Osteoarthrosis as a risk factor for cardiovascular accidents. What are cardiovascular diseases and the causes of their development?

The underlying cause of most cardiovascular diseases is atherosclerosis, which can develop slowly and unnoticed over many years before the first symptoms appear, which usually occurs in middle age. Acute coronary and cerebrovascular accidents often develop suddenly and often lead to death before the patient can receive any medical care.

In the early 50s of the twentieth century, the now generally accepted concept of risk factors affecting morbidity rates, the frequency of complications and mortality from various diseases, incl. cardiovascular. Risk in this case refers to the likelihood of developing a disease, its complications and death from this disease. Numerous studies have shown that modification of cardiovascular risk factors can significantly reduce cardiovascular morbidity and mortality in individuals with diagnosed and undiagnosed cardiovascular diseases.

Main cardiovascular risk factors

Cardiovascular risk factors are usually divided into modifiable and non-modifiable.

TO unmodifiable include age (the older, the greater the risk of CVD), male gender, heredity (cases of premature death from CVD or the development of CVD - myocardial infarction, stroke, angioplasty or coronary artery bypass surgery in blood relatives: men under the age of 55 years and women under under 65 years of age).

Main modifiable Cardiovascular risk factors are considered:

• arterial hypertension (blood pressure ≥ 140/90 mm Hg for people without diabetes and ≥ 130/80 mm Hg for people with diabetes);
• dyslipidemia (occurring in various combinations, increased blood levels of total cholesterol more than 5.0 mmol/l, low-density lipoprotein cholesterol more than 3.0 mmol/l, triglycerides more than 1.7 mmol/l, decreased high-density lipoprotein levels less than 1.0 mmol/l for men and less than 1.2 mmol/l for women);
• diabetes mellitus or impaired glucose tolerance;
• overweight (body mass index more than 25 kg/m2); smoking (including passive smoking);
• smoking (including passive smoking);
• lack of physical activity;
• excessive alcohol consumption, uric acid metabolism disorders, air pollution, country of residence (WHO experts, residence in countries former USSR recognized as a cardiovascular risk factor).

Long-term exposure to these factors contributes to the progression of atherosclerosis, the growth and destabilization of atherosclerotic plaques, which ultimately leads to stenosis and occlusion of the arteries supplying blood to vital organs such as the heart and brain. In addition to those listed, there are quite a lot of other cardiovascular risk factors, but since their role in the development of CVD is much less, they are not used for clinical purposes in most cases.

Interaction of cardiovascular risk factors

The same person often has several cardiovascular risk factors simultaneously. However, it should be taken into account that this is not a summation, but a mutual potentiation of risk. This means that the total risk of CVD, its complications and cardiovascular death in the presence of 2 or more cardiovascular risk factors in the same person exceeds the arithmetic sum of these same risks taken separately.

Assessment of cumulative individual cardiovascular risk

In persons without signs of cardiovascular diseases, an individual assessment of the total cardiovascular risk in clinical practice is currently carried out most often using the EuroSCORE (European Systematic COronary Risk Estimation) scales, which were developed separately for European countries with low and high risk CVD (the latter includes Ukraine), as well as according to the Framingham scale, created in the USA. There are other cardiovascular risk scales - German PROCAM, New Zealand, Sheffield, etc., but they are used much less frequently. All of these scales are used either in the form of special tables or in the form of calculator programs (both online and downloadable), which are available on the Internet.

For the population of Ukraine today, the EuroSCORE scale is considered the most acceptable (Fig. 1). Using this scale, the individual risk (probability) of death from cardiovascular diseases is calculated. The risk is considered high if its level reaches 5% or more.

Rice. 1.

Note: THC - total blood cholesterol

Such individuals require persistent risk adjustment, as well as active targeted identification of possible asymptomatic cardiovascular disease (usually of atherosclerotic origin). In this case, the following non-invasive research methods are predominantly used in clinical practice: electrocardiography (ECG), including automatic 24-hour ambulatory monitoring, cardiac ultrasound (including stress echocardiography, tissue Doppler, etc.), great vessels neck, head and limbs, multispiral CT scan, magnetic resonance imaging. These methods make it possible to identify episodes of ischemia, local disturbances in myocardial contractility and perfusion, hypertrophy, dilatation, disturbances in geometry, contractility and synchrony of contraction of the heart, thickening of the intima-media complex in the vessels, atherosclerotic plaques and calcium deposits in the arteries (including coronary ), stenoses and aneurysms of blood vessels.

However, the limitations of the EuroSCORE scale, which only takes into account cardiovascular risk factors such as gender, age, systolic blood pressure, total cholesterol, and smoking status, should be taken into account. Therefore, according to the latest European recommendations, patients with established CVD, peripheral arterial disease or cerebral atherosclerosis are also included in the high-risk group; persons with diabetes mellitus type II or type I with microalbuminuria; persons with a significant increase in the levels of individual risk factors: total cholesterol - 8 mmol/l (320 mg/dl) or more, low-density lipoprotein cholesterol - 6 mmol/l (240 mg/dl) or more, blood pressure - 180/110 mm Hg and more; immediate blood relatives of patients with early onset atherosclerotic cardiovascular diseases or persons at high risk of CVD (see above).

“New” cardiovascular risk factors

Over the past decade and a half, a number of “new” indicators related to cardiovascular risk factors have been proposed.

These are elevated levels of C-reactive protein (determined by quantitative methods), homocysteinemia, levels of brain natriuretic peptide, tumor-necrotic factor, etc.

Experts in the United States and Europe, despite the certain benefit of identifying these factors in some clinical situations, have now concluded that the information obtained in this way adds little to the total cardiovascular risk calculated on the basis of more “traditional” risk factors, and significantly does not change the tactics of primary and secondary prevention of cardiovascular diseases. At the same time, the cost/effectiveness ratio for routine detection of “new” cardiovascular risk factors in everyday clinical practice is not yet optimal.

Chernobrivenko A.A.,
cardiologist highest category, Ph.D.
head Antihypertensive center of Darnitsky district, Kyiv

Literature

1. ACCF/AHA 2009 Performance Measures for Primary Prevention of Cardiovascular Disease in Adults. A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Performance Measures (Writing Committee to Develop Performance Measures for Primary Prevention of Cardiovascular Disease). // Journal of the American College of Cardiology. - 2009. - Vol. 54, No. 14. - P. 1364-1405.
2. Brook R.D., Franklin B., Cascio W. et al. Air Pollution and Cardiovascular Disease. A Statement for Healthcare Professionals From the Expert Panel on Population and Prevention Science of the American Heart Association. // Circulation. 2004; 109: 2655-2671.
3. Cardiovascular disease risk factors. Canadian Medical Association // Supplement to CMAJ 2000; 162 (9 Suppl).
4. Clinical Implications of Obesity with Specific Focus on Cardiovascular Disease. A Statement for Professionals From the American Heart Association Council on Nutrition, Physical Activity, and Metabolism // Circulation. 2004; 110: 2952-2967.
5. European guidelines on cardiovascular disease prevention in clinical practice: executive summary. // European Journal of Cardiovascular Prevention. - 2007. - Vol. 14. - (Supp. 2) - P. 1-40.
6. Hlatky M.A., Greenland P., Arnet D.K. et al. Criteria for Evaluation of Novel Markers of Cardiovascular Risk. A Scientific Statement From the American Heart Association. // Circulation published online Apr 13, 2009; DOI: 10.1161/CIRCULATIONAHA. 109. 192278
7. Hobbs F.D.R. Guidelines and management of global risk: the European perspective. // European Heart Journal Supplements (2004) 6 (Supplement C), C5-C14.
8. Prevention of Cardiovascular Disease. Guidelines for assessment and management of cardiovascular risk. / World Health Organization. - 2007. - 97 R.

Cardiovascular diseases are common name a whole group of diseases of the heart and circulatory system. Around the world, about 17.5 million people die from heart disease every year. At risk are older people with bad habits, diabetes, high blood pressure and excess weight.

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Common symptoms of heart disease

The first symptoms of the disease appear an unpleasant feeling in the chest and diaphragm. A person experiences high sweating, coughing, fatigue, and swollen limbs. Signs of cardiovascular disease (CVD) vary depending on the type of disease and individual characteristics. All this makes it difficult to timely diagnose such diseases and initiate treatment. Appearance severe cough may be a sign of a cold or viral infections, but in the case of CVD, the use of expectorants has no effect. An important signal is the sudden appearance of a cough when horizontal position bodies, frequent attacks at night. Appearing weakness is a sign of a functional malfunction in the nervous system. The patient experiences high fatigue, sleep disturbances, absent-mindedness, memory problems, causeless anxiety and trembling of the limbs. All these problems are caused by impaired blood circulation and appear in the early stages of the disease.



Increased body temperature, cramps, pallor appear when severe forms CVD and the presence of concomitant inflammatory processes in the body (myo-, peri-, endocarditis). Such disturbances cause a sharp rise in temperature to forty degrees and above. With this development of the disease, there is a threat of hemorrhage in the brain. Increasing pressure at 140/90 is a good reason for immediately taking blood pressure-lowering medications and further maintaining normal blood pressure levels. If the opposite situation is observed, a pulse of less than 50 beats per minute is a sure sign of coronary heart disease and cardiac dysfunction.

The appearance of swelling of the limbs at the end of the day can occur due to kidney problems, a large amount of salt in the body, and heart problems. This happens because the disruption of the heart does not allow it to fully pump blood fluid; as a result, it accumulates in the limbs, which causes swelling. Frequent and sudden dizziness may be signs of an impending stroke. The person feels a throbbing headache, weakness and nausea. Shortness of breath and acute lack of air occur, which also occurs with some types of myocardial infarction. Similar symptoms can also manifest themselves in diseases of the lungs and kidneys, which makes it difficult to determine the true cause.

During physical activity, a person may feel pain in the back, between the shoulder blades and lumbar region. Such symptoms often occur during severe emotional shocks and even during rest. The use of heart medications does not give the desired result, which indicates an impending heart attack. Symptoms may include chest pain, squeezing and burning. A strong Blunt pain, which becomes stronger and weaker. Also, similar signs are observed with the appearance of vascular spasm and angina.

Acute, prolonged chest pain radiating to left hand, a clear symptom of myocardial infarction. If the attack develops quickly, the patient may lose consciousness. With all this, acute chest pain can be a sign of other diseases, such as radiculitis, neuralgia, shingles, etc. All this makes it difficult to take correct measures to provide first aid to the patient. The main symptom of all cardiac disorders is rapid heartbeat, not caused by physical exertion or emotional shock. Such an attack is accompanied by weakness, nausea, and loss of consciousness. These are symptoms of developing angina and tachycardia, heart failure.



Types of Cardiovascular Diseases

The following diseases of the heart and blood vessels are distinguished:

• Cardiac ischemia.
• Vascular atherosclerosis.
• Peripheral circulation disorders.
• Rheumatic carditis.
• Heart disease.
• Thromboembolism.





Cardiac ischemia

The essence of the disease is damage to the myocardium, which causes a decrease or complete cessation of blood supply to the heart muscle. The main reason violation is a narrowing coronary arteries. Symptoms of the disease are manifested by pain in the chest, radiating to the left side of the body, occurring during physical activity, rest, and eating. The pain intensifies over several months, appearing more and more often. This is due to an increase in atherosclerotic spots, which gradually closes the lumen of the artery. Narrowing of the lumen by 90% causes an exacerbation of the disease and is critical.

The disease has mental manifestations, expressed in causeless anxiety, fear of death, apathy, and a feeling of lack of air. As the disease progresses, the occurrence of such conditions becomes more frequent, which only worsens the disease. Feelings of anxiety and fear provoke stress on the heart, increased blood pressure and temperature, which is already a dangerous condition in the presence of CVD.

Conservative treatment of the disease is aimed at improving blood supply to the myocardium, maintaining an acceptable level of blood pressure and improving the general condition of the patient. However, such methods do not always give the desired result. In this case, surgical interventions are used, such as coronary artery bypass grafting, deep artery stenting and myocardial revascularization.

The method of coronary bypass grafting is to connect damaged vessel with the coronary artery, thereby creating a bypass path for the affected area. After this, blood begins to flow into the myocardium in full, which eliminates ischemia and angina. This method is recommended in the presence of concomitant diseases, such as diabetes mellitus, congenital heart disease, damage to a large number of blood vessels, etc.



Atherosclerosis of cerebral vessels

The disease affects the walls of blood vessels with focal inflammation, there is an increasing thickening of the walls of the arteries with cholesterol stains, which leads to a narrowing of the lumen and oxygen starvation of the brain. Symptoms of the disease are expressed in changes in gait, noise in the ears, and flashing dots before the eyes. Impairments of perception and memory are the most characteristic symptoms illness, and memory problems extend only to recent events, without affecting deeper memory. In severe cases, the patient may experience decreased vision and hearing, severe migraines and facial flushing.

Treatment in most cases is prescribed medication, with a strict diet. A number of drugs are prescribed to dilate blood vessels, as well as a complex of vitamins and antioxidants. It is necessary to limit the consumption of fatty, fried, salty foods, chocolate, cocoa, and fatty dairy products.



Peripheral circulation disorder

Under normal conditions, the peripheral circulatory system provides organs with sufficient blood flow to function properly. Functional changes in blood circulation occur as a result of changes in heart rhythm. When the resistance to blood flow by the vessels begins to weaken, the walls of the vessels dilate, which leads to arterial hyperemia. In another case, with increasing resistance circulatory system, there is a difficult flow of blood to the organs and thrombosis, which threatens the development of ischemia. Such disorders occur when there is a decrease in the volume of blood passing from the heart to the veins and back, with heart defects, dysfunction of the heart valves, and enlargement of the heart muscle. All this leads to obstruction of blood flow and blood stagnation.

Symptoms of the disorder appear in more than 80% of patients; in other cases, an atypical course of the disease without severe symptoms may be observed. Typical symptoms are lameness, pain in calf muscles, which manifests itself when walking, weakened sensitivity of the limbs. In more severe stages, pain appears in the buttocks and thighs, and the development of a trophic ulcer and, as a result, gangrene are possible.

Drug treatment involves the use of a whole range of drugs aimed at lowering blood pressure, dilating blood vessels and strengthening their walls. Antiplatelet agents are prescribed, drugs that reduce the risk of myocardial infarction, eliminate muscle pain and prevent blood clots.

Surgical intervention is permissible in the following cases:

• severe intermittent claudication, the elimination of which is impossible with medications;
• critical damage to the arteries and vessels of the lower extremities as a result of ischemia and the development of trophic ulcers;
• acute ischemia, threatening the formation of blood clots and the development of gangrene;
• development of gangrene (the focal nature of the disorder involves the removal of the affected areas of the vessels and their subsequent replacement with borrowed or artificial arteries (shunts); with extensive development of inflammation, amputation of the limb is performed).

In the first three cases it is applied surgical revascularization, allowing blood flow to bypass the affected areas by applying a vascular bypass. In case of gangrene development, general surgical methods for limb removal.

A highly effective way to prevent circulatory disorders is physical therapy, which increases blood pressure, improves heart function and relieves symptoms of intermittent claudication in 70% of cases.



Rheumatic carditis

The disease affects the walls of the heart, resulting in an inflammatory process developing inside the organ. Pathological changes begin with the myocardium and end with the outer lining of the heart - the pericardium. The disorder is not an independent disease; it develops as one of the complications of rheumatism in the form of allergic and inflammatory reactions to the presence of streptococcus in the blood. Most often, the primary source of the disease is located in the upper respiratory tract.

Mild forms of the disease do not have pronounced symptoms and can occur without any noticeable manifestations. When the disease is acute, a person experiences a high temperature of up to 40 degrees and pain in the joints, especially the knees. This condition lasts up to two months; in the absence of timely relief of the disease, more severe symptoms develop: fever, hemoptysis, pressing pain in the chest, fainting, the face becomes pale with a blue tint.

Treatment methods are determined by the degree, form and severity of the disease. Pharmacological treatment is carried out at any stage of the disease and consists of three components:

1. 1. Antimicrobial treatment. Antibiotics are used penicillin group and drugs combined with them to suppress streptococcal infections.
2. 2. Anti-inflammatory therapy. In the acute course of the disease, glucocorticosteroids (Prednisolone, Dexamethasone) are prescribed if the disease persists light form, use anti-inflammatory drugs based on salicylic acid.
3. 3. Maintenance therapy. These are diuretics, sedatives and a course of vitamins.

Prescribed dietary food which will provide required amount useful elements for the patient are excluded from the diet unhealthy food. The menu should contain foods high in animal and plant proteins. Boiled meat and fish, fresh vegetables and fruits. Side dishes should consist of buckwheat, oatmeal and rice porridge. It is undesirable to eat sweet, starchy and spicy foods. Coffee, alcohol and tobacco are strictly prohibited. It is not recommended to consume products containing soy, food dyes, and cholesterol.



Heart disease

Heart disease is a pathology of the heart valves in which the heart ceases to function properly. The disease can be congenital or acquired. Congenital heart disease occurs in only 1-2% of newborns. In this case, anomalies in the development of the organ are observed, which lead to its malfunction. In adulthood, the disorder can develop under the influence of other diseases, such as rheumatism, ischemia, and stroke.

To treat heart defects, both congenital and acquired, a complex of measures is required, including surgery and drug treatment. During surgery to restore the functionality of the heart valves, a valvuloplasty procedure is performed, using animal heart valves, mechanical or biological prostheses for replacement. The operation is performed with artificial circulation and lasts from 4 to 8 hours. The rehabilitation period takes from 6 to 12 months, depending on the severity of the disease and the complexity of the recovery period. Further treatment is carried out conservatively. A daily routine, a course of physical therapy, and diet are established.

Thromboembolism

The disease is a blockage of a blood vessel by a blood clot that has broken off from the walls of the vessel or the heart. As a result, blood stops flowing to the heart, and a rupture of blood vessels occurs, leading to an ischemic heart attack. Most often, thromboembolism occurs during surgical operations, especially if the patient has malignant neoplasms. A blood clot forms in the veins of the systemic circulation, which causes blockage in the left heart chamber and adjacent arteries.

Symptoms of the disease include rapid heartbeat, bluish facial skin, chest pain, hypertension, and abnormal pulsation of the veins. The severity of these symptoms depends on the degree and form of the disease. The acute form can be accompanied by severe pain, muscle spasms, and breathing problems, which most often leads to death. Milder forms are characterized by an increase in the above symptoms.

Thromboembolism is a dangerous condition that threatens death in the absence of immediate help. During a critically acute attack, the patient loses consciousness and can only be saved by using closed heart massage, defibrillation, artificial ventilation lungs. After the acute attack has stopped, an embolectomy procedure is performed, which involves manual removal of the blood clot. The operation carries a high risk and is performed only in critical cases. Next, a set of drugs is prescribed to relieve pain, normalize blood pressure, and prevent recurrent thrombosis of veins or arteries. Individual treatment is used for each stage of the disease.

In 85% of cases with acute thromboembolism, the patient dies before they can provide first aid.

Conclusion

Cardiovascular diseases are a broad group of diseases that can have general symptoms, But different reasons. Most CVDs can be prevented by eliminating risk factors such as poor diet, bad habits, lack of physical activity. According to the Ministry of Health, 76% of diagnoses of serious heart disease occur in overweight people. Of these, 20% are acute and in the vast majority of cases end in death. Heart problems caused by bad habits account for about 40%. Such cases have a severe clinical picture, although the mortality rate is low. The remaining cases of acute manifestations of the disease occur in elderly people and patients with congenital pathologies of the heart and circulatory system.

From the standpoint of state statistics, rheumatic diseases (RD) are not classified as life-threatening, but in clinical practice, systemic connective tissue diseases are often the cause of death in young and middle-aged patients. Rheumatoid arthritis (RA), systemic scleroderma (SSc), systemic lupus erythematosus (SLE), antiphospholipid syndrome(AFS), ankylosing spondylitis (AS) and many others lead to a reduction in the life expectancy of patients, and the 5-year survival rate of patients with severe forms of systemic connective tissue diseases does not exceed 50%, which is comparable to the outcomes of lymphogranulomatosis and common lesions of the coronary arteries.

Research in recent years has shown that the leading cause of decreased life expectancy in RD is cardiovascular complications associated with atherosclerotic vascular lesions and thrombosis. Preclinical forms of atherosclerosis (endothelial dysfunction, thickening of the intimate media complex, increased arterial wall resistance, increased coronary calcium levels) are detected much more often in patients with RD than in the general population. It has been established that the risk of premature development and progression of atherosclerosis in RD is higher than in the population and is associated not only with traditional risk factors, but also with the activity of the inflammatory process, as well as drug therapy.

Every third patient with RA and 30% of patients with SLE have signs of preclinical atherosclerosis. It has been shown that in patients with RA the risk of cardiovascular disease (CVD) is 2-5 times higher than in the general population. This reduces the life expectancy of this category of patients by 5-10 years. Patients with RA are 2 times more likely than patients without RA to develop myocardial infarction and sudden coronary death. 2 years before the diagnosis of RA, these individuals are 3 times more likely to be hospitalized for acute coronary syndrome than those observed in a sample from the general population. When performing coronary angiography in patients with RA, multivessel atherosclerotic lesions of the coronary arteries are detected with a higher frequency than in the control group. It has been proven that the risk of coronary heart disease (CHD) in patients with SLE is 5-6 times higher than in the general population, and in young women with SLE aged 35-44 years – 50 times higher. According to prospective studies, approximately 10% of patients with SLE have clinical manifestations of atherosclerosis (angina pectoris, myocardial infarction, damage to the cerebral and peripheral arteries), and at autopsy, atherosclerosis is detected in more than half of patients.

Some features of cardiovascular pathology in RD are known. Thus, rheumatoid coronaryitis in most cases is asymptomatic and has been described in patients with rheumatoid arthritis with generalized vasculitis. In SLE, young patients develop ischemia or infarction due to coronaryitis or early development of atherosclerosis of the coronary arteries. In the clinic of patients with AS, angina pectoris is a common manifestation. A special place in the structure of cardiovascular disorders in SLE is occupied by thrombosis and thromboembolism associated with secondary APS. Cardiac manifestations of APS include the development of venous, arterial and intracardiac thrombosis with the formation of venous and arterial hypertension, myocardial infarction, chronic ischemic ventricular dysfunction, and valvular pathology.

In systemic vasculitis, unlike other RDs, vascular damage is a cardinal and pathognomonic sign of the disease. The cardiovascular manifestations of systemic vasculitis are based on immune inflammation of the structures of the heart and blood vessels, the development of systemic necrotizing vasculitis, including granulomatous, giant cell with the formation of aneurysmal protrusions (polyarteritis nodosa, Wegener's granulomatosis, Horton's disease), or destructive changes in the aortic arch system and its branches with their stenosis and ischemia of organs (Takayasu disease), or with the formation of granulomas and eosinophilic infiltrates mainly in the walls of the pulmonary vessels (Churg-Strauss syndrome).

Features of cardiovascular pathology in RD are as follows: multiple lesions coronary vessels; early relapses of ACS; increased mortality after the first MI; high frequency of “painless” ischemia and “asymptomatic” MI; connection with the activity of inflammation (increased ESR, CRP, extra-articular manifestations); low percentage of “critical” stenoses, high frequency of “vulnerable” plaques, pronounced signs of inflammation of the vascular wall;

Several possible causes and their relationships are discussed, leading to an increased risk of cardiovascular accidents against the background of accelerated atherosclerotic vascular damage in RD:

1) accumulation of classical cardiovascular risk factors;

2) general immunoinflammatory mechanisms underlying the pathogenesis of RB and atherosclerosis, which is currently considered as a probable “inflammatory” human disease;

3) side effects drug therapy (non-steroidal anti-inflammatory drugs (NSAIDs), glucocorticosteroids, basic anti-inflammatory drugs);

4) insufficient attention to the need to prevent cardiovascular complications in these diseases;

5) factors associated with the progression of RDs themselves.

Numerous studies have emphasized the important role of classical risk factors in the development of atherosclerosis in patients with RD. It has been proven that the determinants of atherosclerotic plaque and thickening of the intima-media complex according to ultrasound examination carotid arteries Patients with RA, SLE and SSc are age, gender, smoking, dyslipidemia, arterial hypertension, insulin resistance, overweight, sedentary lifestyle, family history of cardiovascular diseases. RA and SLE have been shown to be associated with insulin resistance and accumulation of visceral adipose tissue. Both conditions are components of the metabolic syndrome, which is currently considered to be a consequence of subclinical immune inflammation and is a risk factor for atherosclerosis in patients with RD.

Among traditional cardiovascular risk factors, smoking is of particular importance, predisposing to the development of not only CVD, but also seropositive RA, detected in patients before the clinical manifestation of arthritis, and is associated with more severe course RA. In RA, smoking correlates with the development of atherosclerotic lesions of the carotid arteries and the severity of coronary artery calcification. When studying the effect of smoking on the levels of pro-inflammatory cytokines, it was shown that in smoking men the concentration of IL 6 is higher than in non-smokers (9.6 ± 7.6 pg/ml versus 6.2 ± 6.6 pg/ml; p = 0.013). It can be assumed that smoking exerts atherogenic effects by influencing the vascular wall through proinflammatory signals associated with hyperproduction of IL 6. Systemic inflammation plays an important role in the development of disorders associated with the blood cholesterol transport system. It should be noted that in patients with RA several years before the clinical manifestation of the disease, there is an increase in the level of cholesterol (C), triglycerides (TG) and a decrease in the concentration of high-density lipoprotein cholesterol (HDL-C). With active RA disorders lipid spectrum blood are manifested in a decrease in the concentration of atherogenic lipids (C, TG) and anti-atherogenic lipoproteins (HDL-C) and are associated with an increase in inflammatory markers, primarily CRP and IL 6 .

Hyperhomocysteinemia, a potentially modifiable risk factor for atherosclerosis, has been established in patients with RA, SSc and SLE. Hyperhomocysteinemia is associated with thickening of the intima-media complex and increased level coronary calcium, and in patients with stable and unstable plaques, the concentration of homocysteine ​​is significantly different. A connection has been noted between hyperhomocysteinemia and the use of DMARDs with antifolate activity (methotrexate, sulfasalazine). When taking folic acid, normalization of homocysteine ​​levels in RA is observed.

Compared with healthy individuals, patients with RA and SLE have an increase in the concentration of hypercoagulability markers (fibrinogen, tissue plasminogen activator, tissue plasminogen activator inhibitor type 1, D-dimer and von Willebrand factor), which, according to epidemiological studies, are associated with increased risk cardiovascular complications.

Considering the common pathogenesis of atherosclerosis and RD, in recent years immunological markers of atherosclerosis in this category of patients have become the object of intensive research. Particular attention is paid to proteins of the acute phase of inflammation (C-reactive protein (CRP), serum amyloid protein A), indicators of immune activation ( pro-inflammatory cytokines, their soluble receptors), endothelial dysfunction (cellular adhesion molecules, von Willebrand factor), organ-nonspecific autoantibodies (antibodies to phospholipids and oxidized low-density lipoprotein) and immune complexes. Many of them, on the one hand, are “predictors” of cardiovascular disasters in the population, and on the other hand, they reflect the chronic autoimmune inflammatory process in RD or are its participants.

Data have been published on the independent pathogenetic significance of CRP in the processes of atherogenesis and atherothrombosis, an increase in the risk of cardiovascular accidents in healthy people and patients with coronary artery disease. A slight increase in CRP concentration reflects subclinical inflammation in the vascular wall associated with the atherosclerotic process. A series of studies have traced the relationship between atherosclerotic vascular lesions (thickening of the intima-media complex, the presence of atherosclerotic plaques according to vascular ultrasound) and the concentration of CRP in SLE and RA. There is evidence that in men with undifferentiated arthritis, an increase in the concentration of CRP to 5-15 mg/l is associated with an increase in cardiovascular mortality by 3.7 times (within 10 years), with a concentration of CRP > 16 mg/l by 4 times .

Several atherosclerosis-associated autoantigens have been identified, including oxygenated low-density lipoprotein (LDL), heat shock proteins, cardiolipin, and beta2-glycoprotein-1. The most pronounced atherogenic properties are those of oxygenated LDL, heat shock proteins 60/65, which induce a strong local immune response in the plaque. In addition, oxygenated LDL can stimulate apoptosis, which is involved in plaque destabilization processes. Studies have been conducted to study the levels of autoantibodies (to oxygenated LDL, heat shock proteins, cardiolipin, beta2-glycoprotein-1, cardiolipin) as factors in the progression of atherosclerosis in RA, SLE and SSc. An increase in the levels of autoantibodies and immune complexes in this category of patients compared to healthy patients has been proven, which was associated with preclinical manifestations of atherosclerosis according to ultrasound examination of the thickness of the intima-media complex in these patients.

There is no doubt about the role of endothelial dysfunction in the pathogenesis of atherosclerosis. Manifestations of endothelial dysfunction are associated with a lack of production or bioavailability of nitric oxide in the arterial wall, which provides vasodilation, inhibition of the expression of adhesion molecules, platelet aggregation, antiproliferative, antiapoptotic and antithrombotic effects. In atherosclerosis, the balance between humoral factors that have a potential protective effect (nitric oxide, endothelial hyperpolarizing factor, prostacyclin) and factors that damage the vessel wall (endothelin-1, thromboxane A2, superoxide anion) is disturbed. Some criteria for endothelial dysfunction may include: humoral factors associated with the activity of endothelial cells, such as endothelin-1, von Willebrand factor, E-selectin, intercellular adhesion molecules, vascular cell adhesion molecules and others. Endothelial dysfunction is detected in RA and SLE both at early and late stages of the disease, regardless of disease activity and the presence of cardiovascular risk factors. In patients with RA and SLE, there was an increase in the levels of intercellular adhesion molecules, vascular cell adhesion molecules, E-selectin, von Willebrand factor compared to healthy patients, which was significantly associated with the presence of atherosclerotic plaques in the vessels or signs of preclinical atherosclerosis. In patients with RA, a significant decrease in the elasticity of small and large vessels, increase in systemic vascular resistance compared to control.

The balance between pro-inflammatory and anti-inflammatory cytokines and other molecular inflammatory factors may be critical for the progression of atherosclerosis. The following are considered pro-inflammatory and, therefore, pro-atherogenic: CRP, E-selectin, endotoxin, tumor necrosis factor (TNF), interleukins (IL-1b, IL-6, IL-8, IL-12, IL-18), macrophage chemoattractant protein, leukotriene P4, lipoxygenase degradation products. Anti-inflammatory, or atheroprotective, are IL-4 and IL-10. Of the mediators of interleukocyte interaction, the greatest importance in atherosclerosis is given to IL-1, IL-6 and TNF. IL-1, IL-6 and TNF increase the adhesiveness of blood cells to the vascular endothelium and their procoagulant activity, increase the mobility of neutrophils, are a chemoattractant for a number of cells, promote the activation of cells at the site of inflammation, enhance their production of other cytokines, as well as prostaglandins, collagen synthesis and fibronectin, stimulate phagocytosis, generation of superoxide radicals, cause degranulation mast cells, determine the synthesis of proteins in the acute phase of inflammation. All this contributes to the development of exudative and proliferative components of the inflammatory response. TNF has the ability to induce apoptosis in cells, as well as stimulate the synthesis of metalloproteinases and proteolytic enzymes (tryptase and chymase). Many researchers have proven an increase in the levels of IL-1, IL-6 and TNF in patients with RA and SLE compared to the control group, and their increase was associated with the initial signs of the development of atherosclerotic vascular lesions in this category of patients. IL-6 plays a key role in the development of autoimmune inflammation and cardiovascular accidents.

Inflammatory cells infiltrating the plaque are involved in the degradation of the extracellular matrix through phagocytosis and secretion of proteolytic enzymes (plasminogen activators, matrix metalloproteinases), which can cause thinning of the fibrous coating and cause rupture of the atherosclerotic plaque. An increase in the levels of matrix metalloproteinases has been established in patients with RA compared to healthy patients, which indicates an increased risk of instability of atherosclerotic plaques in these patients.

Thus, this analysis allows us to draw the following conclusions:

1. RD – diseases with a proven high cardiovascular risk;

2. The combination of factors (traditional and disease-related) in patients with RD increases the risk of cardiovascular complications;

3. Systemic inflammation is the main risk factor for the development of cardiovascular complications in RD;

Bibliography

1. Ilyina A.E., Varfolameeva E.I., Volkov A.V. and others. The relationship between the thickness of the intima-media complex, risk factors for cardiovascular diseases and the level of CRP in patients with gout. Ter. Arch 2009;10:46-8.

2. Cardiology: National Guide / Ed. Yu.N. Belenkova, R.G. Oganova. – M.: EOTAR – Media, 2007. – 1232 p.

3. Nasonov E.L. The problem of atherothrombosis in rheumatology // Bulletin of the Russian Academy of Medical Sciences. – 2007. – No. 5. – P. 6 – 10.

4. Nasonov E.L. Immunological markers of atherosclerosis // Ter. Archive. – 2008. - No. 5. – 80 – 85.

5. Nasonov E.L., Popkova T.V. Cardiovascular problems of rheumatology. Scientific - practical rheumatol. 2004; 4:4–9.

6. Popkova T.V. Atherosclerotic vascular lesions in systemic lupus erythematosus and rheumatoid

7. Popkova T.V., Novikova D.S., Pisarev V.V. and others. Risk factors for cardiovascular diseases in rheumatoid arthritis. Scientific and practical Rev-matol. 2009; 3:4–11.

8. Rheumatology: national guidelines. Ed. E.L. Nasonova, V.A. Nasonova. M.: GEOTAR-Media, 2008.

10. Avalos I, Rho YH, Chung CP et al. Atherosclerosis in rheumatoid arthritis and systemic lupus erythematosus. Clin Exp Rheumatol 2008; 26 (Suppl. 51): 5–13.

11. Abou-Raya, A, Abou-Raya, S. Inflammation: a pivotal link between autoimmune diseases and atherosclerosis // Autoimmun Rev. 2006. Vol. 5. No. 5. P. 331 – 337.

12. Ahmad, Y, Shelmerdine, J, Bodill, H e.a. Subclinical atherosclerosis in systemic lupus erythematosus (SLE): the relative contribution of classic risk factors and the lupus phenotype // Rheumatology (Oxford). 2007. Vol. 46. ​​No. 6. P. 983 – 988.

13. Bassi, N, Ghirardello, A, Iaccarino, L e.a. OxLDL/beta(2)GPI-anti-oxLDL/beta(2)GPI complex and atherosclerosis in SLE patients // Autoimmun Rev. 2007. Vol. 7. No. 1. P. 52 – 58.

14. Blann, A.D., Lip, G.Y.H. The endothelium in atherothrombotic disease assessment of function, mechanisms and clinical implications // Blood Coagul. Fibrinolysis. 1998. No. 9. P. 297 – 306.

15. Carotti, M, Salaffi, F, Mangiacotti, M e.a. Atherosclerosis in rheumatoid arthritis: the role of high-resolution B

mode ultrasound in the measurement of the arterial intima-media thickness // Reumatismo. 2007. Vol. 59. No. 1. P. 38 – 49.

16. Chung, CP, Avalos, I, Raggi, P, Stein, CM. Atherosclerosis and inflammation: insights from rheumatoid arthritis // Clin Rheumatol. 2007. Vol. 26. No. 8. P. 1228 – 1233.

17. Colombo, BM, Murdaca, G, Caiti, M e.a. Intima-media thickness: a marker of accelerated atherosclerosis in women with systemic lupus erythematosus // Ann N Y Acad Sci. 2007. No. 1108. P. 121 – 126.

18. Chung C.P., Oeser A., ​​Solus J.F. et al. Inflammation-associated insulin resistance: differential effects in rheumatoid arthritis and systemic lupus erythematosis define potential mechanisms. Arthr Rheum 2008; 58(7):2105-12.

19. Dessein PH, Joffe BI, Veller MG et al. Traditional and nontraditional cardiovascular risk factors are associated with atherosclerosis in rheumatoid arthritis. J Rheumatol 2005; 32:435–42.

20. Dessein PH, Tobias M, Veller MG. Metabolic syndrome and subclinical atherosclerosis in rheumatoid arthritis. J Rheumatol 2006; 33:2425–32.

21. Dessein, P.H., Norton, G.R., Woodiwiss, A.J. e.a. Influence of nonclassical cardiovascular risk factors on the accuracy of predicting subclinical atherosclerosis in rheumatoid arthritis // Rheumatol. 2007. Vol. 34. No. 5. P. 943 – 591.

22. Edwards N.L. The role of hyperuricemia and gout in kidney and cardiovascular disease. Cleve Clin J Med 2008;75(Suppl. 5):S13–S16.

23. Frostegard, J. SLE, atherosclerosis and cardiovascular disease // J Intern Med. 2005. Vol. 257. No. 6. P. 485 – 495.

24. Grover, S, Sinha, RP, Singh, U e.a. Subclinical atherosclerosis in rheumatoid arthritis in India // J Rheumatol. 2006. Vol. 33. No. 2. P. 201 – 203.

25. Han C., Robinson D.W., Hackett M.V. et al. Cardiovascular disease and risk factors in patients with rheumatoid arthritis, psoriatic arthritis and ankylosing spondilitis // J. Rheumatol. – 2006. – N 33. – P. 2167 – 2172.

26. Hurlimann, D, Enseleit, F, Ruschitzka, F. Rheumatoid arthritis, inflammation, and atherosclerosis // Rheumatol.2004. Vol. 29. No. 8. P. 760 – 768.

27. Hoshi T., Kitagawa K., Yamagami H. et al. Relation between interleukin-6 level and subclinical intracranial large-artery atherosclerosis. Atherosclerosis 2008; 197(l): 326-32.

28. Kerekes, G. Effects of rituximab treatment on endothelial dysfunction, carotid atherosclerosis, and lipid profile in rheumatoid arthritis / G. Kerekes, P. Soltesz, H. Der // Clin Rheumatol, 2009.– 28.– P. 705– 10.

29. La Montagna, G, Cacciapuoti, F, Buono, R e.a. Insulin resistance is an independent risk factor for atherosclerosis in rheumatoid arthritis // Diab Vasc Dis Res. 2007. Vol. 4. No. 2. P. 130 – 135.

30. McMahon, M, Hahn, BH. Atherosclerosis and systemic lupus erythematosus-mechanistic basis of the association

// Curr Opin Immunol. 2007. Vol. 19. No. 6. P. 633 – 639.

31. Peterson MJ, Symmons DP, McCarrey DW et al. Cardiovascular risk management in patients with rheumatoid arthritis and other types of inflamematory arthritis – EULAR TASK ORCE “Cardiovascular risk management in RA”. Ann Rheum Dis 2008; 67 (suppl. II): 310.

32. Peterson MJ, Symmons PM, McCarey D et al. EULAR evidence-based recommendations for cardiovascular risk management in patients with rheumatoid arthritis and other forms of inflammatory arthritis. Ann Rheum Dis 2009; doi: 10.1136/ard.2009.113696.

33. Ross R. Atherosclerosis – an inflammatory disease // N. Engl. J. Med. – 2005. – N 340. – P. 115 – 126.

34. Roman, MJ, Crow, MK, Lockshin, MD e.a. Rate and determinants of progression of atherosclerosis in systemic lupus erythematosus // Arthritis Rheum. 2007. Vol. 56. No. 10. P. 3412 – 3419.

35. Woods A., Brull D.J., Humphries S.E., Montgomery H.E. Genetics of inflammation and risk of coronary artery disease: the central role of interleukin-6. Eur Heart J 2000; 21(19):1574-83.

Diseases of the cardiovascular system (CVD): review, manifestations, principles of treatment

Cardiovascular diseases (CVD) represent the most pressing problem of modern medicine, because mortality from pathologies of the heart and blood vessels has taken first place along with tumors. Millions of new cases are registered every year, and half of all deaths are associated with some form of circulatory system damage.

Pathology of the heart and blood vessels has not only a medical, but also a social aspect. In addition to the colossal government costs for diagnosing and treating these diseases, the level of disability remains high. This means that a sick person of working age will not be able to fulfill his duties, and the burden of his maintenance will fall on the budget and relatives.

In recent decades, there has been a significant “rejuvenation” of cardiovascular vascular pathology, which is no longer called a “disease of old age.” Increasingly, among patients there are people not only of mature age, but also of young age. According to some reports, among children the number of cases of acquired heart disease has increased up to ten times.

Mortality from cardiovascular diseases, according to the World Health Organization, reaches 31% of all deaths in the world; coronary disease and strokes account for more than half of the cases.

It has been noted that diseases of the cardiovascular system are much more common in countries with an insufficient level of socio-economic development. The reasons for this are the inaccessibility of high-quality medical care, insufficient equipment of medical institutions, shortage of personnel, lack of effective preventive work with the population, most of whom live below the poverty line.

We owe a lot to the spread of CVD modern image life, nutritional patterns, lack of exercise and bad habits, therefore today all kinds of preventive programs are being actively implemented aimed at informing the population about risk factors and ways to prevent pathology of the heart and blood vessels.

Cardiovascular pathology and its varieties

The group of diseases of the cardiovascular system is quite extensive, the list includes:

• – , ;
• ( , );
• Inflammatory and infectious lesions - rheumatic or other in nature;
• Vein diseases – , ;
• Pathology of peripheral blood flow.

Most of us associate CVD primarily with coronary heart disease. This is not surprising, because this pathology is the most common, affecting millions of people on the planet. Its manifestations in the form of angina pectoris, rhythm disturbances, and acute forms in the form of a heart attack are widespread among middle-aged and elderly people.

In addition to cardiac ischemia, there are other, no less dangerous and also quite common types of CVD - hypertension, which only the lazy have never heard of, strokes, peripheral vascular diseases.

In most diseases of the heart and blood vessels, the substrate of the lesion is atherosclerosis, which irreversibly changes the vascular walls and disrupts the normal movement of blood to the organs. – severe damage to the walls of blood vessels, but it appears extremely rarely in the diagnosis. This is due to the fact that clinically it is usually expressed in the form of cardiac ischemia, encephalopathy, cerebral infarction, damage to the blood vessels of the legs, etc., therefore these diseases are considered the main ones.

Coronary heart disease (CHD) is a condition when the coronary arteries, altered by atherosclerosis, deliver an insufficient volume of blood to the heart muscle to ensure exchange. The myocardium experiences a lack of oxygen, hypoxia occurs, followed by -. The response to poor circulation is pain, and structural changes begin in the heart itself - connective tissue grows (), cavities expand.

factors for the development of ischemic heart disease

The extreme degree of lack of nutrition of the heart muscle results in heart attack– myocardial necrosis, which is one of the most severe and dangerous types of coronary artery disease. Men are more susceptible to myocardial infarction, but in old age the gender differences gradually disappear.

Arterial hypertension can be considered an equally dangerous form of damage to the circulatory system.. It is common among people of both sexes and is diagnosed from the age of 35-40. Increased blood pressure contributes to persistent and irreversible changes in the walls of arteries and arterioles, as a result of which they become inextensible and fragile. Stroke is a direct consequence of hypertension and one of the most severe pathologies with a high mortality rate.

High blood pressure also affects the heart: it increases, its walls thicken due to increased load, and the blood flow in the coronary vessels remains at the same level, therefore, with a hypertensive heart, the likelihood of coronary artery disease, including myocardial infarction, increases many times over.

Cerebrovascular pathology includes acute and chronic forms of circulatory disorders in the brain. It is clear that an acute stroke in the form of a stroke is extremely dangerous, since it makes the patient disabled or leads to his death, but chronic variants of damage to the cerebral vessels also cause many problems.

typical development ischemic disorders brain due to atherosclerosis

Encephalopathy against the background of hypertension, atherosclerosis or their simultaneous influence causes disruption of brain function, it becomes increasingly difficult for patients to perform work duties, with the progression of encephalopathy difficulties appear in everyday life, and the extreme degree of the disease is when the patient is incapable of independent existence.

Listed above diseases of the cardiovascular system are so often combined in the same patient and aggravate each other, that it is often difficult to draw a clear line between them. For example, a patient suffers from high blood pressure, complains of heart pain, has already suffered a stroke, and the reason for everything is atherosclerosis of the arteries, stress, and lifestyle. In this case, it is difficult to judge which pathology was primary; most likely, the lesions developed in parallel in different organs.

Inflammatory processes in the heart() – myocarditis, endocarditis, pericarditis – are much less common than the previous forms. Their most common cause is when the body reacts in a unique way to a streptococcal infection, attacking not only the microbe, but also its own structures with protective proteins. Rheumatic heart disease is the lot of children and adolescents; adults usually have a consequence - heart disease.

Heart defects can be congenital or acquired. Acquired defects develop against the background of the same atherosclerosis, when the valve leaflets accumulate fatty plaques, calcium salts, and become sclerotic. Another cause of acquired defect may be rheumatic endocarditis.

When the valve leaflets are damaged, both narrowing of the opening () and expansion () are possible. In both cases, circulatory disturbance occurs in the small or large circle. Stagnation in the systemic circle is manifested by typical symptoms of chronic heart failure, and with the accumulation of blood in the lungs, the first sign will be shortness of breath.

the valvular apparatus of the heart is a “target” for carditis and rheumatism, the main cause of acquired heart defects in adults

Most heart lesions ultimately result in heart failure, which can be acute or chronic. Acute heart failure possible against the background of a heart attack, hypertensive crisis, severe arrhythmia and is manifested by pulmonary edema, acute in the internal organs, cardiac arrest.

Chronic heart failure also referred to as forms of ischemic heart disease. It complicates angina pectoris, cardiosclerosis, previous myocardial necrosis, long-term arrhythmias, heart defects, dystrophic and inflammatory changes in the myocardium. Any form of cardiovascular pathology can result in heart failure.

Signs of heart failure are stereotypical: patients develop edema, the liver becomes enlarged, the skin becomes pale or bluish, shortness of breath is tormented, and fluid accumulates in the cavities. Both acute and chronic forms of heart failure can cause the death of the patient.

Vein pathology in the form of varicose veins, thrombosis, phlebitis, thrombophlebitis, it occurs both among elderly and young people. Largely spread varicose veins contributes to the lifestyle of a modern person (nutrition, physical inactivity, excess weight).

Varicose veins usually affect the lower extremities when the subcutaneous or deep veins legs or thighs, but this phenomenon is also possible in other vessels - the veins of the small pelvis (especially in women), the portal system of the liver.

A special group of vascular pathologies consists of congenital anomalies, such as aneurysms and malformations.- this is a local expansion of the vascular wall, which can form in the vessels of the brain and internal organs. In the aorta, an aneurysm is often atherosclerotic in nature, and dissection of the affected area is extremely dangerous due to the risk of rupture and sudden death.

C, when the developmental disorder occurred vascular walls Neurologists and neurosurgeons are faced with the formation of abnormal weaves and tangles, since these changes pose the greatest danger when located in the brain.

Symptoms and signs of cardiovascular disease

Having very briefly touched upon the main types of pathology of the cardiovascular system, it is worth paying a little attention to the symptoms of these ailments. The most common complaints are:

1. Discomfort in the chest, heart palpitations;

Pain is the main symptom of most heart diseases. It accompanies angina pectoris, heart attack, arrhythmias, and hypertensive crises. Even slight discomfort in the chest or short-term intense pain should be a cause for concern and in case of acute, “dagger” pain, you need to urgently seek qualified help.

In coronary heart disease, pain is associated with oxygen starvation of the myocardium due to atherosclerotic damage to the heart vessels. Stable angina occurs with pain in response to exercise or stress; the patient takes nitroglycerin, which eliminates the pain attack. Unstable angina pectoris is manifested by pain at rest, medications do not always help, and the risk of a heart attack or severe arrhythmia increases, so pain that arises on its own in a patient with cardiac ischemia is the basis for seeking help from specialists.

Acute, severe pain in the chest, radiating to the left arm, under the shoulder blade, or into the shoulder, may indicate a myocardial infarction. P Taking nitroglycerin does not eliminate it, and symptoms include shortness of breath, rhythm disturbances, a feeling of fear of death, and severe anxiety.

Most patients with pathology of the heart and blood vessels experience weakness and get tired quickly. This is due to insufficient oxygen supply to tissues. As chronic heart failure increases, resistance to physical activity sharply decreases; it is difficult for the patient to walk even a short distance or climb a couple of floors.

symptoms of advanced heart failure

Almost all cardiac patients experience shortness of breath. It is especially characteristic of heart failure with damage to the heart valves. Defects, both congenital and acquired, can be accompanied by stagnation of blood in the pulmonary circulation, resulting in difficulty breathing. A dangerous complication of such heart damage can be pulmonary edema, requiring immediate medical attention.

Edema accompanies congestive heart failure. First, they appear in the evening on the lower extremities, then the patient notes their spread upward, the hands and tissues begin to swell abdominal wall, face. In severe heart failure, fluid accumulates in the cavities - the abdomen increases in volume, shortness of breath and a feeling of heaviness in the chest intensify.

Arrhythmias can manifest as a feeling strong heartbeat or freezing. Bradycardia, when the pulse slows down, contributes to fainting, headaches, and dizziness. Rhythm changes are more pronounced during physical activity, anxiety, after a heavy meal and drinking alcohol.

Cerebrovascular diseases with damage brain vessels, manifested by headaches, dizziness, changes in memory, attention, and intellectual performance. Against the background of hypertensive crises, in addition to headaches, palpitations, flickering “spots” before the eyes, and noise in the head are disturbing.

An acute circulatory disorder in the brain - a stroke - is manifested not only by pain in the head, but also by a variety of neurological symptoms. The patient may lose consciousness, paresis and paralysis develop, sensitivity is impaired, etc.

Treatment of cardiovascular diseases

Cardiologists, therapists, and vascular surgeons treat cardiovascular diseases. Conservative therapy prescribed by the clinic doctor, and if necessary, the patient is sent to the hospital. It's also possible surgery certain types of pathology.

The basic principles of therapy for cardiac patients are:

• Normalization of the regime, excluding excessive physical and emotional stress;
• A diet aimed at correcting lipid metabolism, because atherosclerosis is the main mechanism of many diseases; in case of congestive heart failure, fluid intake is limited, in case of hypertension - salt, etc.;
• Giving up bad habits and physical activity - the heart must carry out the load it needs, otherwise the muscle will suffer even more from “underutilization”, so cardiologists recommend walking and feasible exercises even for those patients who have had a heart attack or heart surgery;
, indicated for severe defects, cardiomyopathies, myocardial dystrophies.

Diagnosis and treatment of pathology of the heart and blood vessels are always very expensive activities, and chronic forms require lifelong therapy and observation, therefore it is an important part of the work of cardiologists. To reduce the number of patients with pathology of the heart and blood vessels, early diagnosis of changes in these organs and their timely treatment by doctors in most countries of the world, preventive work is actively carried out.

It is necessary to inform as many people as possible about the role healthy image life and nutrition, movements in maintaining the health of the cardiovascular system. With the active participation of the World Health Organization, various programs are being implemented aimed at reducing morbidity and mortality from this pathology.

Malyarov Sergey Aleksandrovich - Candidate of Medical Sciences, Associate Professor of the Department of Child, Social and Forensic Psychotherapy of NMAPE named after. P.L. Shupika, head of the Center for Psychosomatics and Depression, Universal Clinic “Oberig”, Kyiv

Depressive disorders and cardiovascular diseases are interdependent conditions. Depression is caused by a certain lifestyle and the presence of psychological factors leading to the development of cardiovascular disorders, and is the most important indicator of an unfavorable prognosis of a somatic disorder (Frasure-Smith N. et al., 1995).

In depressed patients, the risk of sudden death due to a cardiovascular accident is much higher than in the general population, and is greatest in the presence of concomitant cardiovascular diseases (Wilson A.C., Kostis J.B., 1992). At the same time, full-blown depressive states are noted much more often in such patients. In the mid-80s of the XX century. Data have been published that in 20–25% of patients with pathological changes in the coronary vessels, confirmed by coronary angiography, signs of depression were determined, sufficient for the diagnosis of an affective disorder. Almost 45% of patients who suffered a myocardial infarction also had a comorbid depressive disorder in the period from 3–4 days to 4 months after the cardiovascular accident.

The prevalence of depression in the general population is 5–30%, in general medical practice - 20–50%. This disease accounts for 20–25% of all mental disorders. Depression is diagnosed in about 35% of somatic patients in a hospital setting, it is detected in 33–42% of oncology patients, in 45–47% of patients during the first 2 weeks after a stroke, in 45% during the first few days after myocardial infarction , in 35% - within 3–4 months after myocardial infarction.

Currently, cardiovascular pathology ranks 1st in terms of morbidity and mortality, and, according to the World Health Organization and the World Bank, by 2020 depression will take 2nd place. It is estimated that currently up to 25% of people in developed countries of the world suffer from emotional disorders and up to 75% will experience them throughout their lives. The high prevalence of these conditions suggests a significant number of patients with a combination of coronary heart disease and depression, but the statistical probability of such a coincidence today looks too simple. There is ample evidence that the interaction of these disorders potentiates the severity of each of them. Thus, mortality within 1 year after myocardial infarction in patients with comorbid depression is 2–3 times higher than in post-infarction patients without depressive symptoms (Carney R.M. et al., 2001).

Today, it is difficult to surprise health care specialists with such statistics. However, professional awareness and the desire to draw special attention to this problem still have little impact on everyday practice. The most important negative point is the cultural aspect of the “false psychologization” of a person’s condition after a cardiovascular accident. It is a generally accepted psychologically understandable assumption that patients with severe cardiovascular pathology cannot help but be depressed.

The greatest practical difficulty lies in the timely appointment simultaneous treatment in the presence of both diseases. After all, depressed patients, due to the psychopathological specificity of their condition, recognize and respond to acute cardiac symptoms in the post-infarction period much later. For the same reason, depressed patients show little initiative in complying with the recommended cardiac rehabilitation regimen.

In addition to psychopathological and behavioral aspects, there are also direct biological factors that worsen the prognosis of combined disorders. In patients with cardiac pathology, an increased metabolism of catecholamines (adrenaline, norepinephrine) is noted. In patients with reduced left ventricular function, changes in the level of endogenous neurotransmitters can provoke cardiac arrhythmia. In depression, there is also an increase in norepinephrine metabolism. The resulting synergistic effect may cause an increased risk of sudden coronary death. In the work of R.M. Carney et al (1993) showed that prolonged attacks of tachycardia occurred more often in depressed patients undergoing cardiac catheterization due to cardiovascular pathology than in patients without concomitant affective pathology.

Changes in heart rate are the most important prognostic indicator both in depression and in the state after acute myocardial infarction. In patients with comorbid post-infarction condition and depressive disorder instability of heart rate is more pronounced, which is the most important indicator of an unfavorable prognosis in patients in the post-infarction period. Actually, antidepressant therapy in patients with cardiovascular pathology leads to normalization of parasympathetic tone, which can be regarded as a cardioprotective effect.

Platelets play a key role in the pathogenesis of acute coronary syndrome, and the use of antiplatelet drugs is the core of therapy. D.L. Musselman et al (1996), conducting cytometry, showed that in patients with depression the level of activity of glycoprotein receptors IIb/IIIa is significantly increased. The use of modern serotonergic antidepressants in the treatment of emotional disorders reduces the level of platelet activity to normal indicators even before the appearance of clinical positive dynamics of depressive symptoms.

It is known that the reaction to stress can provoke ischemia and/or acute arrhythmia, and in patients with depression the reaction to stress is significantly distorted (inadequate to the strength of the stimulus). The stress response manifests itself in α-adrenergic stimulation, which leads to contraction of the vascular wall and an increase in blood pressure. A prolonged and inappropriate stress reaction primarily causes pathological changes microcirculation in the heart muscle. It is believed that psychological stress is greater than acute physical exercise, affects the functioning of the heart muscle and contributes to the onset of inflammatory changes in small vessels. Pathophysiologically, depression can be both a cause and a consequence of chronic inflammatory processes observed in cardiovascular pathology. Depression is associated with an increase in markers of subacute inflammation (C-reactive protein, interleukin-6, tumor necrosis factor-α and redistribution of B and T cells), which, in turn, may contribute to the progression of cardiovascular disorders.

Identifying depressive symptoms in patients with cardiovascular pathology can present certain difficulties due to the fact that typical depressive symptoms(decreased energy, asthenia, sleep disturbance, loss of interest and satisfaction from usual activities) are regarded as common and understandable consequences of severe cardiovascular pathology.

Symptoms are “recognized” as qualitatively and quantitatively corresponding to the affective symptom complex, and are not “recognized” as psychologically ordinary and understandable for the condition of a seriously somatic patient. Key points are the patient’s complaints of a feeling of constant fatigue, inability to relax, a large number of vague somatic complaints, anxious alertness, irritability or hypersensitivity. The patient does not talk about depression only because he is not asked about it.

The main symptoms of depression include:

• decreased mood;
• the patient's loss of interest and lack of satisfaction in all or almost all types of daily activities;
• a sharp decrease in energy (psychological and physical tone), which is accompanied by increased fatigue (asthenia, weakness, exhaustion) and decreased activity.

Other symptoms of depression include:

• decreased ability to concentrate and pay attention, self-esteem and loss of self-confidence;
• ideas of blame and self-destruction, self-harm or suicide;
• pessimistic and gloomy vision of the future;
• sleep disorders, appetite.

It is considered clinically important to identify somatoaffective or vital symptoms that accompany a decrease in the level of activity of a depressive patient. These include decreased interest and satisfaction from usual activities, lack of response to events or activities that normally cause it, early morning awakening (≥2 hours before usual time), worsening in the morning, objective signs of psychomotor retardation or agitation (objectively recorded by a doctor or described by others), noticeable decreased appetite, decreased body weight (an objective criterion is considered to be a loss of 5% of total body weight), a stable and pronounced decrease in sexual needs.

One of the world's leading psychiatric publications published the results of a study that differentiated the prognostic significance of individual clusters of affective symptoms in patients with cardiovascular disorders. The authors emphasize that somatoaffective symptoms in the practice of an internist are almost always considered as naturally inherent in the somatic state of the patient in the post-infarction period. The focus of antidepressant therapy on the rapid reduction of these particular symptoms dramatically improved the prognosis in such patients (de Jonge P. et al., 2006).

In practice, the evidence of the independent existence of a comorbid depressive state in a patient is confirmed by the presence of affective symptoms for most of the day for >2 weeks and their effect on a decrease in daily activity. The key elements of the patient’s condition, which the practitioner should pay attention to, are not just sadness and loss of interest, but the patient’s reports of loss of control over himself and over many aspects of his personal life, a description of anxiety (a feeling of constant tension at the slightest excitement, various changeable, uncertain vegetative and painful sensations), signs of irritability (hot temper and negativism at the slightest provocation, intolerance to noise or bright light), complaints of constant fatigue and exhaustion. In addition, the doctor should discuss with the patient the high likelihood of developing depression against the background of cardiovascular pathology, which will further prevent the patient from being unwilling to discuss symptoms and possible therapeutic intervention in this regard.

The problem of anxiety in patients with cardiovascular pathology also deserves special attention. Thus, at present it is difficult to say that in patients with more severe depressive states the severity of cardiopathology is also more pronounced, however, it can be said that severe and prolonged anxiety disorders lead to more severe disorders of the cardiovascular system.

In primary medical practice over the past decades, a risk assessment procedure has become standard. cardiovascular disorders and its decline in people over 40 years of age. Thus, preventive intervention is suggested in the presence of signs of arterial hypertension, increased cholesterol levels, overweight bodies. It is necessary that regular screening for possible manifestations of depression and anxiety is also incorporated into this model. It is especially important to assess the presence of symptoms in the period after a vascular accident.

The topic of monitoring indicators of the cardiovascular system in patients with affective pathology deserves a separate discussion.

It can be argued that, despite the obvious significance of the problem under discussion, the diagnosis of affective disorders in cardiological practice exists rather as an exception. This is largely due to the erroneous understanding of internists about the complexity and unsafety of using psychotropic drugs in somatically weakened patients.

The decision about when and how to treat patients with depressive and anxiety disorders is determined not on the basis of contrasting the severity of the physical condition, but through a careful assessment of factors such as the severity and duration of the current affective episode, a history of depression, impairments in daily functioning, the quality of microsocial support at the moment, perceived traumatic influence and stress response. The presence of symptoms for >2 weeks is sufficient to establish a diagnosis. Subthreshold depressive symptoms may spontaneously improve within the first 2–4 weeks; in this case, psychological support is sufficient. Selection criterion therapeutic intervention It is not the number of symptoms, but the disruption of everyday functioning, including household and hygienic functions. The most important auxiliary tool can be a standardized self-assessment of the patient - screening tools.

Choice of drug therapy for depressed state in cardiological practice should primarily be determined by an assessment of the possible effect on the state of the cardiovascular system. Medications that have the potential to increase or destabilize heart rate should be avoided.

Despite all the recommendations about caution in the use of psychotropic drugs in somatic practice, standard tricyclic antidepressants are still widely prescribed by internists. Representatives of the first generation of this class of drugs (for example, amitriptyline) have a number of effects on the function of the cardiovascular system. All drugs in this group can cause cardiac conduction disturbances, and orthostatic arterial hypotension detected in the first weeks of their use appears to be especially dangerous in elderly patients. According to working group The Cardiac Arrhythmia Suppression Trial, the use of tricyclic antidepressants increases the risk of mortality in cardiac patients, primarily in patients with coronary heart disease (Lespérance F., Frasure-Smith N., 2000). Most tricyclic antidepressants cause an increase in heart rate in patients with cardiovascular pathology, and in young patients they cause more pronounced instability of heart rhythm than in older people. All this casts doubt on the possibility of their use in cardiological practice.

Most second generation antidepressants have a favorable action profile on cardiovascular system. Greatest evidence base about them positive application in somatic patients has been accumulated for selective serotonin reuptake inhibitors (SSRIs). It has been proven that the latter do not have direct action on heart rate, do not affect blood pressure, do not change cardiac conduction. A number of large-scale studies have found that the use of SSRIs in patients who have suffered a myocardial infarction is associated with a decrease in the incidence of recurrent acute cardiovascular events and, accordingly, with a decrease in mortality. If a doctor has such safe means in his arsenal that can significantly improve the quality of rehabilitation in the post-infarction period, there is every reason to treat depression in patients with cardiovascular pathology.

Dual-spectrum (serotonin-noradrenergic) antidepressants have not been studied in the treatment of cardiac patients, but their ability to sharply increase adrenergic tone requires, at a minimum, caution.

Most tranquilizers, including benzodiazepines (for example, gidazepam, phenazepam) and other sedative-hypnotic drugs, do not have antidepressant activity, but, on the contrary, exhibit depressogenic properties. Therefore, their use should be short-term, if necessary, to correct individual symptoms of anxiety. In all cases of a combination of anxiety and depression, the use of SSRI antidepressants is indicated.

Low-potency neuroleptics (thioridazine, sulpiride), popular among doctors, do not exhibit antidepressant activity, but aggravate the lack of initiative and asthenia in somatic patients. Thioridazine, according to international and domestic standards, is not recommended as a first-choice drug in the treatment of patients with mental disorders due to high cardiotoxicity - conduction disturbances and the risk of a sharp increase in the interval Q–Tc.

There is a problem for the serotonergic group of antidepressants drug interactions, since they are selective inhibitors of certain enzymes of the cytochrome P450 system. You should be careful when prescribing such powerful inhibitors of these enzymes as paroxetine or fluoxetine in combination with warfarin, class 1C antiarrhythmic drugs, beta-adrenergic receptor blockers (Greenblatt D.J. et al., 1998).

Antidepressants of this group, such as escitalopram and citalopram, have a slight effect on the activity of cytochrome enzymes. Therefore, practically no cases of drug interactions have been described for escitalopram, which, under conditions complex therapy makes his choice preferable.

Generally drug therapy for affective disorders in somatic patients includes 2 stages:

• active therapy for 2–4 months, allowing for rapid relief of depressive symptoms and restoration of functioning;
• stabilizing therapy for up to 12 months in patients with newly diagnosed depression, aimed at maintaining functioning and preventing possible exacerbation.

List of used literature

• Carney R.M., Blumenthal J.A., Stein P.K. et al.(2001) Depression, heart rate variability, and acute myocardial infarction. Circulation, 104(17): 2024–2028.
• Carney R.M., Freedland K.E., Rich M.W. et al.(1993) Ventricular tachycardia and psychiatric depression in patients with coronary artery disease. Am. J. Med., 95(1): 23–28.
• de Jonge P., Ormel J., van den Brink R.H. et al.(2006) Symptom dimensions of depression following myocardial infarction and their relationship with somatic health status and cardiovascular prognosis. Am. J Psychiatry 163(1): 138–144.
• Frasure-Smith N., Lespérance F., Talajic M.(1995) Depression and 18-month prognosis after myocardial infarction. Circulation, 91(4): 999–1005.
• Greenblatt D.J., von Moltke L.L., Harmatz J.S., Shader R.I.(1998) Drug interactions with newer antidepressants: role of human cytochromes P450. J. Clin. Psychiatry, 59 Suppl., 15: 19–27.
• Lespérance F., Frasure-Smith N.(2000) Depression in patients with cardiac disease: a practical review. J. Psychosom. Res., 48(4–5): 379–391.
• Musselman D.L., Tomer A., ​​Manatunga A.K. et al.(1996) Exaggerated platelet reactivity in major depression. Am. J Psychiatry 153(10): 1313–1317.
• Wilson A.C., Kostis J.B.(1992) The prognostic significance of very low frequency ventricular ectopic activity in survivors of acute myocardial infarction. BHAT Study Group. Chest, 102(3): 732–736.