2005). "Global burden of hypertension: analysis of worldwide data". Lancet. 365 (9455): 217–23. doi:10.1016/S0140-6736(05)17741-1. PMID 15652604.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  106. ^ Kearney PM, Whelton M, Reynolds K, Whelton PK, He J; Whelton; Reynolds; Whelton; He (January 2004). "Worldwide prevalence of hypertension: a systematic review". J. Hypertens. 22 (1): 11–9. doi:10.1097/00004872-200401000-00003. PMID 15106785.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  107. ^ Burt VL; Whelton P; Roccella EJ; et al. (March 1995). "Prevalence of hypertension in the US adult population. Results from the Third National Health and Nutrition Examination Survey, 1988–1991". Hypertension. 25 (3): 305–13. doi:10.1161/01.HYP.25.3.305. PMID 7875754. Retrieved 5 June 2009. {{cite journal}}: Unknown parameter |author-separator= ignored (help)
  108. ^ a b c d Lloyd-Jones D; Adams RJ; Brown TM; et al. (February 2010). "Heart disease and stroke statistics--2010 update: a report from the American Heart Association". Circulation. 121 (7): e46–e215. doi:10.1161/CIRCULATIONAHA.109.192667. PMID 20019324. {{cite journal}}: |first10= missing |last10= (help); |first11= missing |last11= (help); Unknown parameter |author-separator= ignored (help)
  109. ^ a b Burt VL; Cutler JA; Higgins M; et al. (July 1995). "Trends in the prevalence, awareness, treatment, and control of hypertension in the adult US population. Data from the health examination surveys, 1960 to 1991". Hypertension. 26 (1): 60–9. doi:10.1161/01.HYP.26.1.60. PMID 7607734. Retrieved 5 June 2009. {{cite journal}}: Unknown parameter |author-separator= ignored (help)
  110. ^ Ostchega Y, Dillon CF, Hughes JP, Carroll M, Yoon S; Dillon; Hughes; Carroll; Yoon (July 2007). "Trends in hypertension prevalence, awareness, treatment, and control in older U.S. adults: data from the National Health and Nutrition Examination Survey 1988 to 2004". Journal of the American Geriatrics Society. 55 (7): 1056–65. doi:10.1111/j.1532-5415.2007.01215.x. PMID 17608879.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  111. ^ "Culture-Specific of Health Risk". Stanford. Retrieved 12 April 2014.
  112. ^ Falkner B (May 2009). "Hypertension in children and adolesents: epidemiology and natural history". Pediatr. Nephrol. 25 (7): 1219–24. doi:10.1007/s00467-009-1200-3. PMC 2874036. PMID 19421783.
  113. ^ Luma GB, Spiotta RT; Spiotta (May 2006). "Hypertension in children and adolescents". Am Fam Physician. 73 (9): 1558–68. PMID 16719248.
  114. ^ "Global health risks: mortality and burden of disease attributable to selected major risks" (PDF). World Health Organization. 2009. Retrieved 10 February 2012.
  115. ^ Lewington S, Clarke R, Qizilbash N, Peto R, Collins R; Clarke; Qizilbash; Peto; Collins; Prospective Studies (December 2002). "Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies". Lancet. 360 (9349): 1903–13. doi:10.1016/S0140-6736(02)11911-8. PMID 12493255.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  116. ^ Singer DR, Kite A; Kite (June 2008). "Management of hypertension in peripheral arterial disease: does the choice of drugs matter?". European Journal of Vascular and Endovascular Surgery. 35 (6): 701–8. doi:10.1016/j.ejvs.2008.01.007. PMID 18375152.
  117. ^ a b c d e f g h Esunge PM (October 1991). "From blood pressure to hypertension: the history of research". J R Soc Med. 84 (10): 621. PMC 1295564. PMID 1744849.
  118. ^ a b Kotchen TA (October 2011). "Historical trends and milestones in hypertension research: a model of the process of translational research". Hypertension. 58 (4): 522–38. doi:10.1161/HYPERTENSIONAHA.111.177766. PMID 21859967.
  119. ^ Swales JD, ed. (1995). Manual of hypertension. Oxford: Blackwell Science. pp. xiii. ISBN 0-86542-861-1.
  120. ^ Postel-Vinay N, ed. (1996). A century of arterial hypertension 1896–1996. Chichester: Wiley. p. 213. ISBN 0-471-96788-2.
  121. ^ "The medieval origins of the concept of hypertension". Heart Views. 15 (3): 96–98. 2014. doi:10.4103/1995-705X.144807. Retrieved 25 November 2014.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  122. ^ "Avicenna's doctrine about arterial hypertension". Acta Med Hist Adriat. 2014. PMID 25310615. Retrieved 25 November 2014.
  123. ^ "The Medieval Origins of the Concept of Hypertension". Heart Views. PMID 25538828.
  124. ^ Dustan HP, Roccella EJ, Garrison HH; Roccella; Garrison (September 1996). "Controlling hypertension. A research success story". Arch. Intern. Med. 156 (17): 1926–35. doi:10.1001/archinte.156.17.1926. PMID 8823146.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  125. ^ Novello FC, Sprague JM; Sprague (1957). "Benzothiadiazine dioxides as novel diuretics". J. Am. Chem. Soc. 79 (8): 2028. doi:10.1021/ja01565a079.
  126. ^ Chockalingam A (May 2007). "Impact of World Hypertension Day". Canadian Journal of Cardiology. 23 (7): 517–9. doi:10.1016/S0828-282X(07)70795-X. PMC 2650754. PMID 17534457.
  127. ^ Chockalingam A (June 2008). "World Hypertension Day and global awareness". Canadian Journal of Cardiology. 24 (6): 441–4. doi:10.1016/S0828-282X(08)70617-2. PMC 2643187. PMID 18548140.
  128. ^ Alcocer L, Cueto L; Cueto (June 2008). "Hypertension, a health economics perspective". Therapeutic Advances in Cardiovascular Disease. 2 (3): 147–55. doi:10.1177/1753944708090572. PMID 19124418. Retrieved 20 June 2009.
  129. ^ William J. Elliott (October 2003). "The Economic Impact of Hypertension". The Journal of Clinical Hypertension. 5 (4): 3–13. doi:10.1111/j.1524-6175.2003.02463.x. PMID 12826765.
  130. ^ Coca A (2008). "Economic benefits of treating high-risk hypertension with angiotensin II receptor antagonists (blockers)". Clinical Drug Investigation. 28 (4): 211–20. doi:10.2165/00044011-200828040-00002. PMID 18345711.
  131. ^ a b c Gulati, V.; White, WB. (August 2013). "Review of the state of renal nerve ablation for patients with severe and resistant hypertension". J Am Soc Hypertens. 7 (6): 484–93. doi:10.1016/j.jash.2013.07.003. PMID 23953998.
  132. ^ Bhatt, Deepak L.; Kandzari, David E.; O'Neill, William W.; D'Agostino, Ralph; Flack, John M.; Katzen, Barry T.; Leon, Martin B.; Liu, Minglei; Mauri, Laura; Negoita, Manuela; Cohen, Sidney A.; Oparil, Suzanne; Rocha-Singh, Krishna; Townsend, Raymond R.; Bakris, George L. (2014). "A Controlled Trial of Renal Denervation for Resistant Hypertension". New England Journal of Medicine. 370 (15): 1393–1401. doi:10.1056/NEJMoa1402670. ISSN 0028-4793.
  133. ^ Lobo, M. D.; de Belder, M. A.; Cleveland, T.; Collier, D.; Dasgupta, I.; Deanfield, J.; Kapil, V.; Knight, C.; Matson, M.; Moss, J.; Paton, J. F. R.; Poulter, N.; Simpson, I.; Williams, B.; Caulfield, M. J. (2014). "Joint UK societies' 2014 consensus statement on renal denervation for resistant hypertension". Heart. 101 (1): 10–16. doi:10.1136/heartjnl-2014-307029. ISSN 1355-6037.

Further reading

  • James, Paul A.; Oparil, Suzanne; Carter, Barry L.; Cushman, William C.; Dennison-Himmelfarb, Cheryl; Handler, Joel; Lackland, Daniel T.; Lefevre, Michael L.; MacKenzie, Thomas D.; Ogedegbe, Olugbenga; Smith, Sidney C.; Svetkey, Laura P.; Taler, Sandra J.; Townsend, Raymond R.; Wright, Jackson T.; Narva, Andrew S.; Ortiz, Eduardo (18 December 2013). "2014 Evidence-Based Guideline for the Management of High Blood Pressure in Adults". JAMA. 311 (5): 507–20. doi:10.1001/jama.2013.284427. PMID 24352797.