Interdependence of cardiovascular pathology and affective disorders. Cardiovascular pathology in rheumatic diseases

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(SSD), systemic lupus erythematosus (SLE), antiphospholipid syndrome (APS), 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 outcomes with lymphogranulomatosis and widespread 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 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 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 of the 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 of the carotid arteries of patients with RA, SLE and SSc are age, gender, smoking, dyslipidemia, arterial hypertension, insulin resistance, overweight, sedentary lifestyle life, family history of cardiovascular diseases. RA and SLE have been shown to be associated with insulin resistance and accumulation of visceral adipose tissue. Both states are components metabolic syndrome, which is currently considered as 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 associated with a more severe course of 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). In active RA, disturbances in the lipid spectrum of the blood manifest themselves in a decrease in the concentration of atherogenic lipids (cholesterol, triglycerides) and antiatherogenic lipoproteins (HDL) 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 coronary calcium levels, and homocysteine concentrations are significantly different in patients with stable and unstable plaques. A connection has been noted between hyperhomocysteinemia and the use of DMARDs with antifolate activity (methotrexate, sulfasalazine). Against the background of the reception folic acid normalization of homocysteine levels is observed in RA.

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 last years Immunological markers of atherosclerosis in this category of patients are becoming 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), proteins heat shock, cardiolipin, 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 early and late. late stages 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 and an increase in systemic vascular resistance are observed compared to controls.

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 highest value in atherosclerosis, IL-1, IL-6 and TNF are imparted. 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, the generation of superoxide radicals, cause degranulation of mast cells, and 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. Key role IL 6 belongs to 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;

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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 is not only medical, but also 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 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.

The spread of CVD is largely due to our modern lifestyle, diet, lack of exercise and bad habits, so 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 include angina pectoris, arrhythmias, sharp 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.

No less dangerous form damage to the circulatory system can be considered arterial hypertension. 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 high rate mortality.

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 of ischemic brain disorders 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 high 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. Most common cause they become 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 lesions 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 big circle. Stagnation in a large circle manifests itself typical symptoms chronic heart failure, and when blood accumulates 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, skin they become pale or cyanotic, suffer from shortness of breath, 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. In many ways, lifestyle contributes to the spread of varicose veins. modern man(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:

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, not 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 myocardium due to atherosclerotic lesions of the cardiac 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 left hand, under the shoulder blade, in the shoulder may indicate 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 Such heart damage may cause 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 arms, tissues of the abdominal wall, and face begin to swell. 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 to cerebral vessels, manifested by headaches, dizziness, changes in memory, attention, and intellectual performance. On the background hypertensive crises In addition to the headache, the heart palpitations, the flickering of “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 individual species 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.;

Quitting 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 much as possible more people about the role of a healthy lifestyle 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.

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. At risk in in this case the probability of developing the disease, its complications and death from this disease is understood. 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 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 recognize living in the countries of the former USSR 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, to the high-risk group according to the latest European recommendations also include patients with established CVD, peripheral arterial disease or cerebral atherosclerosis; 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.

This is an elevated level C-reactive protein(determined by quantitative methods), homocysteinemia, brain natriuretic peptide level, 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 of the highest category, Ph.D.
head Antihypertensive center of Darnitsky district, Kyiv

Literature

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.

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.

Cardiovascular disease risk factors. Canadian Medical Association // Supplement to CMAJ 2000; 162 (9 Suppl).

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.

European guidelines on cardiovascular disease prevention in clinical practice: executive summary. // European Journal of Cardiovascular Prevention. - 2007. - Vol. 14. - (Supp. 2) - P. 1-40.

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

Hobbs F.D.R. Guidelines and management of global risk: the European perspective. // European Heart Journal Supplements (2004) 6 (Supplement C), C5-C14.

Prevention of Cardiovascular Disease. Guidelines for assessment and management of cardiovascular risk. / World Health Organization. - 2007. - 97 R.

Cardiovascular diseases are among the most dangerous pathologies, which kill tens of thousands of people around the world every year. Despite the great diversity of heart diseases, many of their symptoms are similar to each other, which is why it often becomes quite difficult to make an accurate diagnosis when a patient first contacts a therapist or cardiologist.

In recent years, CVS pathologies are increasingly affecting young people, for which there are reasons. In order to promptly identify deviations, you need to know about the risk factors for developing heart disease and be able to recognize their symptoms.

The causes of the development of cardiovascular diseases can be associated both with pathologies occurring in the human body and with the influence of certain factors. Thus, patients who are most susceptible to such diseases are:

suffer from hypercholesterolemia;

have a genetic predisposition to cardiovascular diseases;

abuse alcohol;

suffer from CFS.

In addition, the risk group includes:

diabetics;

patients suffering from obesity;

people leading a sedentary lifestyle;

persons with a family history.

The development of cardiovascular pathologies is directly influenced by stress and overwork. People who smoke are also susceptible to disruptions in the functioning of the cardiovascular system.

Types of diseases

Among all existing heart diseases, the leading ones are occupied by:

IHD, accompanied coronary insufficiency. It often develops against the background of vascular atherosclerosis, spasm or thrombosis.

Inflammatory pathologies.

Non-inflammatory diseases.

Congenital and acquired heart defects.

Cardiac arrhythmias.

The list of the most common CVD diseases includes:

angina pectoris;

myocardial infarction;

rheumatic heart disease;

myocardiostrophy;

myocarditis;

atherosclerosis;

strokes;

Raynaud's syndrome;

arteritis;

embolism of cerebral vessels;

phlebeurysm;

thrombosis;

thrombophlebitis;

mitral valve prolapse;

endocarditis;

aneurysm;

arterial hypertension;

hypotension.

Diseases of the heart and blood vessels often occur against each other. This combination of pathologies significantly aggravates the patient’s condition, reducing his quality of life.

Important! Cardiovascular diseases must be treated. In the absence of proper assistance, the risk of target organ damage increases, which can lead to serious complications, including disability and even death!

Heart damage due to kidney disease

Pathologies of the cardiovascular system and kidneys have the same risk factors that contribute to their development. Obesity, diabetes, genetics - all this may well cause disruption of the functioning of these organs.

CVD can be a consequence of kidney disease, and vice versa. That is, between them there is a so-called “ Feedback" This means that for people with heart disease, the risk of kidney damage increases significantly. This combination of pathological processes leads to extremely severe consequences, including the death of the patient.

In addition, when the functioning of the cardiovascular system and kidneys is impaired, non-traditional renal factors come into force.

These include:

overhydration;

anemia;

failure in the exchange of calcium and phosphorus;

systemic inflammatory diseases;

hypercoagulability.

Numerous studies have shown that even minor dysfunction paired organ may cause damage to the cardiovascular system. This condition is called cardiorenal syndrome, and can have serious consequences.

In many cases, patients who have been diagnosed with chronic renal failure suffer from cardiac pathologies. This is a disease that is accompanied by a violation of the filtration function of the renal glomeruli.

In most cases, this disease leads to the development of secondary arterial hypertension. It, in turn, causes damage to target organs, and, above all, the heart suffers.

Important! Heart attack and stroke are the most common consequences of this pathological process. The progression of CKD leads to a rapid transition of arterial hypertension to next stage development with all the complications accompanying this pathological process.

Symptoms of CVD

Impaired heart muscle function or blood vessels causes the development of circulatory failure. This deviation is accompanied by both cardiac and vascular failure (HF).

Chronic manifestations of HF are accompanied by:

decreased blood pressure;

constant weakness;

attacks of dizziness;

cephalgia of varying intensity;

chest pain;

pre-fainting states.

Heart pathologies accompanied by such symptoms manifest themselves less clearly than vascular diseases. Thus, acute vascular insufficiency leads to the development of:

collapse;

state of shock;

syncope.

The pathological conditions described above are extremely difficult for patients to tolerate. Therefore, you should not underestimate the danger of CVD, and when the first signs of their development appear, you should contact a specialist and undergo a comprehensive examination.

In fact, the symptoms of CVD are quite diverse, so it is extremely problematic to consider them comprehensively. However, there are a number of signs that are the most common in pathological lesions of the heart muscle and blood vessels.

To non-specific clinical manifestations Cardiovascular pathologies include:

Important! If such pain makes itself felt even when the person is at rest, you should immediately consult a doctor. Such a deviation may be evidence of an impending heart attack!

In addition to the above symptoms, many CVDs are characterized by the occurrence of:

rapid heartbeat;

shortness of breath, which can sometimes develop into poisoning - attacks of suffocation;

stabbing pain in the heart;

motion sickness in transport;

fainting in a stuffy room or in hot weather.

Many of the symptoms described above are characteristic of overwork - mental or physical. Based on this, most patients decide to “wait it out” and do not seek help from a doctor. But in this case, time is not best medicine, since postponing a visit to a specialist threatens not only the health, but also the life of the patient!

CVD in children and adolescents

Damage to the heart and blood vessels is not exclusively an “adult” problem. Often such diseases are diagnosed in children, and they include:

Congenital. This group of cardiovascular pathologies includes malformations of large blood vessels and heart muscle. As a rule, such pathologies are diagnosed during the period of intrauterine development of the fetus, or during the first few months of a newborn’s life. Often these diseases can only be cured by surgery.

Acquired. Such diseases can develop at any period of a child’s life. Their occurrence can be provoked by childhood infectious diseases, or by pathologies suffered by a woman during pregnancy.

The most common diseases of the cardiovascular system, occurring in children of primary and school age, include arrhythmia, heart disease and vascular disease.

Adolescents require special attention from parents because, due to changes in their hormonal levels, the risk of developing heart and vascular diseases is especially high.

Thus, most often children in puberty suffer from mitral valve prolapse and neurocirculatory dystonia (VSD). Each of these pathological conditions requires mandatory seeking medical help.

Often such deviations are not separate pathologies, but indicate the development of other, more serious and dangerous diseases in the body. In this case, the period of puberty, which already exposes the body of adolescents to severe stress, can cause the development of severe cardiovascular diseases.

Cardiovascular diseases are one of the most common groups of pathological processes, accompanied by a high percentage of population mortality. Their dangerous consequences can only be prevented if a person is attentive to his health.

People who have a genetic predisposition to CVD or are at risk should be extremely careful. The best option for them is to undergo preventive examinations with a cardiologist and therapist every 6-12 months with all the necessary diagnostic procedures (ECG, Holter BP, Holter CG, etc.).

As you know, any disease is easier to prevent, and all medical specialists, without exception, emphasize this!

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 administration of 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 inadequate stress reaction primarily causes pathological changes in microcirculation in the heart muscle. It is believed that psychological stress, to a greater extent than sudden physical exertion, affects the functioning of the heart muscle and contributes to the onset of inflammatory changes in the heart muscle. 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. The 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 in usual activities, lack of response to events or activities that normally cause it, early morning awakening (≥2 hours before usual time), deterioration in the morning, objective signs of psychomotor retardation or agitation ( objectively recorded by a doctor or described by others), a noticeable decrease in appetite, a decrease in 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 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 (temper and negativity 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, it has become a standard procedure for assessing the risk of cardiovascular disorders and reducing it in people over the age of 40 years. Thus, preventive intervention is suggested in the presence of signs of arterial hypertension, increased cholesterol levels, overweight bodies. Regular screening is essential possible manifestations depression and anxiety were 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.

Decisions about when and how to treat patients with depressive and anxiety disorders are not determined based on severity. somatic condition, but by carefully assessing factors such as the severity and duration of the current affective episode, a history of depression, impairments in daily functioning, the quality of current microsocial support, the expected psychotraumatic 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. The criterion for choosing a therapeutic intervention is not the number of symptoms, but the disruption of daily functioning, including household and hygienic ones. 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 disease, and cause more pronounced instability in young patients heart rate than in older people. All this casts doubt on the possibility of their use in cardiological practice.

Most second generation antidepressants have a favorable profile of action on the cardiovascular system. The largest evidence base on their positive use in somatic patients has been accumulated for selective serotonin reuptake inhibitors (SSRIs). It has been proven that the latter do not have a direct effect on heart rate, do not affect blood pressure, and 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, correction individual symptoms 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.

For the serotonergic group of antidepressants, there is a problem of drug interaction, 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 makes it a preferable choice in complex therapy.

In general, 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.