Treatment of arterial hypertension in diabetes mellitus. Treatment of hypertension in diabetes mellitus. Principles of combined antihypertensive therapy for diabetes mellitus

Hypertension and diabetes mellitus are independent risk factors for the development of microangiopathy, peripheral vascular disease, cardiovascular disease and cerebrovascular disease.
Blood pressure should be measured for every person with diabetes when visiting a doctor and at least once every 6 months. If hypertension is detected, appropriate treatment is prescribed as described above. Target blood pressure values< 130/90 мм рт.ст. При назначении антигипертензивных препаратов следует контролировать возможные побочные их влияния на гипергликемию и гипогликемию, электролитный баланс, функцию почек, обмен липидов, состояние ССБ и нейропатические симптомы, включая ортостатическую гипотонию и импотенцию.

Classification, diagnosis and target blood pressure values ​​for diabetes mellitus

It should be noted that to determine the degree of increase in blood pressure, it is necessary to simultaneously evaluate systolic and diastolic blood pressure. If systolic blood pressure (SBP) and diastolic blood pressure (DBP) levels fall into different categories, then the higher BP is selected to formulate a diagnosis. An isolated increase in systolic blood pressure may occur. For diabetes mellitus, the target blood pressure value is< 130/80 мм рт.ст., что снижает вероятность развития и прогрессирования микро- и макрососудистых осложнений сахарного диабета.

There are two methods for diagnosing hypertension:

1. Blood pressure measurement using the Korotkoff method (mandatory study):

• rapid inflation of air into the cuff to a level exceeding the level of disappearance of Korotkoff sounds > 20 mmHg;
• rate of decrease in cuff pressure< 2 мм рт.ст. в секунду;
• measuring on each arm twice with an interval > 1 minute and calculating the average of all measurements;
• If the shoulder circumference is > 32 cm, a special wide cuff should be used.

2. Daily blood pressure monitoring (indication - difficulties in achieving target blood pressure).

In T1DM, the most common cause of hypertension is diabetic nephropathy, and in T2DM, essential hypertension (hypertension).

Treatment of arterial hypertension

Currently, as soon as the doctor makes a decision to adjust blood pressure for diabetes mellitus, antihypertensive drugs are also prescribed along with lifestyle changes (weight loss, low-salt diet and physical activity program). But some doctors still prefer to start only with lifestyle changes, at least for 3 months, and if this does not normalize blood pressure, then only then add antihypertensive drug therapy.
Despite early initiation of antihypertensive therapy, monotherapy is often ineffective and a combination of drugs is necessary. The following drugs have been proven to effectively reduce blood pressure and morbidity/mortality in patients with diabetes: ACE inhibitors, diuretics, ARBs and beta blockers. Data on calcium channel blockers (CCBs) are less certain, except in the elderly. These drugs reduce blood pressure and stroke, but some studies have shown to be less effective than ACE inhibitors plus diuretics for cardiovascular events, progression of diabetic nephropathy, and especially heart failure.

ACE inhibitors
Interaction with other drugs. Because ACE inhibitors reduce aldosterone levels, this leads to a slight increase in serum potassium levels and increases the risk of hyperkalemia when drugs that increase serum potassium (potassium-sparing diuretics, potassium supplements, or heparin) are coadministered. Nonsteroidal anti-inflammatory substances may reduce the antihypertensive effect of ACE inhibitors by inhibiting the synthesis of vasodilatory prostaglandins. In patients with impaired renal function, the combination of ACE inhibitors with non-steroidal anti-inflammatory substances may further impair renal function. Although aspirin reduces the effect of ACE inhibitors, the benefits of aspirin treatment in patients with cardiovascular disease justify this combination.
Before starting treatment with ACE inhibitors, if possible, stop taking diuretics for 2-3 days. The starting dose prescribed in conjunction with diuretics is usually 2 times lower than without them.
Therapeutic effectiveness, disadvantages and side effects. Many studies have shown that in patients with diabetes mellitus, ACE inhibitors reduce urinary albumin excretion and the rate of progression of DN to a greater extent than other antihypertensive drugs that maintain blood pressure at a comparable level. In this regard, ACE inhibitors become the first choice drugs in patients with DN at any stage, including microalbuminuric. Ramipril, for example, despite a minimal reduction in blood pressure, significantly reduced the risk of cardiovascular disease.
They can cause coughing, but the most serious side effect of ACE inhibitors is hyperkalemia, which occurs primarily with severe manifestations of DN or may be a manifestation of hyporeninemic hypoaldosteronism syndrome. When renin levels are reduced, circulating aldosterone levels are also reduced, which impairs potassium excretion by the renal tubules. Any drug that worsens a deficiency in aldosterone secretion or action may result in clinically significant hyperkalemia.
Serum creatinine levels may increase in some patients at the start of treatment with an ACE inhibitor, especially with bilateral renal artery stenosis or with severe renal damage. In patients with impaired renal function or suspected renovascular hypertension, serum creatinine and potassium levels should be monitored ~1 week after initiation of therapy. A noticeable increase in any of them should be a reason to stop treatment. If a patient at the stage of chronic renal failure is prescribed an ACE inhibitor and after two weeks such treatment leads to hyperkalemia of more than 6 mmol/l or an increase in creatinine levels by more than 30% of the initial level, then the drug is discontinued.
Contraindications and restrictions. ACE inhibitors are contraindicated in patients with renal artery stenosis, pregnant women and those planning pregnancy, as they have a teratogenic effect and also increase neonatal morbidity and mortality. It should be prescribed with caution to patients with a history of hyperkalemia, as well as to elderly patients who are prone to developing hypotension.

Angiotensin II receptor blockers
Angiotensin II receptor blockers (ARBs) also slow the progression of DN, particularly at the stage of microalbuminuria. If the patient does not tolerate ACE inhibitors well, then an ARB can be prescribed in this case, since they have a renoprotective effect in patients with DN.
Interaction with drugs. Because ARBs may cause slight increases in serum potassium, the risk of hyperkalemia is increased when they are combined with potassium-sparing diuretics, potassium supplements, and heparin. Nonsteroidal anti-inflammatory drugs (NSAIDs) may reduce the antihypertensive effects of ARBs by inhibiting the synthesis of vasodilatory prostaglandins. In addition, in patients with impaired renal function, coadministration of ARBs and NSAIDs may worsen renal damage. ARBs should be used with caution in patients receiving lithium as they may cause lithium toxicity.
Therapeutic effectiveness, disadvantages and side effects. In general, ARBs are well tolerated and do not cause metabolic deterioration in diabetic patients. They are usually prescribed to patients with proteinuria who do not tolerate ACE inhibitors well. Data obtained in a limited number of patients with valsartan showed that it reduces proteinuria in patients with hypertension and kidney disease. However, more research is needed to prove their protective effect in diabetic patients.
Drugs should be prescribed with caution in cases of impaired renal and liver function. Since the mechanisms of action of ACE inhibitors and ARBs are similar, ARBs are prescribed with caution in patients with renal artery stenosis and a history of hyperkalemia.
Elderly patients are more likely to develop hypotension during ARB treatment and are more likely to have renal and hepatic dysfunction, which significantly prolongs the duration of action of ARBs.
Common side effects include dizziness, diarrhea, peripheral edema and myalgia. Serious side effects include hypotension and hyperkalemia. Some patients experienced deterioration in renal function. Unlike ACE inhibitors, ARBs rarely cause cough.

Direct renin inhibitor (aliskiren)
The secretion of renin by the kidneys is stimulated by a decrease in circulating blood volume and kidney perfusion. Renin, in turn, converts angiotensinogen into angiotensin I, the precursor of angiotensin II, and the latter triggers a cascade of reactions leading to an increase in blood pressure. Thus, suppression of renin secretion can reduce the production of angiotensin P. When taking thiazide diuretics, ACE inhibitors and ARBs, plasma renin activity increases. Therefore, inhibition of renin activity may be a potentially effective strategy to suppress the entire renin-angiotensin system. Aliskiren is the first of a new class of drugs - a direct renin inhibitor, which has been proven to have antihypertensive activity. The improved bioavailability of oral aliskiren compared to previously offered drugs of this type, and the long half-life allows this drug to be taken once a day.
Aliskiren effectively reduces blood pressure both in monotherapy and in combination with thiazide diuretics (hydrochlorothiazide), ACE inhibitors (ramipril, lisinopril). ARB (valsartan) or CCB (amlodipine). When aliskiren is taken with these antihypertensive agents, plasma renin activity does not increase, but remains at or even below basal levels. Alixiren has placebo-like safety and tolerability and does not interact with a wide range of drugs except furosemide. Currently, there is limited data on the long-term effectiveness and tolerability of aliskiren in diabetic patients with hypertension. As a result, the exact role of this drug in the treatment of hypertension in patients with diabetes has not been fully established.

(module direct4)

Diuretics
Diuretics have been used for several decades to treat hypertension. They reduce sodium levels in the body through their natriuretic action and reduce the increased plasma volume often associated with hypertension in diabetic patients. Despite the fact that diuretics impair glucose tolerance and worsen lipid metabolism, they are undoubtedly effective in treating hypertension and reducing the volume of circulating fluid in diabetes. Convincing evidence has been obtained for thiazide diuretics that they reduce cardiovascular risk and are particularly effective in patients with impaired renal function or diabetic nephropathy.

Drugs in this group:

1. thiazide and thiazide-like (hydrochlorothiazide, indapamide);
2. loop (bumetanide, furosemide);
3. potassium-sparing (triamterene, amiloride);
4. aldosterone receptor blockers (spironolactone, epleron).

The mechanism of action depends on the class of diuretic. Thiazide drugs increase the excretion of sodium, chlorine and water, inhibiting the transport of sodium ions in the renal tubule. Loops inhibit the reabsorption of sodium and chloride in the ascending loop of Henle by blocking the binding of chloride to the Na+/K+/2C1 cotran-sporter, which increases diuresis. Potassium-sparing diuretics, such as triamterene and amiloride, inhibit the sodium-potassium ion exchange system in the distal renal tubules independently of aldosterone. In contrast, spironolactones suppress the action of aldosterone in the distal renal tubules, increasing the excretion of sodium, chlorine and water.
Pharmacokinetics vary greatly among different drugs.
Interaction with drugs. The hypotensive effect of diuretics may be potentiated by other antihypertensive drugs. Hypokalemia caused by diuretics may aggravate cardiac arrhythmias caused by cardiac glycosides, for example. NSAIDs may interfere with the action of diuretics because they themselves cause sodium and fluid retention.
Therapeutic effectiveness. In a large randomized controlled trial, diuretics were shown to reduce morbidity and mortality by reducing the incidence of stroke and heart failure.
Among diuretics, aldosterone antagonists appear to reduce proteinuria when used alone and have additive effects when combined with ACE inhibitors or ARBs in both T1DM and T2DM. In addition, with this combination, a more significant decrease in blood pressure was observed, which is explained not only by a specific vascular effect, but also by an anti-inflammatory mechanism.
Treatment with Eplerenone, a selective aldosterone blocker, is effective in diabetic patients who have already received treatment with an ACE inhibitor. This resulted in a significant reduction in albumin excretion, and it was concluded that the combination of these two drugs had additive antiproteinuric effects, with rates of hyperkalemia comparable to placebo.
In clinical practice, this combination should be used with extreme caution in patients with reduced GFR. They should relatively limit potassium in the diet and avoid taking non-steroidal anti-inflammatory drugs and cyclooxygenase-2 inhibitors, and in some cases additionally prescribe kaliuretic diuretics. The risk of hyperkalemia is slightly less when combined with an ARB.
Thus, if renal failure is observed with a combination of T1DM and hypertension, loop diuretics are usually prescribed. Thiazide diuretics are unable to stimulate natriuresis when serum creatinine levels rise to 2 mg%.
Potassium-sparing and osmotic diuretics are usually not used to treat hypertension in diabetes mellitus.
Side effects, restrictions and contraindications. Treatment with thiazide diuretics is complicated by hypokalemia, hyponatremia, reduced circulating blood volume, hypercalcemia and hyperuricemia. Increased diuresis may cause dehydration, dizziness, muscle cramps, or orthostatic hypotension. Orthostatic hypotension is most pronounced during treatment with loop diuretics. It may be necessary to prescribe additional potassium supplements in patients receiving loop diuretics, as in some patients receiving thiazides. In diabetic patients, carbohydrate metabolism may worsen. The administration of diuretics may also be accompanied by slight increases in LDL-C levels, triglycerides, sexual dysfunction and orthostatic hypotension.
Thiazides are contraindicated in patients with chronic renal failure and gout.
Diuretics should not be prescribed until the patient's existing electrolyte disturbances have been corrected, and they are contraindicated in patients with anuria. Particular caution should be exercised when prescribing diuretics to patients prone to hypotension and hypovolemia.
Elderly patients are especially sensitive to the hypotensive effect of diuretics. In this regard, treatment should begin with small doses and very gradually titrate the dose to the required antihypertensive dose.

Beta adrenergic blockers
Although beta blockers have been shown to significantly reduce cardiovascular morbidity and mortality in population-based, randomized and controlled studies, in real-world clinical situations the risks and benefits of such treatment and the choice of specific drug must be carefully weighed. Although beta blockers obscure the clinical manifestations of hypoglycemia in diabetes mellitus, their administration to diabetic patients who have previously suffered a myocardial infarction has been shown to significantly reduce the incidence of cardiovascular events.

Drugs in this group:

1. non-selective beta-1 and beta-2 (nadolol, pindolol, propranolol, timolol);
2. cardioselective beta-1 (atenolol, betaxolol, bisoprolol, metoprolol succinate, nebivolol);
3. combined beta-1, beta-2 and alpha-1 (carvedilol, labetalol).

The mechanism of action of beta blockers is to compete with catecholamines for binding to sympathetic receptors. Beta-1 selective, or “cardioselective,” drugs primarily block beta-1 receptors in the heart and blood vessels. Non-selective beta blockers interact with beta 1 and beta 2 receptors. At the same time, beta-2 blockers interact with receptors in the bronchi and vascular smooth muscles and, accordingly, have less antihypertensive potential and can cause bronchospasm. Blocking beta-1 receptors reduces heart rate, cardiac output, diastolic and systolic blood pressure.
The pharmacokinetics of different drugs is very different.
Interaction with drugs. Beta blockers may enhance the hypotensive effect of other antihypertensive drugs. They may also block the action of sympathomimetics. Since beta blockers slow AV conduction, the administration of other drugs with a similar effect may cause AV blockade.
Therapeutic effectiveness. In patients with a history of myocardial infarction, beta blockers reduce the risk of death by 25%. Since patients with diabetes and a history of heart attack have an increased risk of death compared with those without diabetes, it can be expected that beta blockers may be useful in patients with diabetes.
Beta-adrenergic blockers reduce proteinuria to a lesser extent than ACE inhibitors or ARBs. Cardioselective beta-1 blockers delay the progression of DN, but to a lesser extent than renin-angiotensin system (RAS) inhibitors.
However, it has been established that the newer vasodilatory alpha/beta blockers, such as Carvedilol and beta-1 selective Nebivolol, have a more pronounced positive effect on hemodynamics and renal function in DN than metoprolol, due to their greater beta-1 blocking activity .
However, non-selective beta blockers may mask sympathodependent symptoms - precursors of hypoglycemia. Beta blockers also predispose to the development of hyperkalemia by inhibiting renin synthesis and impairing potassium uptake into extrarenal tissues, and may potentiate hypertriglyceridemia. Selective beta-1 blockers are preferred over non-selective beta blockers in patients with diabetes mellitus because they are less likely to cause hypoglycemia and hyperkalemia.
Limitations, side effects and contraindications. Abrupt withdrawal of beta blockers can lead to the development of myocardial ischemia, myocardial infarction, ventricular arrhythmia, or rebound hypertension. If beta blockers are planned to be discontinued, it should be done gradually.
Elderly patients may have unpredictable reactions to beta blockers. They are less sensitive to the antihypertensive effects of these drugs and are especially sensitive to their side effects.
One of the specific side effects of beta blockers in patients with diabetes is a deterioration in carbohydrate metabolism. This effect depends on the dose and duration of treatment and may be additive to the side effects of thiazide and/or loop diuretics. Non-selective beta blockers disrupt carbohydrate metabolism to a greater extent than cardioselective ones.
In addition, while taking beta blockers, which are mostly non-selective, hypoglycemia becomes more severe, and the sympathodependent symptoms of hypoglycemia precursors - tachycardia, palpitations, hunger, tremor and agitation - are obscured.
Sweating is a common side effect of beta blockers and may be exacerbated by symptoms of hypoglycemia.
Beta blockers are contraindicated in patients with severe bradycardia, sinus node weakness, or severe AV block unless they have a pacemaker installed to prevent the development of fatal cardiac arrhythmias. Beta blockers should not be prescribed to patients with decompensated systolic heart failure. Beta blockers are also contraindicated in patients with severe peripheral circulatory disorders, as isolated cases of gangrene have been described.

Alpha adrenergic blockers
The hypotensive effect of drugs in this group is comparable to drugs from other classes. But there have been no long-term controlled studies with these drugs in diabetes. In this regard, these drugs for diabetes mellitus are recommended for use in cases of resistant hypertension to other classes of drugs.
Mechanism of action. Alpha blockers competitively inhibit alpha-1 adrenergic receptors in the sympathetic nervous system.
Pharmacokinetics depends on the type of drug.
Interaction with drugs. First of all, when prescribed with other antihypertensive drugs, they further reduce blood pressure. Other substances that can enhance the hypotensive effect of alpha-blockers: diuretics, MAO inhibitors, and alcohol. Coadministration of an alpha blocker with a phosphodiesterase-5 inhibitor, such as sildenafil (Viagra), may cause postural hypotension. In this regard, sildenafil can be taken no earlier than 4 hours after taking the alpha blocker.
Therapeutic effect. The multicenter controlled trial ALLHAT compared the effectiveness of doxazosin, on the one hand, and beta-blockers, calcium channel blockers, ACE inhibitors, and diuretics, on the other. But the study was stopped prematurely because the incidence of cardiovascular events increased in patients receiving alpha-blockers. Due to this, as well as such side effects as orthostatic hypotension, alpha blockers are currently not considered as suitable drugs for the treatment of hypertension in patients with diabetes mellitus.
Alpha blockers reduce insulin resistance in type 2 diabetes, although they are not considered an “antidiabetic” drug. In limited studies, alpha blockers have been shown to moderately reduce LDL-C, and doxazosin has positive effects on triglycerides, total cholesterol, and HDL.
Limitations, side effects and contraindications. When prescribing alpha blockers, it is necessary to carefully monitor blood pressure, in particular the development of postural hypotension. Doxazosin should be used with caution in patients with liver disease as it is predominantly metabolized by the liver.
The use of alpha blockers is contraindicated in pregnant and breastfeeding women. Elderly patients are prone to developing hypotension during treatment with alpha-blockers, and therefore their blood pressure should be carefully monitored and the dose increased very gradually.
Of the side effects, the most serious is orthostatic hypotension, especially at the beginning of treatment. Common side effects include dizziness, weight gain, drowsiness, peripheral edema, blurred vision, and shortness of breath. Rarely, serious side effects such as angina, palpitations and sinus tachycardia have been observed. Sinus bradycardia has also been described.

Calcium channel blockers

Drugs in this group are divided into two subgroups:

1. dihydropyridine (BCP-DHP);
2. non-dihydropyridine (BCP-NDHP).

CCB-DHPs have a predominantly vasodilatory effect and minimally affect cardiac contractility and AV conduction. In contrast. CCB-NDGPs primarily affect myocardial contractility.
Pharmacokinetics depends on the class of the drug.
Therapeutic effect. Nondihydropyridine calcium channel blockers (diltiazem and verapamil) have been shown to reduce microalbuminuria and proteinuria to the same extent as ACE inhibitors and ARBs; Moreover, these drugs may also have an additive effect with respect to the antiproteinuric effect of ACE. However, they have not been shown to have a specific protective effect on renal function, and therefore they can be considered as an additional rather than primary therapy for DN.
Limitations, side effects and contraindications. Common side effects observed with CCB treatment are dizziness, peripheral edema (especially common in CCB-BPH), hot flashes and headache. CCB-BHD causes reflex tachycardia, but it rarely develops when taking amlodipine, since the onset of its action is gradual. In some patients, nifedipine causes gingival hyperplasia, and therefore in such patients it is very important to maintain oral hygiene.
CCBs are contraindicated in patients with or suspected of hypotension. Caution should be used when prescribing CCBs to patients with bradycardia, heart failure, cardiogenic shock, aortic stenosis, and kidney and liver diseases. CCB-NDHPs are contraindicated in patients with cardiac conduction disorders, in particular with sinus node weakness and Wolff-Parkinson-Bythe syndrome. CCBs may also increase symptoms of gastroesophageal reflux by relaxing the esophageal sphincter.
Elderly patients are especially sensitive to the hypotensive effects of CCBs.

Central action
Centrally acting drugs used to treat hypertension include Clonidine (Clonidine) and Methyldopa (Dopegyt), alpha-2 receptor agonists. Clonidine and methyldopa are recommended for use in diabetic patients with resistant hypertension that is not controlled by other agents. But they should be used with caution in diabetes, as they cause hypotension and a tendency for patients to fall.

Arterial hypertension means an increase in blood pressure above 140/90 mm. This condition greatly increases the risk of heart attack, stroke, kidney failure, etc. With diabetes, the dangerous threshold for hypertension is reduced: a systolic pressure of 130 and a diastolic pressure of 85 millimeters indicates the need for therapeutic measures.

Why does diabetes increase blood pressure?

The causes of arterial hypertension in diabetes mellitus are different and depend on the type of disease. Thus, in the insulin-dependent form of the disease, arterial hypertension in most cases develops due to diabetic kidney disease. A small number of patients have primary arterial hypertension, or isolated systolic hypertension.

If the patient has non-insulin-dependent diabetes, then hypertension develops in some cases much earlier than other metabolic diseases. In such patients, essential arterial hypertension is a common cause of the disease. This means that the doctor cannot determine the cause of its occurrence. Quite rare causes of hypertension in patients are:

• pheochromocytoma (a disease characterized by increased production of catecholamines, which causes tachycardia, pain in the heart and arterial hypertension);
• Itsenko-Cushing syndrome (a disease caused by increased production of adrenal hormones);
• hyperaldosteronism (increased production of the hormone aldosterone by the adrenal glands), characterized by a negative effect on the heart;
• another rare autoimmune disease.

The disease also contributes to:

• magnesium deficiency in the body;
• prolonged stress;
• intoxication with salts of heavy metals;
• atherosclerosis and the resulting narrowing of the large artery.

Features of hypertension in insulin-dependent diabetes

This form of the disease is often accompanied by kidney damage. It develops in a third of patients and has the following stages:

• microalbuminuria (appearance of albumin in urine);
• proteinuria (the appearance of large protein molecules in the urine);
• chronic renal failure.

Moreover, the more protein is excreted in urine, the higher the pressure. This happens because diseased kidneys are less able to eliminate sodium. This increases the fluid content in the body and, as a result, increases blood pressure. As glucose levels rise, there is even more fluid in the blood. This creates a vicious circle.

It consists in the fact that the body tries to cope with poor kidney function, while increasing the pressure in the renal glomeruli. They gradually die off. This is how kidney failure progresses. The main task of a patient with insulin-dependent diabetes mellitus is to normalize glucose levels and thereby delay indefinitely the onset of the terminal stage of chronic renal failure.

Signs of hypertension in non-insulin-dependent diabetes

Even before the symptoms of this disease appear, the patient begins the process of insulin resistance. Tissue resistance to this hormone gradually decreases. The body tries to overcome low sensitivity of body tissues to insulin by producing more insulin than needed. And this, in turn, contributes to high blood pressure.

Thus, the main factor in the development of hypertension in diabetes mellitus is the insulin level. However, in the future, hypertension occurs due to the progression of atherosclerosis and deterioration of kidney function. The lumen of the vessels gradually narrows, causing them to pass less and less blood.

Hyperinsulinism (that is, high levels of insulin in the blood) has a bad effect on kidney function. They are getting worse at removing fluid from the body. And an increased amount of fluid in the body leads to the development of edema and hypertension.

How does hypertension manifest in diabetes?

It is known that blood pressure is subject to a circadian rhythm. At night it decreases. In the morning it turns out to be 10–20 percent lower than in the afternoon. In diabetes mellitus, this circadian rhythm is disrupted, and it turns out to be high all day long. Moreover, at night it is even higher than during the day.

This disorder is associated with the development of one of the dangerous complications of diabetes – diabetic neuropathy. Its essence is that high sugar negatively affects the functioning of the autonomic nervous system. In this case, the vessels lose the ability to narrow and expand depending on the load.

The type of hypertension is determined by daily monitoring. This procedure will indicate when it is necessary to take antihypertensive medications. At the same time, the patient must significantly limit salt intake.

Medicines for hypertension and diabetes

Anti-hypertension medications should be taken in order to reduce it to 130/80 mm recommended for diabetes. Treatment with diet gives good blood pressure values: the tablets are well tolerated and give the most satisfactory results.

This indicator is a kind of guideline in the treatment of hypertension. If medications do not reduce blood pressure in the first weeks of treatment due to side effects, then you can slightly reduce the dosage. But after about a month, intensive treatment must be resumed and medications taken in the prescribed dosage.

Gradually lowering high blood pressure helps avoid symptoms of hypotension. After all, in patients with diabetes, arterial hypertension is complicated by orthostatic hypotension. This means that with a sharp change in body position, a sharp drop in tonometer readings is observed. This condition is accompanied by fainting and dizziness. Its treatment is symptomatic.

Sometimes it can be difficult to choose pills for hypertension if you have diabetes. This is due to the fact that changes in carbohydrate metabolism leave their mark on the action of all medications, including antihypertensives. When choosing treatment and medications for a patient, the doctor must be guided by many important nuances. Properly selected tablets meet certain requirements.

1. These medications sufficiently relieve the symptoms of arterial hypertension in diabetes mellitus and have few side effects.
2. These medications do not impair proper blood sugar control or raise cholesterol levels.
3. The tablets protect the kidneys and heart from the harmful effects of high blood sugar.

What groups of drugs are used

1. Diuretics, or diuretics. These medications are good at lowering high blood pressure due to arterial hypertension. The body gets rid of excess water and salts well. Medicines in this group are used for heart failure, as they reduce the load on the heart and blood vessels. Diuretic drugs fight edema well. Your doctor will help you choose the most appropriate medications.
2. Beta blockers. These medications effectively affect the sympathetic nervous system. They are effectively used to treat the disease as a primary remedy. Modern beta blockers have minimal side effects.
3. ACE inhibitors. Such drugs act on the production of the enzyme responsible for hypertension in humans.
4. Angiotensin II receptor blockers. Such drugs provide support to the heart in conditions of high sugar. They also effectively protect the liver, kidneys and brain from possible complications.
5. Calcium antagonists. These medications inhibit the entry of this metal ions into the heart cells. Thus, you can achieve optimal tonometer readings and avoid complications from the cardiovascular system.
6. Vasodilators work well to relax the walls of blood vessels and thus lower blood pressure. However, currently such drugs occupy an insignificant place in the treatment of hypertension, as they have serious side effects and have an addictive effect.

The role of diet in the treatment of hypertension

Consuming perhaps fewer carbohydrates if you have hypertension and diabetes is a realistic and achievable step in staying healthy. Such treatment will reduce the need for insulin and at the same time bring the cardiovascular system to normal.

Treatment kills several problems at once:

• reduces insulin and blood sugar levels;
• prevents the development of all kinds of complications;
• protects the kidneys from the toxic effects of glucose;
• significantly slows down the development of atherosclerosis.

Low-carbohydrate treatment is ideal when the kidneys are not yet releasing proteins. If they begin to work normally, blood counts for diabetes return to normal. However, with proteinuria, such a diet should be used with caution.

You can eat enough sugar-lowering foods. This:

• meat products;
• eggs;
• seafood;
• green vegetables and mushrooms;
• cheeses and butter.

Essentially, when hypertension and diabetes are combined, there is no alternative to low-carbohydrate eating. This treatment is used regardless of the type of diabetes. Sugar levels drop to normal levels within a few days. You will have to constantly monitor your diet so as not to risk increasing your glucose levels. Low-carb meals are filling, tasty and healthy.

At the same time, this diet normalizes the tonometer readings. This is a guarantee of excellent health and the absence of life-threatening complications.

Hypertension is a major comorbidity in diabetics. According to medical statistics, more than half of people with diabetes have problems with blood pressure. Hypertension complicates the treatment and course of the underlying disease, and complications can lead to death.

Treatment of hypertension and diabetes is complex and consists of medications, diet and lifestyle changes.

For type 1 and type 2 diabetes, the normal blood pressure level is considered to be no higher than 130/85 mmHg. The main cause of high blood pressure in patients with diabetes is metabolic disorders. This leads to decreased production of essential hormones. High levels of sugar in the blood impair the integrity and elasticity of the walls of blood vessels. Result: impaired cellular metabolism, accumulation of fluid and sodium, increased blood pressure and the risk of stroke, acute heart failure, and heart attack.

Glomerular microangiopathy, or damage to small blood vessels, causes poor kidney function in patients with type 1 diabetes. This leads to the removal of protein from the body along with urine. This explains the constant high level of blood pressure, which results in kidney failure. If arterial hypertension is not associated with type 1 diabetes, then in such patients all renal functions are preserved.

In the second type of diabetes, affected kidneys lead to the development of dangerous pathologies in 20% of patients. An increase in pressure is provoked by the development of insulin resistance - a decrease in the sensitivity of tissues to the action of insulin. To compensate for this, the body begins to produce more insulin, which leads to a significant increase in blood pressure. As insulin production increases, the load on the pancreas increases. After a few years of intense work, it can no longer cope with the load, and the blood sugar level rises even more. This is the beginning of type 2 diabetes.

• The sympathetic nervous system is activated,
• The kidneys are unable to cope with the task of removing excess sodium and fluid from the body,
• Sodium and calcium settle in cells,
• Excess insulin provokes thickening of the walls of blood vessels, which leads to loss of elasticity and poor patency.

As diabetes develops, the lumen in the vessels becomes narrower, which impedes blood flow.

Another danger is body fat, which affects most patients. Fat releases substances into the blood that increase blood pressure. This process is called metabolic syndrome.

Pathogenesis of hypertension

Unfavorable factors that increase the likelihood of hypertension include:

• Lack of microelements, vitamins,
• Poisonings,
• Frequent stress, lack of sleep,
• Excess weight,
• Poor nutrition
• Atherosclerosis.

The group of patients at increased risk includes older people.

The main feature of hypertension in diabetes mellitus is a decrease in high blood pressure during the day and an increase in blood pressure at night.

In patients with diabetes, high blood pressure increases the likelihood of developing dangerous and severe complications:

• The risk of developing kidney failure, gangrene and incurable ulcers increases 20 times,
• The risk of vision deterioration up to blindness increases 16 times,
• The risk of heart attack and stroke increases 5 times.

Many patients suffering from diabetes experience a complication in the form of orthostatic hypotension. It is characterized by sharp drops in blood pressure when getting up (from a bed, sofa, chair, etc.). This is accompanied by darkening of the eyes, nausea, severe dizziness and fainting. It appears due to a violation of vascular tone, which is called diabetic neuropathy.

Treatment of hypertension in diabetes mellitus type 1 and 2

If you have high blood pressure, you should consult your doctor and not self-medicate. This can be fatal.

For diabetics, the attending physician uses:

• Medication methods: drugs are prescribed that lower blood sugar and blood pressure,
• Diets: for diabetes, they are aimed at reducing the intake of salt, sugar,
• Physical therapy to combat excess weight,
• Organizing a healthy lifestyle for the patient.

Drug treatment of hypertension

The choice of medications should be careful and based on glucose levels, sugar levels and concomitant pathologies. The drug can be prescribed only in accordance with the rules:

• He should lower blood pressure gradually over 2-4 months,
• The medicine for hypertension should not have many side effects and lead to negative consequences,
• The medicine should not increase sugar levels or worsen its balance,
• The drug should not increase blood levels of triglyceridor and cholesterol,
• The medication should support the normal functioning of the heart, kidneys, and blood vessels.

It is more difficult to select medications to lower blood pressure in type 2 diabetes: the disrupted process of carbohydrate metabolism gives many restrictions on the use of drugs.

Diuretics

A group of these drugs helps the body get rid of excess fluid, which leads to a decrease in blood pressure. Thiazide drugs (hydrochlorothiazide, hypothiazide) with constantly elevated sugar levels reduce the risk of heart attack and stroke. But they must be taken with caution: the daily dose is no more than 12.5 mg. An overdose (over 50 mg) will lead to a significant increase in sugar levels. This type of drug has the effect of counteracting the occurrence of complications: acute renal failure. Contraindications: renal failure in the chronic stage. The same contraindications apply to potassium-sparing drugs.

Loop types of diuretics are rarely prescribed: they lead to diuresis and remove large amounts of potassium. This can lead to heart rhythm disturbances and a decrease in potassium ions in the blood. In combination with ACE inhibitors, they are prescribed to patients with renal failure. Lasix and Furosemide are the safest - they do not provoke an increase in sugar, but also do not protect the kidneys.

In cases where hypertension is accompanied by 2 types of diabetes, a combination of diuretics with a group of ACE inhibitors is prescribed. The simultaneous use of diuretic drugs and beta blockers without medical supervision can provoke a sharp increase in glucose levels. For older people, taking diuretics with beta blockers reduces the risk of fractures.

The administration of thiazide-like diuretics with ACE inhibitors is accompanied by a mild diuretic effect and practically does not remove potassium from the body. A small dosage of these medications does not have a significant effect on lowering sugar, hypertension and cholesterol levels.

Inhibitors

ACE inhibitors (enalapril) are designed to block enzymes that promote the production of angiotensin II. This hormone reduces the diameter of blood vessels and causes the adrenal glands to secrete more aldosterone, which retains sodium and fluid. The use of inhibitors expands the lumen in the blood vessels, as a result of which excess fluid and sodium are eliminated faster. This leads to a decrease in blood pressure.

ACE inhibitors and angiotensin II receptor blockers facilitate the functioning of the cardiovascular system in patients with end-stage renal disease. Taking medications leads to a slowdown in the development of pathologies. Medicines in this group do not provoke lipid metabolism disorders and normalize tissue sensitivity to the effects of insulin. For their safe use, it is necessary to follow a salt-free diet: ACE inhibitors prevent potassium excretion.

Beta blockers

Selective beta blockers are prescribed for hypertension and diabetes accompanied by ischemia and heart failure. This drug is also prescribed for grade 3 headache. Beta blockers are prescribed for a history of coronary heart disease and for the prevention of myocardial infarction. In diseases of the cardiovascular system, they significantly reduce the risk of death. A group of selective drugs lowers blood pressure and does not have negative symptoms. A decrease in blood pressure occurs due to the blockade of β1 receptors, and is accompanied by a decrease in the frequency and strength of heart contractions.

Non-selective beta blockers are not prescribed for diabetes because they lead to an increase in sugar and bad cholesterol. Blockade of β2 receptors, which are not found in the heart and liver, leads to negative results:

• Asthma attacks
• Vascular spasms,
• Stopping the process of fat breakdown.

This group of drugs is most effective for high blood pressure. Potassium antagonists are blockers of calcium channels in cell membranes, slowing down the flow of calcium ions to smooth muscle cells. Long-term use does not cause addiction and deterioration of metabolism, this leads to an increase in the level of uric acid and sugar.

Regular use has positive effects:

• Increased physical endurance,
• Reducing the oxygen demand of the heart muscle during exercise,
• Blockage of calcium channels, which prevents smooth muscle cells from entering fluid.
• Antagonists and beta blockers cannot be prescribed simultaneously.

Contraindications to the use of antagonists are old age: the older the person, the more time it takes to remove the drug from the body. Side effects may include a sharp drop in blood pressure, tachycardia, and edema. The drugs are rarely prescribed for heart failure, coronary heart disease, and unstable angina.

Agonists

A group of stimulants leads to a weakening of the functions of the sympathetic nervous system, a decrease in the number of heart contractions and a decrease in blood pressure. As a result of long-term use, the functioning of the heart and blood vessels improves. They are contraindicated in bradycardia, heart failure, and liver disease.

Alpha blockers

The use of alpha-adrenergic receptors leads to a decrease in blood pressure without an increase in heart rate. They are contraindicated in heart failure and orthostatic hypotension.

Drugs of the alpha-blocker group are often used as an adjuvant in combination treatment, and as a one-time relief of a sharp increase in blood pressure. The use of drugs provokes vasodilation and narrowing of veins and arteries, reducing sympathetic tone. They are prescribed as a prevention of crises, strokes, and prostate diseases.

Non-drug treatment of hypertension

Diet

Hypertensive patients with diabetes need to adhere to a special diet. Doctors usually prescribe low-carbohydrate diets, which are aimed at lowering sugar levels and normalizing blood pressure.

Basic nutrition rules:

• Taking essential vitamins
• Reducing the daily portion of salt to 5 g,
• Refusal of fatty foods
• Refusal of foods rich in sodium (salted fish, caviar, olives, lard, smoked meats and sausages),
• Eating at least 5 times a day,
• The last meal should be two hours before bedtime,
• An increase in foods containing calcium in the diet (sesame seeds, hard cheese, greens, nuts, soybeans, beans, fruits, dairy products),
• Consumption of low-fat varieties of river and sea fish and seafood
• Including vegetable broths in the diet,
• Including plenty of fruits, dried fruits and vegetables in your diet.

Healthy lifestyle

It is often difficult to convince patients of the effectiveness and necessity of a healthy lifestyle. In such cases, patients are scheduled to visit a psychologist. The standard is to quit smoking and alcohol. Based on the test results and general condition, the doctor prescribes a complex of physical therapy.

Long walks in the fresh air and Nordic walking, yoga, swimming, and therapeutic horse riding have a positive effect. People with diabetes and hypertension need sun and air baths. It is recommended to refrain from working at night and in the evening, and from increased emotional and physical stress. If your job is sedentary, you need to find time during the day to do simple gymnastics to restore blood flow in the cervical spine. For every three hours of work there should be 20-25 minutes of rest.

Hypertension is when blood pressure is so elevated that treatment would provide far more benefit to the patient than the harmful side effects. If your blood pressure is 140/90 or higher, it is time to actively seek treatment. Because hypertension several times increases the risk of heart attack, stroke, kidney failure or blindness. In type 1 or type 2 diabetes, the blood pressure limit drops to 130/85 mmHg. Art. If you have higher blood pressure, you need to make every effort to lower it.

In diabetes mellitus type 1 or 2, hypertension is especially dangerous. Because if diabetes is combined with high blood pressure, then the risk of a fatal heart attack increases by 3-5 times, stroke - by 3-4 times, blindness - by 10-20 times, kidney failure - by 20-25 times, gangrene and leg amputation - 20 times. At the same time, high blood pressure is not so difficult to normalize, unless your kidney disease has not yet progressed too far.

Read about cardiovascular diseases:

Causes of hypertension in diabetes

In type 1 and type 2 diabetes, the causes of arterial hypertension may be different. In type 1 diabetes mellitus, hypertension in 80% of cases develops as a result of kidney damage (diabetic nephropathy). In type 2 diabetes, hypertension usually develops in the patient much earlier than carbohydrate metabolism disorders and diabetes itself. Hypertension is one of the components that is a precursor to type 2 diabetes.

Causes of hypertension in diabetes and their frequency

Notes on the table. Isolated systolic hypertension is a specific problem in elderly patients. Read more in the article “Isolated systolic hypertension in the elderly.” Another endocrine pathology - this may be pheochromocytoma, primary hyperaldosteronism, Itsenko-Cushing syndrome or another rare disease.

Essential hypertension - this means that the doctor is not able to determine the cause of the increase in blood pressure. If hypertension is combined with obesity, then most likely the cause is intolerance to dietary carbohydrates and increased levels of insulin in the blood. It's called metabolic syndrome and is highly treatable. It could also be:

• magnesium deficiency in the body;
• chronic psychological stress;
• intoxication with mercury, lead or cadmium;
• narrowing of a large artery due to atherosclerosis.

And remember that if the patient truly wants to live, then medicine is powerless :).

High blood pressure in type 1 diabetes

In type 1 diabetes, the main and very dangerous cause of increased blood pressure is kidney damage, in particular diabetic nephropathy. This complication develops in 35-40% of patients with type 1 diabetes and goes through several stages:

• stage of microalbuminuria (small molecules of albumin protein appear in the urine);
• stage of proteinuria (the kidneys filter worse and worse, and large proteins appear in the urine);
• stage of chronic renal failure.

According to the Federal State Institution Endocrinology Research Center (Moscow), among patients with type 1 diabetes without kidney pathology, 10% suffer from hypertension. In patients at the stage of microalbuminuria, this value increases to 20%, at the stage of proteinuria - 50-70%, at the stage of chronic renal failure - 70-100%. The more protein is excreted in the urine, the higher the patient's blood pressure- this is a general rule.

Hypertension with kidney damage develops due to the fact that the kidneys poorly excrete sodium in the urine. There is more sodium in the blood, and fluid accumulates to dilute it. Excessive circulating blood volume increases blood pressure. If, due to diabetes, the concentration of glucose in the blood is increased, then it pulls even more fluid with it so that the blood is not too thick. Thus, the volume of circulating blood increases further.

Hypertension and kidney disease form a dangerous vicious cycle. The body tries to compensate for weak kidney function, and therefore blood pressure rises. This, in turn, increases the pressure inside the glomeruli. This is the name given to the filter elements inside the kidneys. As a result, the glomeruli gradually die off, and the kidneys work worse and worse.

This process ends in kidney failure. Fortunately, in the early stages of diabetic nephropathy, the vicious cycle can be broken if the patient is treated diligently. The main thing is to lower blood sugar to normal. Medicines also help -, and. You can read more about them below.

Long before the development of “real” type 2 diabetes, the disease process begins with. This means that tissue sensitivity to the action of insulin is reduced. To compensate for insulin resistance, too much insulin circulates in the blood, and this itself increases blood pressure.

Over the years, the lumen of blood vessels narrows due to atherosclerosis, and this becomes another significant “contribution” to the development of hypertension. At the same time, the patient's abdominal obesity (around the waist) increases. It is believed that adipose tissue releases substances into the blood that further increase blood pressure.

This whole complex is called . It turns out that hypertension develops much earlier than type 2 diabetes. It is often detected in a patient immediately when diabetes is diagnosed. Fortunately, it is great for helping to control type 2 diabetes and hypertension at the same time. You can read the details below.

Hyperinsulinism is an increased concentration of insulin in the blood. It occurs in response to insulin resistance. If the pancreas has to produce an excess amount of insulin, then it “wears out” intensively. When it stops coping over the years, blood sugar rises and type 2 diabetes occurs.

How hyperinsulinism increases blood pressure:

• activates the sympathetic nervous system;
• the kidneys are less able to excrete sodium and fluid in the urine;
• sodium and calcium accumulate inside cells;
• Excess insulin contributes to thickening of the walls of blood vessels, which reduces their elasticity.

Features of manifestations of hypertension in diabetes

Diabetes mellitus disrupts the natural daily rhythm of blood pressure fluctuations. Normally, a person’s blood pressure in the morning and at night during sleep is 10-20% lower than during the day. Diabetes leads to the fact that many hypertensive patients do not lower their blood pressure at night. Moreover, when hypertension and diabetes are combined, nighttime pressure is often higher than daytime pressure.

This disorder is believed to occur due to . Elevated blood sugar affects the autonomic nervous system, which regulates the body's functioning. As a result, the ability of blood vessels to regulate their tone, that is, to narrow and relax depending on the load, deteriorates.

The conclusion is that when hypertension and diabetes are combined, not only one-time pressure measurements with a tonometer are required, but also daily 24-hour monitoring. It is carried out using a special device. Based on the results of this study, the timing and dosage of blood pressure medications can be adjusted.

Practice shows that patients with type 1 and type 2 diabetes are usually more sensitive to salt than hypertensive patients who do not have diabetes. This means that limiting salt in the diet can have a powerful healing effect. If you have diabetes, to treat high blood pressure, try eating less salt and see what happens after a month.

High blood pressure in diabetes mellitus is often complicated by orthostatic hypotension. This means that the patient's blood pressure drops sharply when moving from a lying position to a standing or sitting position. Orthostatic hypotension manifests itself after standing up abruptly with dizziness, darkening of the eyes, or even fainting.

Like disruption of the circadian rhythm of blood pressure, this problem arises due to the development of diabetic neuropathy. The nervous system gradually loses the ability to control vascular tone. When a person gets up quickly, the load immediately increases. But the body does not have time to increase blood flow through the vessels, and because of this, the state of health worsens.

Orthostatic hypotension makes it difficult to diagnose and treat high blood pressure. It is necessary to measure blood pressure in diabetes in two positions - standing and lying down. If a patient has this complication, then he should get up slowly each time, “according to how he feels.”

Our website was created to promote a low-carbohydrate diet for type 1 and type 2 diabetes. Because Eating less carbohydrates is the best way to reduce and maintain normal blood sugar. Your need for insulin will decrease and this will help improve your hypertension treatment results. Because the more insulin circulates in the blood, the higher the blood pressure. We have already discussed this mechanism in detail above.

Get recipes for a low-carbohydrate diet for type 1 and type 2 diabetes

To what level should blood pressure be reduced in diabetes?

Hypertensive patients with diabetes mellitus are patients at high or very high risk of cardiovascular complications. It is recommended to reduce their blood pressure to 140/90 mm Hg. Art. in the first 4 weeks if they tolerate the prescribed medications well. In the following weeks, you can try to reduce your blood pressure to about 130/80.

The main thing is how does the patient tolerate drug therapy and its results? If it’s bad, then blood pressure should be reduced more slowly, in several stages. At each of these stages - by 10-15% of the initial level, for 2-4 weeks. When the patient adapts, the dosage is increased or the amount of medication is increased.

Reducing blood pressure gradually can help avoid episodes of hypotension and thus reduce the risk of myocardial infarction or stroke. The lower limit of the normal blood pressure threshold is 110-115/70-75 mmHg. Art.

There are groups of patients with diabetes in whom the “upper” blood pressure should be reduced to 140 mm Hg. Art. and below may be too difficult. Their list includes:

• patients whose target organs are already damaged, especially the kidneys;
• patients with cardiovascular complications;
• elderly people, due to age-related vascular damage by atherosclerosis.

It can be difficult to choose blood pressure pills for a patient who has diabetes. Because impaired carbohydrate metabolism imposes restrictions on the use of many medications, including those for hypertension. When choosing a drug, the doctor takes into account how the patient controls his diabetes and what concomitant diseases, besides hypertension, he has already developed.

Good blood pressure pills for diabetes should have the following properties:

• significantly lower blood pressure, and at the same time have as few side effects as possible;
• do not worsen blood sugar control, do not increase levels of “bad” cholesterol and triglycerides;
• Protect your heart and kidneys from the damage caused by diabetes and high blood pressure.

Currently, there are 8 groups of drugs for hypertension, of which 5 are basic and 3 are additional. Tablets that belong to additional groups are prescribed, as a rule, as part of combination therapy.

Groups of blood pressure medications

Diuretics (water medications) for blood pressure

Classification of diuretics

You can find detailed information about all these diuretic medications. Now let's discuss how diuretics treat hypertension in diabetes.

Hypertension in patients with diabetes often develops because the volume of circulating blood is increased. Diabetics are also hypersensitive to salt. Because of this, diuretics are often prescribed to treat high blood pressure in diabetes. And diuretic medications help many patients well.

Doctors value thiazide diuretics because these drugs reduce the risk of heart attack and stroke in patients with hypertension by approximately 15-25%. Including those with type 2 diabetes. It is believed that in small doses (equivalent to hydrochlorothiazide< 25 мг в сутки) они не ухудшают контроль сахара в крови и не повышают “плохой” холестерин.

Thiazide and thiazide-like diuretics are contraindicated in patients at the stage of chronic renal failure. Loop diuretics, on the other hand, are effective in renal failure. They are prescribed if hypertension is combined with edema. But there is no evidence that they protect the kidneys or heart. Potassium-sparing and osmotic diuretics are not used at all for diabetes.

For hypertension in combination with diabetes mellitus, small doses of thiazide diuretics are usually prescribed along with or. Because diuretics on their own, without other medications, are not effective enough in this situation.

Beta blockers

Medicines from the group of beta blockers are:

• selective and non-selective;
• lipophilic and hydrophilic;
• with and without internal sympathomimetic activity.

All these are important properties, and it is advisable for the patient to spend 10-15 minutes to understand them. And at the same time, learn about contraindications and side effects of beta blockers. After this, you will be able to understand why the doctor prescribed this or that drug.

Beta blockers must be prescribed to a patient with diabetes mellitus if he is diagnosed with any of the following:

• cardiac ischemia;
• heart failure;
• acute post-infarction period - to prevent recurrent myocardial infarction.

In all of these situations, beta blockers significantly reduce the risk of death from cardiovascular disease and other causes.

At the same time, beta blockers can mask the symptoms of impending severe hypoglycemia, as well as make it difficult to recover from a hypoglycemic state. Therefore, if a diabetic has impaired recognition of hypoglycemia, then these medications can only be prescribed to him with extreme caution.

Selective beta blockers have the least negative effect on metabolism in diabetes. This means that if, according to indications, the patient needs to take beta blockers, then cardioselective drugs must be used. Beta blockers with vasodilatory activity - nebivolol (Nebilet) and carvedilol (Coriol) - can even improve carbohydrate and fat metabolism. They increase tissue sensitivity to insulin.

Note. Carvedilol, although not a selective beta blocker, is one of the newer drugs that is widely used, works effectively, and probably does not impair metabolism in diabetes.

Modern beta blockers, rather than drugs of the previous generation, are recommended to be given preference in the treatment of patients with diabetes, as well as patients at risk of developing type 2 diabetes. In contrast, non-selective beta blockers that do not have vasodilatory activity (propranolol) increase the risk of developing type 2 diabetes.

Angiotensin II receptor blockers (angiotensin receptor antagonists)

You can find detailed information about these relatively new medications. To treat high blood pressure and kidney problems in diabetes, angiotensin II receptor blockers are prescribed if a patient develops a dry cough. This problem occurs in approximately 20% of patients.

Angiotensin II receptor blockers are more expensive than ACE inhibitors, but do not cause a dry cough. Everything that is written in this article above in the section on ACE inhibitors also applies to angiotensin receptor blockers. The contraindications are the same, and the same tests must be taken while taking these medications.

It is important to know that angiotensin II receptor blockers reduce left ventricular hypertrophy of the heart better than ACE inhibitors. Patients tolerate them better than any other high blood pressure medications. They have no more side effects than placebo.

This is a relatively new drug. It was developed later than ACE inhibitors and angiotensin receptor blockers. Rasilez was officially registered in Russia
in July 2008. Results from long-term studies of its effectiveness are still awaited.

Rasilez is a direct renin inhibitor.

Rasilez is prescribed together with ACE inhibitors or angiotensin II receptor blockers. Such combinations of drugs have a pronounced effect on protecting the heart and kidneys. Rasilez improves blood cholesterol levels and increases tissue sensitivity to insulin.

Alpha blockers

For long-term treatment of arterial hypertension, selective alpha-1 blockers are used. Drugs in this group include:

• prazosin
• doxazosin
• terazosin

Pharmacokinetics of selective alpha-1-blockers

Side effects of alpha-blockers:

• orthostatic hypotension, up to fainting;
• swelling of the legs;
• withdrawal syndrome (blood pressure jumps strongly with a “ricochet”);
• persistent tachycardia.

Some studies have shown that alpha blockers increase the risk of heart failure. Since then, these drugs have not been particularly popular, except in certain situations. They are prescribed along with other drugs for hypertension if the patient has benign prostatic hyperplasia.

For diabetes, it is important that they have a beneficial effect on metabolism. Alpha-blockers lower blood sugar, increase tissue sensitivity to insulin, and improve cholesterol and triglyceride levels.

At the same time, heart failure is a contraindication for their use. If the patient exhibits orthostatic hypotension, alpha-blockers should not be prescribed.

Which tablets to choose for the treatment of hypertension in diabetes mellitus?

In recent years, more and more doctors are inclined to believe that To treat high blood pressure, it is better to prescribe not one, but 2-3 drugs at once. Because patients usually have several mechanisms for the development of hypertension operating simultaneously, and one medicine cannot affect all causes. Blood pressure pills are divided into groups because they act differently.

A single medicine can lower blood pressure to normal in no more than 50% of patients, and only if hypertension was initially moderate. At the same time, combination therapy allows you to use smaller doses of drugs and still get better results. In addition, some pills reduce or completely eliminate each other's side effects.

Hypertension is dangerous not in itself, but because of the complications it causes. Their list includes: heart attack, stroke, kidney failure, blindness. If high blood pressure is combined with diabetes, the risk of complications increases several times. The doctor assesses this risk for a particular patient and then decides whether to start treatment with one tablet or immediately use a combination of drugs.

Explanations for the figure: BP - blood pressure.

The Russian Association of Endocrinologists recommends the following strategy for the treatment of moderate hypertension in diabetes. First of all, an angiotensin receptor blocker or an ACE inhibitor is prescribed. Because drugs from these groups protect the kidneys and heart better than other drugs.

If monotherapy with an ACE inhibitor or angiotensin receptor blocker does not sufficiently reduce blood pressure, it is recommended to add a diuretic. Which diuretic to choose depends on the preservation of the patient’s kidney function. If there is no chronic renal failure, thiazide diuretics can be used. The drug Indapamide (Arifon) is considered one of the safe diuretics for the treatment of hypertension. If renal failure has already developed, loop diuretics are prescribed.

Explanations for the picture:

• BP - blood pressure;
• GFR is the glomerular filtration rate of the kidneys, for more details see “What tests do you need to take to check your kidneys”;
• CRF - chronic renal failure;
• BCC-DHP—dihydropyridine calcium channel blocker;
• BCC-NDHP—non-dihydropyridine calcium channel blocker;
• BB - beta blocker;
• ACE inhibitor - ACE inhibitor;
• ARA is an angiotensin receptor antagonist (angiotensin-II receptor blocker).

It is advisable to prescribe drugs that contain 2-3 active ingredients in one tablet. Because the fewer pills there are, the more willingly patients take them.

A short list of combination medications for hypertension:

• Korenitek = enalapril (Renitec) + hydrochlorothiazide;
• fozide = fosinopril (monopril) + hydrochlorothiazide;
• co-diroton = lisinopril (diroton) + hydrochlorothiazide;
• hyzaar = losartan (cozaar) + hydrochlorothiazide;
• noliprel = perindopril (Prestarium) + thiazide-like diuretic indapamide-retard.

ACE inhibitors and calcium channel blockers are thought to enhance each other's ability to protect the heart and kidneys. Therefore, the following combination medications are often prescribed:

• tarka = trandolapril (hopten) + verapamil;
• prestance = perindopril + amlodipine;
• equator = lisinopril + amlodipine;
• exforge = valsartan + amlodipine.

We strongly caution patients: Do not self-prescribe medications for hypertension. You may suffer severe side effects, including death. Find a qualified doctor and see him. The doctor sees hundreds of patients with hypertension every year, and therefore he accumulates practical experience of how medications work and which ones are more effective.

Hypertension and diabetes mellitus: conclusions

We hope you found this article about hypertension in diabetes mellitus helpful. High blood pressure in diabetes is a huge problem for doctors and for patients themselves. All the more relevant is the material presented here. In the article “Causes of hypertension and how to eliminate them. Tests for hypertension” you can find out in detail what tests you need to take for effective treatment.

After reading our materials, patients will be able to better understand hypertension in type 1 and type 2 diabetes in order to adhere to effective treatment strategies and prolong their life and capacity. Information about blood pressure pills is well structured and will serve as a convenient “cheat sheet” for doctors.

We would like to emphasize once again that it is an effective remedy to lower blood sugar in diabetes, as well as normalize blood pressure. This diet is useful for patients with diabetes, not only type 2, but even type 1, except in cases of severe kidney problems.

Follow our or. If you limit carbohydrates in your diet, you will be more likely to lower your blood pressure. Because the less insulin circulates in the blood, the easier it is to do this.

Type 2 diabetes mellitus, arterial hypertension and the risk of cardiovascular complications

O.A. Kislyak, T.O. Myshlyaeva, N.V. Malysheva

Russian State Medical University

Diabetes mellitus (DM) is one of the most common chronic diseases and represents a serious health problem, since diabetes mellitus causes a decrease in quality of life, early disability and high mortality. All countries are experiencing an increase in the incidence of diabetes mellitus. The number of people with diabetes mellitus is currently approaching 200 million people, with the bulk (90%) of patients being patients with type 2 diabetes mellitus. According to forecasts, if such growth rates continue, by 2010 the number of people with diabetes mellitus on the planet will reach 221 million people, and by 2025, more than 300 million people will have diabetes mellitus.

Type 2 diabetes mellitus is characterized by the development of severe disabling complications leading to complete disability and premature mortality. According to the Cost of Diabetes in Europe - Type 2 (CODE-2) study, which studied the prevalence of various diabetic complications in patients with diabetes mellitus (average age of those examined was 67 years), 59% of patients had complications, with 23% of those examined having 2, and 3% - 3 complications of type 2 diabetes. Cardiovascular pathology was found in 43%, cerebrovascular pathology in 12% of patients. It has been established that with type 2 diabetes mellitus, the risk of developing cardiovascular pathology is 3-4 times higher than without it. Patients with type 2 diabetes have the same risk of premature death as patients who have had a myocardial infarction without diabetes. In most developed countries of the world, diabetes mellitus ranks 3-4 in the overall mortality structure and is the leading cause of blindness and decreased vision in the adult population.

Despite the advances in medicine, diabetes remains one of the priority diseases, the social and medical significance of which is obvious. The main cause of mortality in diabetes mellitus is vascular complications, in the pathogenesis of which the main role belongs to hyperglycemia and its metabolic effects. The risk of macro- and microangiopathy in patients with type 2 diabetes mellitus directly depends on the level of glycemia. An analysis of the results of the United Kingdom Prospective Diabetic Study (UKPDS) showed that an increase in glycated hemoglobin levels of only 1% increases the risk of diabetes-related mortality by 21%, myocardial infarction by 14%, peripheral vascular disease by 43%, and microvascular disease. complications - by 37%, development of cataracts - by 19%. The incidence of any complications of diabetes mellitus, including death of patients, increases in proportion to the average level of glycated hemoglobin HbA1c.

Mortality from cardiovascular diseases among patients with type 1 and type 2 diabetes mellitus is 35 and 75%, respectively. Life expectancy in patients with type 2 diabetes mellitus is shorter, and mortality (taking into account age) is almost twice as high as in patients without this disease.

The high cardiovascular risk in diabetes is due to several factors. First, many cardiovascular disease (CVD) risk factors are present in patients already at the pre-diabetes stage (Fig. 1). As is known, insulin resistance (IR) plays a leading role in the development of type 2 diabetes mellitus. In the modern interpretation, insulin resistance should be understood as a primary selective and specific violation of the biological action of insulin, accompanied by a decrease in glucose consumption by tissues (mainly skeletal muscles) and leading to chronic compensatory hyperinsulinemia. In conditions of insulin resistance, there is a decrease in the supply of glucose to insulin-dependent tissues (muscle, fat), an increase in the production of glucose by the liver, which contribute to the development of hyperglycemia. With adequate ability of β-cells to compensate for increased glucose levels by excess production of insulin, the state of normoglycemia is maintained. However, subsequently, as the severity of insulin resistance increases, the insulin secretory ability of b-cells is depleted and they cease to cope with the increasing load of glucose. Initially, this is manifested by the development of hyperglycemia in the postprandial (after eating) period. An example of postprandial hyperglycemia is impaired glucose tolerance. With further progression of impaired insulin secretion by pancreatic beta cells and persisting insulin resistance, impaired glucose tolerance develops into type 2 diabetes mellitus. It has been established that annually impaired glucose tolerance develops into type 2 diabetes mellitus in 4-9% of patients. Thus, macrovascular complications

Rice. 2. Global cardiometabolic risk

disorders that are a manifestation of CVD occur much earlier than the development of the full picture of DM.

Secondly, factors such as obesity, arterial hypertension and dyslipidemia can also play a decisive role in the development of complications of diabetes mellitus caused by atherosclerosis. Many people with type 2 diabetes have several risk factors for cardiovascular disease before diagnosis, including, in addition to diabetes, hyperlipidemia, hypertension and excess body weight. Thus, every second patient with diabetes is diagnosed with dyslipidemia, and almost all patients in this category are overweight. This “polygenic syndrome”, which includes hypertriglyceridemia, decreased levels of high-density lipoproteins, abdominal obesity, arterial hypertension (AH), impaired fasting glycemia, as a separate concept was first introduced into scientific use under the names “metabolic trisyndrome”, “abundance syndrome” , and later as “metabolic syndrome”. At first, the possible connection between the components of this syndrome was ignored by many, until in 1988 G.M. Jaewen et al. did not put forward a hypothesis about insulin resistance as the root cause of the development of the so-called metabolic syndrome. Great interest in the problem of metabolic syndrome in the last decade is explained by its wide distribution in the population (up to 20%), as well as by the fact that all its components relate to established risk factors for cardiovascular diseases, including acute coronary syndrome and stroke. The increase in the total individual cardiovascular risk several times with a combination of its factors determines the high medical and social significance of metabolic syndrome. Moreover, the presence of metabolic syndrome is currently considered as the main cause of high global cardiometabolic risk, combining the risk of CVD and the risk of developing diabetes (Fig. 2).

The most common condition in patients with type 2 diabetes mellitus is arterial hypertension. Thus, the iKRB8 study analyzed which cardiovascular diseases patients who were first diagnosed with diabetes mellitus already had. It turned out that arterial hypertension occurred in almost 65% of patients; quite often patients had already suffered a myocardial infarction in the past (34%) or had

ECG changes (33%). Peripheral vascular diseases (macroangiopathy) were recorded in 46% of patients, and stroke in 38% of patients.

Arterial hypertension is observed in approximately 75-80% of patients with type 2 diabetes mellitus and is the cause of death in more than 50% of patients. It is a proven fact that the association of diabetes mellitus and arterial hypertension significantly increases the risk of adverse outcomes in patients. The combination of these diseases is to a certain extent natural. Arterial hypertension and diabetes mellitus are pathogenetically related. Their frequent coexistence is facilitated by the interaction of common hereditary and acquired factors. Among them, the following are considered the most important: genetic predisposition to high blood pressure and diabetes mellitus; sodium retention in the body, as well as angiopathy and nephropathy, which contribute to increased blood pressure and the development of diabetes; obesity, especially abdominal obesity, which can cause or worsen insulin resistance.

Analyzing the causes and frequent coexistence of hypertension and diabetes, many researchers paid attention to possible common mechanisms of their development, namely a similar complex of metabolic disorders. Several factors are involved in the pathogenesis of arterial hypertension against the background of insulin resistance in patients with type 2 diabetes mellitus. Normally, insulin causes vasodilation, which in healthy individuals, against the background of increased sympathetic activity, also caused by the action of insulin, is not accompanied by a change in blood pressure levels. In patients with insulin resistance, the vasodilating effect of insulin is blocked, and the development of hyperinsulinemia activates a number of mechanisms that increase the tonic tension of the vascular wall. Insulin resistance is accompanied by activation of the sympathetic nervous system. Activation of the sympathetic system leads to increased contractility of cardiomyocytes and vascular smooth muscle cells. This is accompanied by an increase in cardiac output, an increase in total peripheral vascular resistance (TPVR) and blood pressure levels. Under conditions of hyperglycemia, an increase in the filtration of glucose in the renal glomeruli is accompanied by an increase in its reabsorption along with sodium in the proximal tubules of the nephron. As a result, hypervolemia occurs, leading to an increase in peripheral vascular resistance, cardiac output and blood pressure levels. Endothelial dysfunction plays an important role in the development of arterial hypertension in type 2 diabetes mellitus. With hyperinsulinemia, the production of vasoconstrictor substances by the endothelium increases, in particular endothelin-1, thromboxane A2, and a decrease in nitric oxide and prostacyclin, which have vasodilating effects. In addition, patients with diabetes have increased sensitivity to angiotensin II and norepinephrine, which have a vasoconstrictor effect. These changes may also be due to insufficient nitric oxide production. It is believed that impaired vasodilation and increased vasoconstriction lead to an increase in vascular tone, an increase in total peripheral vascular resistance and, as a consequence, to arterial hypertension. Activation of glucose metabolism in insulin-sensitive cells of the ventromedial hypothalamus, induced by hyperinsulinemia, is accompanied by an increase in the activity of the sympathetic centers of the brain. In addition, an increase in the central activity of the sympathetic nervous system leads to the suppression of inhibitory

Cardiology

Diabetes

Normal blood pressure, hypertension, hypertension + diabetes mellitus

Rice. 3. Prevalence of LVH in different population groups

influences from the baroreceptor apparatus of large vessels. But, perhaps, the central link in the pathogenesis of hypertension in diabetes is the high activity of the renin-angiotensin-aldosterone system (RAAS).

The daily profile of blood pressure in patients with diabetes mellitus has its own characteristics and differs from the daily profile of patients with arterial hypertension without metabolic disorders. Thus, against the background of metabolic disorders, a higher average level of both systolic and diastolic blood pressure is revealed per day, during the day and at night. A significantly larger number of patients have an insufficient reduction in blood pressure at night and nocturnal hypertension. Another feature of the daily blood pressure profile in patients with diabetes is an increase in the variability of systolic and diastolic blood pressure during the day and night hours. Patients with type 2 diabetes mellitus and arterial hypertension are also characterized by a large magnitude and speed of the morning rise in blood pressure. Regardless of the average blood pressure level, excess blood pressure variability and higher

Activation of PPA1?y in the experiment

^mol/L EC50 Pioglitazone 0.2 ^mol/L EC50 Telmisartan 5.02 ^mol/L EC50 Irbesartan 26.97 ^mol/L EC50 Losartan >50 ^mol/L

,<У.

h["Ts.O" ~ o

Rice. 4. Activation of PPARy by telmisartan

Benson S.C. et al. Hypertension. 2004; 43:993-1002

The rate of morning rise in blood pressure correlates with more severe total target organ damage and is considered a factor of unfavorable prognosis in patients with arterial hypertension. On the other hand, it has been shown that diabetes mellitus (regardless of arterial hypertension and obesity) is combined with left ventricular myocardial hypertrophy (LVH) and increased arterial wall stiffness (Fig. 3).

The frequent coexistence of arterial hypertension and diabetes mellitus, associated with a high risk of cardiovascular events, dictates the need to determine principles for the management of patients with arterial hypertension and type 2 diabetes.

Many studies have shown that strict blood pressure control is important for preventing cardiovascular complications in patients with diabetes. The importance of effective blood pressure control to prevent cardiovascular complications in patients with diabetes has been proven in many completed studies. According to the UKPDS multicenter randomized trial involving patients with type 2 diabetes mellitus and high blood pressure, strict glycemic control significantly reduces the incidence of microvascular complications, and strict blood pressure control (less than 144/82 mm Hg) significantly and significantly reduces the risk of any clinical complications associated with diabetes by 24%; diabetes-related mortality by 32%; stroke by 44%, diabetic retinopathy and kidney failure by 37%, decreased visual acuity by 47%. One of the most important conclusions of this study is that the risk of mortality and the development of micro- and macrovascular complications of diabetes was significantly reduced with strict blood pressure control compared with blood glucose control. The HOT (Hypertension Optimal Treatment) study proved that achieving a lower target blood pressure (diastolic blood pressure less than 80 mm Hg) in patients with type 2 diabetes was accompanied by an additional reduction in cardiovascular risk by 51%. No less impressive results were obtained in the ADVANCE study (Action in Diabetes and Vascular Disease: Preterax and Diamicron MR Controlled Evaluation). The results of the ADVANCE study showed that intensive antihypertensive therapy reduced overall mortality by 14% and the risk of cardiovascular mortality by 18%. In addition, the likelihood of cardiovascular complications is reduced by 14% and renal complications by 21%.

In all patients with diabetes, intensive non-pharmacological measures should be used where appropriate, with particular attention to weight loss and reducing salt intake.

The target blood pressure level should be<130/80 мм рт. ст., и антигипертензивное лечение должно начинаться уже при высоком нормальном уровне АД.

All effective and well-tolerated drugs can be used to lower blood pressure. Combinations of two or more medications are often necessary.

Available evidence confirms that lowering blood pressure has a protective effect on the occurrence and progression of nephropathy. Some additional nephroprotection can be achieved by using blockers of the renin-angiotensin system (receptor antagonists).

angiotensin receptors or angiotensin-converting enzyme inhibitors).

Blockers of the renin-angiotensin system should be the main component of combination therapy and are preferred in monotherapy.

The presence of microalbuminuria requires the use of antihypertensive therapy even at a high normal initial blood pressure level. Blockers of the renin-angiotensin system have a pronounced antiproteinuric effect, and their use should be preferred.

The treatment strategy should address all cardiovascular risk factors, including the use of statins.

Due to the many cases of orthostatic hypotension, blood pressure measurements should also be taken in an upright position.

Thus, the most important principle that must be observed when choosing an antihypertensive drug for diabetes is the prescription of drugs that block the RAAS. Currently, drug effects on the RAAS can be considered an established therapeutic technique used for the treatment of arterial hypertension and the prevention of cardiovascular morbidity and cardiovascular mortality (CVM). Both angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs), which reduce the effects of angiotensin II, have proven effective in controlling hypertension. However, ACEIs reduce the effects of AT11 by blocking the last step in the conversion of angiotensin I to ATP, and ARBs (also known like sartans) do not interfere with the formation and circulation of ATP, but specifically inhibit the binding of the peptide to AT1 receptors. In addition to a clear hypotensive effect, both of these classes of drugs have the ability to have an organoprotective effect and prevent the development of new cases of diabetes.

The history of the creation of ARBs is associated with clarification of the role of various ATP receptors, and therefore alternative approaches to ACEIs to blockade of the RAAS through the AT1 receptor system have emerged. It is currently known that ATP realizes its effects through two types of receptors - AT1 and AT2. The main properties of AT1 receptors are the mediation of vasoconstriction and an increase in blood pressure, sodium reabsorption in the renal tubules, cell proliferation, including smooth muscle cells in the blood vessels and heart, which leads to all the adverse effects in the cardiovascular continuum. Of interest are the data that in abdominal obesity and arterial hypertension there is an increase in the expression of AT1 receptor genes, which apparently enhances the negative effects of AT II.

The properties of AT2 receptors are largely opposite. Their activation promotes cell differentiation, tissue regeneration, apoptosis and possibly vasodilation, and inhibits cell growth. Therefore, the use of ARBs blocks AT1 receptors while maintaining the ability of circulating angiotensin II to interact with AT2 receptors, which contributes to additional organoprotective effects. The fundamental differences between ARBs and ACEIs are precisely the preservation of the function of AT2 receptors. Therefore, this new group of drugs has taken a leading place among antihypertensive drugs in many countries and is becoming more widespread every year. For this group of drugs in a number of clinical studies

Losartan Telmisartan

Glucose Insulin HOMA HbAic

fasting index

Rice. 5. The effect of telmisartan on indicators associated with insulin resistance Vitale C. et al. Cordiovasc Diabetol. 2005; 4:6

niums (LIFE, RENAAL, DETAIL, AMADEO, IRMA-2, etc.) have demonstrated pronounced organoprotective properties, which is manifested in the regression of target organ damage associated with diabetes and metabolic syndrome, such as left ventricular hypertrophy and microalbuminuria.

ARBs are not only effective, pathogenetically substantiated means for controlling blood pressure in diabetes, but can influence not only blood pressure, but also other components of the metabolic syndrome and diabetes (impaired fat and carbohydrate metabolism). This effect is, to one degree or another, characteristic of most ARBs. It is known that the process of adipocyte differentiation greatly depends not only on the influence of ATII, but also on the activity of PPARy (peroxisome proliferator-activated receptors), which have recently been given great importance. It is well known that peroxisome proliferator-activated receptor γ (PPARy) is an established therapeutic target in the treatment of insulin resistance, diabetes mellitus and metabolic syndrome. Currently, PPARy receptor agonists (pioglitazone, rosiglitazone) are increasingly used in diabetes and metabolic syndrome. The ability of the drug from the ARB group telmisartan (Mikardis) to significantly activate PPARy receptors has been established. It turned out to be the only ARB capable of activating PPARy receptors at physiological concentrations (Fig. 4).

Recent studies show that telmisartan has a pronounced positive effect on insulin resistance and carbohydrate metabolism characteristics

Before treatment

After treatment

III!,! 0.75 2.4 1.9 1.68 1.59

HDL (mmol/l)

Rice. 6. Dynamics of lipid metabolism parameters in patients with hypertension

and metabolic syndrome during treatment with telmisartan

(Fig. 5). There is evidence of a clear positive effect of telmisartan on lipid metabolism. Thus, in our study of the effects of telmisartan in patients with metabolic syndrome, it was revealed that telmisartan at a dose of 80 mg for 8 weeks had a pronounced effect on lipid metabolism, namely on the level of total cholesterol, VLDL and, most importantly, on the level of triglycerides (Fig. 6). If before the start of the study, TG levels > 1.69 mmol/l were determined in 77% of patients, then after 8 weeks of treatment with telmisartan, elevated TG levels persisted in only 45% of patients. These positive metabolic effects of telmisartan were accompanied by its clear and complete antihypertensive effect. Our study revealed that even monotherapy with telmisartan at a dose of 80 mg per day had an antihypertensive effect in

women with both mild and moderate arterial hypertension and metabolic syndrome. Not only the average numbers of SBP and DBP decreased significantly in all periods of the day, but also the pressure load according to the TI indicator (hypertension time index), which, as is known, is especially important in terms of the effect of elevated blood pressure on the condition of target organs. And finally, we identified a reliable and significant decrease in the level of microalbuminuria in the examined patients, which indicated its pronounced organ-protective effect.

The OCTAXET program, which is investigating the effects of RAAS blockade using telmisartan on many components of the cardiovascular continuum, and is expected to end in 2008, will provide new data on the results of treatment of patients with cardiovascular disease and diabetes.

1. King H, Aubert RE, Herman WH. Global burden of diabetes, 1995-2025 Prevalence, numerical estimates, and projections. Diabetes Care 1998; 21: 1414-31.

2. Stratton IM, Adler AI, Neil AW, Matthews DR, Manley SE, Cull CA, Hadden D, Turner RC, Holman RR: Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes: prospective observational study (UKPDS 35). BMJ 321:405-412, 2000.

3. UK Prospective Diabetes Study (UKPDS) Group. Tight blood pressure control and risk of macrovascular and microvascular complications

in type 2 diabetes. UKPDS 38. Br. Med. J., 1998, 317, 705-713.

4. Chazova I.E., Mychka V.B. Metabolic syndrome. MEDIA MEDICA, Moscow, 2004, 163 p.

5. Mancia G. The association of hypertension and diabetes: prevalence, cardiovascular risk and protection by blood pressure reduction. Acta Diabetol.2005; 42:S17-S25.

Shestakova M.V. Diabetes mellitus and arterial hypertension.

In the book: Guide to arterial hypertension. Edited by Academician E.I. Chazov, professor I.E. Chazovoy. MEDIA MEDICA, Moscow, 2005, 415-433.

7. Hansson L, Zanchetti A, Carruthers SG et al. Effects of intensive blood-pressure lowering and low dose aspirin in patient with hypertension: principal results of the HOT randomized trial. Lancet 1998; 351: 1755-62.

8. ADVANCE trial study group rationale and design of the study: ADVANCE randomized trial of blood pressure lowering and intensive glucose control in high-risk individuals with type 2 diabetes mellitus. J Hypertens 2001;

9. 2007 Guidelines for the management of arterial hypertension. The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). J. Hypertens 2007, 25, 1 105-1 187.