When the children’s oval window closes

Cardialgia is any pain behind the sternum or in the left half of the chest (in the region of the heart) that is different in its characteristics from angina and, accordingly, is not a symptom of coronary heart disease. You may not hear this term often, but the prevalence of cardialgia is higher than angina. According to my observations in the clinic when patients complain of pain in the heart, the ratio of cardialgia and angina is about 20: 1. Cardialgia is often the antipode of angina, as it is necessary to carry out the most important differential diagnosis by category "dangerous" pain (angina pectoris) – "not dangerous" pain (cardialgia). Cardialgia, although it can be quite intense, is not a threat in the vast majority of cases.

The main proportion (90%) of cardialgia accounts for cardioneurosis (especially against the background of the syndrome of connective tissue dysplasia) and hypertension. In this case, its characteristics are as follows:

– pain can be any sensations (often whining, colitis, crushes);

– more often it is located not behind the breastbone, but in the precordial region;

– last long – for hours or even days, sometimes briefly "pierces";

– can give to the left shoulder and arm, causing the sensation of numbness of the left hand, fingers;

– often intensified with deep breathing, accompanied by a feeling of unsatisfied breath ("sighs of relief");

– sedatives (for example, validol, Corvalol) can be effective for stopping it, and nitroglycerin is useless;

– it is not associated with physical activity, on the contrary, more often it occurs and is strengthened at rest;

– Chronologically appears on the background or after the experience;

– can be very colorfully (pretentiously) subjectively perceived – a hot ball in the chest, a lump in the region of the heart, something hot inside and

When the children's oval window closes

I want to emphasize (!) That with menopausal and alcoholic heart damage, the characteristic features of pain in the precardiac region can be very similar to those described above!

Cardialgia is one of the possible symptoms of so many diseases (several dozen) and in most cases is not dangerous. Neurotic disorders (they account for 90% of cardialgia), mitral valve prolapse, alcoholic heart damage, esophageal or stomach pathology, intercostal neuralgia, osteochondrosis, male or female menopause, and herpes chest disease – this is an incomplete list of diseases that can manifest pain in the region of the heart. Summary: if you are worried about pain in the heart, then it is highly likely that it is either not related to the heart, or due to cardiac neurosis.

Arterial hypertension is a syndrome manifested by a steady or periodic increase in blood pressure (BP). It is known that the upper limit of normal blood pressure are the numbers 135 \ 85

Insidiousness of the disease lies in the fact that a person may almost not feel elevated blood pressure. Factors that are part of a poor lifestyle – chronic stress, unresolved neurosis, sedentary lifestyle, overweight, prolonged lack of rest (workaholism), controlling the type of behavior – contribute to the emergence and consolidation of arterial hypertension. Treatment of arterial hypertension with medications can be difficult if the causes of it are not corrected. Arterial hypertension is a syndrome that can be part of one of the 3 diseases: 1) hypertension (90%) is a disease of a wrong lifestyle; most often, it is based on chronic emotional overstrain with anger subconsciously directed inward (intrapersonal conflict); 2) NDC in hypertensive type (5%) – cardioneurosis with hypertensive reactions; 3) secondary arterial hypertension (5%) – when high blood pressure is one of the symptoms of a disease (for example, renal hypertension). There is a special form of arterial hypertension, which, with reservations, can be attributed to age: it is called " sclerotic arterial hypertension ". As a rule, this form of hypertension develops in people older than 70-75 years, quite well subjectively tolerated, considered less malignant (in terms of complications with heart attack and stroke). Its specific feature is the large difference between upper and lower pressure. If during hypertension, both systolic and diastolic blood pressure rises simultaneously (for example, 200/110

Heart failure is a pathological condition in which the heart, per unit of time, cannot transfer the required volume of blood into the arterial bed. Normally, the volume of blood flowing to the heart is equal to the flow rate (continuity of flow). The violation of this balance is the basis of the development of heart failure (HF). The heart consists of 4 chambers: the right and left atria, the right and left ventricle. The failure of at least one of them (when the inflow and outflow are not equivalent) over time leads to the manifestation of symptoms of HF. Possible causes of heart failure: 1) abnormal functioning of the valvular apparatus of the heart (heart defects), 2) weak contraction of the heart chamber (s) – blood is ejected from them in small quantities (for example, myocardial infarction, myocarditis, perennial atrial fibrillation), 3) chambers (s) and the hearts do not relax well (increased "rigidity" myocardium) – in "rigid" blood does not flow sufficiently into the chamber: for example, diastolic dysfunction of the left ventricle in hypertension, when due to the rigidity of the left ventricle the blood begins to stagnate in the left atrium. The last phenomenon is easy to understand by the example of the suction action of a pipette: imagine a compressed pipette dipped into water, at the time of decompression, water will flow into it. So if the pipette (heart) does not fully open, there is little water (blood) in it.

The earliest symptoms of HF: unmotivated weakness and shortness of breath with habitual physical exertion. The combination of similar symptoms, of course, occurs in other diseases, but CH debuts with them. CH is always a consequence. Diseases that most often lead to the development of HF: coronary heart disease, arterial hypertension, congenital or acquired heart defects, atrial fibrillation. These pathological conditions affect the whole heart or its individual chambers. Thus, to prevent the development of HF, it is necessary to treat "forerunner disease". In the advanced stage of HF it manifests as shortness of breath at rest (up to suffocation), swelling of the legs, severe weakness, paleness of the skin, and blueness of the lips. HF inevitably leads to death. Another thing is that its adequate treatment in the early stages leads to long-term remission, allowing you to live for decades; in advanced cases, despite the most modern and comprehensive therapy, the patient seems to have no more than 5 years (at best). Life example: famous Soviet actor

Hypercholesterolemia – blood cholesterol levels higher than normal values ​​- 5.5-6.5 mmol / l. This is the so-called total cholesterol. Biochemically and laboratory cholesterol is divided into "good" (HDL) and "bad" (LDL, VLDL). Level "good" it is desirable to have a high "bad" correspondingly low. In cardiology, another term is often used: dyslipidemia. Under dyslipidemia understand any change in the normal ratio of blood lipids, predisposing to atherosclerosis. For example, total cholesterol is normal, and its malignant fraction is elevated, or cholesterol is normal, and the concentration of neutral fat (triglycerides) is high. That is, dyslipidemia is a broader concept. Hypercholesterolemia is primary and secondary. Primary hypercholesterolemia is a genetically determined disease; like any congenital abnormality is very rare. Hereditary hypercholesterolemia can be suspected when a person has very high blood cholesterol, without cause, usually above 11 mmol / l and there are xanthomas. Secondary hypercholesterolemia occurs against the background of an acquired disease, one of the manifestations of which is elevated cholesterol. The most common cause of secondary hypercholesterolemia can be considered unhealthy diet (dietary lipemia) – the predominance in the diet of foods high in cholesterol and saturated fatty acids. Another common cause of secondary hypercholesterolemia is diabetes. Incorrectly treated diabetes mellitus is always accompanied by dyslipidemia, thereby predisposing to atherosclerosis. Sometimes the motives of secondary hypercholesterolemia are not obvious, in which case it is most often a manifestation of a wrong lifestyle. What fundamentally distinguishes secondary hypercholesterolemia from the primary: it is never too high (usually the concentration of total cholesterol does not exceed 9-11 mmol / l), and therefore not so malignant (atherogenic). Let’s stop on clinical value "cholesterol problem". An excessive concentration of cholesterol in the blood over the years leads to its deposition (on the principle of concentration gradient) in the walls of those arteries that experience the greatest hemodynamic effect (arteries of the heart, aorta and its large branches) – over time, atherosclerosis of these vessels develops.

For a cardiologist, the most interesting is the concentration in the blood "bad" cholesterol – LDL. Situations where total cholesterol is normal, and "bad" increased – common and definitely need attention. In general, the problem of hypercholesterolemia may be somewhat exaggerated. So much so that in recent years, some researchers have assumed that common cholesterol values ​​of up to 7.5 mmol / l are considered normal. Such disagreements are caused by the fact that it is still unclear why people with high cholesterol levels, including "bad", remain clinically healthy, living to old age; on the other hand, there are many examples of people who become ill with atherosclerosis, having normal blood cholesterol. Summary: elevated blood cholesterol is just a risk factor for atherosclerotic diseases (stroke and myocardial infarction); Whether they manifest or not is impossible to predict; in combination with other risk factors (eg, smoking, diabetes, overweight), the danger increases many times over. Figures of total cholesterol above 8 mmol / l require an unambiguous correction (even in young healthy individuals), since with such a concentration of cholesterol the probability of the onset of premature atherosclerotic disease is extremely high. In the blood test "for cholesterol" First of all, pay attention to the concentration of LDL and HDL.

Atherosclerosis is a systemic disease of the large arteries of the elastic type, which is based on the deposition of lipids (primarily cholesterol) in the inner wall (intima) of these arteries. There are several alternative, somewhat mutually exclusive, theories of the pathogenesis of atherosclerosis. However, the main thing that unites them: without cholesterol, there is no atherosclerosis. Since atherosclerosis is recognized as a multifocal, polyetiological disease, then, speaking of its origin, it is correct to use the term risk factor, and not the cause. The risk factors for atherosclerosis are divided into modifiable (acquired) and non-modifiable. The first are those that can "to abolish": hypercholesterolemia, smoking, arterial hypertension, diabetes mellitus and some others. To the second – uncorrectable circumstances: age, male gender, unfavorable heredity. The most logical atherogenesis is due to the high level of blood cholesterol: an excess of cholesterol along the concentration gradient enters the walls of the arteries, where it is captured by the cells; cells, gradually overloaded with cholesterol, die; cholesterol is in the extracellular space, where, accumulating, begins to form an atherosclerotic plaque. However, hypercholesterolemia occurs in no more than 2/3 of cases of atherosclerosis. This means that other risk factors for atherosclerosis are non-lipid. The most significant of these are smoking and uncontrolled arterial hypertension. In both cases, arterial wear is significantly increased: nicotine activates the sympathetic nervous system (blood volume is ejected from the heart with force, "injuring" arterial walls), and in case of arterial hypertension arterial walls are under the permanent influence of high blood pressure, which also injures them. Excessive hemodynamic effects on the arterial wall leads to the fact that their inner shell begins to need a large amount of building material (cholesterol, one of the essential components of the biological membrane), which begins to enter it in an excess amount – and this is, in fact, the beginning of atherogenesis . With regard to diabetes – another major risk factor for atherosclerosis – it should be recognized that it is almost always accompanied by dyslipidemia. Therefore, it is likely that the basic mechanism of atherogenesis in diabetes mellitus is the deposition of lipids in the arterial wall according to the principle of concentration gradient. First of all, the aorta, its branches, the places of the natural bends of arteries and bifurcations (divisions) are subjected to atherosclerosis – that is, the large vessels whose wall experiences the greatest hemodynamic effects, and where the turbulence and the turbulent blood flow occurs. Formed atherosclerotic plaque may have an eccentric or concentric configuration. The eccentric plaque is flattened, does not affect the blood flow and therefore is clinically asymptomatic. Concentric plaque narrows the lumen of the artery. A hemodynamically significant contraction of at least 70% is considered. The hemodynamic significance of stenosis is understood as such a narrowing, when an increase in the load on an organ fed by a given artery is accompanied by its ischemia, due to a decrease in blood flow. In the advanced stage of atherosclerosis, the arterial lumen is completely obliterated (blocked) – the blood flow through such a vessel is stopped.

Thus, the main pathophysiological phenomenon of atherosclerosis is ischemia or, in other words, lack of blood (oxygen) in the area that is supplied by this artery. The subjective manifestations of the phenomenon of ischemia depend on which organ suffers. For example, in the heart muscle, ischemia is manifested mainly by chest pain (angina pectoris, acute myocardial infarction); in the brain – dizziness, weakness, impaired speech, etc.; in the arteries of the lower extremities – intermittent claudication. On the one hand, atherosclerosis is strongly associated with the general aging of the body, on the other hand, atherosclerosis can affect people of any age. In the latter case, it usually develops in the presence of risk factors. I repeat once again the primary ones: hypercholesterolemia, smoking, uncontrolled arterial hypertension, diabetes mellitus, obesity. In addition, persons with a controlled type of behavior, for example, bosses, and subjects experiencing a chronic lack of positive emotions are subject to early atherosclerosis ("ossification" arteries). Typical look "coronary" personality: a professional who places high demands on others with insufficiently effective control for subjective or objective reasons, which causes a feeling of internal dissatisfaction and irritation. In elderly people, who, probably for existential reasons, gradually cease to enjoy life, atherosclerosis can develop rapidly. Finally, we must not forget about the hereditary predisposition to atherosclerosis; as an example, an earlier disease (up to 50 years) a close relative of myocardial infarction. In this case, the heredity itself is a risk factor. The most known atherosclerotic diseases or their clinical forms: angina pectoris, coronary heart disease, stroke, intermittent claudication. Main "pathophysiological drama" Atherosclerosis is the tearing of a plaque and the formation of a thrombus in this place, which in seconds can completely block the lumen of the artery. According to this scenario, most heart attacks and strokes develop. And "overstrain" small size plaque, including hemodynamically insignificant, eccentric.

The clinical deceit of atherosclerosis is that it can be asymptomatic for many years, and then chronologically unpredictable, without a precursor, leading to a life-threatening condition: myocardial infarction or stroke. In this connection, it is extremely important to engage in primary prevention of atherosclerosis, which boils down to a healthy lifestyle: do not overeat, regularly load yourself physically, monitor your weight, do not smoke, monitor blood pressure, avoid stressful work. Regardless of gender, aortic atherosclerosis is always the first to develop – it is asymptomatic. Then in men, atherosclerosis affects the coronary arteries; for the time being, it may be asymptomatic, but subsequently it is necessarily complicated by angina pectoris or myocardial infarction. In women, following atherosclerosis of the aorta, atherosclerosis of the brain arteries often develops – there is a risk of developing dyscirculatory encephalopathy, stroke; however, cerebral atherosclerosis can also be asymptomatic for many years. In men, coronary atherosclerosis affects the cerebral arteries (risk of stroke) or the ileal-femoral segment arteries (intermittent claudication) – with about the same probability. In women after cerebral atherosclerosis, coronary arteries are affected and coronary artery disease develops. Intermittent claudication for women is not typical.

Before the appointment of statin therapy, it is necessary to assess the genesis of atherosclerosis: lipid or non-lipid. In lipid atherosclerosis, statin therapy is mandatory, it is highly effective. In non-lipid atherosclerosis, the protective effect of statin therapy is questionable; in this case, emphasis should be placed on combating non-lipid risk factors for atherosclerosis: smoking, hypertension and

The earliest clinical marker of latent (asymptomatic) atherosclerosis is an increase in the thickness of the intima-media complex (CMM): the total thickness of the inner and middle layers of the artery. This parameter is determined mainly by ultrasound of the carotid arteries. Regardless of age, it should not exceed 1 mm. However, it is still more correct to normalize the CIM value based on age and sex: for men under 40 years old CIM should be no more than 0.7 mm, from 40 to 50 years old – 0.8 mm, over 50 years old – 0.9 mm, for women up to 45 years old – 0.7 mm, from 45 to 60 years old – 0.8 mm, over 60 years old – 0.9 mm. Pathological values ​​of CMM thickness are associated with accumulation of atherogenic lipids in the artery wall. Identification of this fact allows you to take preventive anti-atherogenic measures.

Myocardial infarction – a clinical form of coronary heart disease, characterized by the development of necrosis (necrosis) of the heart muscle. In the absolute majority of cases, myocardial infarction (MI) develops due to the occurrence of acute cardiac artery thrombosis, which entails a complete cessation of blood flow through it:

The earliest and most frequent symptom of MI is severe, often unbearable, chest pain, accompanied by severe perspiration. Other possible sensations (shortness of breath, weakness) appear either with the pain, or somewhat later. MI is a terrible complication of coronary heart disease: among the causes of death in people of middle and older age groups, this disease, along with strokes and oncopathology, takes the leading place. The course of the disease is variable: MI can lead to death, despite the provision of the fastest and most complete medical care; on the other hand, some people suffer a heart attack "on foot" – in such a situation, he is diagnosed retrospectively. In most cases, however, only emergency medical care can save a person, if not from death, then from serious complications (immediate and remote) of myocardial infarction. Myocardial infarction can be transferred several times, some die from the first. Transferred to MI is a serious call signaling that there is some cause (risk factor) in a person’s life that provoked such a terrible disease – for example, smoking. If such a patient quits smoking, he reduces the risk of recurring (always, at least, disabling) myocardial infarction tenfold, and thus gives himself a chance for a long life. There are a number of other risk factors associated with the early development of myocardial infarction and that fit into the idiom called " wrong lifestyle ". Therefore, if this disease has befallen you, the question must be asked: why did I get sick? In extreme old age, myocardial infarction is often fatal, reflecting the natural processes of aging and dying of the body.

Over the years in the infarction ward, I have seen hundreds of patients with acute myocardial infarction. For myself (behind the scenes) I divide myocardial infarction into senile and non-aging. "Senile heart attack" occurs in persons of the appropriate age and, as it were, for no apparent reason (as the relatives of the patient think so). Old age is a relative concept, since one person can look at 80 at the age of 60 and vice versa. People who look hardened outwardly are usually old and inside (atherosclerosis of the vessels); they can get acute myocardial infarction just like that. because age came up dangerous. In this case, myocardial infarction is one of the dramatic manifestations of aging, general vascular wear, and wilting of the body. Of course, patients with "senile" a heart attack can safely survive it, be discharged from the hospital and live for many more years. An essence in another: the similar heart attack carries only an age shade. I focus on this attention, because it is not uncommon to hear questions from the patient or from his relatives, they say, why he fell ill, "did not drink, did not smoke, did not go on girls"! I answer them that this is just old age. This is exactly how completely healthy old people get into our department, who "never hurt anything". Conditional age limit when a heart attack is more likely "senile": from 70 years regardless of gender. A completely different philosophical message has "non-jobless heart attack". Myocardial infarction can get sick at any age; For example, in my practice I met a 26-year-old patient with a heart attack. Almost every day, people of 40-50 years old come to our department with a heart attack. Such relatively young patients almost always have some apparent cause of such an early occurrence of the disease. Each "non-classical" myocardial infarction develops against the background of a risk factor, which for a particular patient becomes the cause of the disease. Major risk factors "non-historic" myocardial infarction: a long smoking period (from 10-15 years), long-term uncontrolled arterial hypertension, high blood cholesterol (which is often associated with overweight, leadership position at work, choleric temperament), chronic stress and uncorrected diabetes. Each of these risk factors can significantly accelerate the development of atherosclerosis, which means "bring a person to trouble". "Non-static" myocardial infarction is a kind of message to the patient, because his lifestyle is incompatible with longevity. Therefore, it is necessary to eliminate the risk factors from your life – only in this case there can be no second heart attack. If the risk factor is not eliminated, a repeated heart attack, more likely fatal, will be (!). In real life, I know patients who had a heart attack in the late 80s, however, "hand in mind", they prosper to this day. So much in the hands of man.

Coronary heart disease (CHD) is the most common heart disease and the most common cause of heart death. Atherosclerosis of the arteries of the heart is the basis of CHD. For many years, the disease may be asymptomatic and manifest, for example, with acute myocardial infarction. However, more often, coronary artery disease debuts with angina and is limited to it for many years.

There are other options for the onset of CHD: sudden death, arrhythmias, paroxysmal dyspnea – but this is an exception. In our country, there is hyperdiagnosis of ischemic heart disease: almost any pain behind the sternum or in the region of the heart is interpreted as angina pectoris. However, given that such a formidable diagnosis is in itself a responsible task, strong clinical arguments are needed to prove IHD. Ideally, a diagnostic search should be conducted in order to complicate the study and increase its sensitivity. 1. Patient survey: angina pectoris – a clinical diagnosis and with a probability of 90-95% is established using the usual detailed survey. 2. If there is doubtful pain in the region of the heart, the patient should perform an exercise test with simultaneous ECG recording (treadmill test, bicycle ergometry) – it can reveal a correlation between the load and ischemic changes on the ECG. 3. If the test results are negative or ambiguous, then it is advisable to complete the diagnostic search by performing coronary angiography. This diagnostic technique allows to visualize hemodynamically significant contractions in the arteries of the heart and, with a probability of 99%, confirm or refute angina (IHD, atherosclerosis of the cardiac arteries). Unfortunately, in Russian medicine, the first 2 stages are often incorrect and you have to face a situation where the patient has obviously non-cardiac pain, but is sent to coronary angiography (invasive diagnosis with a certain percentage of serious complications), in which stenosis in the heart arteries is not found.

Coronary angiography is a diagnostic procedure, which consists in introducing a contrast agent into the arteries of the heart, which, under the control of fluoroscopy, makes it possible to evaluate their patency and identify narrowings.

Coronary angiography invasive manipulation: a puncture is performed on one of the large peripheral arteries (usually the femoral or radial arteries), through which the conductor is brought to the heart. Like any invasive technique, coronary angiography has its own percentage of complications, including lethal ones; therefore, it is always associated with some risk and requires the mandatory hospitalization of the patient in the hospital for at least 1-2 days. Coronary angiography is painless and is performed without anesthesia under local anesthesia (puncture site). In experienced hands, complications in its implementation are less than 1%. Coronary angiography is the gold standard for diagnosing coronary heart disease; another thing is that its conduct must be justified from a clinical point of view. So there are situations when the pain in the chest is clearly non-cardiac, but the doctor, apparently from his professional helplessness, sends the patient to coronary angiography. Nevertheless, its role in modern cardiology is very large: sometimes only coronary angiography allows to complete a long diagnostic search.

Stenting – in relation to cardiology: modern treatment of coronary artery disease, which is to install a thin, mesh metal tube in the area of ​​the cardiac artery, narrowed atherosclerotic plaque. This technique refers to minimally invasive – it does not imply general anesthesia and chest opening. Manipulation is performed through the puncture of one of the peripheral arteries (radial or femoral); a special conductor is introduced through which the stent (under the control of fluoroscopy) "is delivered" to destination; the last stage is balloon expansion of the stent; the result: the narrowed area of ​​the artery again pass. The procedure is performed under local anesthesia (the puncture site is anesthetized and, as a rule, a sedative is injected into the patient). According to the patients, this operation is absolutely painless.

The stent is high-thrombogenic and without the use of special drugs will inevitably be thromboed. Therefore, after stenting for at least 1 year, the patient should take an antiplatelet drug that will prevent stent clotting. For the current period, the stent from the inside overgrows with endothelium (the natural artery sheath) and ceases to be thrombogenic. Neglect of these drugs is fraught with the development of stent thrombosis (acute artery occlusion), leading to myocardial infarction.

Aspirin (acetylsalicylic acid) is a drug that has anti-inflammatory, analgesic, antipyretic effects. In the middle of the last century, it was found that, among other things, acetylsalicylic acid interferes with platelet aggregation (adhesion) and the formation of arterial thrombi. Therefore, the main point of application of aspirin in cardiology is the prevention of thrombosis in the arteries of the heart — protection against life-threatening complications of IHD and myocardial infarction. "Aspirin boom" still going on. Numerous studies have shown that regular use of acetylsalicylic acid reduces the risk of myocardial infarction and general vascular mortality by several times. Currently, the diagnosis of coronary artery disease, angina automatically means lifelong appointment of aspirin. All men over 50 years old and women over 60 years old are recommended to take aspirin daily, even in the absence of the disease, since even this category of individuals has been shown to have a protective effect (reducing mortality from strokes and heart attacks). However, acetylsalicylic acid is not a panacea for thrombosis, since the thrombotic cascade is a multifactorial process; In addition, there are subjects insensitive to aspirin – in about 5-10% of people it does not cause an antiplatelet effect. This medical reality (in any case in Khabarovsk) does not allow for laboratory diagnostics for the presence of individual sensitivity (anti-platelet effect) to aspirin, therefore, when indicated, it is given to everyone in 100% of cases. Now various forms of aspirin are held in high esteem. "cachet"reducing it "ulcerogenic" Effect. I like to prescribe Cardiomagnyl (aspirin + alkali).

Plavix (clopidogrel, zilt and others) is a drug from the group of antiplatelet agents. It is a worthy addition (not an alternative!) Aspirin in terms of preventing blood clots in the arteries. It has its own individual niche application. Basically, Plavix is ​​administered after stenting of the coronary arteries to prevent stent thrombosis (along with aspirin); The second most common situation in which Plavix is ​​shown is the individual intolerance to aspirin or insensitivity to it (the latter circumstance is difficult to prove). After stenting, Plavix is ​​prescribed for at least a year; during this time, the stent overgrows from the inside with natural artery tissue and ceases to be thrombogenic. The problem of resistance (lack of anti-platelet effect) to Plavix is ​​actual – about 5% of people are insensitive to it. Plavix can be dispensed with 1) with a stable course of IHD in the absence of stenting, 2) one year after stenting. All of the above applies to the ultra-modern antiplatelet Brillint; This is an improved analogue of plavix – no resistance to it is observed. However, it is more expensive.

Cordarone is a modern, powerful antiarrhythmic drug. The strength of the antiarrhythmic effect exceeds all other drugs in this group. Effectively suppresses beats, various tachyarrhythmias. But. It has a number of remote side effects that develop after 5-10 years of regular intake of cordarone. It is necessary to highlight the main ones: the defeat of the thyroid gland, sclerotic processes in the lungs, impaired vision, skin pigmentation. I repeat, they have been developing over many years, but in fact are irreversible. The toxicity of cordarone is determined by the presence of an iodine molecule in its composition: with one tablet we get the amount of iodine ten times greater than its daily need. Cordarone complications do not pose an immediate threat, so if its intake is necessary (for example, for health reasons), the resulting side effects are medically corrected, and the medicine is used further. When prescribing cordarone, a doctor must always weigh the risks and benefits of taking them. I use it in the following clinical situations: 1) life-threatening ventricular arrhythmias (in such a situation only he is practically effective) – the situation is pan or gone, 2) briefly before the intended radical antiarrhythmic heart surgery (for example, before radiofrequency ablation during atrial fibrillation or WPW syndrome) – the duration of admission from several months to a year, 3) to provide emergency care in hospital conditions. For example, to relieve an attack of atrial fibrillation, Cordarone is administered intravenously, 4) in elderly people with symptomatic arrhythmias (older than 70-80 years). In the latter case, the benefits obviously exceed the risk. Statistically, persons of this age group live no more than 10-15 years. By administering cordaron to them, we provide miraculous healing from painfully tolerated arrhythmias, and patients most likely do not live to see its side effects, dying from natural causes. Often. in clinical practice, you encounter situations when cordarone is given for a long time, for example, in innocuous ventricular premature beats. In my opinion, this is absolutely unacceptable! Cordarone is a toxic drug that should be prescribed, I repeat, according to strict indications.

Coronary artery bypass surgery (CABG) is a surgical treatment of coronary artery disease, which consists in forming bypass vascular pathways (shunts) in places where atherosclerotic plaques are located. Imagine a heart artery consisting of consecutive sections A, B, C; the blood goes from A through B to C. The department B is clogged (clogged with an atherosclerotic plaque). From the superficial veins of the patient’s lower limbs (one or two veins are cut out) they create a shunt, one end of which is fixed to section A, the other to C; as a result, the blood flow goes through the shunt from A to C, bypassing V. AKSH is a serious abdominal surgery, combined with general anesthesia, opening of the chest, cardiopulmonary bypass, and other attributes of cardiac surgery. At present, a stent operation is a worthy alternative to CABG. However, there are clinical situations where only AKSH can offer the patient – as a rule, these are advanced cases with multiple lesions of the coronary arteries, when stenting is impossible or dangerous.

Pulmonary embolism (pulmonary embolism) is a life-threatening condition in which thrombotic masses are occluded in the pulmonary artery branch by occluding blood, obturating (overlapping) the lumen of the vessels. This leads to a sharp decrease in blood flow through the lungs and a symmetrical decrease in systemic blood flow; oxygenation of blood drops significantly. The cardinal symptom of pulmonary embolism is sudden, unmotivated dyspnea at rest; or dyspnea appears when walking for short distances, which the person had previously seamlessly overcome. Imagine you ran a sprint; in this case, the appearance of dyspnea seems as natural as its absence at rest. So in patients with pulmonary embolism, shortness of breath is as if they are "the cars were unloaded", although in reality they did little or nothing. Depending on the amount of thromboembolism, the clinical picture of the disease varies from barely perceptible shortness of breath, to sudden, sharpest shortness of breath, ending in a quick death. In clinical practice, most often we have to deal with cases of submassive pulmonary embolism when pulmonary thrombosis is significant, but timely provision of medical care helps save the patient’s life. The logical question is: where do these blood clots come from? In 90% of cases, blood clots form in the large veins of the lower extremities; in the rest – in the veins of the pelvis. The only place where can "settle down" detached thrombus – branches of the pulmonary artery. Risk factors for vein thrombosis and pulmonary embolism: female gender, overweight, sedentary lifestyle, taking oral contraceptives, old age, prolonged immobilization (for example, after a broken leg), cancer, smoking. The combination of several factors increases the risk of disease. According to my observations, patients with pulmonary embolism enters in a cardiology hospital can be divided into 3 clinical and social groups: 1) elderly people (in this case, the processes of uncontrolled thrombus formation in the veins are associated with the general aging of the body); 2) patients who have been forced for a long time (weeks, months) are on bed rest – for example, after a fracture of the bones of the pelvis, legs, spine; 3) middle-aged women – 40 – 50 (60) years – with risk factors: overweight, smoking, sedentary lifestyle, taking oral contraceptives (a combination of 1-2 risk factors is enough to increase the risk of pulmonary embolism at times). Life example: actress

Heart defects are a diverse group of heart diseases, which are united by the presence of macroscopic changes in the chambers and (or) heart valves, leading to impaired intracardiac and systemic hemodynamics. Heart defects are divided into congenital and acquired. Congenital malformations due to fetal anomaly. A classic example of such a defect is atrial septal defect, when there is a message between the atria, normally present only in the fetus. In accordance with the principle of pressure gradient, an additional intracardiac blood flow occurs (from left to right), which leads to an overload of the right heart chambers. Depending on the size of the defect, the defect can appear already from an early age, or it can clinically manifest in an adult state. So there are cases when the defect is an accidental find, for example, in a physically strong middle-aged man with a planned ultrasound of the heart. There are several dozen congenital heart defects; for those who want to familiarize themselves with them in detail, I recommend turning to the special literature. Acquired heart defects are the result of a disease that was transferred after birth. Currently, it makes sense to talk about two types of such defects: rheumatic and senile. The first develop on the background of recurrent angina (usually in adolescence), which are complicated by systemic autoimmune inflammation of the connective tissue, especially the heart valves (rheumatism); the latter are a classic example of age-related (involutive) damage to the cardiac valve apparatus due to the deposition of calcium salts in them. Regardless of the cause, valvular heart disease is always isolated (one or more); there is either their deformation and destruction with the development of failure, or the fusion of the valve cusps with the development of stenosis. In case of insufficiency, the valve allows blood to flow back into the chamber from which blood flowed into it; at a stenosis there is an obstacle for outflow of blood. The only and inevitable consequence of heart disease is the development of heart failure. The earliest symptom of the disease is shortness of breath, appearing and growing gradually, gradually. Currently, rheumatic heart defects are successfully corrected surgically; success in treating senile malformations depends on the age of the patient – in elderly people, the risk of not undergoing complex abdominal surgery is very high, so they often show only drug treatment of heart failure. Acquired heart defects can be asymptomatic for a long time (10–20 years) and can be detected by chance, for example, during a medical examination: a doctor listens for a heartbeat. Diagnosing blemish does not mean performing an immediate surgical operation. Such a patient should be kept on record with a cardiologist. Only when a heart defect manifests symptoms of heart failure (and this happens sooner or later), the question of its surgical correction is raised; if the operation is not done in a timely manner, the patient lives no more than 5-7 years from the moment the first symptoms appear.

Hypotension, in contrast to arterial hypertension, is a syndrome of low blood pressure. Hypotension may be primary and secondary. In the latter case, it is one of the symptoms of a disease: for example, heart failure, hypocorticoidism, etc. We are more interested in primary (unreasonable) arterial hypotension, which has an unofficial name: hypotonic disease. Criteria for diagnosis: 1) consistently low blood pressure (below 100/60 mm. Hg. Art.), 2) unknown etiology of the disease, 3) its manifestation in adolescence (14-18 years old), 4) the presence of certain symptoms. A combination of all criteria is mandatory. For example, low blood pressure in the absence of symptoms is not a disease. Complaints of patients with hypotonic disease are not specific: weakness (cardinal symptom!), Poor exercise tolerance, episodes of pre-unconscious states, periodic dizziness. In general, this is a relatively rare problem; even less often, it is a reason for seeking medical attention. Young women constitute the main contingent of such patients. In patients with hypotonic disease, there is a vegetative imbalance when the regulatory mechanisms controlling blood pressure do not increase it enough or, sometimes, even paradoxically reduce it. Treatment of the disease presents certain difficulties, since there are no drugs in the pill form that increase blood pressure (at least in Khabarovsk). Therefore, non-pharmacological agents are the main treatment: 1) dietary intake with high salt content, 2) the volume of fluid consumed should be at least 2 liters per day, 3) mandatory regular (preferably daily) physical activity of an aerobic nature (jogging, walking, swimming yoga and

ECG (electrocardiography) is a method of superficial recording of the electrical activity of the heart. The heart is a generator of electric current, which creates an electric field around it. With the help of electrodes on the surface of the body, it is possible to register the potential difference at each time point of the heart’s work and convert it into a curve using special equipment. The heart is in constant motion due to continuous intracellular processes of depolarization (current generation) and repolarization (discharge); the continuity of the electromechanical work of the heart determines that the direction of the current (electromotive force) is constantly changing along a standard trajectory. Registration of the change in the direction of the electromotive force leads to the formation of characteristic teeth on the ECG. Any significant pathology of the heart leads to local or diffuse disturbances of electrical processes that can affect the ECG – the direction of the electromotive force deviates from the standard trajectory. In cardiology, the diagnostic significance of an ECG may be completely different. Conditionally divide it into 3 categories: 1) the role of the ECG is exceptional and paramount – applies to all arrhythmic diseases and syndromes; 2) the role of the ECG is very important, but there are alternative diagnostic methods – myocardial infarction, pulmonary embolism, pericarditis; 3) the role of the ECG is only auxiliary – cardiomyopathy, hypertensive disease, cardioneurosis, myocardiodystrophy, hypertrophy, heart disease, etc.

Mitral valve prolapse (PMK) – sagging of the mitral valve cusps into the cavity of the left atrium at the time of the contraction of the left ventricle.

One of the most common congenital abnormalities of the heart. Differs from blemish by the fact that in the overwhelming majority of cases, MVP does not lead to impaired hemodynamics, without posing any threat to life. PMK is one of the manifestations of connective tissue dysplasia syndrome. At the heart of this syndrome is fragility, weakness of the connective tissue, which is present in almost any organ, including the structure of the mitral valve. The cause of this syndrome is prenatal developmental pathology when "Something went wrong". Depending on the depth of sagging of the valves, the PMK is of three degrees. Grade 1 prolapse accounts for over 90% of cases and is almost always insignificant hemodynamically. The clinical (hemodynamic) significance of MVP is determined by the severity of mitral regurgitation (insufficiency). The higher the degree of prolapse, the more blood regurgitates (returns) to the left atrium, which accordingly increases the clinical significance of this anomaly. Observations require patients: 1) with prolapse 2 or 3 degrees; 2) if the valves of the mitral valve are myxomatous changed; 3) if the MVP is combined with multiple additional chords in the left ventricle. The designated category of persons is at risk in terms of the formation of future developed heart disease (heart disease or arrhythmia syndrome). Persons with PMK of 1 degree and without additional anomalies do not need medical examination – they are healthy. Ultrasound of the heart allows you to visualize PMK, assess its degree and hemodynamic significance.

WPW syndrome (phenomenon) is a microporcus of the heart, the essence of which is the presence of an additional pathway between the atria and the ventricles. Normally, electrical communication between them is carried out through the so-called atrioventricular node. As a result, intrauterine developmental disorders in the heart (in addition to the above-mentioned node), additional muscle-conducting bundles (Kent bundles), which connect the atria and ventricles, function. As a rule, a bunch of one, at least – two or more. This abnormality leads to the fact that electrical excitation from the atria to the ventricles proceeds along 2 paths: normal (AV node) and abnormal (Kent beam). The clinical significance of this microfluoric heart is determined by the possible occurrence of attacks of unmotivated heartbeat (atrioventricular reciprocal tachycardias – circulation of an electrical impulse involving the Kent beam). WPW syndrome is detected on a normal ECG and in the absence of heart palpitations it is called a WPW phenomenon. A person can live for decades with such "bad cardiogram"while remaining subjectively completely healthy. The first paroxysm of tachycardia in life automatically translates the phenomenon of WPW into a syndrome – that is, into a disease. The WPW phenomenon begins to be detected on an ECG, most often between 10 and 30 years old. The time of his transition to the syndrome (the appearance of paroxysms of the heartbeat) is variable and unpredictable. Someone "transformation" takes several months, someone decade. The sooner the electrocardiographic manifestation of the WPW phenomenon occurs, the higher the likelihood of the occurrence of arrhythmia during the lifetime. In other words, if the WPW phenomenon appears on the ECG in older age groups (over 40 years), then the likelihood of arrhythmias in them is very small, since they simply may not live to the stage of the syndrome, dying from any natural causes. The treatment tactics for WPW syndrome is different in Russia and abroad. In economically developed countries, when it is detected in people of young and middle age, an active therapeutic tactic is becoming increasingly established: radiofrequency ablation of the Kent beam at the asymptomatic stage of the disease (at the stage of the phenomenon) is recommended. This approach is based on the fact that WPW syndrome has been found to increase the risk of sudden cardiac death by a fraction of a percent. Therefore, beam ablation saves the patient from future arrhythmias and levels other cardiac risks. In Russia, the ablation operation in WPW syndrome is performed only when there are attacks of reciprocal arrhythmia (at least one) – that is, at the stage of the syndrome. My recommendations to patients with the phenomenon of WPW: 1) live a normal life – the first heart attack, if there is, it will take you by surprise, so you should not think about it. The attack itself carries almost no threat to life. When it appears, 2) immediately go into a state of physical rest, call an ambulance to relieve the seizure and documentation of arrhythmia through an ECG, 3) after stopping the first paroxysm of heartbeat, you should plan to go to the clinic to a cardiologist.

Pulmonary hypertension is a syndrome based on an increase in blood pressure in the pulmonary artery; as a result, the right heart chambers are forced to work with increased stress in order to "push through" blood through "plot" high pressure. I recall that blood from peripheral veins flows into the right chambers of the heart, from there through the pulmonary artery enters the system of pulmonary capillaries, where it is enriched with oxygen (blood); from the lungs, blood along the pulmonary vein system is delivered to the left heart. In pulmonary hypertension, an obstruction of blood flow is formed at the level of the pulmonary artery or / and its branches. This is always a secondary pathology. Diseases that may be complicated by pulmonary hypertension: 1) Valvular defects and diseases of the left heart chambers are the most common cause of pulmonary hypertension. With the defeat of the left ventricle (for example, after myocardial infarction), he becomes unable to pump all the volume of blood that flows to him from the lungs. The blood begins to stagnate in the pulmonary artery system, which leads to an increase in pressure in it. Theoretically, any serious organic disease of the left ventricle, mitral or aortic valve defects may eventually be complicated by pulmonary hypertension; 2) Pulmonary embolism – a very common cause of pulmonary hypertension. Thrombotic masses entering the pulmonary artery system overlap a part of its lumen, which leads to a significant increase in pressure in it and a decrease in blood flow through the lungs; 3) Diseases of the bronchoalvolar system leading to the development of pulmonary hypertension. This group includes pathologies affecting the lung tissue and / or small bronchi: bronchial asthma, chronic obstructive bronchitis, etc. A natural consequence of a long pathological process in the lungs and bronchi is tissue sclerosis, which results in the replacement of small pulmonary arteries by the connective tissue, which in turn reduces the overall "cross section" the channel of the pulmonary artery and gradually leads to an increase in pressure in it; 4) Congenital heart defects. Most of them are accompanied by an overload of the right heart chambers. "by volume"leading to pulmonary hypertension; 5) Systemic diseases (amyloidosis, sarcoidosis, etc.), which after many years can give complications to the lungs in the form of diffuse sclerosis of its parenchyma and replacement of pulmonary arterioles with connective tissue. In this case, the pathophysiology of pulmonary hypertension is the same as in primary diseases of the bronchoalveolar system.

The main clinical manifestation of pulmonary hypertension is shortness of breath with little exertion. The presence of pulmonary hypertension indicates a far advanced stage of the underlying disease, reflecting the neglect of the process and an unfavorable prognosis. Effective treatment of persistent pulmonary hypertension does not exist – it is necessary to promptly treat the underlying disease.

Shortened interval syndrome P-Q is a phenomenon recognized by a specialist exclusively on an ECG. This syndrome, when identified, often serves as a reason for referral to a cardiologist. About the essence of the syndrome. Electrical communication of atrial myocardium and ventricular myocardium is performed through the AV node. An electrical impulse passes through it with a small delay (a fraction of a second), which (delay) on the ECG is reflected in the form of the so-called P-Q interval.

This delay is necessary for the successive contraction of the heart chambers (first the atria, then the ventricles), which makes intracardiac hemodynamics more beneficial. It (interval) has an upper and lower limit of the norm. Its magnitude less than normal in cardiology is indicated by shortened PQ syndrome. Is it dangerous? Previously (another 10-15 years ago) it was believed that this ECG pattern was associated with the occurrence of heart attack (paroxysmal tachycardia); He was treated the same way as WPW. However, it was subsequently proved that this syndrome does not provoke any arrhythmias and in fact is simply an ECG abnormality. A short interval P-Q is the norm for children of small age, therefore if it (interval) remains as such in an adult, then this is considered a sign "infantilism" AV node. The only clinical significance of this phenomenon is that if an adult develops atrial fibrillation (atrial fibrillation) in the future, it is highly likely that it (arrhythmia) will occur with a high frequency of ventricular contraction due to the inability of the AV node to "the delay" pulses. Persons with shortened P-Q syndrome do not need cardiac examinations.

Sinus arrhythmia. Heart rate regularity is relative. Normally, there is a slight variability (we are talking about fractions of a second), which is not subjectively felt, but is easily detected on an ECG. This is sinus arrhythmia. There are 2 of its clinical varieties: 1) physiological – is present in any healthy person. The extreme variant of such an arrhythmia is respiratory (cyclic) sinus arrhythmia: during inhalation, the heart rate increases, and on exhalation it decreases. When the respiratory arrhythmia heart rate fluctuations, in addition to being associated with the act of breathing, are more pronounced. Cyclic sinus arrhythmia is characteristic of young people with cardiac neurosis and trained athletes. 2) non-cyclic sinus arrhythmia is often detected in elderly people with systemic atherosclerosis, when the functioning of the brain centers for regulating heart rhythm is impaired. It is not associated with breathing and is probably one of the manifestations of aging of the body.

Sinus arrhythmia in a young man of 17 years during the night of sleep.

Sinus arrhythmia, whatever its origin, does not require treatment. On the contrary, one should be wary of an excessively regular heart rhythm (rigid sinus rhythm), when natural fluctuations are practically not observed. It is always worth remembering the fundamental law of dialectic unity: opposites must combine, dynamically balance, complement each other. In other words, the sinus rhythm should not be too regular (the predominance of one opposite), since it is associated with ventricular arrhythmias and an increased risk of cardiovascular death. However, I hasten to reassure you: a rigid sinus rhythm is characteristic of heavy chronicles of the heart. To summarize: even if the doctor meets with pronounced manifestations of sinus arrhythmia, attention will not be focused on it.

The open oval window is a natural anatomical message between the right and left atrium, normally present only in the fetus.

After birth, this hole overgrows for a year. If it remains open, then it is a heart disease. The timing of the clinical manifestation of a defect (symptoms of heart failure) depends on the size of the defect (window). If the defect is small, the symptoms may appear only in adulthood (over 40 years); in the case of a significant defect – symptoms occur in childhood. Diagnosed with a defect using ultrasound of the heart. Sometimes, if the defect is very small or the visualization of the heart is bad, the usual ultrasound of the heart is not informative – then a transesophageal ultrasound of the heart is used. Treatment of blemish only operational. Currently they are trying to use a minimally invasive technique – catheter implantation. "patches" in place of an open oval window.

"Diffuse changes in the myocardium of the left ventricle". This idiom is often found in the description of the electrocardiogram with which the patient comes to the cardiologist for an appointment. With this phrase, functional diagnostics doctors are taught to describe any difficult to interpret and non-specific ECG changes reflecting the electrical activity of the left ventricle. My attitude towards him is extremely negative. As I mentioned on the pages of the site, a normal ECG is generally low in sensitivity and low specificity for many heart conditions. I think that this sounds surprising to the patient, but the ECG can change stereotypically with many heart and non-heart (!) Diseases. So, such changes that do not fit into a particular ECG diagnosis are usually interpreted as "diffuse changes in the myocardium of the left ventricle". This mainly concerns the tine. "T" on ECG. There is even an expression: "many diseases, and T wave one". But in a different way, one can say: with a multitude of diseases, the T wave changes equally. I have a negative attitude to the discussed phrase, because I noticed: it disturbs and disturbs patients who, after reading such an ECG conclusion, become suspicious; although the changes on the ECG, in fact, may not reflect at all "poor heart condition". Sometimes one incorrectly said or incorrectly written word can provoke or aggravate neurosis. Expression "diffuse changes. " I usually replace with "nonspecific changes in the myocardium of the left ventricle", or, I describe the ECG literally, for example: "negative T teeth there, there, there. "

Radiofrequency catheter ablation (RFA). Modern surgical treatment of cardiac arrhythmias that are not amenable to drug correction. With this method, all instrumental manipulations are carried out through the puncture of one of the large veins (usually the subclavian). Through a vein, a medical catheter is delivered to an arrhythmic focus, which is affected by high-frequency energy – this leads to destruction "focal arrhythmia".

The most important advantage of the RFA over traditional abdominal cardiac surgery is its minimally invasiveness – manipulation is performed without opening the chest, without general anesthesia, without subsequent long-term healing of the surgical suture and physical rehabilitation. RFA was originally used for the radical treatment of patients with WPW syndrome. Indeed, the destruction of an additional beam with the help of local exposure to high-frequency electrical energy led to a brilliant clinical result: complete recovery of the patient. In the future, the range of indications for the performance of the RFA significantly expanded. Now it is used to treat atrial fibrillation and flutter, idiopathic ventricular and atrial extrasystoles, AV-reciprocal tachycardia, etc. Those patients who used to suffer from all their lives from heart attack and interruption of the heart with the implementation of the RFA technique had a chance for full recovery. The maximum therapeutic effect (no recurrence in the late postoperative period) with RFA can be traced in patients without signs of organic myocardial damage.

Sinus tachycardia – increased heart rate over 90 beats per minute. At rest, the heart of a healthy person is reduced with a frequency of 50-80 beats per minute. Causes of sinus tachycardia: 1. The natural reaction of the body (heart) to physical or psycho-emotional (anger, cry, fear) stress. Did everyone run a hundred? Did everyone take the exam at school? These are situations where the body needs more energy; In this case, an increase in heart rate ensures the delivery of the required amount of oxygen to the organs and tissues. 2. Sinus tachycardia is often observed in persons with cardiac neurosis, characterized by constant, background agitation – patients may complain of palpitations. 3. Unmotivated sinus tachycardia is sometimes observed with alcohol abuse, dyshormonal cardiomyopathy, pregnancy, hyperthyroidism, and some other clinical situations. 4. Sinus tachycardia occurs in patients with severe organic lesion of the myocardium, complicated by heart failure; for example: after myocardial infarction, prolonged diastolic dysfunction of the left ventricle. In such situations, an increase in rhythm is a compensatory mechanism that arises in response to "heart muscle weakness" – The affected heart is forced to contract more often in order to provide the body with oxygen. 5. Severe diseases of the bronchopulmonary system, when the lungs cannot provide the necessary amount of oxygen in the blood – respiratory failure. Then the heart begins to contract more often in order to compensate for blood hypo-oxygenation.

Blockade of the bundle of His. Often, patients are deducted on the ECG issued by them conclusion "about the blockade of some kind of legs". Awareness of availability "heart block" many leads to a state of cognitive dissonance. Part of the cardiac conduction system, which provides electrical excitation from the atria to the ventricles, are the so-called bundle of his.

They are two: right (goes to the right ventricle) and left (goes to the left ventricle). The left leg has a front and rear branch. Carrying on each of the legs can be slow or interrupted completely. In the first case they talk about an incomplete blockade, in the second – about a complete one. The blockade of the left leg is absolutely not characteristic of a healthy heart. Other variants of blockades (right leg, anterior or posterior branch of the left leg) can be either a manifestation of the disease or occur in healthy people, in the form of an innocent congenital anomaly of the cardiac conduction system detected on an ECG. However, the last category of persons, in my opinion, need unobtrusive monitoring by a cardiologist to track the dynamics of ECG blockade and well-being – occasionally such conduction disturbances progress.

Early ventricular repolarization syndrome (RRF). Almost a quarter of all people on the ECG show the so-called early ventricular repolarization syndrome. Patients often come to the cardiologist with the question, what does it mean? This ECG phenomenon reflects the local heterogeneity of cardiac repolarization and is innate. In the overwhelming majority of cases, it is absolutely safe and should be treated as, for example, mitral valve prolapse 1 tbsp., Shortened P-Q interval syndrome, an additional cord of the left ventricle — that is, as an innocent cardiac anomaly. However, for a fraction of a percent (

0.1%) this syndrome increases the risk of sudden cardiac death through the launch of idiopathic ventricular fibrillation – from the outside it looks like the sudden death of a completely healthy young man. We regularly hear about such shocking episodes from the media. Medical journals also describe incidents of malignant fatal RRZh syndrome. However, the a priori probability of its unfavorable course is less than 1%. One of the possible markers of the potential danger of the syndrome is a change in the degree of prematurity of repolarization (that is, on different ECG manifestations of the syndrome have varying degrees of severity), especially in combination with syncopal anamnesis.

"Vitamins for the heart". Repeatedly, in my practical activities, I had to deal with the patient’s perseverance, urging me to assign him some "vitamins for the heart". Special pressure is felt from persons with cardioneurosis. I do not know where all this people are reading, but no "vitamins strengthen the heart muscle" not. Apparently, the media (including the Internet) advertising these drugs in the context of their "cardiometabolic effect". Often, such patients have previously been with cardiologists; they prescribed Magnesium B6, Preductal, Mildronate, Magnerot, Kudesan and others. Apparently, such drugs are regarded by someone as "vitamins for the heart". The indicated drugs have their niche in cardiology, and in short it looks as follows: antiarrhythmic effect (we are talking about magnesium-sensitive extrasystole); anti-ischemic effect (Prepuctal-type drugs are indicated for patients with severe angina); the placebo effect – the patient wants to be treated – let him be treated (!), but these drugs will act at the level of auto-suggestion.

Warfarin is an anticoagulant; prevents the formation of blood clots, helps dissolve existing ones. Unlike aspirin, the main point of application of warfarin is: 1) prevention of venous thrombosis, 2) prevention of thrombus formation in the cavities of the heart. In cardiology, warfarin is used in 3 clinical situations: pulmonary embolism, atrial fibrillation (atrial fibrillation) and the presence of a prosthetic heart valve. In pulmonary embolism, venous thrombi forming in the veins of the pelvis and lower extremities, coming off with blood flow are recorded in the branches of the pulmonary artery. Appointment of anticoagulants in such a situation is one of the mandatory components of treatment aimed at preventing the prolongation of thrombosis in the veins and lysis of thrombotic masses brought into the pulmonary artery. In atrial fibrillation, there is no effective atrial contraction, which creates conditions for stasis, blood turbulence in the so-called left atrial appendage. The auricle of the left atrium is a trabecular, closed cavity in which thrombotic masses easily form. From the intra-atrial thrombus, chronologically unpredictable, can come off "pieces" and fly (embolism) in different organs; the most dramatic situation – cerebral artery thromboembolism – means a stroke. However, not everyone who suffers from atrial fibrillation in the left atrium forms blood clots. The risk group includes: 1) persons with a permanent form of atrial fibrillation or with often recurring (more often once a month) arrhythmia attacks (especially subjects over 60 years old; the older, the higher the risk of thrombosis); 2) patients with dilated left atrium (determined by ultrasound of the heart); 3) patients with additional risk factors for increased thrombosis: diabetes, obesity, myocardial infarction, etc. Prosthetic heart valve is extremely thrombogenic; The potential complication is the same as in atrial fibrillation: thromboembolism. Patients with a prosthetic valve take warfarin in high dosages. Warfarin treatment is carried out only under the supervision of the INR (internationally normalized attitude). INR is a relative indicator reflecting the strength of the anticoagulant effect of warfarin. Blood is donated to the INR in any small laboratory. INR is considered therapeutic from 2 to 3.5 – only with this range of INR, new blood clots are not formed, and old ones dissolve. If the INR is less than 2, consider that warfarin is idle. With an INR of more than 3.5, there is a threat of bleeding – in this case, the risk of its use exceeds the benefit. The need to regularly take a blood test for INR, along with the lability of this parameter, is the cornerstone in the treatment of warfarin. Sometimes, it is difficult to achieve the target value of the INR, and when it is reached after some time, it suddenly falls outside the acceptable limits. With "titled" INR blood test is taken only once every 4-6 months. In recent years, new anticoagulants have been created that do not require laboratory monitoring (no need to go to the clinic to take a blood test) – this is their huge advantage over warfarin. Pradaks and Xarelto are widely used in Russia. The main disadvantage of these drugs is the price: a monthly course of treatment will cost about 3000-4000 rubles, which is 10 times the cost of treatment with warfarin. I emphasize that if the target INR has been achieved during warfarin therapy and it remains constant all the time, then the effectiveness of anticoagulant treatment is absolutely comparable to that of new anticoagulants. So for "budget" Patients warfarin is still the drug of choice. Life with Vafarin.

Dishormonal (climacteric) cardiomyopathy. Climax – natural wilting of the human reproductive function. Most people experience this period safely or with moderately unpleasant symptoms. Pathological menopause is accompanied by a whole range of painful sensations, which noticeably worsen the quality of life and force you to see a doctor. One of the manifestations of the pathological course of menopause may be dishormonal cardiomyopathy. Sex hormones, being natural cardioprotectors, play an important role in the metabolism of the heart muscle, so their lack during the period of extinction of reproductive function underlies the development of cardiomyopathy. This disease is a combination of nonspecific menopause symptoms (vegetative crises and changes in the neuropsychic sphere) and cardiac symptoms. Vegetative manifestations: hot flashes, excessive sweating, numb feeling in different parts of the body, dizziness. Neuropsychiatric symptoms: irritability, tearfulness, insomnia, unstable mood, dissatisfaction with inhalation, unmotivated weakness. Cardiac symptoms consist of symptoms, as in cardiac neurosis (cardialgia, palpitations, extrasystoles) and ECG changes ("bad ECG"). The chronology of the appearance of subjective symptoms in female and male menopause is different. In women, the symptoms of dyshormonal cardiomyopathy can start from 35-37 years old (that is, long before the menstrual cycle and the menopause itself) or, on the contrary, appear on the 6th decade of life (that is, several years after the onset of menopause). Thus, I emphasize that the onset of symptoms of the pathological female menopause does not always correlate with "typical menopausal age" – 40-50 years. The age of male menopause is less predictable, but unlike female, its symptoms more or less clearly correlate with a decrease in libido and a progressive impairment of copulatory ability (erectile dysfunction, up to impotence). Another thing is that men suffering from dyshormonal cardiomyopathy often hide their intimate problems from a cardiologist without understanding their connection with heart symptoms, which makes diagnosis difficult. Treatment of pathological menopause resembles that of cardioneurosis. First, it is necessary to lucidly explain the essence of the problem, its safety and complete reversibility of the disease (dyshormonal cardiomyopathy passes on its own after 1-5 years). Secondly, sedatives are prescribed if necessary (starting with herbal tinctures, ending with prescription drugs). Thirdly, with arrhythmic symptoms (palpitations, interruptions), it is possible to prescribe cardiotropic drugs that stop these sensations. Fourth, with the ineffectiveness of the above measures, hormone replacement therapy is shown to the patient under the supervision of a urologist or gynecologist. However, the need for hormone therapy of pathological menopause does not arise in recent years, since it is almost always possible to cope. "non-hormonal means". In conclusion, I emphasize once again: dyshormonal cardiomyopathy is a functional, fully reversible heart disease, the outcome of which is complete recovery.

Extraesophageal EFI of the heart (electrophysiological study). The method of studying some of the electrophysiological parameters of the heart, possible due to the anatomical fit of the middle third of the esophagus to the heart, more precisely to the left atrium. Research methodology: through the oral cavity a special electrode is inserted into the esophagus to the place of its contact with the heart; then, according to a special protocol, electrical impulses are passed from the esophagus to the heart. The nature of the heart’s response (determined by ECG) to the impulse imposed on it from the outside is the object of study. CPEFI is shown 1) in case of suspected sick sinus syndrome (heart block), 2) in case of suspected atrioventricular conduction disorder (heart block), 3) in case of suspected reciprocal supraventricular arrhythmias involving the AV node, 4) in case of suspected syndrome WPW. The doctor may suggest that you conduct CPEBI if you are worried about fainting (semi-conscious consciousness) and heart attacks of unclear etiology; as a rule, this specific study is preceded by Holter ECG monitoring, which did not provide a definite answer to the questions posed. In addition, the transesophageal electrode is sometimes used for therapeutic purposes: through transesophageal stimulation of the heart, some supraventricular tachyarrhythmias are stopped.

Extraesophageal ultrasound of the heart. It is known that with ordinary ultrasound of the heart, called transthoracic, the sensor is applied to the chest. At the same time from the structures of the heart ultrasonic sensor "separated" skin, intercostal muscles, ribs, lungs. In the way that "get to your destination", ultrasound needs to go through several anatomical obstacles of different density, which reduces the quality of the ultrasound image.

There is an alternative methodology for imaging the heart through ultrasound, which is possible due to the anatomical fit of the middle third of the esophagus to the heart. Through the oral cavity, a special transesophageal sensor is inserted into the esophagus until it touches the heart; from this place ultrasound with minimal distortion "gets" to the heart structures – visualization of the heart is almost perfect. Conducting transesophageal ultrasound of the heart is shown in cases where a conventional ultrasound does not provide answers to questions posed. These include: 1) diagnosis of blood clots in the heart cavities (mainly in the left atrial appendage with atrial fibrillation), 2) assessment of the function of the prosthetic valve (for example, if its endocarditis or thrombosis is suspected) (3) , dissecting aneurysm), 4) suspicion of infective endocarditis, unconfirmed by conventional ultrasound, 5) accurate diagnosis of some congenital heart defects (atrial septal defect, bicuspid aortic valve), long-term non-hemodynamic omy.

Abnormally located chord (ARCH). From the free ends of the cusps of the mitral valve are the so-called chords, which are attached by the other end to the walls of the left ventricle. The chord is a thin (2-3 mm) connective tissue cord, indirectly involved in the opening and closing of the valve.

When the left ventricle contracts (systole) – the tension of the chords weakens – the valve closes tightly; when the left ventricle relaxes (diastole) – chords "to reach out" behind "straightened" ventricle – the valve opens. Breaking the chord (for example, in myocardial infarction) leads to the fact that in the systole of the ventricle the mitral valve begins to prolapse (sag) into the cavity of the left atrium; in such a situation, the valve closes untightly and part of the blood returns (regurgitates) to the left atrium. The ARCH is the chord that "stretched" between the walls of the left ventricle. Such a chord does not perform any function, because of its abnormal location; she is simply present in the heart, as an additional burden. Approximately 80% (!) Of people have at least one ARCH. According to modern concepts, the clinical significance of ARCH is close to zero — that is, its presence does not threaten anything. The only exceptions are cases of polychordality (when more than one APH is found in the left ventricle) or when the APX is not a connective tissue, but a muscle cord ("fat" chord). It is assumed that such subjects increase the risk of sudden cardiac death at a young age (under 30 years) by a fraction of a percent. If, for example, to take 10,000 people without ARCH and 10,000 with ARCH, then in the second group 1 people will chronologically unpredictably die suddenly in their youth. Persons with polychordality or presence "muscular" chords have an even higher risk of sudden cardiac death. ARCH is diagnosed by ultrasound of the heart. However, even with the presence of ARCH, it is not always possible to detect it – much depends on the experience and pedantry of the doctor.

Systolic (upper) blood pressure (SBP) is the maximum pressure in the arterial system developed during systole (contraction) of the left ventricle. Its value depends mainly on 1) the stroke volume of the heart (the volume of blood pushed out by the left ventricle during one systole); 2) the elasticity of the large arteries (especially the aorta) and 3) the circulating blood volume. The upper limit of the norm of the GARDEN is the value equal to 139

over 80 years old) – the blood supply to the cerebral blood pressure regulation centers is disturbed.

Diastolic (lower, "renal"a) blood pressure (DBP) is the minimum pressure in the arteries during diastole (relaxation) of the heart. Its value depends on 1) the tone of the peripheral arteries, 2) the elasticity of the large arteries (especially the aorta) and 3) "suction" action of the aortic valve. The hemodynamic influence of these factors leads to the fact that the blood flow becomes more or less uniform (continuous) throughout the entire cardiac cycle — thus, relatively high blood pressure is maintained during diastole. The upper limit of the norm dad is a value equal to 89

Diastolic dysfunction of the left ventricle. Often, in the conclusion of an ultrasound of the heart, patients can read about the so-called diastolic dysfunction of the left ventricle (DDLS). The diastolic function of the left ventricle is its ability to relax after systole (contraction); it is during this period that the left ventricle is filled with blood, followed by another contraction. DDLS – the inability of the left ventricle to stretch, relax and adequately fill with blood without "inclusions" compensatory mechanisms.

Violation of the diastolic function of the left ventricle leads to the fact that in the left atrium (from this chamber blood flows in the left ventricle) pressure starts to rise due to stagnation of blood in it; further, if DDLS is maintained, the pressure in the vascular system of the lungs rises and

The ability for normal relaxation of the heart chambers in general and of the left ventricle in particular depends on the following factors: myocardial stiffness, pressure inside the pericardial cavity, heart rate.

– Myocardial stiffness is the most common cause of DDLS. Any condition leading to increased density and, consequently, poor myocardial distensibility (advanced age, obesity, prolonged arterial hypertension, left ventricular myocardial hypertrophy, some heart defects, chronic coronary artery disease and

– Increased pressure inside the pericardial cavity. Basically, this refers to emergency cardiology, when for some reason a fluid accumulates in the pericardial cavity, which squeezes the heart and prevents it from relaxing. Examples: a knife wound to the heart, pericarditis (for example, in myocardial infarction) with a large amount of fluid effusion, long-term systemic diseases (oncoprocesses, some rheumatic diseases, uremia, etc.) complicated by pericardial effusion. Relatively rare cause of DDLJ.

– Frequent rhythm of the heart. The more often the heart contracts, the shorter the period of diastole (relaxation); accordingly, the left ventricle for such a short diastole is filled with a smaller blood volume – the pressure in "preceding" ventricular chambers will rise. Often, it is in this scenario that the clinic of diastolic heart failure develops in overweight people. In this case, a drug-induced reduction in heart rate leads to the normalization of intracardiac hemodynamics and a reduction (relief) of symptoms.

It is necessary to distinguish the concepts of DDLS and diastolic heart failure (HF). DDLS may be asymptomatic for a long time (years), for example, in hypertension. DDLS, as a manifestation of a pathological condition, with inadequate treatment always leads to diastolic HF. The main and very first symptom of diastolic HF is shortness of breath with habitual physical exertion. DDLS is reliably diagnosed by ultrasound of the heart.

Parasystole is a premature contraction of the heart, which, unlike an extrasystole, does not depend on a normal heart contraction, since "not linked" with him. In other words, if extrasystole is a result of the main rhythm, the manifestation of which is the presence of a coherence interval (the appearance of an extrasystolic contraction at strictly defined time intervals) and submission to the phenomenon "over frequency suppression", the parasystole functions as an independent, alternative heart rate driver. Parasystole has its own automatism, which sets its frequency. Thus, with a parasystole in the heart there are two pacemakers that do not depend on each other: normal (sinus node) and ectopic (parasystolic). If, for example, the automatism of the parasystolic center exceeds the automatism of the sinus node, then the number of parasystoles will exceed the number of normal contractions.

The figure depicts 2 parasystoles: they are not connected (not linked) with the main rhythm, appear according to their own automatism. If, for example, the sinus node stops functioning (acute blockade of the sinus node), the beats will disappear, but the parasystole will not.

Parasystole, like extrasystole, is a purely electrocardiographic diagnosis. The clinical significance of parasystole and extrasystole is similar. But there are differences:

– The ratio of parasystoles and extrasystoles approximately 1:20 (according to my observation

– Parasystole is often refractory to medication effects, which makes it very difficult to treat. If parasystoles are very many, then the technique comes to the rescue

– Parasystole is worse subjectively transferred, as it introduces an even greater imbalance in the normal chronology of the heart rhythm, arising "by own decree".

– A very frequent parasystole will lead to arrhythmogenic dilatation of the heart with a greater probability than a very frequent extrasystole.

– Depolarization of parasystoles is determined by calcium current, and arrythmia – by sodium. Modern antiarrhythmics effectively inhibit sodium current and low calcium.

– Against the background of organic heart disease, parasystole is more malignant than extrasystole. In other words, it is more likely than extrasystole to cause fatal ventricular arrhythmias.

Sudden cardiac death (SCD) is a death of a non-violent nature due to cardiac pathology, when circulatory arrest occurs within no more than an hour after the onset of acute clinical symptoms. SCD includes 4 periods: prodromal (the appearance of some kind of precursors of sudden death), the onset of acute symptoms of the disease, circulatory arrest, biological death. The clinical picture of the Air Force is variable. In many patients, the prodromal period is absent and the disease makes its debut with acute symptoms: chest pain, shortness of breath, half-swoon or faint. If the onset of the disease begins with fainting, then in most cases this is a manifestation of a sudden cessation of blood circulation. Then the period of acute symptoms and circulatory arrest chronologically merge into a single whole, and from the outside it looks like "walked, fell and died". SCD can occur against the background of a known heart disease or be the first and only manifestation of latent pathology, which can only be established after opening. The main thing is always an unexpected death.

From a social and medical point of view, ARIA should be divided into deaths up to 30 years and after 30 years. In children and young people under 30 years old, BCC occurs

1 case per 50,000 people, and the main causes of ARIA are the following diseases:

– Arrhythmogenic dilatation of the right ventricle

– Anomalies of the coronary arteries

– Congenital heart defects

After 30 years, ARIA is much more common.

1 case per 1000 people and, as a rule, lead to it:

– Dilated cardiomyopathy (expansion of the heart chambers), which may be idiopathic (of unknown etiology) or secondary to the background of the disease (uncontrolled arterial hypertension, myocarditis, alcoholic heart damage, etc.)

– Sleep apnea / hypoponet syndrome (typical for people with obesity)

The BCC peak occurs at the age of 35-45 years. The ratio of men and women is approximately 7: 1. Speaking about the chronology of events that lead to ARIA it is necessary to highlight: the presence of a disease (for example, one of the above), the effect of a transient trigger factor, an arrhythmic trigger, the development of a circulatory arrest. Consider the whole drama of the BCC events on the example of one of the most common cardiovascular diseases – CHD. The patient for many years has asymptomatic atherosclerosis of the coronary arteries. At some point (usually due to stress or intense physical exertion, a triggering factor) occurs. "tear" atherosclerotic plaque, in place of which a thrombus forms in seconds, completely covering the lumen of the cardiac artery. One of the possible consequences (manifestations) of acute thrombosis of the heart artery is ventricular fibrillation (arrhythmic trigger). The occurrence of this arrhythmia is always accompanied by cessation of blood circulation and loss of consciousness (clinical death). Without emergency medical care, such a patient dies within 5 minutes (biological death). If ventricular fibrillation develops some time after an acute cardiac artery thrombosis, it is preceded by the clinical symptoms of myocardial infarction: severe chest pain and / or shortness of breath. If ventricular fibrillation occurs immediately after cardiac artery thrombosis, then, even before he realizes the symptoms of myocardial ischemia (pain, shortness of breath), the person loses consciousness and dies. How ventricular fibrillation develops in real life is shown in the figures:

This patient was reanimated because he was in the hospital.

Arrhythmic triggers leading to ARIA are divided into:

– Bradyarrhythmic (rapidly progressive decrease in heart rate)

Ventricular tachyarrhythmias triggering SCD are a uncoordinated contraction of the heart with a very high frequency. This is about:

– Ventricular tachycardia, turning into ventricular fibrillation

– Ventricular tachycardia type "pirouette"turning into ventricular fibrillation

– Primary ventricular fibrillation

All of the above tachyarrhythmias are triggered by ventricular extrasystoles (for more on the role of extrasystoles in ARIA here).

Bradycardia, as the cause of SCD, is less common. The following figure shows how the heart can suddenly stop:

This patient suffered from fainting (sinokopami) that occurred 2-3 times a month. With Holter ECG monitoring, it was possible to fix the moment of cardiac arrest for 8 seconds – another faint occurred. After the implantation of the pacemaker, the syncopes disappeared. If the cause of the suffering was not established in time, then one of the fainting would end in death.

Another observation from personal experience, proving the role of bradycardia, as the probable cause of ARIA. Male, 47 years old, obese, severe arterial hypertension. When Holter ECG monitoring during the night period, pauses in the work of the heart with a duration of 2-4 seconds were detected, which chronologically coincides with respiration stops for a few seconds:

Diagnosed with sleep apnea. Without proper care, the probability of SCD in a dream for this patient over the next 5 years is about 50%.

According to literary data "contribution" Each arrhythmic trigger in the occurrence of ARIA is as follows:

1- Primary ventricular fibrillation

2- Ventricular tachycardia type "pirouette"turning into ventricular fibrillation

4- Ventricular tachycardia, turning into ventricular fibrillation

Prevention of ARIA is the timely detection of the disease, which can lead to such a dramatic outcome. It is clear that for various reasons it is not always possible. First, in at least half of the cases, ARD develops without a prodromal period, that is, absolutely suddenly against the background of subjective health. Secondly, if there is a prodromal period, then it can manifest itself as unimportant, in the patient’s mind, symptoms (for example, non-intensive, sporadic pain in the chest or an episode of faintness); accordingly, he does not seek medical assistance.

In the case of a known heart disease, measures are taken to control it, which in itself reduces the risk of air force by several times. If we are talking about heart disease, we offer its prompt correction; in the diagnosis of coronary artery disease – myocardial revascularization and drug therapy aimed at restoring adequate blood flow in the arteries; intravital diagnosis of canalopathy means the implantation of a cardioverter-defibrillator; with clinically significant sleep apnea syndrome – CPAP therapy and

If, however, VSS happened in non-hospital conditions ("a man in the street fell, lost consciousness and wheezed"), then the order of assistance is as follows: given that in at least 80% of cases the cause of fainting is ventricular tachyarrhythmia, it is necessary to produce a so-called external defibrillation as soon as possible (passing a single high-voltage electric current through the chest) in the heart and restores the heart rhythm. If you do not perform defibrillation within 5 minutes, the chances of saving a person are subsequently close to zero, because during this time the electrical fibrillation activity of the heart is completely extinguished. Here is an example of successful defibrillation and resuscitation of a person:

In some large cities of developed countries in public places (for example, in the subway) there are portable defibrillators and employees, most importantly, trained to use them. In Russian reality, external defibrillators can only be found in the hospital and at the SMP brigades; therefore, the BCC outside the hospital can end safely only in one case: "an ambulance was passing by". However, in the absence of a defibrillator under your hands, you should immediately call an ambulance, cover your head with ice, begin an indirect heart massage and breathe mouth to mouth (it is clear that several people have to do all this agreed). Even in the case of competently conducted resuscitation actions and a quick arrival of the SMP (no more than 10 minutes), the chances of a successful outcome of resuscitation are no more than 10%. Nothing can replace emergency defibrillation.

One of the main outpatient principles for the prevention of sudden cardiac death with known organic heart disease is limiting exercise. It’s not about "vegetable lifestyle"; just to avoid any exertion, accompanied by significant dyspnea: running, brisk walking, walking uphill, heavy fitness and

Sinus rhythm is the normal heart rhythm of a person when electrical stimulation is generated in a special area of ​​the right atrium called the sinus node. Sinus node is a cluster of cells capable of spontaneous depolarization. From the sinus node electrical excitation extends to the rest of the myocardium. The frequency of sinus rhythm (heart rate – HR) at rest ranges from 60 to 90 per minute. HR less than 60 min. – is called sinus bradycardia (this is a variant of sinus rhythm), which is normally recorded during the rest period, during sleep. Heart rate over 90 min. – is called sinus tachycardia (this is also a variant of sinus rhythm), which is normally detected during physical and emotional stress, reaching 150-170 cuts per minute at the peak. – according to the needs of the body.

The bicuspid aortic valve is a congenital heart disease, which occurs in about 1 in 800-1000 people – that is, it is not so rare. The aortic valve, which normally has 3 doors, in the course of a person’s life experiences significant hemodynamic loads – blood from the left ventricle is forcefully released into the aorta, "hitting" herewith, about its walls and opened valve flaps; in the period of diastole (relaxation of the heart), a certain volume of blood from the aorta rushes back into the left ventricle, but by this time the aortic valve leaves are tightly closed, which prevents retrograde reflux of blood (blood "is facing" with closed valve). Normal, tricuspid aortic valve, functioning in this mode "non-stop", only in old age (older than 60 years) can undergo sclerotic changes, calcification. And even then, only in rare cases, its degenerative, age-related involution reaches the degree of defect (senile aortic defect).

Bicuspid aortic valve is defective. It is subjected to the same impacts as the tricuspid, but has less on the leaf. So 2 doors will take on "load for three". Bicuspid aortic valve is much easier to be infected (bacterial endocarditis) and much more sensitive to rheumatic lesions. But even if these diseases do not develop (which often happens in socially adapted people), the double-leaf valve still wears out (is sclerosed) in a natural way much earlier than the three-fold valve, which is manifested in the formation of a heart defect: aortic insufficiency. In people whose activity is associated with significant physical exertion (for example, athletes), a developed defect can be formed by 40-45 years; on the contrary, in persons far from sports, the clinical picture of aortic insufficiency manifests by 55-60 years. It is important to understand that in any case, a bicuspid aortic valve will lead to a particular complication, and thus shorten life expectancy. The most dramatic outcome of an undiagnosed bicuspid aortic valve in time is sudden cardiac death. Lifetime diagnosis of this defect means the mandatory limitation of intense physical exertion (running, heavy fitness and

Nitroglycerin was isolated in the middle of the 19th century. Initially, this chemical substance was used in technical needs, in particular, as explosives. Later it was found that nitroglycerin is a powerful vasodilator – relaxes the smooth muscles that are present in many hollow organs and in the walls of blood vessels. However, researchers were confused by its short duration.

5 minutes. Therefore, it is not widely used as an antispasmodic. However, it was found that nitroglycerin is able to quickly and effectively stop an attack of angina. This phenomenon has long been attributed to its direct vasodilating effect – the expansion of the coronary arteries. Scientists have continued rational research and found that the strength of the effect of nitroglycerin on the veins and arteries is very different and correlates approximately as 10: 1. In other words, nitroglycerin is primarily a powerful venous dilator, and affects arteries only in superior concentrations. The postulation of this phenomenon puzzled the medical community, since it was necessary to explain its exceptional effect in an attack of angina pectoris. Currently, it has been proven that nitroglycerin suppresses angina pectoris pain through a mechanism for reducing cardiac preload. In the physiology of the cardiovascular system, there is the concept of preload and afterload on the heart. Preloading is the entire volume of blood that flows to the heart from the veins per unit of time – depends primarily on the tone of the peripheral veins. Afterload is the entire volume of blood that "pushes out" heart into the arterial bed per unit of time – determined by the level of peripheral resistance of the arteries; simply put – current blood pressure. Nitroglycerin, reducing preload (expanding veins), contributes to the deposition of blood in the veins, which leads to a decrease in the volume of blood flowing to the heart, and hence to facilitate its work. In this and only this, its miraculousness lies in the attack of angina. Another niche of using nitroglycerin in cardiology: the relief of the phenomena of acute left ventricular failure (pulmonary edema, cardiac asthma). With a serious lesion of the left ventricle or its valve apparatus (myocardial infarction, myocarditis, some defects, etc.), there is a stagnation of blood in the vessels of the lungs; however, the preload remains at the same level. The following pathological situation arises: the affected heart is not able to pump all the volume of blood flowing to it; the blood begins to stagnate in the vessels of the lungs, which leads to edema of the pulmonary parenchyma – this is the manifestation of cardiac asthma, subjectively felt as shortness of breath, asphyxiation. The use of nitroglycerin in such a situation will quickly reduce the preload, which eliminates the dissonance ratio "inflow-outflow". So, in cardiology, nitroglycerin is used only in 2 cases: to relieve angina and left ventricular failure. The use of nitroglycerin for any pain in the chest, of course, is not justified. Since nitroglycerin acts for no more than 5 minutes, then if the pain passes through a longer period of time (usually patients say: "he relieves pain in 10-20 minutes") – it means we have some kind of cardialgia, and the pain passes by itself or through the placebo effect. Given the enormous prevalence of cardialgia in general (the ratio of cardialgia and angina with outpatient admission of at least 20: 1), the use of nitroglycerin can be quite reasonable in a simple diagnostic test: pain → taking nitroglycerin tablets → evaluating the response to it over the next 5 minutes. With angina, the effect is fast and full. Otherwise it is cardialgia. If we have a chronicle in front of us, then the lack of response to nitroglycerin means 3 possible clinical situations: cardialgia, prolonged angina attack (preinfarction state), myocardial infarction debut. There are diseases of the esophagus, manifested by chest pains very similar in characteristics to angina, and the pain in them can positively (including quickly) respond to nitroglycerin. In such a situation, only a comprehensive assessment of a painful attack (its appearance mainly in the prone position, concomitant symptoms of dyspepsia, a normal ECG at the height of the attack, etc.) eliminates its angina pectoris. The main side effect of nitroglycerin is headache. It is explained simply: the veins of the brain are dilated → a transient microflow of brain tissue arises → there is a feeling of pain in the head. With its chronic intake, the headache disappears. For the prevention of angina attacks, long-acting nitroglycerin tablets (up to 6-10 hours) are used: Pektrol, Cardiket, Monochinkwe, etc.

Corvalol is a sedative actively used in cardiology to relieve symptoms of cardiac neurosis. I note that, unlike others "cordial" drops, Corvalol has in its composition Phenobarbital – that is, a pharmacological substance with a pronounced sedative effect. Valerian, Motherwort, and other tinctures are just a mixture of soothing herbs, so it’s not entirely clear what effect they have: placebo or drug? The presence of Phenobarbital in Corvalol automatically classifies it as an effective sedative. Another thing is that the concentration of Phenobarbital in Corvalol is minimal, so to speak, homeopathic. However, in my opinion, even such an insignificant concentration of it is enough to rank "cordial" sedative drops, he held a non-competitive first place. Calculation of Corvalol drops when taking it "on demand" this is: "drop on year of life". That is, for example, if we have a 40-year-old subject, then he should take at least 40-45 drops. The use of Corvalol in a smaller dosage is one of the main reasons for its inefficiency. It is possible to drip more, less – at best, expect a placebo effect. Corvalol and related remedies (Valokardin, Valoserdin) are used mainly for acute relief of cardioneurotic symptoms: cardialgia, palpitations in the face of anxiety, etc. Some patients refer to intolerance to Corvalol because of the presence of alcohol in it. I treat with understanding such patients. Now there are a lot of other non-prescriptive sedatives at their disposal (Novopassit, Persen, etc.), but their effectiveness has been questioned by many experts.

Pheochromocytoma is a tumor of the adrenal medulla producing catecholamines (adrenaline, norepinephrine). Catecholamines are adrenergic hormones that are synthesized in the pair endocrine organ – adrenal glands. Catecholamines are released into the blood continuously in a certain basic amount to maintain the tone of the sympathetic nervous system (↑ blood pressure, ↑ pulse, ↑ bronchus tone and

The main clinical phenomenon of pheochromocytoma is the uncontrolled release of catecholamines into the bloodstream, which is accompanied by a sudden adrenergic hypertensive crisis. Its characteristics: an abrupt increase in blood pressure to high numbers (upper pressure, as a rule, exceeds 200 mm Hg), palpitations, severe headache, trembling in the body, sweating, at the end of an attack, urge to urinate or defecate. A crisis is stopped as suddenly as it appears. The traditional drug treatment used in the treatment of hypertension does not prevent catecholamine crises with pheochromocytoma – that is, it is absolutely not effective. In the interictal period, the patient may feel healthy, but if he takes antihypertensive drugs, then most likely the blood pressure will be symptomatically low. The classic, crisp course of pheochromocytoma is observed in the debut of the disease (months or years); subsequently, as pathology progresses, blood pressure remains elevated even after a hypertensive crisis. Pheochromocytoma, being a syndrome of secondary hypertension, has a progressive, malignant course of uncontrolled arterial hypertension. And if radical treatment is not carried out in time, then one of the crises ends "catecholamine shock" (syndrome of uncontrollable hemodynamics) and death of the patient. Almost always, it is the cardiologist who first encounters a patient with pheochromocytoma, since high blood pressure is its only manifestation. Unfortunately, the clinical picture of pheochromocytoma can be erased: crises are not expressed explicitly or there is a persistent increase in blood pressure, which mimics the usual hypertension. In such a situation, the doctor should be alerted by the extremely low effectiveness of prophylactic antihypertensive therapy (resistant hypertension), including with a combination of 3-4 drugs. The pheochromocytoma is diagnosed laboratory and instrumentally. If there is a reasonable suspicion of her taking a blood test for free metanephrins (catecholamine metabolites) – a positive result with a 95% probability will indicate a pheochromocytoma. Visually, this tumor is diagnosed by computed or magnetic resonance tomography of the abdominal organs. If the clinic of the disease is typical, then the stage of laboratory diagnosis can be neglected and immediately refer the patient to tomography. Treatment of the disease only operational (removal of the tumor); before the operation, the patient is already medically compensated in the hospital (for several days), stabilizing blood pressure through the use of a combination of alpha and beta adrenergic blockers.

Atrioventricular reciprocal tachycardias. Translated from Latin: atrium – atria, ventriculum – ventricles. This is a group of paroxysmal cardiac tachyarrhythmias, which are united by the obligatory passage (circulation) of an electrical impulse through an atrioventricular node (AV node). There are 2 main syndromes that can be complicated by AV tachycardia: the WPW phenomenon and the dissociation of the AV node. Both morphological abnormalities are congenital, often in the context of connective tissue dysplasia syndrome. The first reason – the phenomenon of WPW – as mentioned above, is the presence in the heart of an additional path (Kent beam), with the participation of which the impulse rotates:

If the loop circulates, as shown in the figure, counterclockwise, then we have Atrioventricular orthodromic tachycardia. The word orthodromicity emphasizes the initial passage of the pulse through the AV node (antegrade), then retrograde (from bottom to top) through the pathway to the atria. The circulation of the impulse in the opposite direction means that it first moves anterograde along an additional path, then retrogradely through the AV node to the atria; such tachyarrhythmia is called Atrioventricular antidromic tachycardia.

The second reason is the dissociation of the AV node – that is, the separation of the AV node on the path with different speed of conduction (in healthy people the AV node is homogeneous): simplified, on a fast path, and slow. At some point, the electric impulse is usually conducted (from top to bottom, anterograde) on the fast path, but not carried out (blocked) on the slow, but the pulse passed on the fast path enters the slow path from the other side (bottom up, retrograde) and again penetrates the fast path – the loop is closed, the possibility arises for multiple circulation of the electric pulse along the formed loop.

This is how the Atrioventricular nodal reciprocal tachycardia starts.

Persons who have the above-described congenital conditions for AV tachycardia can be completely healthy for many years. Signs of the phenomenon of WPW and (or) dissociation of the AV node can be detected on a normal ECG; however, they are often absent, making it impossible to foresee arrhythmia in the future. As soon as the first episode of arrhythmia occurs in the life, the congenital anomaly of the cardiac conduction system becomes a disease. AV-tachycardia is a sudden paroxysm of unmotivated heartbeat, triggered by atrial extrasystole. Its frequency is determined by the frequency of circulation (revolutions) of the pulse per minute; typically 140 to 220 per minute. For a particular patient, the heart rate varies insignificantly: plus or minus 10 beats, and during an attack that has already occurred without interference, the frequency remains stable throughout the entire paroxysm. The duration of the attack can be completely different: from a few seconds to several hours. Treatment of AV-tachycardia is only operative through RFA. As a rule, the patient is referred to a heart surgeon when the attacks of the heartbeat become so frequent that they significantly worsen the quality of life. In WPW syndrome, an additional route is burned; in the case of AV-node dissociation, it is a slow way. The probability of success of the operation (no recurrence in the long term) is more than 95%. Before surgery, for the prevention of paroxysmal palpitations, the patient may take an antiarrhythmic agent, and the occurring seizures can be stopped by means of vagal tests.

Hypertrophic cardiomyopathy (HCM) is a genetically determined disease characterized by hypertrophy of all or part of the left ventricular myocardium. There is 1 case for 500 newborns. Hypertrophic changes in the myocardium proper and manifest after birth – most often in adolescence; however, the development of hypertrophy can occur in young children or, conversely, in adult subjects (up to 30-35 years). There are 3 possible morphologies of hcmp: symmetrical hypertrophy of all LV walls, asymmetric hypertrophy of the interventricular septum with minor hypertrophy of the remaining walls, isolated asymmetric hypertrophy of the interventricular septum.

Variants of the clinical course of hcmp: asymptomatic and symptomatic. Not less than 1/3 of patients with HCM disease secretly, and a person will know about it at best when conducting a planned ultrasound of the heart; and for some, the diagnosis is completely established after death "from non-cardiac causes" at autopsy. Symptomatic course of the disease is very variable. The most frequent is the gradual development of heart failure through the mechanism of diastolic dysfunction of the left ventricle; As a rule, the symptoms of heart failure appear rather late – in the fifth or sixth dozen of life, they progress slowly. A more rare variant of the course of hcmp is the appearance of obstructive syncope. The cause of syncopes lies in the transient obstruction of blood flow at the level of the outflow tract of the left ventricle due to the powerful hypertrophy of the IVF.

As a rule, fainting occurs during exercise. This course of hcmp is malignant, so any of the fainting can end in death. The thromboembolic variant, as a complication of endocarditis of one of the valves, belongs to the extremely rare variant of the course of HCM. The most dramatic complication of HCM is sudden cardiac death (SCD). The mechanism of BCC – ventricular fibrillation. Among the causes of the sudden death of young athletes GMKP is one of the first places. The very possibility of launching a fatal ventricular arrhythmia in HCM is laid in the impaired architectonics of hypertrophied myocardium:

When the children's oval window closes

Histological section of healthy myocardium and HCM.

In a healthy myocardium, the muscle bundles are arranged longitudinally – this is a variant of the norm; in the myocardium in the case of hcmp, the muscle bundles have a chaotic orientation. Such "friability" myocardial fibers predetermines the possibility of circulation of an electric impulse along a complex, unpredictable trajectory. In all patients with HCM deaths, suddenly from acute arrhythmia, long before the onset of sudden death, ventricular premature beats are recorded, as the only manifestation of electrical "abnormalities" hearts. Unfortunately, it is still impossible to predict how clinically diagnosed asymptomatic HCM will clinically proceed. In any case, with the diagnosis made, one should start with limiting heavy physical exertion, eliminate professional sport; and if we have a child, then send him in life in the humanitarian direction. There are several precursors of VSS in HCM; each of them separately probably does not play a predictor role, however the more there is in one patient, the higher the risk of arrhythmic death: ventricular tachycardia with Holter monitoring ECG, unexplained syncope, cases of SCD in close relatives, maximum LV wall myocardium more than 3 cm, paradoxical decrease in blood pressure during exercise. Patients with asymptomatic HCM need lifelong cardiac examinations: once a year, an ultrasound of the heart and a Holter.

Hypertension in pregnant women. Arterial hypertension during pregnancy can occur in the following clinical forms:

– Arterial hypertension that occurred before pregnancy or occurred in the first half of pregnancy (up to week 20); it usually persists after delivery. It is referred to as hypertension or, which is the same, essential hypertension.

– Gestational arterial hypertension (hypertension of pregnant women) – induced by pregnancy, appears in its second half (after 20 weeks). Often it has a severe course; it is complicated by damage to other organs: pre-eclampsia (nephropathy), eclampsia (nephropathy + brain swelling). If arterial hypertension that occurred before pregnancy (hypertension) becomes malignant after 20 weeks, then they also speak of gestational hypertension.

– Unclassified arterial hypertension – if hypertension is detected after the 20th week of pregnancy, but the previous parameters of blood pressure are unknown, then gestational hypertension is diagnosed. If after pregnancy it does not pass, then the diagnosis of hypertension is set.

The main problem of arterial hypertension in pregnant women (regardless of its type) is an extremely poor arsenal of therapeutic agents that is acceptable to safe use. In this regard, in the United States a classification of teratogenicity (toxic effects on the fetus) of FDA (Foodand Drug Administration) drugs was developed:

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