Arterial hypertension

Arterial hypertension is an increase in blood pressure at rest: systolic (up to 140 mm Hg and above), diastolic (up to 90 mm Hg and above), or both.

Arterial hypertension of unknown cause (primary, essential) is the most common; hypertension with a known cause (secondary arterial hypertension) is most often a consequence of kidney disease. The patient usually does not notice the presence of hypertension until it becomes severe or persistent. The diagnosis is established by measuring blood pressure. Other tests are used to determine the cause, assess risk, and identify other cardiovascular risk factors. Treatment of arterial hypertension involves lifestyle changes and medications such as diuretics, beta-blockers, ACE inhibitors, angiotensin II receptor blockers, and calcium channel blockers.

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Epidemiology

In the United States, hypertension affects approximately 50 million people. Only 70% of these people know they have hypertension, 59% are treated, and only 34% have adequate blood pressure (BP) control. Among adults, hypertension is more common in African Americans (32%) than in Caucasians (23%) or Mexicans (23%). Morbidity and mortality are also higher in African Americans.

Blood pressure increases with age. About two-thirds of people over 65 suffer from hypertension. People over 55 with normal blood pressure have a 90% risk of developing hypertension over time. Since high blood pressure is common in older people, this “age-related” hypertension may seem natural, but high blood pressure increases the risk of complications and mortality. Hypertension can develop during pregnancy.

According to the diagnostic criteria for arterial hypertension adopted by the World Health Organization jointly with the International Society of Hypertension (WHO-ISH) and the First Report of the Experts of the Scientific Society for the Study of Arterial Hypertension of the All-Russian Scientific Society of Cardiologists and the Interdepartmental Council on Cardiovascular Diseases (DAG-1), arterial hypertension is a condition in which the level of systolic blood pressure is equal to or exceeds 140 mm Hg and/or the level of diastolic blood pressure is equal to or exceeds 90 mm Hg in 3 different blood pressure measurements.

According to the modern classification of arterial hypertension, renal arterial hypertension is understood as arterial hypertension pathogenetically associated with kidney disease. This is the largest group of diseases from secondary arterial hypertension, which makes up about 5% of all patients suffering from arterial hypertension. Even with normal renal function, renal arterial hypertension is observed 2-4 times more often than in the general population. With a decrease in renal function, the frequency of its development increases, reaching 85-90% in the stage of terminal renal failure. Only those patients who suffer from salt-wasting kidney diseases remain with normal arterial pressure.

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Causes arterial hypertension

Arterial hypertension can be primary (85-95% of all cases) or secondary.

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Primary arterial hypertension

Hemodynamic and physiological variables (such as plasma volume, plasma renin activity) are altered, supporting the hypothesis that primary hypertension is unlikely to have a single cause. Even if one factor initially predominates, many factors are likely to contribute to the persistent high blood pressure (mosaic theory). In afferent systemic arterioles, dysfunction of the sarcolemmal ion pumps in smooth muscle cells may lead to chronically elevated vascular tone. Heredity may be a predisposing factor, but the exact mechanism is unclear. Environmental factors (e.g., dietary sodium intake, obesity, stress) are likely to be significant only in individuals with a hereditary predisposition.

Secondary arterial hypertension

Causes of hypertension include renal parenchymal diseases (eg, chronic glomerulonephritis or pyelonephritis, polycystic kidney disease, connective tissue diseases, obstructive uropathy), renovascular diseases, pheochromocytoma, Cushing's syndrome, primary hyperaldosteronism, hyperthyroidism, myxedema, and coarctation of the aorta. Excessive alcohol consumption and use of oral contraceptives are common causes of treatable hypertension. Sympathomimetics, glucocorticoids, cocaine, or licorice root are common contributors to elevated blood pressure.

The connection between the kidneys and arterial hypertension has attracted the attention of researchers for over 150 years. The first researchers to make a significant contribution to this problem were R. Bright (1831) and F. Volhard (1914), who pointed out the role of primary renal vascular damage in the development of arterial hypertension and presented the connection between the kidneys and increased arterial pressure as a vicious circle, where the kidneys were both the cause of arterial hypertension and the target organ. In the middle of the 20th century, the position on the primary role of the kidneys in the development of arterial hypertension was confirmed and further developed in the studies of domestic (E.M. Tareev, G.F. Lang, A.L. Myasnikov, etc.) and foreign scientists (H. Goldblatt, A.C. Guyton et al.). The discovery of renin, produced by the kidney during its ischemia, and renal prostaglandins: vasodilators and natriuretics, formed the basis for the development of knowledge about the renal endocrine system, capable of regulating arterial pressure. Sodium retention by the kidneys, leading to an increase in the volume of circulating blood, determined the mechanism of increased arterial pressure in acute nephritis and chronic renal failure.

A.S. Guyton et al. (1970-1980) made a major contribution to the study of arterial hypertension. In a series of experiments, the authors proved the role of primary renal sodium retention in the genesis of essential arterial hypertension and postulated that the cause of any arterial hypertension is the inability of the kidneys to provide sodium homeostasis at normal arterial pressure values, including the excretion of NaCl. Maintenance of sodium homeostasis is achieved by "switching" the kidney to a mode of operation under conditions of higher arterial pressure values, the level of which is then fixed.

Later, direct evidence of the role of the kidneys in the development of arterial hypertension was obtained in the experiment and in the clinic. They were based on the experience of kidney transplantation. Both in the experiment and in the clinic, transplantation of a kidney from a donor with arterial hypertension caused its development in the recipient, and, conversely, with the transplantation of "normotensive" kidneys, previously high arterial pressure became normal.

A significant milestone in the study of the problem of kidneys and arterial hypertension was the work of B. Brenner et al., which appeared in the mid-1980s. While maintaining the primary retention of sodium by the kidneys as the main mechanism of pathogenesis of arterial hypertension, the authors associate the cause of this disorder with a decrease in the number of renal glomeruli and a corresponding decrease in the filtering surface of the renal capillaries. This leads to a decrease in the excretion of sodium by the kidneys (renal hypotrophy at birth, primary kidney diseases, the condition after nephrectomy, including in kidney donors). At the same time, the authors thoroughly developed the mechanism of the damaging effect of arterial hypertension on the kidneys as a target organ. Arterial hypertension affects the kidneys (primarily shrunken kidney as a result of arterial hypertension or arterial hypertension accelerates the rate of development of renal failure) due to disturbances of intrarenal hemodynamics - increased pressure inside the renal capillaries (intraglomerular hypertension) and the development of hyperfiltration. Currently, the last two factors are considered as leading in non-immune hemodynamic progression of renal failure.

Thus, it was confirmed that the kidneys can be both a cause of arterial hypertension and a target organ.

The main group of diseases that lead to the development of renal arterial hypertension are renal parenchymatous diseases. Renovascular arterial hypertension, which occurs as a result of renal artery stenosis, is distinguished separately.

Parenchymatous kidney diseases include acute and chronic glomerulonephritis, chronic pyelonephritis, obstructive nephropathy, polycystic kidney disease, diabetic nephropathy, hydronephrosis, congenital renal hypoplasia, kidney injury, renin-secreting tumors, renoprivative conditions, primary sodium retention (Liddle, Gordon syndromes).

The frequency of detection of arterial hypertension in parenchymatous kidney diseases depends on the nosological form of renal pathology and the state of renal function. In almost 100% of cases, the arterial hypertension syndrome accompanies a renin-secreting kidney tumor (reninoma) and lesions of the main renal vessels (renovascular hypertension).

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Pathogenesis

Because arterial pressure is dependent on cardiac output (CO) and total vascular resistance (TPR), pathogenic mechanisms must involve increased CO, increased TPR, or both.

In most patients, CO is normal or slightly increased, and OPSS is increased. Such changes are characteristic of primary arterial hypertension and hypertension caused by pheochromocytoma, primary aldosteronism, renovascular pathology, and renal parenchymatous diseases.

In other patients, CO is increased (possibly due to constriction of the large veins), and TPR remains relatively normal for the corresponding CO; as the disease progresses, TPR increases, and CO returns to normal, probably due to autoregulation. In some diseases that increase CO (thyrotoxicosis, arteriovenous shunts, aortic regurgitation), especially when stroke volume increases, isolated systolic arterial hypertension develops. Some elderly patients have isolated systolic hypertension with normal or decreased CO, probably due to decreased elasticity of the aorta and its main branches. Patients with persistently high diastolic pressure always have decreased CO.

With increasing arterial pressure, there is a tendency for the plasma volume to decrease; sometimes the plasma volume remains the same or increases. The plasma volume in arterial hypertension increases due to primary hyperaldosteronism or renal parenchymatous diseases and can decrease significantly in arterial hypertension associated with pheochromocytoma. With increasing diastolic arterial pressure and the development of arteriolar sclerosis, there is a gradual decrease in renal blood flow. Until the late stages of the disease, the OPSS remains normal, as a result of which the filtration fraction increases. Coronary, cerebral and muscular blood flow is maintained until severe atherosclerotic vascular lesions occur.

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Changes in sodium transport

In some forms of hypertension, sodium transport across the cell wall is impaired because of abnormalities or inhibition of Na,K-ATPase or increased permeability of the cell wall to Na. This results in elevated intracellular sodium levels, making the cell more sensitive to sympathetic stimulation. Ca ions follow Na ions, so accumulation of intracellular calcium may also be responsible for the increased sensitivity. Because Na,K-ATPase can recycle norepinephrine back into sympathetic neurons (thus inactivating this neurotransmitter), inhibition of this mechanism may also enhance the effects of norepinephrine, contributing to increased blood pressure. Defects in sodium transport may occur in healthy children if their parents have hypertension.

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Sympathetic nervous system

Sympathetic stimulation increases blood pressure, usually to a greater extent in patients with borderline blood pressure values (120-139/80-89 mm Hg) or hypertension (systolic BP 140 mm Hg, diastolic BP 90 mm Hg, or both) than in normotensive patients. Whether this hyperreactivity occurs in the sympathetic nerves or in the myocardium and muscularis mucosae of the vessels is unknown. A high resting heart rate, which may result from increased sympathetic activity, is a well-known predictor of hypertension. Some hypertensive patients have higher than normal levels of circulating plasma catecholamines at rest.

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Renin-angiotensin-aldosterone system

This system is involved in the regulation of blood volume and, consequently, arterial pressure. Renin, an enzyme synthesized in the juxtaglomerular apparatus, catalyzes the conversion of angiotensinogen to angiotensin I. This inactive substance is converted by ACE, primarily in the lungs but also in the kidneys and brain, to angiotensin II, a potent vasoconstrictor that also stimulates the autonomic centers in the brain, increasing sympathetic activity, and stimulates the release of aldosterone and ADH. Both of these substances promote sodium and water retention, increasing arterial pressure. Aldosterone also promotes the excretion of K ⁺; low plasma potassium levels (< 3.5 mmol/L) increase vasoconstriction by closing potassium channels. Angiotensin III circulating in the blood stimulates aldosterone synthesis as intensely as angiotensin II, but has much less pressor activity. Since they also convert angiotensin I to angiotensin II, ACE inhibitors do not completely block the formation of angiotensin II.

Renin secretion is controlled by at least four nonspecific mechanisms:

• vascular receptors of the kidneys that respond to changes in pressure in the affected wall of the arterioles;
• macula densa receptors that respond to changes in NaCl concentration in the distal tubules;
• circulating angiotensin, renin secretion;
• The sympathetic nervous system, like the renal nerves, stimulates the secretion of renin indirectly through b-adrenergic receptors.

In general, it has been proven that angiotensin is responsible for the development of renovascular hypertension, at least in the early stages, but the role of the renin-angiotensin-aldosterone system in the development of primary hypertension has not been established. It is known that in African Americans and elderly patients with arterial hypertension, the content of renin tends to decrease. The elderly also have a tendency to decrease the amount of angiotensin II.

Arterial hypertension associated with renal parenchyma damage (renal hypertension) is the result of a combination of renin-dependent and volume-dependent mechanisms. In most cases, no increase in renin activity is detected in the peripheral blood. Arterial hypertension is usually moderate and sensitive to sodium and water balance.

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Vasodilator insufficiency

Insufficiency of vasodilators (e.g. bradykinin, nitric oxide) as well as excess of vasoconstrictors (such as angiotensin, norepinephrine) can lead to the development of arterial hypertension. If the kidneys do not secrete vasodilators in the required amount (due to damage to the renal parenchyma or bilateral nephrectomy), arterial pressure can increase. Vasodilators and vasoconstrictors (mainly endothelial) are also synthesized in endothelial cells, therefore endothelial dysfunction can be a powerful factor in arterial hypertension.

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Pathological changes and complications

There are no pathological changes in the early stages of hypertension. Severe or long-term hypertension affects target organs (primarily the cardiovascular system, brain, and kidneys), increasing the risk of coronary artery disease (CAD), MI, stroke (mainly hemorrhagic), and renal failure. The mechanism involves the development of generalized atherosclerosis and increased atherogenesis. Atherosclerosis leads to hypertrophy, hyperplasia of the middle vascular coat, and its hyalinization. These changes mainly develop in small arterioles, which is noticeable in the kidneys and eyeball. In the kidneys, changes lead to narrowing of the lumen of the arterioles, increasing the total peripheral vascular resistance. Thus, hypertension leads to a further increase in blood pressure. Since the arterioles are narrowed, any minor narrowing against the background of an already hypertrophied muscular layer leads to a decrease in the lumen to a much greater extent than in unaffected arteries. This mechanism explains why the longer arterial hypertension exists, the less likely it is that specific treatment (for example, surgical intervention on the renal arteries) for secondary arterial hypertension will lead to normalization of arterial pressure.

Due to increased afterload, left ventricular hypertrophy gradually develops, leading to diastolic dysfunction. As a result, the ventricle dilates, leading to dilated cardiomyopathy and heart failure (HF) due to systolic dysfunction. Thoracic aortic dissection is a typical complication of hypertension. Almost all patients with abdominal aortic aneurysm have hypertension.

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Symptoms arterial hypertension

Before complications develop in target organs, there are no symptoms of hypertension. Excessive sweating, facial flushing, headache, malaise, nosebleeds, and increased irritability are not signs of uncomplicated hypertension. Severe hypertension may occur with pronounced cardiovascular, neurological, renal symptoms, or retinal damage (e.g., clinically manifested coronary atherosclerosis, heart failure, hypertensive encephalopathy, renal failure).

An early symptom of high blood pressure is the fourth heart sound. Retinal changes may include narrowing of the arterioles, hemorrhages, exudation, and, in the presence of encephalopathy, edema of the papilla of the optic nerve. Changes are divided into four groups according to the increasing probability of a poor prognosis (there are classifications of Keys, Wegener, and Barker):

• Stage I - constriction of arterioles;
• Stage II - constriction and sclerosis of arterioles;
• Stage III - hemorrhages and exudation in addition to vascular changes;
• Stage IV - swelling of the optic nerve papilla.

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Diagnostics arterial hypertension

Diagnosis of arterial hypertension is carried out based on the results of changes in blood pressure. Anamnesis, physical examination and other research methods help to identify the cause and clarify the damage to target organs.

Blood pressure should be measured twice (the first time with the patient lying or sitting, and again after the patient has been standing for at least 2 minutes) on 3 different days. The results of these measurements are used for diagnostics. Blood pressure is assessed as normal, prehypertension (borderline hypertension), stage I and stage II arterial hypertension. Normal blood pressure is significantly lower in children.

Ideally, blood pressure should be measured after the patient has rested for more than 5 minutes at different times of the day. The cuff of the tonometer is placed on the upper arm. A properly selected cuff covers two-thirds of the biceps brachii; it covers more than 80% (but not less than 40%) of the arm circumference. Thus, obese patients need a large cuff. The specialist measuring blood pressure pumps air above the systolic pressure and then slowly releases it, auscultating the brachial artery. The pressure at which the first heart sound is heard during the cuff release is systolic blood pressure. The disappearance of the sound indicates diastolic blood pressure. Blood pressure is measured on the wrist (radial artery) and thigh (popliteal artery) using the same principle. Mercury tonometers are the most accurate in measuring blood pressure. Mechanical tonometers must be calibrated regularly; automatic tonometers often have a large error.

Blood pressure is measured on both arms; if the pressure on one arm is significantly higher than on the other, the higher figure is taken into account. Blood pressure is also measured on the legs (using a larger cuff) to detect coarctation of the aorta, especially in patients with a reduced or poorly conducted femoral pulse; with coarctation, blood pressure on the legs is significantly lower. If blood pressure figures are within the borderline arterial hypertension range or vary significantly, it is advisable to take more blood pressure measurements. Blood pressure figures may be elevated only from time to time until arterial hypertension becomes stable; this phenomenon is often considered "white coat hypertension", in which blood pressure increases when measured by a physician in a medical facility and remains normal when measured at home and with 24-hour blood pressure monitoring. At the same time, pronounced sharp increases in blood pressure against the background of usual normal figures are not common and may indicate pheochromocytoma or unrecognized use of narcotic substances.

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Anamnesis

The anamnesis includes the duration of hypertension and the highest BP values previously recorded; any indications of the presence or manifestations of PVS, HF or other concomitant diseases (e.g. stroke, renal failure, peripheral arterial disease, dyslipidemia, diabetes mellitus, gout) and family history of these diseases. The anamnesis includes the level of physical activity, smoking, alcohol consumption and stimulants (prescribed and self-administered). Dietary habits are clarified regarding the amount of salt and stimulants consumed (e.g. tea, coffee).

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Objective examination

Physical examination includes measurement of height, weight, and waist circumference; fundus examination for retinopathy; auscultation of murmurs in the neck and over the abdominal aorta; and a complete cardiac, neurological, and respiratory examination. Abdominal palpation is performed to detect renal enlargement and abdominal masses. Peripheral pulses are determined; a weakened or poorly conducted femoral pulse may indicate coarctation of the aorta, especially in patients younger than 30 years.

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Instrumental diagnostics of arterial hypertension

In more severe hypertension and in younger patients, imaging studies are more likely to yield findings. In general, when hypertension is diagnosed for the first time, routine investigations are performed to identify target organ damage and cardiovascular risk factors. Investigations include urinalysis, urine albumin to creatinine ratio, blood tests (creatinine, potassium, sodium, serum glucose, lipid profile), and ECG. Thyroid-stimulating hormone levels are often measured. Ambulatory blood pressure monitoring, radionuclide renography, chest radiography, pheochromocytoma screening, and renin-Na-dependent serum assays are not routinely needed. Plasma renin levels are of no value for diagnosis or drug selection.

Depending on the results of the initial examination and investigation, additional methods of investigation may be used. If microalbuminuria, albuminuria or proteinuria, cylindruria or microhematuria are detected in the urine analysis, and also if the creatinine content in the blood serum is increased (123.6 μmol/l in men, 106.0 μmol/l in women), ultrasound examination of the kidneys is used to determine their size, which can be of great importance. In patients with hypokalemia not associated with the administration of diuretics, primary hyperaldosteronism or excessive consumption of table salt should be suspected.

On the electrocardiogram, one of the early symptoms of “hypertensive heart” is a widened, peaked P wave, reflecting atrial hypertrophy (however, this is a nonspecific sign). Left ventricular hypertrophy, accompanied by the appearance of a pronounced apical impulse and a change in QRS voltage with or without signs of ischemia, may appear later. If any of these signs are detected, an echocardiogram is often performed. Patients with an altered lipid profile or signs of PVS are prescribed tests to identify other cardiovascular risk factors (eg, C-reactive protein).

If coarctation of the aorta is suspected, chest X-ray, echocardiography, CT or MRI are performed to confirm the diagnosis.

Patients with labile blood pressure, characterized by significant increases, with clinical symptoms such as headache, palpitations, tachycardia, increased respiratory rate, tremor, and pallor, should be examined for the possible presence of pheochromocytoma (eg, plasma free metanephrine assay).

Patients with symptoms suggestive of Cushing's syndrome, connective tissue disorders, eclampsia, acute porphyria, hyperthyroidism, myxedema, acromegaly, or CNS disorders require appropriate evaluation (see other sections of the guide).

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Treatment arterial hypertension

Primary hypertension has no cause, but in some cases of secondary hypertension, the cause can be addressed. In all cases, controlling blood pressure can significantly reduce complications. Despite treatment for hypertension, blood pressure is reduced to target levels in only one-third of hypertensive patients in the United States.

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Lifestyle changesFor all patients, the target BP is < 140/90 mmHg; for patients with diabetes or kidney disease, the target is < 130/80 mmHg or as close to this level as possible. Even elderly and geriatric patients can tolerate a diastolic pressure of 60-65 mmHg without increasing the risk and frequency of cardiovascular events. Ideally, patients or their family members should measure BP at home, which they should be trained to do, but their performance should be regularly monitored, and tonometers should be regularly calibrated.

Recommendations include regular physical activity in the fresh air, at least 30 min per day 3-5 times per week; weight loss to achieve a BMI of 18.5 to 24.9; smoking cessation; a diet for high blood pressure rich in fruits, vegetables, low-fat foods with a reduced amount of saturated and total fats; sodium intake < 2.4 g / day (< 6 g table salt) and limiting alcohol intake to 30 ml per day for men and 15 ml per day for women. Stage BI (mild arterial hypertension), without signs of target organ damage, lifestyle changes can be effective without prescribing drugs. Patients with uncomplicated hypertension do not need to limit activity as long as BP is under control. Dietary changes can also help control diabetes mellitus, obesity and dyslipidemia. Patients with prehypertension should be convinced of the need to follow these recommendations.

Clinical guidelines for the management of hypertension

Clinical guidelines for the management of hypertension may vary by country and health organization. Below are general principles of treatment and clinical guidelines that can be used in the management of hypertension:

1. Lifestyle changes:

   • Patients with hypertension are advised to make the following lifestyle changes:
   • Follow a diet low in salt (sodium) and fat, including increased intake of fruits, vegetables, whole grains, and magnesium.
   • Maintain and control a healthy weight.
   • Practice regular physical activity, such as walking or swimming.
   • Limit alcohol consumption and avoid smoking.

2. Drug treatment:

   • Medication may be used if lifestyle changes are not effective enough or if blood pressure is high and requires urgent reduction.
   • Medications used to treat hypertension may include diuretics, beta blockers, angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), calcium channel blockers, and other classes of drugs.
   • Medication treatment should be carried out under the supervision of a physician, and patients should strictly follow the instructions for taking medications.

3. Regular monitoring:

   • Patients with hypertension are advised to measure their blood pressure regularly and keep records of the results.
   • Regular medical examinations allow you to monitor your condition and the effectiveness of treatment.

4. Target indicators:

   • Blood pressure targets may vary depending on age and underlying medical conditions, but it is generally recommended to aim for a blood pressure reading of less than 140/90 mmHg.

5. Risk factor control:

   • Managing other cardiovascular risk factors, such as diabetes mellitus, hyperlipidemia, and obesity, is also important to prevent complications of hypertension.

6. Compliance with appointments:

   • Patients should strictly follow the doctor's recommendations and take medications regularly.
   • It is important to tell your doctor about any side effects or problems with your medications.

7. Consultations and regular visits to the doctor:

   • Patients with hypertension are advised to consult their doctor regularly to assess their condition and adjust their treatment.

These recommendations can serve as a general guideline, and a specific hypertension management plan should be developed individually for each patient based on their medical history and characteristics. Patients should discuss their treatment plan and recommendations with their physician to determine the best approach to hypertension management.

Forecast

The higher the BP and the more pronounced the changes in the retinal vessels or other manifestations of target organ damage, the worse the prognosis. Systolic BP is a better predictor of fatal and non-fatal complications than diastolic BP. Without treatment of arterial hypertension, the one-year survival rate of patients with retinosclerosis, cloud-like exudates, narrowing of arterioles and hemorrhages (stage III retinopathy) is below 10%, and in patients with the same changes and edema of the optic nerve papilla (stage IV retinopathy) - below 5%. PVS becomes the most common cause of death in treated patients with arterial hypertension. Ischemic and hemorrhagic strokes are frequent complications of arterial hypertension in patients for whom treatment is incorrectly selected. In general, effective BP control prevents the development of most complications and increases life expectancy.

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