Arterial hypertension

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Classification according to ICD-10
I10.0 high blood pressure
I11.0 Hypertensive heart disease with (congestive) heart failure
I11.9 Hypertensive heart disease without (congestive) heart failure
ICD-10 online (WHO version 2019)

The arterial hypertension , often shortened hypertension (from ancient Greek ὑπέρ hyper over (default) "and τείνειν teinein , hypertension, hypertension or in everyday language, tighten ') high blood pressure called, is a medical condition wherein the blood pressure of the arterial vascular system increases chronically is. According to the definition of the WHO , a systolic blood pressure of more than 140  mmHg and / or a diastolic blood pressure of more than 90 mmHg is considered to be hypertension in adults . Temporary increases in blood pressure due to illness, medication , pregnancy or physical exertion are not included in this definition .


Causes of arterial hypertension can be disorders of the endocrine system , the cardiovascular system and kidney damage . However, most of the diseases are based on largely unknown factors.

Arterial hypertension usually only shows unspecific symptoms. Consequential damage such as coronary artery disease with the consequence of heart attacks as well as kidney failure and strokes are responsible for a large number of deaths in industrialized countries. Various groups of drugs are available to treat the symptoms. In combination with lifestyle changes, they can effectively lower blood pressure and significantly reduce the risk of complications.

Inheritance also plays a major role. For example, if the parents already suffer from hypertension, the risk of being affected by high blood pressure increases many times over.


The incidence ( prevalence ) of arterial hypertension has been consistently high in industrialized countries since the 1980s. It is 10–50% of the total population, with the incidence increasing significantly with age. Over 20% of Central Europeans have a greatly increased systolic blood pressure of over 160 mmHg, and for those over 80 years of age this percentage is even 30%. This makes it one of the most frequent consultation occasions in a general medical practice. However, arterial hypertension also occurs in younger people. In the age group of 25 to 29 year olds, the pressure in the vessels is too high in around every tenth woman and around every fourth man. The frequency of high blood pressure increases sharply with increasing age. In the over 60s, only about one in four has normal blood pressure values. The ratio of affected women to men changes with age. While it is 2: 3 in adolescent adulthood, women predominate at around 4: 3 among 60-year-olds.

The highest hypertension prevalence in Europe was found earlier in Germany, which is also in the stroke - mortality stood with a European leader. In the meantime, however, this has changed, at least with regard to hypertension: As in most other western industrialized countries with high per capita incomes, the situation in Germany improved from 1975 to 2015, while high blood pressure remains a problem in Eastern Europe .

Employment can be an important factor that increases blood pressure . Of workers with an average age of 44 years, only 35% had normal blood pressure, and of the hypertensive patients only 7.5% had normal blood pressure values ​​under antihypertensive therapy. This was shown by long-term blood pressure measurements during work, which were carried out repeatedly over a period of five years. The target values ​​for blood pressure are mostly not achieved in Germany: only a maximum of every fifth hypertension patient in Germany has a blood pressure below 140/90 mmHg or, if there is an increased risk (e.g. diabetes), below 130/80 mmHg. Of the 20 million people who suffered from hypertension in Germany, only 10% of men and 21% of women were treated correctly. 75% of hypertensive diabetics were treated, but only 7.5% achieved the target value of below 130/80 mmHg.

Etiology and pathogenesis (causes and course)

For the vast majority of diseases, no clear cause ( etiology ) can be identified. In this case, it is referred to as primary or essential hypertension . If, on the other hand, an underlying disease can be identified, hypertension is referred to as secondary.

A number of causes lead to temporary increases in blood pressure, which many authors classify as secondary hypertension, but which do not meet the definition in the narrower sense and are reversible if the causal factors are eliminated. These causes include diseases of the central nervous system (inflammation, increased intracranial pressure, poisoning), the effects of drugs ( ovulation inhibitors , corticosteroids , non-steroidal anti-inflammatory drugs ), luxury foods ( licorice ) and drugs ( cocaine , amphetamines ). During pregnancy, too, diseases with high blood pressure often occur (around 10%). A distinction is made between pregnancy-induced hypertension (SIH) and grafted forms, in which pre-existing hypertension worsens, and pre-existing forms that exist independently of the pregnancy. Pregnancy-induced hypertension with protein loss ( preeclampsia ) is a relevant cause of maternal and child mortality during pregnancy and requires targeted treatment and monitoring.

Primary hypertension

No physical cause of the high blood pressure can be identified in up to 95% of patients. This primary or essential (also: essential) hypertension is multifactorial and has not yet been conclusively clarified. A genetic component plays a role, various mutations are known, which, however, cannot in themselves explain a disease (polygenic cause). In addition, extremely rare forms of hypertension are known that are based on the modification of a single gene (monogenic). The fact that the majority of hypertensive patients have a positive family history also suggests a genetic cause. that is, other family members are also affected. Various lifestyle factors (constitution, consumption of alcohol, tobacco and excessive consumption of table salt, stress, hormonal reasons) play a strongly promoting role.

Various theories exist on the pathogenesis of primary hypertension. Often the hypertension occurs as part of a metabolic syndrome . The associated insulin resistance and the consecutive hyperinsulinemia possibly contribute to the increase in blood pressure through two mechanisms. On the one hand, insulin causes a direct retention of salt and water in the kidneys; on the other hand, insulin has a proliferative effect on vascular muscle cells, which leads to an increase in resistance in the blood circulation. Disturbances of the ion transport on the membrane of vascular cells are held responsible for an increased reactivity of the arterial resistance vessels. In patients with arterial hypertension, a reduced activity of endothelial NO synthase with reduced NO production ( nitric oxide ) can often be detected. These changes appear to play a role in hypertension, but one that is not fully understood. The body's own control system RAAS , on the other hand, seems to play only a subordinate role in primary hypertension.

Psychotherapy - especially behavioral methods such as biofeedback - has been proven in various studies to be effective in the treatment of high blood pressure and it is usually used in combination with antihypertensive medication. In 1950, the psychoanalyst Franz Alexander described essential hypertension as one of the seven classic psychosomatic diseases ( Holy Seven ). Even if Alexander's point of view was questioned on individual points by later research (see Holy Seven ), the importance of psychosomatic factors for blood pressure is now widely recognized.

Primary hypertension is a diagnosis of exclusion and should only be made when other causes can be ruled out. It must be treated with antihypertensive measures for a long time or for life.

Secondary hypertension

Secondary hypertension is a high blood pressure disorder caused by other underlying diseases. This is the case in 5–15% of all hypertensive patients. The most common causes of secondary hypertension are diseases of the kidneys , the endocrine system (here in particular primary hyperaldosteronism ) and sleep apnea syndrome .

Angiography of renal artery stenosis
  • In kidney diseases, a distinction is made between diseases of the renal arteries and kidney tissue. Diseases of the kidney tissue ( renoparenchymatous form ) are caused by chronic inflammation ( glomerulonephritis , interstitial nephritis ), by diabetic damage ( nephropathy ), cystic kidneys or by mechanical compression of the kidneys ( Page kidney ). Pathogenetically, this results in a reduced ability to excrete salt and thus an increase in blood pressure. The narrowing of the renal artery ( renal artery stenosis ), known as the renovascular form , is caused by arteriosclerosis , connective tissue diseases ( fibromuscular dysplasia ) or inflammation. As a result, the kidneys are not supplied with enough blood, which activates the renin-angiotensin-aldosterone system (RAAS). This causes vascular constriction , activation of the sympathetic nervous system and reduced salt excretion in the kidneys, which in turn results in increased blood volume. All of these mechanisms contribute to an increase in blood pressure ( gold leaf mechanism ). The treatment of renovascular hypertension consists in widening the narrowing of the arteries with a catheter ( angioplasty ). However, if the stenosis persists for a long time, the resulting kidney tissue damage can cause the hypertension to persist even after such treatment ( renal fixation ).
  • Disorders in the hormonal balance can be caused by a number of different diseases. In Conn syndrome , increased aldosterone levels lead to an increase in blood pressure. The normokalemic variant (with normal potassium levels) of Conn's syndrome could, according to recent studies, account for a large part of secondary hypertension. In a pheochromocytoma , the excessive production of adrenaline and noradrenaline causes activation of the sympathetic nervous system, in Cushing's syndrome the increased corticosteroid hormones cause increased salt reabsorption in the kidneys. Other, rarer causes are adrenogenital syndrome , acromegaly (increased growth hormone production) and hyperparathyroidism (overactive parathyroid glands). The use of contraceptives can also cause hypertension.
  • In an aortic coarctation (congenital malformations of the aorta), there is a narrowing of the aorta at the aortic arch, so the curvature of the aorta above the heart . This narrowing causes blood pressure to rise. Due to the reduced blood flow to the kidneys, which are located below this constriction, arterial hypertension occurs through the same mechanisms as in renal artery stenosis (see above).
  • In sleep apnea syndrome , the sympathetic wake-up reactions that occur lead to an increase in blood pressure, especially at night. Treatment of sleep apnea syndrome ( CPAP therapy ) usually improves hypertension significantly.
  • The Pica loop syndrome is another very rare cause of secondary hypertension.

Clinical picture


Hypertension is often symptom-free or causes only uncharacteristic symptoms. A headache that occurs in the morning is typical and can be reduced by raising the head end of the bed. Other possible symptoms are dizziness , nausea , nosebleeds ( epistaxis ), fatigue and insomnia. If the blood pressure is very high, shortness of breath ( dyspnoea ) during exercise, angina pectoris and visual disturbances can occur. Noticeable changes in the feeling of thirst , the frequency of urination, the tendency to sweat or the ability to exercise can also be signs of high blood pressure. However, arterial hypertension can also be asymptomatic for a long time (without symptoms). They often only becomes apparent by the series loss figures, which is why they sometimes also called "silent killer" ( silent killer is called).

Gradient forms

In unstable and exertion -dependent hypertension , the blood pressure values are only increased temporarily or during exertion, whereas this is permanently the case with stable hypertension . As malignant or accelerated hypertension is defined as a severe form with systolic blood pressure above 180 mmHg and / or diastolic blood pressure greater than 110 mmHg, which is associated mostly with a distinct symptoms. In the literature and in the American and European guidelines, however, there are different information on the definition and limit values ​​for the need for treatment of malignant hypertension. In addition to nausea and vomiting, symptoms such as headache, impaired vision and consciousness, seizures and other neurological symptoms are in the foreground. In some cases, changes in the fundus of the eye of a higher degree, an abolished day-night rhythm in long-term blood pressure measurements and the development of renal insufficiency are included in the definition.

The hypertensive crisis is a sudden dysregulation of blood pressure in the systemic circulation with a critical increase in blood pressure, usually to over 230/130 mmHg. There is a risk of acute organ damage such as brain damage (high pressure encephalopathy ), acute heart failure , pulmonary edema , heart attack or, rarely, an aortic tear ( aortic dissection ). If such damage occurs, one speaks of a hypertensive emergency , which requires a rapid lowering of blood pressure with medication.

Consequences and complications


High blood pressure is recognized as a risk factor for the development of atherosclerosis . If obesity (severe overweight) and another risk factor - such as diabetes mellitus (diabetes) or lipid metabolism disorders (increased cholesterol or LDL values) - are added to the risk factor, there is a significantly increased risk of cardiovascular disease in the course of life -Suffering from disease .

According to the German Hypertension League, 45% of deaths in men and 50% of deaths in women are caused by cardiovascular diseases associated with arterial hypertension, such as coronary artery disease (CHD), myocardial infarction , heart failure , kidney failure , and stroke arterial disease .

The incidence of CHD deaths depends approximately linearly on blood pressure; it increases from 10 / 10,000 person-years (with normal blood pressure) to 60 / 10,000 person-years (systolic pressure> 180 mmHg). Since slight and medium increases in blood pressure are much more common than extreme pressures of more than 180 mmHg, significantly more people with medium blood pressure values ​​suffer cardiovascular events overall. However, this also means that people with only slightly elevated blood pressure must also be identified and treated in order to significantly reduce the high number of cardiovascular-related deaths.

After cigarette smoking, arterial hypertension is the second most important and at the same time the most common risk factor for the occurrence of cardiovascular disease. Nowadays, every second (51%) German and Austrian dies from cardiovascular disease. 16,000 Austrians alone die of a heart attack every year .

Classification according to ICD-10
I11.0 Hypertensive heart disease with (congestive) heart failure
I11.9 Hypertensive heart disease without (congestive) heart failure
ICD-10 online (WHO version 2019)

Hypertensive heart disease (CHD)

In addition to the increased risk of arteriosclerosis, a permanently high blood pressure causes damage to the heart muscle . The muscles become thicker and stiffer, so that the heart can no longer relax so easily and suck in blood during diastole (diastolic compliance disorder ). This leads to poor filling of the heart and symptoms of cardiac insufficiency ( diastolic heart failure ), in particular shortness of breath under stress or with a fast heartbeat ( tachycardia ). Furthermore, the cardiac arrhythmia atrial fibrillation occurs more frequently and can lead to a worsening of symptoms due to the sometimes considerably high heart rate.

According to echocardiographic criteria, the CHD is divided into four stages (relaxation disorder, pseudonormalization, reversible and fixed restriction). In addition to the information on elasticity , the wall thickness of the left ventricle, the enlargement of the left atrium and the level of pulmonary arterial pressure are also included in the assessment.

Even with optimal treatment, this consequence of high blood pressure is largely irreversible, but the symptoms can be significantly improved. The therapy consists in

  • Normalization of blood pressure at rest and during exercise,
  • Relief of the heart through diuretics (lowering of pulmonary arterial pressure) and
  • Lowering the heart rate (prolonging the diastole and thus the filling time of the heart).

Further organ damage

High blood pressure can also lead to changes in the retinal vessels of the eye , so that a fundus hypertonicus or, in the case of a high blood pressure crisis, a rare hypertensive retinopathy can occur.

The kidneys are also damaged by persistent high blood pressure, and kidney function is impaired ( hypertensive nephropathy ).

High blood pressure - one of the "four big risk factors"

In addition to diabetes mellitus including secondary diseases, which often also include high blood pressure, tobacco smoking and hypercholesterolemia  , high blood pressure is one of the “four major risk factors”. A large meta-study by Northwestern University in Chicago - published in 2012 in the New England Journal of Medicine  - analyzed these risks on the basis of 18 studies that examined a total of more than 250,000 people (aged 45 to 75) and followed them for at least ten years ( longitudinal study ). One result: even one of these “major risk factors” can increase the normal risk of cardiovascular diseases - in particular heart attacks and strokes - to around ten times. People with two or more of these risk factors are at an even higher risk.

“A male non-smoker without diabetes with normal blood pressure (not more than 120 to 80) and a normal cholesterol level (maximum 180 milligrams per deciliter) [...] only has a cardiovascular disease risk of 1.4 percent. Someone who has one of these values, who smokes or is diabetic, on the other hand, has to reckon with a heart attack 40 percent in the course of his life. "

Given these data, doctors recommend that people with high blood pressure avoid other of these risk factors (e.g. smoking) if possible. More than 250,000 people in Germany suffer a heart attack every year. Almost every heart attack patient who is hospitalized survives, but heart failure or a serious arrhythmia that can lead to premature death is often left behind.


The diagnostic measures pursue three goals: The presence of arterial hypertension is diagnosed and objectified by measuring blood pressure ; Causes of secondary hypertension are sought; Consequential damage is documented and the cardiovascular risk is determined. In addition to anamnesis and physical examination , laboratory and urine diagnostics, EKG , echocardiography , ophthalmoscopy (fundus examination ) and other diagnostic means are used.

The phenomenon that people with otherwise normal blood pressure repeatedly have elevated blood pressure values ​​when measured by medical personnel is often referred to as white coat hypertension . The following sources of error or influencing factors are mentioned: urge to stool or urinate: effect on the systolic value up to +27 mmHg, diastolic up to +22 mmHg, white coat effect: systolic. up to + 22 / diastol. up to +14, speaking: + 17 / + 13, smoking: + 10 / + 8, drinking coffee: + 10 / + 7, acute cold (drafts): + 11 / + 8, lack of back support: + 8 / + 6– 10, cuff too narrow: −8 / + 8, legs crossed: variable, emotional stress: variable. Therefore, these occasional measurements should be supplemented by self-measurements by the patient and, if possible, by 24-hour measurements. It is also possible to record load-dependent blood pressure peaks by examining them on a bicycle ergometer .


In 1999 the World Health Organization presented a classification of arterial hypertension, which the German medical societies also follow (see table). The degrees of severity presented in this classification are explicitly intended as flexible guide values. Rather, the diagnosis of hypertension should take into account the overall cardiovascular risk. Although this increases linearly with systolic and diastolic blood pressure, it is also dependent on other risk factors such as age, smoking, increased cholesterol levels, obesity, a positive family history, previous illnesses such as diabetes, strokes, heart, kidney and vascular diseases. As a consequence, it may be necessary to treat high-normal blood pressure when such factors are present.

rating systolic (mmHg) diastolic (mmHg)
optimal blood pressure <120 <80
normal blood pressure 120-129 80-84
high-normal blood pressure 130-139 85-89
mild hypertension (level 1) 140-159 90-99
moderate hypertension (level 2) 160-179 100-109
severe hypertension (stage 3) > 180 > 110
isolated systolic hypertension > 140 <90

In the United States, the American Heart Association (AHA) and the American College of Cardiology (ACC) redefined target blood pressure values ​​in November 2017. The guidelines referred to as an update of the JNC7 report from 2003 now classify blood pressure values ​​of 130 to 139 mmHg systolic and 80 to 89 mmHg diastolic as grade 1 hypertension. The German High Pressure League e. V. DHL® is now checking the updated target blood pressure values ​​of the American experts.

The WHO continues to classify hypertension clinically into three grades according to organ damage to blood vessels, eyes , heart , kidneys, etc. Grade I is a hypertension without end organ damage, grade II is mild damage ( fundus hypertonicus grade I and II, plaque formation in larger vessels, slight kidney and heart damage). Grade III includes severe organ damage with manifest cardiovascular complications: angina pectoris , myocardial infarction , heart failure , neurological symptoms ( TIA , stroke ), peripheral occlusive disease , aortic dissection , fundus hypertonicus III and IV, renal insufficiency .

In the ICD-10 (as of 2008) only a subdivision into benign and malignant hypertension is made.


The treatment of arterial hypertension is a building block in reducing cardiovascular mortality.

In reality, high-pressure patients are sometimes inadequately supplied with medication. In one study, only every second patient was treated for the given hypertension indication. Both general practitioners and cardiologists misjudged the quality of their high-pressure therapy. In 60% of the cases they thought they had "adjusted optimally" to the disease, while this was actually the case in only 35% of the cases. A new study, on the other hand, shows that physical activity can lower blood pressure just as well as drug treatment. Therefore, drugs should not simply be recommended unreservedly.

General measures

The change in lifestyle plays an important role as the basis of therapy. This applies equally to patients before the start of drug therapy and to those who are already being treated. Attending a heart school can be useful for a permanent lifestyle change .

Factors that have been shown to lower blood pressure and cardiovascular risk include:

  • The completion of the smoking does not cause a direct reduction in blood pressure, but is probably the most important measure to reduce the risk of complications. People who quit smoking in middle age have just as long a life expectancy as non-smokers. Smoking also makes some antihypertensive drugs less effective, such as beta blockers.
  • Alcohol consumption and the occurrence of high blood pressure correlate positively with one another, and the risk of stroke is significantly increased with high alcohol consumption. Alcohol also reduces the effectiveness of drug therapy. The maximum amount of alcohol per day should not exceed 30 g for men and 20 g for women. By restricting consumption, blood pressure can be lowered by 2-4 mmHg.
  • A weight reduction in overweight ( obesity ) can significantly reduce blood pressure (5-20 mmHg per 10 kg) and affects insulin resistance, diabetes mellitus, elevated blood lipids and heart failure positively. A combination with other general measures increases the effects. A lifestyle change with weight reduction through a change in diet and exercise not only lowers blood pressure, but also significantly reduces left ventricular muscle mass by reducing preload and afterload on the heart. The increase in performance on the ergometer and the reduced exertional dyspnea are also due to a decrease in left ventricular hypertrophy (LVH) and an improvement in diastolic function. In every second patient, blood pressure decreases with weight. Why only about half of the patients respond measurably to weight loss is currently the subject of research. The blood sugar, on the other hand, decreases more significantly than the blood pressure in every patient who loses weight.
  • Regular physical activity lowers blood pressure by 4–9 mmHg, even at low intensity. The best effect is achieved when exercising for at least 30 minutes several times a week. Biking , swimming , running , hiking and weight training, etc., are suitable . Contrary to popular belief, strength training does not increase blood pressure; instead, moderate training even shows a slight decrease in pressure in hypertensive patients. Physical activity is a sensitive predictor of cardiovascular mortality.
  • Excessive consumption of table salt can contribute to the frequency and extent of high blood pressure. However, the connection between table salt and high blood pressure is not entirely certain. A reduction in daily consumption to less than six grams can lower blood pressure by up to 8 mmHg, and even more in combination with other measures. The effect of antihypertensive agents is increased by such a reduction. Anyone who consumes 2.5 g less table salt (1 g sodium) per day reduces their risk of cardiovascular disease by a quarter. According to a model calculation in the New England Journal of Medicine , in the United States alone, avoiding 3 g of salt per day would mean 44,000 to 92,000 fewer deaths per year. The authors of the study expect 54,000 to 99,000 fewer heart attacks and 32,000 to 66,000 fewer strokes per year.
  • In one study it could be shown that salt deactivates the eNOS enzyme, even in concentrations that are achieved through salt consumption in today's western diet.
  • Furthermore, a damaged endothelial glycocalyx has an influence on the exposure of sodium to the endothelial cells and is therefore the cause of the so-called salt sensitivity, which is present in an estimated 30% of all those affected by high blood pressure.
  • The body needs enough potassium to prevent and counteract hypertension and strokes. A balanced ratio of sodium and potassium is particularly important for regulating blood pressure. Reducing the daily consumption of table salt and increasing your potassium intake are therefore a relatively simple way of doing something for your health. In order to get more potassium, it is recommended to eat more fruits and vegetables, because they contain a lot of potassium citrate, which has been shown to lower blood pressure.
  • Increasing the consumption of fruit , vegetables and fish as well as reducing saturated fatty acids is another effective means of bringing about a reduction in blood pressure (8-14 mmHg) and limiting the overall cardiovascular risk.

Here the secondary plant substances , especially the flavonoids ( taxifolin ), play a growing role. Epidemiological and in vivo studies indicate a positive influence on various cardiovascular diseases. These include in particular the inhibition of ROS-forming enzymes, inhibition of platelet function , inhibition of leukocyte activation, and properties that lower blood pressure and expand blood vessels.

  • A study that examined the influence of fish meals containing omega-3 fatty acids showed a significant reduction in blood pressure.
  • In an experimental study on sun exposure, irradiation of the subjects' forearms with UVA rays led to an increased release of nitric oxide in the skin with an expansion of the blood vessels and a measurable decrease in blood pressure.
  • A meta-analysis confirmed that the intake of the amino acid L-arginine as a substrate for nitric oxide formation is associated with a significant reduction in blood pressure

Medical therapy

In general, the following applies (as of 2020): If the blood pressure repeatedly exceeds 140/90 in the practice measurement, drug therapy is indicated in order to lower the blood pressure below this threshold. If the therapy is well tolerated, the blood pressure should even be lowered below 130/80, but not below 120/70. Lowering blood pressure to 130/80 and below is particularly desirable in diabetics. If there are no other cardiovascular risk factors and the blood pressure does not exceed 160/100, medical blood pressure lowering can be dispensed with in exceptional cases. Conversely, if the cardiovascular risk is very high, antihypertensive drugs can be used even with high blood pressure values. After the age of 65, blood pressure should not be reduced below 130/80. After the age of 80, drug therapy is only recommended from a systolic pressure of 160 mmHg.

First choice antihypertensive drugs are:

While therapy was often started with a single active ingredient in the past, the combination of an ACE inhibitor / AT1 antagonist and another active ingredient has been recommended since 2018. Many such active ingredient combinations are now available as a fixed combination in one tablet. The dose is carefully increased until the therapy goal is achieved. If the maximum dose of a double combination is not sufficient, another double combination or a triple combination can be selected.

The selection of active ingredients depends on the age and the accompanying illnesses of the person concerned. For example, thiazides are beneficial in osteoporosis , but unfavorable in metabolic diseases such as diabetes mellitus or gout . Calcium antagonists are beneficial for circulatory disorders, but unfavorable for heart failure . Some drugs are not approved during pregnancy and can harm the unborn child (see: Pregnancy hypertension ). Beta blockers are no longer among the blood pressure lowerers of choice for people with healthy hearts, but are still often used as the recommended medication for heart failure and coronary artery disease .

Second choice agents are potassium channel openers , α 1 antagonists , α 2 agonists , renin inhibitors and NO donors .

Treatment-resistant arterial hypertension

Therapy-resistant arterial hypertension is defined as high blood pressure that is not within the target range despite therapy with three or more high-pressure medications, including at least one diuretic. About 20–30% of hypertensive patients are resistant to therapy, especially in older people or if they are overweight. Often the therapy resistance is based on a secondary form of hypertension. The most common cause is hyperaldosteronism , other causes are obstructive sleep apnea syndrome , chronic kidney disease , renal artery stenosis or pheochromocytoma . The aldosterone / renin quotient should therefore be determined in all patients with therapy-resistant high blood pressure in order to rule out hyperaldosteronism, even if the serum potassium is normal. By adding spironolactone in a low dose (25 mg / d) to the standard therapy, a further reduction in blood pressure can be achieved, regardless of the level of the aldosterone / renin quotient. The most common side effect of spironolactone is gynecomastia with tenderness of the chest, which occurs in around 10% of the men treated. Because of the risk of hyperkalaemia , potassium controls are necessary, especially in patients with chronic kidney disease, diabetes mellitus, elderly patients or concomitant administration of an ACE inhibitor or AT 1 antagonist.

If increased blood pressure cannot be adjusted with medication, interventional renal sympathetic denervation , also known as renal denervation , has been propagated as a therapeutic method since 2009 . In this method, afferent sympathetic nerve fibers in the renal arteries are selectively obliterated using minimally invasive methods ( catheter ablation ). Radical severing of the nerves has long been known, but in contrast to the selective method, it led to considerable side effects. Compared to the previous studies with significantly lower patient numbers, the first prospective randomized study (so-called SYMPLICITY HTN-3 study ) from 2014 with 535 patients could not confirm the previously assumed safety and effectiveness of invasive renal nerve obliteration. The difference in systolic blood pressure of 15 mmHg in the verum group compared to the placebo group six months after the procedure as a postulated study goal could not be demonstrated.

The Barorezeptorstimulation is another invasive method with uncontrolled hypertension. Here, pressure receptors in the area of ​​the carotid fork (fork of the carotid artery) are stimulated via implanted electrodes.

Seven clinical studies have shown that stimulating the baroreceptors with a pacemaker-like device lowers blood pressure in people with treatment-resistant hypertension.

The observed decrease in systolic blood pressure at the longest available follow-up is 36 mmHg (359 patients). In the first 6 months, the average drop in blood pressure was 21 mmHg (307 patients). For patients in Europe, Baroreflex activation therapy devices have received the CE mark for the treatment of resistant hypertension.

Further therapeutic options

In 2007 a first study of a vaccine (CYT006-AngQb) against arterial hypertension was presented. This should induce the production of antibodies in the patient that are specifically directed against angiotensin II and should reduce the activation of the renin-angiotensin-aldosterone system. Further studies on this vaccine were discontinued in 2009 because it was inferior to previous therapy methods.

Arterial hypertension in animals

High blood pressure plays a role in veterinary medicine, especially in domestic cats . Almost a fifth of cats over the age of seven suffer from high blood pressure. The proportion is even higher in animals with chronic kidney disease , hyperthyroidism and diabetes . Consequences of untreated blood pressure are primarily retinal hemorrhages, detachments and edema, which can lead to blindness, as well as kidney, brain and heart damage.


  • Tinsley R. Harrison et al. a .: Harrison's Principles of Internal Medicine . Mcgraw-Hill Professional, New York 2001, 2005, ISBN 0-07-007272-8 .
  • Gerd Herold and colleagues: Internal Medicine 2020. Self-published, Cologne 2020, ISBN 978-3-9814660-9-6 .
  • Ernst Mutschler: drug effects . 8th edition. Wissenschaftliche Verlagsgesellschaft, Stuttgart 2001, ISBN 3-8047-1763-2 .
  • T. Strasser, L. Wilhelmsen (Eds.): Assessing hypertension control and management: hypertension management audit project; a WHO / WHL study . World Health Organization, Regional Office for Europe, Copenhagen. World Hypertension League, Geneva, World Health Organization. Regional Office for Europe (Editor), Copenhagen 1993, DNB 369206258


Web links

Wiktionary: Hypertension  - explanations of meanings, word origins, synonyms, translations

Individual evidence

  1. Renate Wahrig-Burfeind (Ed.): True. Illustrated dictionary of the German language . ADAC-Verlag, Munich 2004, ISBN 3-577-10051-6 , pp. 404 .
  2. W. Fink, G. Haidinger: The frequency of health disorders in 10 years of general practice . In: Z. Allg. Med. 83.200, 102-108. Quoted from What family doctors mainly deal with . In: MMW update. Med. , No. 16., 2007.
  3. a b c Renz cushion u. a., 2004
  4. Data from the Framingham study , cited from Harrison et al. a., 2005.
  5. a b cure high pressure therapy in Germany. In: Medical Tribune , January 26, 2007, p. 24.
  6. ^ The Lancet: Number of people living with high blood pressure has almost doubled worldwide over past 40 years. In: EurekAlert !, accessed on February 1, 2017 (English).
  7. ^ NCD Risk Factor Collaboration (NCD-RisC): Worldwide trends in blood pressure from 1975 to 2015: a pooled analysis of 1479 population-based measurement studies with 19.1 million participants . In: The Lancet . tape 389 , no. 10064 , 2017, p. 37-55 , doi : 10.1016 / S0140-6736 (16) 31919-5 .
  8. DMW 131, 2006, 2580, quoted in Ärzte-Zeitung, November 22, 2006, p. 1.
  9. ^ According to Lars-Christian Rump, in Ärzte-Zeitung , November 26, 2007, p. 4, target values ​​for blood pressure are often not achieved.
  10. Unsatisfactory supply situation, MMM update. (Med no. 49-50 / 2007 8149. born.), P.6, quoted by Lars-Christian Rump, president of Hypertension -Tagung 2007 in Bochum .
  11. a b c d e f Harrison u. a., 2005.
  12. ^ A b Alvin P. Shapiro: Hypertension and Stress: A Unified Concept. Psychology Press, 2013, ISBN 978-1-134-79345-7 , p. 68 google-books ). Wolfgang Linden: Psychological Perspectives of Essential Hypertension: Etiology, Maintenance, and Treatment (= Karger biobehavioral medicine series , Volume 3). Karger, Basel / New York 1984, ISBN 978-3-8055-3662-2 , especially p. 6, with follow-up after up to 24 months ( online at google-books ); Gene L Stainbrook, John W Hoffman, Herbert Benson: Behavioral therapies of hypertension: psychotherapy, biofeedback, and relaxation / meditation. In: Applied Psychology. Volume 32, No. 2, April 1983, pp. 119-135. Online publication: from January 22, 2008, doi: 10.1111 / j.1464-0597.1983.tb00899.x .
  13. ^ Franz Alexander : Psychosomatic medicine. Its principles and applications. Norton, New York 1950 ( DNB 993025870 ). German: Psychosomatic Medicine. Basics and areas of application. De Gruyter, Berlin 1951.
  14. German Society for Cardiology - Heart and Circulatory Research e. V. / German Hypertension League e. V. ESC / ESH Pocket Guidelines. Management of arterial hypertension, 2018 version.
  15. Martin Reincke, Lysann Seiler, Lars C. Rump: normokalemic primary aldosteronism . In: Deutsches Ärzteblatt . tape 100 , no. 4 . Deutscher Ärzte-Verlag , January 24, 2003, p. A-184 / B-169 / C-165 .
  16. ↑ High blood pressure: arteriosclerosis, heart attack and other consequences. Retrieved June 29, 2020 .
  17. Compliance failure | Findings interpreter. Retrieved June 29, 2020 .
  18. ^ Lifetime Risks of Cardiovascular Disease . Friday Packet for January 26, 2012
  19. ^ A b Franziska Draeger: Heart attack: lifestyle has more influence on the risk of heart attack than expected. In: . January 26, 2012, accessed December 27, 2014 .
  20. Der Hausarzt , 15/09, p. 54 f.
  21. ^ WHO / ISH-Guidelines-Subcommittee: 1999 World Health Organization-International Society of Hypertension Guidelines for the Management of Hypertension. Guidelines Subcommittee . In: Journal Hypertens. Volume 17, 1999, SD. 151-183, PMID 10067786 .
  22. a b c d Guidelines for the Management of Arterial Hypertension. German Hypertension League e. V. 2019.
  23. American Heart Association (AHA) / American College of Cardiology (ACC): 2017 Guideline for High Blood Pressure in Adults. November 13, 2017. Retrieved November 19, 2017 .
  24. Quoted from Also cardiologist messes up with hypertension. P. 11 and cure high pressure therapy in Germany . P. 24. In: Medical Tribune of January 26, 2007.
  25. a b Huseyin Naci, Maximilian Salcher-Konrad, Sofia Dias, Manuel R Blum, Samali Anova Sahoo, David Nunan, John PA Ioannidis: How does exercise treatment compare with antihypertensive medications? A network meta-analysis of 391 randomized controlled trials assessing exercise and medication effects on systolic blood pressure. In: British Journal of Sports Medicine. S. bjsports-2018-099921, doi: 10.1136 / bjsports-2018-099921 .
  26. a b c A. V. Chobanian et al. a .: The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure, the JNC 7 report . In: JAMA. May 21, 2003, Volume 289, Number 19, pp. 2560-2572; Erratum in: JAMA. July 9, 2003, Volume 290, Number 2, p. 197, PMID 12748199 .
  27. ^ R. Doll, R. Peto, J. Boreham, I. Sutherland: Mortality in relation to smoking. 50 years' observations on male British doctors . In: BMJ. June 26, 2004, Volume 328, Number 7455, p. 1519, PMID 15213107 .
  28. IB puddey, LJ Beilin, V Rakic: Alcohol, hypertension and the cardiovascular system, a critical appraisal . In: Addict Biol. Vol. 2, 1997, pp. 159-170.
  29. A. Wirth, Sonnenhang ia, 0-49214 Bad Rothenfelde, MMW , No. 22/2010, p. 41e
  30. Strength training for patients with high blood pressure - Active against high blood pressure. Retrieved December 7, 2017 .
  31. L. Sandvik et al. a .: Physical fitness as a predictor of mortality among healthy, middle-aged Norwegian men . In: N Engl J Med. 25 February 1993, Volume 25, Number 328, pp. 533-537, PMID 8426620 .
  32. ^ MR Law: Epidemiologic evidence on salt and blood pressure. In: American journal of hypertension. Volume 10, Number 5, Part 2, May 1997, pp. 42S-45S, ISSN  0895-7061 , PMID 9160779 (review).
  33. K. Stolarz-Skrzypek, T. Kuznetsova u. a .: Fatal and nonfatal outcomes, incidence of hypertension, and blood pressure changes in relation to urinary sodium excretion. In: JAMA , Volume 305, Number 17, May 2011, pp. 1777-1785, ISSN  1538-3598 , doi: 10.1001 / jama.2011.574 , PMID 21540421 .
  34. JA Cutler, D. Follmann, PS Allender: Randomized trials of sodium reduction: an overview. In: The American journal of clinical nutrition , Volume 65, Number 2, Suppl, February 1997, pp. 643S-651S, ISSN  0002-9165 . PMID 9022560 .
  35. ^ NR Cook, JA Cutler et al. a .: Long-term effects of dietary sodium reduction on cardiovascular disease outcomes: observational follow-up of the trials of hypertension prevention (TOHP). In: BMJ (Clinical research ed.) , Volume 334, Number 7599, April 2007, pp. 885-888, ISSN  1756-1833 . doi: 10.1136 / bmj.39147.604896.55 . PMID 17449506 . PMC 1857760 (free full text).
  36. K. Bibbins-Domingo, GM Chertow a. a .: Projected effect of dietary salt reductions on future cardiovascular disease. In: The New England Journal of Medicine , Volume 362, Number 7, February 2010, pp. 590-599, ISSN  1533-4406 , doi: 10.1056 / NEJMoa0907355 , PMID 20089957 , PMC 3066566 (free full text).
  37. J. Li, J. White, L. Guo et al. a. (2009): Salt Inactivates Endothelial Nitric Oxide Synthase in Endothelial Cells. In: Journal of Nutrition , Volume 139, No. 3, pp. 447-451, doi: 10.3945 / jn.108.097451 .
  38. A New Concept in Understanding Vascular Salt Sensitivity. Full text (PDF)
  39. ^ Federal health reporting: Hypertension. Issue 43, Robert Koch Institute / Federal Statistical Office.
  40. FJ He, ND Markandu et al. a .: Effect of short-term supplementation of potassium chloride and potassium citrate on blood pressure in hypertensives. In: Hypertension. Volume 45, Number 4, April 2005, pp. 571-574, ISSN  1524-4563 . doi: 10.1161 / 01.HYP.0000158264.36590.19 . PMID 15723964 .
  41. a b D. Q. Bao, TA Mori and a .: Effects of dietary fish and weight reduction on ambulatory blood pressure in overweight hypertensives. In: Hypertension , Volume 32, Number 4, October 1998, pp. 710-717, ISSN  0194-911X . PMID 9774368 .
  42. FM Sacks, LP Svetkey u. a .: Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. In: The New England Journal of Medicine . Volume 344, Number 1, January 2001, pp. 3-10, ISSN  0028-4793 , doi: 10.1056 / NEJM200101043440101 , PMID 11136953 .
  43. P. Mladenka, L. Zatloukalová u. a .: Cardiovascular effects of flavonoids are not caused only by direct antioxidant activity. In: Free radical biology & medicine. Volume 49, Number 6, September 2010, pp. 963-975, ISSN  1873-4596 . doi: 10.1016 / j.freeradbiomed.2010.06.010 . PMID 20542108 . (Review).
  44. Donald Liu, Bernadette O Fernandez, Alistair Hamilton, Ninian N Lang, Julie MC Gallagher, David E Newby, Martin Feelisch, Richard B Weller: UVA Irradiation of Human Skin Vasodilates Arterial Vasculature and Lowers Blood Pressure Independently of Nitric Oxide Synthase. In: Journal of Investigative Dermatology . 2014, Volume 134, pp. 1839-1846, doi: 10.1038 / jid.2014.27 , PMID 24445737 .
  45. JY Dong, LQ Qin, Z. Zhang and a .: Effect of oral L-arginine supplementation on blood pressure: A meta-analysis of randomized, double-blind, placebo-controlled trials. In: American Heart Journal . Vol. 162, No. 6, 2011, pp. 959-965, PMID 22137067 .
  46. E. Pimenta et al .: Mechanisms and treatment of resistant hypertension . In: J Clin Hypertens (Greenwich) . No. 10 (3) , 2008, p. 239-244 , PMID 18326968 .
  47. ^ DA Calhoun et al .: 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 . In: Hypertension . tape 51 , no. 6 , 2008, p. 1403-1419 , doi : 10.1161 / HYPERTENSIONAHA.108.189141 , PMID 18391085 ( ). ( Memento of the original from May 26, 2008 in the Internet Archive ) Info: The archive link was automatically inserted and not yet checked. Please check the original and archive link according to the instructions and then remove this notice.  @1@ 2Template: Webachiv / IABot /
  48. ^ DA Calhoun: Low-dose aldosterone blockade as a new treatment paradigm for controlling resistant hypertension . In: J Clin Hypertens (Greenwich) . 9 (1 Suppl 1), 2007, p. 19-24 , PMID 17215651 .
  49. Interventional renal sympathetic nerve denervation ( Memento of the original from May 5, 2013 in the Internet Archive ) Info: The archive link was inserted automatically and has not yet been checked. Please check the original and archive link according to the instructions and then remove this notice. in @1@ 2Template: Webachiv / IABot /
  50. Sclerotherapy of renal nerves defeats resistant high blood pressure. In: November 17, 2010, accessed December 27, 2014 .
  51. Felix Mahfoud, Frank Himmel, Christian Ukena, Heribert Schunkert, Michael Böhm, Joachim Weil: Treatment strategies for refractory arterial hypertension . In: Deutsches Ärzteblatt . tape 108 , no. 43 . Deutscher Ärzte-Verlag , October 28, 2011, p. 725–731 , doi : 10.3238 / arztebl.2011.0725 .
  52. DL Bhatt, DE Kandzari u. a .: A controlled trial of renal denervation for resistant hypertension. In: The New England Journal of Medicine . Volume 370, Number 15, April 2014, pp. 1393-1401, ISSN  1533-4406 . doi: 10.1056 / NEJMoa1402670 . PMID 24678939 .
  53. Vera Zylka-Menhorn: Renal Denervation: Unexpected study result . In: Deutsches Ärzteblatt . No. 4 , January 24, 2014, p. A124 ( [accessed on January 28, 2014]).
  54. ^ M Wallbach, MJ Koziolek: Baroreceptors in the carotid and hypertension-systematic review and meta-analysis of the effects of baroreflex activation therapy on blood pressure. . In: Nephrology, dialysis, transplantation: official publication of the European Dialysis and Transplant Association - European Renal Association . November 9, 2017. doi : 10.1093 / ndt / gfx279 . PMID 29136223 .
  55. ^ IJ Scheffers, AA Kroon, J. Schmidli, J. Jordan, JJ Tordoir, MG Mohaupt, FC Luft, H. Haller, J. Menne, S. Engeli, J. Ceral, S. Eckert, A. Erglis, K. Narkiewicz, T. Philipp, PW de Leeuw: Novel baroreflex activation therapy in resistant hypertension: results of a European multi-center feasibility study. . In: Journal of the American College of Cardiology . 56, No. 15, October 5, 2010, pp. 1254-8. doi : 10.1016 / j.jacc.2010.03.089 . PMID 20883933 .
  56. CVRx ® Receives CE Mark Approval of the Barostim neo System ™ for the Treatment of Heart Failure
  57. ^ MJ Brown: Success and failure of vaccines against renin-angiotensin system components. In: Nature reviews. Cardiology. Volume 6, number 10, October 2009, pp. 639-647, ISSN  1759-5010 , doi: 10.1038 / nrcardio.2009.156 , PMID 19707182 . (Review).
  58. ^ Feline Hypertension , Cornell University
  59. ^ MP Littman: Spontaneous systemic hypertension in 24 cats. In: Journal of veterinary internal medicine / American College of Veterinary Internal Medicine. Volume 8, Number 2, March-April 1994, pp. 79-86, PMID 8046680 .
  60. S. Brown, C. Atkins, R. Bagley, et al. a .: Guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats. In: Journal of veterinary internal medicine / American College of Veterinary Internal Medicine. Volume 21, Number 3, May-June 2007, pp. 542-558, PMID 17552466 .
  61. ^ CA Brown, JS Munday, S. Mathur, SA Brown: Hypertensive encephalopathy in cats with reduced renal function. In: Veterinary pathology. Volume 42, Number 5, September 2005, pp. 642-649, doi: 10.1354 / vp.42-5-642 , PMID 16145210 .
  62. ^ Clarke Atkins: Hypertension . In: Veterinary Focus , 2012, Volume 22, Number 1, pp. 17-23; (PDF).