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Hypertension Classification and external resources

pressures, defined as mean arterial pressures 50% or more above average, a person can expect to live no more than a few years unless appropriately treated.[2] Beginning at a systolic pressure of 115 mm Hg and diastolic pressure of 75 mm Hg (commonly written as 115/75 mm Hg), cardiovascular disease (CVD) risk doubles for each increment of 20/ 10 mm Hg.[3]

Automated arm blood pressure meter showing arterial hypertension (shown a systolic blood pressure 158 mmHg, diastolic blood pressure 99 mmHg and heart rate of 80 beats per minute).

In individuals older than 50 years, hypertension is considered to be present when a person’s blood pressure is consistently at least 140 mm Hg systolic or 90 mm Hg diastolic. Patients with blood pressures over - 130/ 80 mm Hg along with Type 1 or Type 2 diabetes, or kidney disease require further treatment.[3] Resistant hypertension is defined as the failure to reduce BP to the appropriate level after taking a three-drug regimen.[3] Guidelines for treating resistant hypertension have been published in the UK,[4] and US.[5] In the United States, prehypertension is defined as blood pressure from 121/81 mm Hg to 139/89 mm Hg and although not a disease category, it is a designation chosen to identify individuals at high risk of developing hypertension.[3]

ICD-10 ICD-9 OMIM DiseasesDB MedlinePlus eMedicine MeSH

I10.,I11.,I12., I13.,I15. 401.x 145500 6330 000468 med/1106 ped/1097 emerg/267 D006973

Hypertension, also referred to as high blood pressure, HTN or HPN, is a medical condition in which the blood pressure is chronically elevated. In current usage, the word "hypertension" without a qualifier normally refers to systemic, arterial hypertension.[1] Hypertension can be classified as either essential (primary) or secondary. Essential hypertension indicates that no specific medical cause can be found to explain a patient’s condition. About 95% of hypertension is essential hypertension. Secondary hypertension indicates that the high blood pressure is a result of (i.e., secondary to) another condition, such as kidney disease or tumours (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. Even moderate elevation of arterial blood pressure leads to shortened life expectancy. At severely high

Essential (primary) hypertension
By definition, essential hypertension has no identifiable cause. However, several risk factors have been identified, including obesity,[6] salt sensitivity, renin homeostasis, insulin resistance, genetics, and age.

The risk of hypertension is 5 times higher in the obese as compared to those of normal weight and up to two-thirds of cases can be attributed to excess weight. More than 85% of cases occur in those with a Body mass index greater than 25.[6]A definitive link


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between obesity and hypertension has been found using animal and clinical studies, from these it has been realized that many mechanisms are potential causes of obesity induced hypertension.These mechanisms include the activation of the sympathetic nervous system as well as the activation of the renin–angiotensin-aldosterone system.[7]

that interfere with the Renin-angiotensin system. How high renin levels predispose to hypertension: Increased renin → Increased angiotensin II → Increased vasoconstriction, thirst/ADH and aldosterone → Increased sodium resorption in the kidneys (DCT and CD) → Increased blood pressure. Some authorities claim that potassium might both prevent and treat hypertension.[11]

Sodium sensitivity
Sodium is an environmental factor that has received the greatest attention. Approximately one third of the essential hypertensive population is responsive to sodium intake.[8] When sodium intake exceeds the capacity of the body to excrete it through the kidneys, vascular volume expands secondary to movement of fluids into the intra-vascular compartment. This causes the arterial pressure to rise as the cardiac output increases. Local autoregulatory mechanisms counteract this by increasing vascular resistance to maintain normotension in local vascular beds. As arterial pressure increases in response to high sodium chloride intake, urinary sodium excretion increases and the excretion of salt is maintained at expense of increased vascular pressures.[9] The increased sodium ion concentration stimulates ADH and thirst mechanisms, leading to increased reabsorption of water in the kidneys, concentrated urine, and thirst with higher intake of water. Also, the water movement between cells and the interstitium plays a minor role compared to this. The relationship between sodium intake and blood pressure is controversial. Reducing sodium intake does reduce blood pressure, but the magnitude of the effect is insufficient to recommend a general reduction in salt intake.[10]

Insulin resistance
Insulin is a polypeptide hormone secreted by cells in the islets of Langerhans, which are contained throughout the pancreas. Its main purpose is to regulate the levels of glucose in the body antagonistically with glucagon through negative feedback loops. Insulin also exhibits vasodilatory properties. In normotensive individuals, insulin may stimulate sympathetic activity without elevating mean arterial pressure. However, in more extreme conditions such as that of the metabolic syndrome, the increased sympathetic neural activity may over-ride the vasodilatory effects of insulin. Insulin resistance and/or hyperinsulinemia have been suggested as being responsible for the increased arterial pressure in some patients with hypertension. This feature is now widely recognized as part of syndrome X, or the metabolic syndrome.

Hypertension is one of the most common complex disorders.The etiology of hypertension differs widely amongst individuals within a large population.[12] Hypertension may be secondary to other diseases but over 90% of patients have essential hypertension which is of unknown origin. It is observed though that: • Having a personal family history of hypertension increases the likelihood that an individual develops HPT. • Essential hypertension is four times more common in black than white people, accelerates more rapidly and is often more severe with higher mortality in black patients. More than 50 genes have been examined in association studies with hypertension, and the number is constantly growing.One of these gene is angiotensinogen (AGT) gene, studied extensively by Kim et al. They showed that increasing the number of AGT

Role of renin
Renin is an enzyme secreted by the juxtaglomerular apparatus of the kidney and linked with aldosterone in a negative feedback loop. The range of renin activity observed in hypertensive subjects tends to be broader than in normotensive individuals. In consequence, some hypertensive patients have been defined as having low-renin and others as having essential hypertension. Lowrenin hypertension is more common in African Americans than white Americans, and may explain why African Americans tend to respond better to diuretic therapy than drugs


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increases the blood pressure and hence this may cause hypertension.[12] Twins have been included in studies measuring ambulatory blood pressure, from these studies it has been suggested that essential hypertension contains a large genetic influence.[12] Supporting data has emerged from animal studies as well as clinical studies in human populations.The majority of these studies support the concept that the inheritance is probably multifactorial or that a number of different genetic defects each have an elevated blood pressure as one of their phenotypic expressions.However, the genetic influence upon hypertension is not fully understood at the moment. It is believed that linking hypertension-related phenotypes with specific variations of the genome may yield definitive evidence of heritability.[13] Another view is that hypertension can be caused by mutations in single genes, inherited on a mendelian basis.[14]

link between hypertension and vitamin D levels in the blood plasma.[17]

Secondary hypertension
Secondary hypertension results from an identifiable cause. With treatment of the underlying cause, secondary hypertension can resolve without the need for anti-hypertensive medications.

Sleep apnea
Sleep apnea is a common, under-recognized cause of hypertension.[18] It is often best treated with nocturnal nasal continuous positive airway pressure, but other approaches include the Mandibular advancement splint (MAS), UPPP, tonsilectomy, adenoidectomy, septoplasty, or weight loss.

Consumption of liquorice (which can be of potent strength in liquorice candy) can lead to a surge in blood pressure.[19] People with hypertension or history of cardio-vascular disease should avoid liquorice raising their blood pressure to risky levels. Frequently, if liquorice is the cause of the high blood pressure, a low blood level of potassium will also be present. Liquorice extracts are present in many medicines (for example cough syrups, throat lozenges and peptic ulcer treatments).

Hypertension can also be age related, if this is the case it is likely to be multifactorial. One possible mechanism involves a reduction in vascular compliance due to the stiffening of the arteries. This can build up due to isolated systolic hypertension with a widened pulse pressure. A decrease in glomerular filtration rate is related to aging and this results in decreasing efficiency of sodium excretion. The developing of certain diseases such as renal microvascular disease and capillary rarefaction may relate to this decrease in efficiency of sodium excretion. There is experimental evidence that suggests that renal microvascular disease is an important mechanism for inducing salt-sensitive hypertension.[15]

Some renal tumors can cause hypertension. The differential diagnosis of a renal tumor in a young patient with hypertension includes Juxtaglomerular cell tumor, Wilms’ tumor, and renal cell carcinoma, all of which may produce renin.[20] The tumor pheochromocytoma (most often located in the adrenal medulla) increases secretion of catecholamines such as epinephrine and norepinephrine, causing excessive stimulation of adrenergic receptors, which results in peripheral vasoconstriction and cardiac stimulation. This diagnosis is confirmed by demonstrating increased urinary excretion of epinephrine and norepinephrine and/or their metabolites (vanillylmandelic acid).

Vitamin D
It has been suggested, as a result of several studies, that vitamin D deficiency is associated with cardiovascular risk factors.[16] It has been observed that individuals with a vitamin D deficiency have higher systolic and diastolic blood pressures than average. Vitamin D inhibits renin secretion and its activity, it therefore acts as a "negative endocrine regulator of the renin-angiotensin system". Hence a deficiency in vitamin D leads to an increase in renin secretion. This is one possible mechanism of explaining the observed

Renal hypertension
Hypertension produced by diseases of the kidney. This includes diseases such as polycystic kidney disease or chronic glomerulonephritis. Hypertension can also be


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produced by diseases of the renal arteries supplying the kidney. This is known as renovascular hypertension; it is thought that decreased perfusion of renal tissue due to stenosis of a main or branch renal artery activates the renin-angiotensin system.

Medications commonly associated with rebound hypertension include centrally-acting antihypertensive agents, such as clonidine and beta-blockers.

Adrenal hypertension
Hypertension is a feature of a variety of adrenal cortical abnormalities. In primary aldosteronism there is a clear relationship between the aldosterone-induced sodium retention and the hypertension.

Apparent mineralocorticoid excess syndrome
autosomal recessive disorder results from mutations in gene encoding 11β-hydroxysteroid dehydrogenase which normal patient inactivates circulating cortisol to the less-active metabolite cortisone. Cortisol at high concentrations can cross-react and activate the mineralocorticoid receptor, leading to aldosterone-like effects in the kidney, causing hypertension. This effect can also be produced by prolonged ingestion of liquorice, which can inhibit the 11β-hydroxysteroid dehydrogenase enzyme and cause secondary apparent mineralocorticoid excess syndrome.

Cushing’s syndrome
Cushing’s syndrome is a condition where both adrenal glands can overproduce the hormone cortisol. Hypertension results from the interplay of several pathophysiological mechanisms regulating plasma volume, peripheral vascular resistance and cardiac output, all of which may be increased. More than 80% of patients with Cushing’s syndrome have hypertension.

Glucocorticoid remediable aldosteronism
is an autosomal dominant disorder in which the increase in aldosterone secretion produced by ACTH is no longer transient, causing of primary hyperaldosteronism, the Gene mutated will result in an aldosterone synthase that is ACTH-sensitive, which is normally not. Compare these effects to those seen in Conn’s disease, an adrenocortical tumor which causes excess release of aldosterone.

Coarctation of the aorta
The congenital abnormality aortic coarctation can result in hypertension.

Certain medications, especially NSAIDs (Motrin/Ibuprofen) and steroids can cause hypertension. Licorice (Glycyrrhiza glabra) inhibits the 11-hydroxysteroid hydrogenase enzyme (catalyzes the reaction of cortisol to cortisone) which allows cortisol to stimulate the Mineralocorticoid receptor (MR) which will lead to effects similar to hyperaldosteronism, which itself is a cause of hypertension.[21]

Polycystic kidney disease
is a cystic genetic disorder of the kidneys, PKD is characterized by the presence of multiple cysts (hence, "polycystic") in both kidneys, can also damage the liver, pancreas, and rarely, the heart and brain. It can be autosomal dominant or autosomal recessive, with the autosomal dominant form being more common and characterized by progressive cyst development and bilaterally enlarged kidneys with multiple cysts, with concurrent development of hypertension, renal insufficiency and renal pain.

Rebound hypertension
High blood pressure that is associated with the sudden withdrawal of various antihypertensive medications is called Rebound Hypertension. The increases in blood pressure may result in blood pressures greater than when the medication was initiated. Depending on the severity of the increase in blood pressure, rebound hypertension may result in a hypertensive emergency. Rebound hypertension is avoided by gradually reducing the dose (also known as "dose tapering"), thereby giving the body enough time to adjust to reduction in dose.

Although few women of childbearing age have high blood pressure, up to 10% develop hypertension of pregnancy. While generally benign, it may herald three complications of pregnancy: pre-eclampsia, HELLP syndrome


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and eclampsia. Follow-up and control with medication is therefore often necessary.

For instance, measurements in control of hypertension should be at least 1 hour after caffeine, 30 minutes after smoking or strenuous exercise and without any stress. Cuff size is also important. The bladder should encircle and cover two-thirds of the length of the (upper) arm. The patient should be sitting upright in a chair with both feet flat on the floor for a minimum of five minutes prior to taking a reading. The patient should not be on any adrenergic stimulants, such as those found in many cold medications. When taking manual measurements, the person taking the measurement should be careful to inflate the cuff suitably above anticipated systolic pressure. The person should inflate the cuff to 200 mmHg and then slowly release the air while palpating the radial pulse. After one minute, the cuff should be reinflated to 30 mmHg higher than the pressure at which the radial pulse was no longer palpable. A stethoscope should be placed lightly over the brachial artery. The cuff should be at the level of the heart and the cuff should be deflated at a rate of 2 to 3 mmHg/s. Systolic pressure is the pressure reading at the onset of the sounds described by Korotkoff (Phase one). Diastolic pressure is then recorded as the pressure at which the sounds disappear (K5) or sometimes the K4 point, where the sound is abruptly muffled. Two measurements should be made at least 5 minutes apart, and, if there is a discrepancy of more than 5 mmHg, a third reading should be done. The readings should then be averaged. An initial measurement should include both arms. In elderly patients who particularly when treated may show orthostatic hypotension, measuring lying sitting and standing BP may be useful. The BP should at some time have been measured in each arm, and the higher pressure arm preferred for subsequent measurements. BP varies with time of day, as may the effectiveness of treatment, and archetypes used to record the data should include the time taken. Analysis of this is rare at present. Automated machines are commonly used and reduce the variability in manually collected readings.[26] Routine measurements done in medical offices of patients with known hypertension may incorrectly diagnose 20% of patients with uncontrolled hypertension[27] Home blood pressure monitoring can provide a measurement of a person’s blood pressure at different times throughout the

Binswanger’s disease
It is a rare neurological disease causing dementia, it is a rare form of form of multi-infarct dementia, its is one of the neurological syndromes associated with hypertension.

Most of the mechanisms associated with secondary hypertension are generally fully understood. However, those associated with essential (primary) hypertension are far less understood. What is known is that cardiac output is raised early in the disease course, with total peripheral resistance (TPR) normal; over time cardiac output drops to normal levels but TPR is increased. Three theories have been proposed to explain this: • Inability of the kidneys to excrete sodium, resulting in natriuretic factors such as Atrial Natriuretic Factor being secreted to promote salt excretion with the side-effect of raising total peripheral resistance. • An overactive Renin-angiotensin system leads to vasoconstriction and retention of sodium and water. The increase in blood volume leads to hypertension. • An overactive sympathetic nervous system, leading to increased stress responses. It is also known that hypertension is highly heritable and polygenic (caused by more than one gene) and a few candidate genes have been postulated in the etiology of this condition.[22][23][24]

Measuring blood pressure
Diagnosis of hypertension is generally on the basis of a persistently high blood pressure. Usually this requires three separate measurements at least one week apart. Exceptionally, if the elevation is extreme, or end-organ damage is present then the diagnosis may be applied and treatment commenced immediately. Obtaining reliable blood pressure measurements relies on following several rules and understanding the many factors that influence blood pressure reading.[25]


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day and in different environments, such as at home and at work.[28] Home monitoring may assist in the diagnosis of high or low blood pressure. It may also be used to monitor the effects of medication or lifestyle changes taken to lower or regulate blood pressure levels. Home monitoring of blood pressure can also assist in the diagnosis of white coat hypertension. The American Heart Association[29] states, "You may have what’s called ’white coat hypertension’; that means your blood pressure goes up when you’re at the doctor’s office. Monitoring at home will help you measure your true blood pressure and can provide your doctor with a log of blood pressure measurements over time. This is helpful in diagnosing and preventing potential health problems." Some home blood pressure monitoring devices also make use of blood pressure charting software. These charting methods provide printouts for the patient’s physician and reminders to take a blood pressure reading. However, a simple and cheap way is simply to manually record values with pen and paper, which can then be inspected by a doctor. Systolic hypertension is defined as an elevated systolic blood pressure. If systolic blood pressure is elevated with a normal diastolic blood pressure, it is called isolated systolic hypertension. Systolic hypertension may be due to reduced compliance of the aorta with increasing age.[30]


Investigations commonly performed in newly diagnosed hypertension
Tests are undertaken to identify possible causes of secondary hypertension, and seek evidence for end-organ damage to the heart itself or the eyes (retina) and kidneys. Diabetes and raised cholesterol levels being additional risk factors for the development of cardiovascular disease are also tested for as they will also require management. Blood tests commonly performed include: • Creatinine (renal function) - to identify both underlying renal disease as a cause of hypertension and conversely hypertension causing onset of kidney damage. Also a baseline for later monitoring the possible side-effects of certain antihypertensive drugs. • Electrolytes (sodium, potassium) • Glucose - to identify diabetes mellitus • Cholesterol Additional tests often include: • Testing of urine samples for proteinuria again to pick up underlying kidney disease or evidence of hypertensive renal damage. • Electrocardiogram (EKG/ECG) - for evidence of the heart being under strain from working against a high blood pressure. Also may show resulting thickening of the heart muscle (left ventricular hypertrophy) or of the occurrence of previous silent cardiac disease (either subtle electrical conduction disruption or even a myocardial infarction). • Chest X-ray - again for signs of cardiac enlargement or evidence of cardiac failure.

Distinguishing primary vs. secondary hypertension
Once the diagnosis of hypertension has been made it is important to attempt to exclude or identify reversible (secondary) causes. • Over 91% of adult hypertension has no clear cause and is therefore called . Often, it is part of the metabolic "syndrome X" in patients with insulin resistance: it occurs in combination with diabetes mellitus (type 2), combined hyperlipidemia and central obesity. • 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.[31]

The degree to which hypertension can be prevented depends on a number of features including: current blood pressure level, changes in end/target organs (retina, kidney, heart - among others), risk factors for cardiovascular diseases and the age at presentation. Unless the presenting patient has very severe hypertension, there should be a relatively prolonged assessment period within which should be repeated measurements of blood pressure. Following this, lifestyle advice and non-pharmacological options should


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be offered to the patient, before any initiation of drug therapy. The process of managing hypertension according the guidelines of the British Hypertension Society suggest that non-pharmacological options should be explored in all patients who are hypertensive or pre-hypertensive. These measures include; • Weight reduction and regular aerobic exercise (e.g., walking) are recommended as the first steps in treating mild to moderate hypertension. Regular exercise improves blood flow and helps to reduce resting heart rate and blood pressure.[32] Several studies indicate that low intensity exercise may be more effective in lowering blood pressure than higher intensity exercise.[33] These steps are highly effective in reducing blood pressure, although drug therapy is still necessary for many patients with moderate or severe hypertension to bring their blood pressure down to a safe level. • Reducing dietary sugar intake • Reducing sodium (salt) in the diet may be effective: It decreases blood pressure in about 33% of people (see above). Many people use a salt substitute to reduce their salt intake. • Additional dietary changes beneficial to reducing blood pressure includes the DASH diet (dietary approaches to stop hypertension), which is rich in fruits and vegetables and low-fat or fat-free dairy foods. This diet has been shown to be effective based on research sponsored by the National Heart, Lung, and Blood Institute.[34] In addition, an increase in daily calcium intake has the benefit of increasing dietary potassium, which theoretically can offset the effect of sodium and act on the kidney to decrease blood pressure. This has also been shown to be highly effective in reducing blood pressure. • Discontinuing tobacco use and alcohol consumption has been shown to lower blood pressure. The exact mechanisms are not fully understood, but blood pressure (especially systolic) always transiently increases following alcohol or nicotine consumption. Besides, abstention from cigarette smoking is important for people with hypertension because it reduces the risk of many dangerous outcomes of hypertension, such as stroke and heart

attack. Note that coffee drinking (caffeine ingestion) also increases blood pressure transiently but does not produce chronic hypertension. • Reducing stress, for example with relaxation therapy, such as meditation and other mindbody relaxation techniques,[35] by reducing environmental stress such as high sound levels and over-illumination can be an additional method of ameliorating hypertension. Jacobson’s Progressive Muscle Relaxation and biofeedback are also used,[36] particularly, device-guided paced breathing,[37][38] although meta-analysis suggests it is not effective unless combined with other relaxation techniques.[39]

Unless hypertension is severe, lifestyle changes such as those discussed in the preceding section are strongly recommended before initiation of drug therapy. Adoption of the DASH diet is one example of lifestyle change repeatedly shown to effectively lower mildly-elevated blood pressure. If hypertension is high enough to justify immediate use of medications, lifestyle changes are initiated concomitantly. There are many classes of medications for treating hypertension, together called antihypertensives, which — by varying means — act by lowering blood pressure. Evidence suggests that reduction of the blood pressure by 5-6 mmHg can decrease the risk of stroke by 40%, of coronary heart disease by 15%-20%, and reduces the likelihood of dementia, heart failure, and mortality from vascular disease. The aim of treatment should be blood pressure control to <140/90 mmHg for most patients, and lower in certain contexts such as diabetes or kidney disease (some medical professionals recommend keeping levels below 120/80 mmHg).[40] Each added drug may reduce the systolic blood pressure by 5-10 mmHg, so often multiple drugs are necessary to achieve blood pressure control. A series of UK guidelines advocate treatment initiation thresholds and desirable targets to be reached as set out in the following table. Of particular note is that for patients with blood pressures between 140-159/80-99 and without additional factors, that only


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lifestyle actions and regular blood pressure and risk-factor review is proposed. UK Hypertension guidelines[4] Thresholds Group for starting treatment >160/100 >140/90 all those with such persisting readings If also:[4] Cardiovascular risk >20% per 10 years Or have established cardiovascular disease Or have evidence end organ damage Or chronic kidney disease without high levels albuminuria[41] Type 2 Diabetes alone[42] Type 1 Diabetes alone[43]


• Additional diuretics such a furosemide or low-dosages of spironolactone • Alpha blockers such as prazosin, or terazosin. Doxazosin has been shown to Target of treatment increase risk of heart failure, and to be less effective than a simple diuretic.[45] • Beta blockers such as atenolol, labetalol, metoprolol (Lopressor, Toprol-XL), <140/90 propranolol. Whilst once first line agents, now less directly used for this in the United Kingdom due to the risk of <140/90 diabetes.[46] • Direct renin inhibitors such as aliskiren (Tekturna) Finally several agents may be given simultaneously: • Combination products (which usually contain HCTZ and one other drug)

Choice of initial medication
Unless the blood pressure is severely elevated, consensus guidelines call for medicallysupervised lifestyle changes and observation before recommending initiation of drug therapy. All drug treatments have side effects, and while the evidence of benefit at higher blood pressures is overwhelming, drug trials to lower moderately-elevated blood pressure have failed to reduce overall death rates. If lifestyle changes are ineffective or the presenting blood pressure is critical, then drug therapy is initiated, often requiring more than one agent to effective lower hypertension. Which type of many medications should be used initially for hypertension has been the subject of several large studies and various national guidelines. The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) study showed better cost-effectiveness and slightly better outcomes for the thiazide diuretic chlortalidone compared with a calcium channel blocker and an ACE inhibitor in a 33,357-member ethnically mixed study group.[47] The 1993 consensus recommendation for use of thiazide diuretics as initial treatment stems in part from the ALLHAT study results, which concluded in 2002 that "Thiazide-type diuretics are superior in preventing 1 or more major forms of CVD and are less expensive. They should be preferred for first-step antihypertensive therapy."[47] A subsequent smaller study (ANBP2) did not show the slight advantages in thiazide diuretic outcomes observed in the ALLHAT study, and actually showed slightly better

>140/80 >135/85 >130/80

<140/80 <130/80

Type 1 Diabetes with <130/80 microalbuminuria[43] Or Type 2 Diabetes with kidney, eye or cerebrovascular damage[42] chronic kidney disease with high levels albuminuria[41] <125/75


Commonly used drugs include the typical groups of:[4] • ACE inhibitors such as captopril, enalapril, fosinopril (Monopril), lisinopril (Zestril), quinapril, ramipril (Altace) • Angiotensin II receptor antagonists may be used where ACE inhibitors are not tolerated: eg, telmisartan (Micardis, Pritor), irbesartan (Avapro), losartan (Cozaar), valsartan (Diovan), candesartan (Amias) • Calcium channel blockers such as nifedipine (Adalat)[44] amlodipine (Norvasc), diltiazem, verapamil • Diuretics: eg, bendroflumethiazide, chlortalidone, hydrochlorothiazide (also called HCTZ) Other additionally used groups include:


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outcomes for ACE-inhibitors in older white male patients.[48] Thiazide diuretics are effective, recommended as the best first-line drug for hypertension by many experts, and much more affordable than other therapies, yet they are not prescribed as often as some newer drugs. Arguably, this is partly because they are offpatent, less profitable, and thus rarely promoted by the drug industry.[49] The consensus recommendations of thiazide diuretics as first-line therapy for hypertension stand against the backdrop that all blood pressure treatments have side-effects. Potentially serious side effects of the thiazide diuretics include hypercholesterolemia, and impaired glucose tolerance with consequent increased risk of developing Diabetes mellitus type 2. The thiazide diuretics also deplete circulating potassium unless combined with a potassium-sparing diuretic or supplemental potassium. On this basis, the consensus recommendations to prefer use of thiazides as first line treatment for essential hypertension have been repeatedly and strongly questioned.[50][51][52] However as the Merck Manual of Geriatrics notes, "thiazide-type diuretics are especially safe and effective in the elderly."[53] Current UK guidelines suggest starting patients over the age of 55 years and all those of African/Afrocaribbean ethnicity firstly on calcium channel blockers or thiazide diuretics, whilst younger patients of other ethnic groups should be started on ACE-inhibitors. Subsequently if dual therapy is required to use ACE-inhibitor in combination with either a calcium channel blocker or a (thiazide) diuretic. Triple therapy is then of all three groups and should the need arise then to add in a fourth agent, to consider either a further diuretic (eg spironolactone or furosemide), an alpha-blocker or a betablocker.[4] Prior to the demotion of betablockers as first line agents, the UK sequence of combination therapy used the first letter of the drug classes and was known as the "ABCD rule".[54][4]

are more likely to have a much better outcome than someone who does not.


Diagram illustrating the main complications of persistent high blood pressure. While elevated blood pressure alone is not an illness, it often requires treatment due to its short- and long-term effects on many organs. The risk is increased for: • Cerebrovascular accident (CVAs or strokes) • Myocardial infarction (heart attack) • Hypertensive cardiomyopathy (heart failure due to chronically high blood pressure) • Hypertensive retinopathy - damage to the retina • Hypertensive nephropathy - chronic renal failure due to chronically high blood pressure • Hypertensive encephalopathy - confusion, headache, convulsion due to vasogenic edema in brain due to high blood pressure.

The level of blood pressure regarded as deleterious has been revised down during years of epidemiological studies. A widely quoted and important series of such studies is the Framingham Heart Study carried out in an American town: Framingham, Massachusetts. The results from Framingham and of similar work in Busselton, Western Australia have been widely applied. To the extent that people are similar this seems reasonable, but

It is based upon several factors including genetics, dietary habits, and overall lifestyle choices. If an individual conscious of their condition takes the necessary preventive measures to lower their blood pressure, they


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there are known to be genetic variations in the most effective drugs for particular subpopulations. Recently (2004), the Framingham figures have been found to overestimate risks for the UK population considerably. The reasons are unclear. Nevertheless the Framingham work has been an important element of UK health policy.

Saunders. pp. 220. ISBN 0-7216-0240-1. OCLC 213041516. [3] ^ Chobanian AV, Bakris GL, Black HR, et al (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. http://hyper.ahajournals.org/ cgi/content/full/42/6/1206. [4] ^ "CG34 Hypertension - quick reference guide" (PDF). National Institute for Health and Clinical Excellence. 28 June 2006. http://www.nice.org.uk/nicemedia/ pdf/cg034quickrefguide.pdf. Retrieved on 2009-03-04. [5] 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" (PDF). Hypertension 51 (6): 1403–19. doi:10.1161/ HYPERTENSIONAHA.108.189141. PMID 18391085. http://hyper.ahajournals.org/ cgi/reprint/51/6/1403.pdf. [6] ^ Haslam DW, James WP (2005). "Obesity". Lancet 366 (9492): 1197–209. doi:10.1016/S0140-6736(05)67483-1. PMID 16198769. [7] Rahmouni K, Correia ML, Haynes WG, Mark AL (January 2005). "Obesityassociated hypertension: new insights into mechanisms". Hypertension 45 (1): 9–14. doi:10.1161/ 01.HYP.0000151325.83008.b4. PMID 15583075. [8] http://www.jstage.jst.go.jp/article/jphs/ 100/5/370/_pdf A Missing Link Between a High Salt Intake and Blood Pressure Increase: Makoto Katori and Masataka Majima, Department of Pharmacology, Kitasato University School of Medicine, Kitasato, Sagamihara, Kanagawa, Japan February 8, 2006 [9] Harrison’s Principles of Internal Medicine, Chapter 24: Hypertensive Vascular Disease [10] Jürgens G, Graudal NA (2004). "Effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterols, and triglyceride". Cochrane

Children and adolescents
As with adults, blood pressure is a variable parameter in children. It varies between individuals and within individuals from day to day and at various times of the day. The epidemic of childhood obesity, the risk of developing left ventricular hypertrophy, and evidence of the early development of atherosclerosis in children would make the detection of and intervention in childhood hypertension important to reduce long-term health risks; however, supporting data are lacking. Most childhood hypertension, particularly in preadolescents, is secondary to an underlying disorder. Renal parenchymal disease is the most common (60 to 70%) cause of hypertension. Adolescents usually have primary or essential hypertension, making up 85 to 95% of cases.[55]

Sushruta (6th century BCE) explained hypertension in a manner which matches the modern symptoms of the disease.[56]

See also
• • • • • • • Exercise hypertension White coat hypertension Home blood pressure monitoring Spontaneously hypertensive rat Prehypertension Pulse pressure Pulmonary hypertension

[1] Maton, Anthea; Jean Hopkins, Charles William McLaughlin, Susan Johnson, Maryanna Quon Warner, David LaHart, Jill D. Wright (1993). Human Biology and Health. Englewood Cliffs, New Jersey, USA: Prentice Hall. ISBN 0-13-981176-1. OCLC 32308337. [2] Guyton & Hall (2005). Textbook of Medical Physiology (7th ed.). Elsevier-


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External links
Hypertension at the Open Directory Project • High Blood Pressure Blog Informative blog on the topic of high blood pressure • High Blood Pressure from the Heart and Stroke Foundation of Canada • High Blood Pressure from MedlinePlus • A guide to lowering high blood pressure from the National Heart, Lung, and Blood Institute • High Blood Pressure (from the American Heart Association)

Major studies
• The Framingham Heart Study • Information on ALLHAT

Retrieved from "http://en.wikipedia.org/wiki/Hypertension" Categories: Hypertension, Aging-associated diseases, Cardiology, Cardiovascular diseases, Medical conditions related to obesity, Nephrology This page was last modified on 20 May 2009, at 00:11 (UTC). All text is available under the terms of the GNU Free Documentation License. (See Copyrights for details.) Wikipedia® is a registered trademark of the Wikimedia Foundation, Inc., a U.S. registered 501(c)(3) taxdeductible nonprofit charity. Privacy policy About Wikipedia Disclaimers


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