Stable exertional angina. Unstable angina Unstable angina etiology and pathogenesis
Currently, several concepts are combined under the concept of unstable angina: New onset angina, progressive exertional angina(characterized by an increase in angina attacks and / or an increase in their duration and strength), angina that first occurred at rest. Each patient with unstable angina is subject to hospitalization, since the further development of the disease is unpredictable.
Etiology and pathogenesis of unstable angina pectoris.
The etiology of unstable angina is similar to that of exertional angina. The main mechanism for the development of unstable angina is the rupture of the fibrous plaque capsule in the coronary artery, which provokes the formation of a thrombus with incomplete closure of the vessel lumen. The presence of a thrombus in the coronary artery prevents adequate blood supply to the myocardium, which leads to the appearance of a pain syndrome and an extensive clinic of unstable angina.
The rupture of a fibrous plaque is facilitated by the accumulation of a large amount of lipids and an insufficient content of collagen in it, inflammation and hemodynamic factors.
Classification of unstable angina.
Class I - first-time angina or worsening of existing angina within a month.
Class II - angina at rest during the previous month.
Class III - angina at rest during the last two days.
Clinical picture of unstable angina pectoris.
Unstable angina is manifested by typical attacks, but characteristic signs of angina pectoris can also be identified.
Over the past 1-2 months, the number, severity and duration of angina attacks (the so-called "crescendo angina") have increased.
Attacks have never occurred before, appeared no more than 1 month ago (first-time angina pectoris).
Attacks of stenocardia began to appear at rest or at night.
An important clinical sign of unstable angina is the absence or weakening of the effect of nitroglycerin, which previously stopped angina attacks.
Diagnosis of the disease.
The main clinical manifestation of unstable angina is pain. A brief description of the methods for diagnosing unstable angina:
- ECG does not give a full opportunity to draw a conclusion, since even with a normal ECG, the presence of unstable angina is not excluded, but an ECG at rest helps to differentiate large-focal myocardial infarction.
- Daily ECG monitoring allows you to identify changes characteristic of unstable angina, especially episodes of painless myocardial ischemia.
- Enzyme diagnostics. The indicators of this diagnosis make it possible to differentiate unstable angina pectoris from myocardial infarction, since there is no significant increase in enzyme activity in unstable angina pectoris.
- echocardiography is ineffective in diagnosing unstable angina pectoris, since the pathological movement of the walls of the left ventricle, detected by this method, can only be detected during a painful episode.
- coronary angiography is indicated for patients in the case when the issue of surgical treatment of unstable angina pectoris is being discussed, or for patients with adverse signs of the course of the disease. Angiographic examination can reveal blood clots in the coronary arteries.
Recently, the Voll method is gaining more and more popularity - this is the use of special equipment for diagnostics. For example, the BIORS bioscanner can significantly reduce the work of doctors and facilitate the process of establishing the disease. To do this, special sensors are installed on the patient's body, which read information about the state of health due to fluctuations in the electric field on the skin.
Treatment of unstable angina.
With unstable angina pectoris, it is necessary to stop (remove the identified symptoms) pain syndrome. This is achieved by introducing a solution of nitroglycerin at a dose of 5-10 mcg / min intravenously with an increase every 15 minutes by 5-10 mcg / min (up to 200 mcg / min) until the pain disappears or a side effect appears in the form of arterial hypotension. After 24 hours, transfer to oral nitrates is carried out.
Beta-blockers reduce myocardial oxygen demand. They are administered intravenously on the first day to all patients in the absence of contraindications.
The prognosis of unstable angina.
With unstable angina within 3 months, myocardial infarction develops in 10-20% of cases with a mortality of 4-10%. In addition to the development of myocardial infarction, it is possible
7. Angina pectoris: classification, clinic, diagnosis, treatment.
Angina pectoris is a clinical syndrome manifested by a feeling of discomfort or pain in the chest of a compressive, pressing nature, which is most often localized behind the sternum and can radiate to the left arm, neck, lower jaw, epigastric region.
For the past two decades, the classification of coronary artery disease, proposed by WHO in 1979 and adapted by VKSC AMN in 1983, has been widely used in cardiology practice:
Angina pectoris;
First-time angina pectoris;
Stable angina pectoris (functional class must be indicated):
Class I - latent. Angina pectoris occurs only with intense and prolonged physical exertion;
Class II - mild degree. Attacks occur when climbing stairs, uphill, in a cold wind, in frosty weather, when walking more than two kilometers and climbing more than one floor;
Class III - moderate. Attacks occur when walking over a distance of more than 1 kilometer and climbing one floor. Occasionally there are seizures at rest;
Class IV - heavy. Inability to perform any physical activity, attacks regularly occur at rest.
Progressive angina (unstable);
Spontaneous (variant, vasospastic) angina.
Classification of progressive angina pectoris according to the severity of occurrence
Class I. Severe or progressive angina pectoris of recent onset, history of exacerbation of coronary heart disease less than 2 months;
Class II. Angina pectoris of exertion and rest is subacute. Patients had anginal attacks during the previous month, but no later than 48 hours;
Class III. Acute rest angina. Patients had anginal attacks at rest during the last 48 hours.
Classification of unstable angina depending on the conditions of its occurrence
Class A. Secondary unstable angina. The development of unstable angina occurs under the influence of factors that aggravate ischemia (fever, anemia, hypotension, infection, tachyarrhythmia, uncontrolled hypertension, respiratory failure, thyrotoxicosis);
Class B. Primary unstable angina, develops without the influence of the above factors;
Class C. Early postinfarction NS. Develops within two weeks after an extensive myocardial infarction.
Most patients with angina feel discomfort or pain in the chest area. Discomfort is usually pressing, squeezing, burning in nature. Often, such patients, trying to describe the area of discomfort, apply a clenched fist or an open palm to the chest. Often the pain radiates ("gives off") to the left shoulder and the inner surface of the left arm, neck; less often - in the jaw, teeth on the left side, right shoulder or arm, interscapular region of the back, as well as in the epigastric region, which may be accompanied by dyspeptic disorders (heartburn, nausea, colic). Extremely rarely, pain can be localized only in the epigastric region or even in the head region, which makes diagnosis very difficult.
Attacks of angina pectoris usually occur during physical exertion, strong emotional arousal, after taking an excess amount of food, staying in conditions of low temperatures or with an increase in blood pressure. In these situations, the heart muscle needs more oxygen than it can get through the narrowed coronary arteries. In the absence of coronary artery stenosis, spasm, or thrombosis, chest pain related to exercise or other circumstances that increase the oxygen demand of the heart muscle may occur in patients with severe left ventricular hypertrophy caused by aortic valve stenosis, hypertrophic cardiomyopathy, as well as aortic regurgitation or dilated cardiomyopathy.
An attack of angina pectoris usually lasts from 1 to 15 minutes. It disappears with the termination of the load or the intake of short-acting nitrates (for example, nitroglycerin under the tongue).
Diagnostics
Laboratory tests help determine the possible cause of myocardial ischemia.
Clinical blood test. Changes in the results of a clinical blood test (decrease in hemoglobin levels, shifts in the leukocyte formula, etc.) make it possible to identify concomitant diseases (anemia, erythremia, leukemia, etc.) that provoke myocardial ischemia.
Determination of biochemical markers of myocardial damage. In the presence of clinical manifestations of instability, it is necessary to determine the level of troponin or the MB fraction of creatine phosphokinase in the blood. An increase in the level of these indicators indicates the presence of an acute coronary syndrome, and not stable angina.
Blood chemistry. All patients with angina pectoris should have a lipid profile (total cholesterol, HDL, LDL and triglyceride levels) assessed to assess cardiovascular risk and the need for correction. Also determine the level of creatinine to assess kidney function.
Glycemic assessment. To detect diabetes mellitus as a comorbidity in angina pectoris, fasting glucose levels are assessed or a glucose tolerance test is performed.
In the presence of clinical signs of thyroid dysfunction, the level of thyroid hormones in the blood is determined.
Instrumental methods.
ECG at rest. All patients with suspected angina should have a resting 12-lead ECG. Although the results of this method are normal in about 50% of cases of observation of patients with angina, signs of coronary heart disease (for example, a history of myocardial infarction or repolarization disorders), as well as other changes (left ventricular hypertrophy, various arrhythmias) can be detected. This allows you to determine a further plan for examination and treatment. An ECG may be more informative if it is recorded during an angina attack (usually during hospital observation).
ECG with exercise. Apply treadmill test or bicycle ergometry with ECG monitoring in 12 standard leads. The main diagnostic criterion for ECG changes during such tests is horizontal or downward ST depression ≥0.1 mV, persisting for at least 0.06-0.08 s after the J-point, in one or more ECG leads. The use of exercise tests is limited in patients with an initially altered ECG (for example, with left bundle branch block, arrhythmias, or WPW syndrome), since it is difficult to correctly interpret ST-segment changes.
Daily ambulatory ECG monitoring. This method is less informative than stress tests, but it can detect myocardial ischemia during normal daily activities in 10-15% of patients with stable angina who do not develop ST segment depression during stress tests. This method is especially valuable for the diagnosis of vasospastic angina pectoris.
Resting echocardiography - detects or excludes other disorders (such as valvular heart disease or hypertrophic cardiomyopathy) as the cause of symptoms, as well as assesses ventricular function, heart cavity sizes, etc.
Scintigraphy with physical or pharmacological stress is carried out with the isotopes of thallium-201, technetium-99 sestamibi or tetrofosmin in combination with physical activity. If patients cannot perform physical activity, scintigraphy is used in combination with pharmacological tests (administration of dobutamine, dipyridamole or adenosine).
Stress echocardiography. It has both advantages and disadvantages compared to myocardial scintigraphy and is an alternative to the latter. Echocardiography is performed in combination with pharmacological or physical activity.
Coronary angiography
Given the possible complications of this invasive procedure and the high cost, coronary angiography is indicated in the following cases:
in patients who have a high likelihood of needing myocardial revascularization;
in patients undergoing cardiac arrest or with life-threatening ventricular arrhythmias;
if the diagnosis is not confirmed by non-invasive methods.
Treatment of angina pectoris has two main goals.
The first is to improve the prognosis and prevent the occurrence of MI and VS, and, accordingly, increase life expectancy.
The second is to reduce the frequency and intensity of angina attacks and thus improve the patient's QoL. Therefore, if different therapeutic strategies are equally effective in alleviating the symptoms of the disease, a treatment with a proven or very likely advantage in improving the prognosis in terms of preventing complications and death should be preferred.
The choice of treatment depends on the clinical response to initial medical therapy, although some patients immediately prefer and insist on coronary revascularization.
Lifestyle change.
The most important role in achieving the first goal is played by changing the patient's lifestyle. Improving the prognosis of the disease can be achieved by the following activities:
To give up smoking
moderate physical activity
Diet and weight loss: limiting salt and saturated fat intake, regular consumption of fruits, vegetables and fish.
Treatment of dyslipidemia.
Dieting is important as initial therapy in patients with elevated lipid levels, but according to various studies, this is not enough to reduce the risk of cardiovascular complications. Therefore, lipid-lowering drugs are prescribed - inhibitors of HMG-CoA reductase (statins). The goal of treatment is to lower total cholesterol to 4.5 mmol/L (175 mg/dL) or lower and lower LDL cholesterol to 2.5 mmol/L (100 mg/dL) or lower.
Antiplatelet agents.
All patients with angina pectoris are prescribed acetylsalicylic acid for life at a dose of 75-150 mg / day in the absence of contraindications. The dose should be minimally effective, since with an increase in the dose, the risk of developing gastrointestinal side effects (bleeding, ulcerogenicity) increases.
In the presence of contraindications to acetylsalicylic acid, it is possible to prescribe clopidogrel, which in studies has shown greater efficacy and less likely to cause the development of gastrointestinal bleeding. However, the high cost of clopidogrel creates certain difficulties. The addition of esomeprazole (80 mg/day) to acetylsalicylic acid has also been shown to be better than switching to clopidogrel for the prevention of recurrent ulcer bleeding in patients with peptic ulcer and vascular disease.
β-blockers
β-blockers are effective in relieving angina attacks and are recommended as first-line drugs to relieve anginal episodes. Their antianginal effect is due to a decrease in myocardial oxygen demand due to a decrease in heart rate (HR) and blood pressure. The diastole is also lengthened and thus the time of blood supply to the ischemic zones of the myocardium increases. Cardioselective β-blockers are most preferred (they cause side effects less often than non-selective ones), among which the most widely used are metoprolol, bisoprolol and atenolol. The effectiveness of taking a β-blocker is judged by the following clinical parameters: Heart rate at rest<60/мин, а при максимуме физической активности <110/мин. β-адреноблокаторы при ишемической болезни сердца кроме симптоматического воздействия оказывают значительное влияние на дальнейший прогноз пациента: их применение снижает риск развития фибрилляции желудочков (основная причины внезапной коронарной смерти) и инфаркта миокарда (в том числе повторного).
Calcium channel blockers
There are 2 subgroups of calcium channel blockers: non-dihydropyridine derivatives (eg, verapamil and diltiazem) and dihydropyridine derivatives (eg, nifedipine and amlodipine). The mechanism of action of these subgroups is different, but they all have antianginal effects and are effective in the treatment of angina pectoris. All calcium channel blockers are prescribed in the form of prolonged forms, which are taken 1 time per day. Dihydropyridine derivatives can be added to β-blockers in patients who fail to achieve the desired effect. The combination of non-dihydropyridine calcium channel blockers and β-blockers is not recommended, as excessive bradycardia may occur. Non-dihydropyridine calcium channel blockers can replace β-blockers in the presence of contraindications for the appointment of the latter (for example, bronchial asthma, COPD, severe atherosclerosis of the lower extremities).
Currently, 3 drugs of this group are used: nitroglycerin, isosorbide dinitrate and isosorbide mononitrate. When prescribing these drugs, you need to know that nitrates are classified into short-acting dosage forms (<1 ч), умеренного продлённого действия (<6 ч) и значительного продлённого действия (6-24 ч).
With angina pectoris of functional class I, short-acting nitrates (tablets, capsules, nitroglycerin or isosorbide dinitrate aerosols) are prescribed, which are taken 5-10 minutes before the intended physical activity to prevent the development of an angina attack. If an attack of angina is not stopped by taking short-acting nitrates, myocardial infarction or non-cardiac pain should be suspected.
With angina pectoris II functional class, in addition to short-acting nitrates, moderate prolonged-acting forms can be used.
With angina pectoris of III functional class, isosorbide mononitrate (significantly prolonged action) is prescribed. It is taken continuously throughout the day with a nitrate-free period of 5-6 hours (usually at night) to avoid nitrate tolerance.
With angina pectoris of IV functional class, angina attacks can also occur at night. At the same time, extended forms of nitrates are prescribed so as to ensure their round-the-clock effect and, more often, in combination with other antianginal drugs (for example, β-blockers).
Ivabradine is an inhibitor of If channels of sinus node cells, selectively reducing sinus rhythm. Its appointment is possible in the presence of contraindications and side effects of β-blockers. Assign a dose of 2.5-10 mg twice a day. Studies have shown that the combination of atenolol (50 mg/day) and ivabradine enhances the anti-ischemic effect and is safe. Side effect: a slight deterioration in vision when taking high doses.
Surgical treatment involves coronary artery bypass grafting (CABG) or balloon angioplasty and stenting of the coronary arteries.
When performing CABG, a bypass shunt is placed between the aorta and the coronary artery. Autografts (the patient's own veins and arteries) are used as a shunt. The most "reliable" shunt is considered to be a shunt from the internal mammary artery (mammary coronary bypass grafting).
A less traumatic method of surgical treatment is balloon angioplasty and stenting, the meaning of which is to dilate the affected area of the coronary artery with a special balloon and implant a special metal structure - a stent. Due to the low efficiency, balloon vasodilation in its pure form (without subsequent stent implantation) is practically not used today. The implantable stent can be "naked" (bare metal stent), or carry on its surface a special medicinal substance - a cytostatic agent (drug eluting stent). Indications for a particular method of surgical treatment are determined individually in each case after the obligatory performance of coronary angiography.
Feel bad, decided to measure the pressure and saw terrible numbers on the tonometer: your pressure is 180/100. What to do? What to take? Take pills or call an ambulance right away?
Or maybe your mother, grandmother complain of dizziness, headaches and high blood pressure. Such situations are familiar to most people.
What are the causes of hypertension, how to act competently in such situations, what medicines to take, what the consequences of a sharp jump in pressure can be and how to prevent them - we will analyze in detail in our article.
Many people think that a person necessarily feels an increase in pressure: heaviness in the head, darkening in the eyes, nausea, pain or discomfort in the heart area. But often hypertension is completely asymptomatic, and the patient learns about his disease during a routine routine examination by a general practitioner or when referring to a doctor with a completely different disease.
Pressure above 140/90 at rest is a clear sign of hypertension, and 180/100 is already the third, severe degree of arterial hypertension according to the classification of the World Health Organization. The greater the difference between the two indicators, the higher the risk of stroke (for example, a pressure of 180/100 is much more dangerous than 180/120).
Pressure 180/100: what to do?
If measures are not taken in time, hypertension can lead to heart failure, cerebral hemorrhage, and decreased visual acuity. You can’t ignore the body’s signals, self-medicate, hope that it will “go away on its own”: high blood pressure can cause atrial fibrillation, stroke, heart attack.
If you are a hypertensive with experience, your home first aid kit should always have something to take at a pressure of 180/100. It:
Alternative methods of treating hypertension can be used as a prophylaxis or with a slight increase in pressure. And the numbers 180/100 are a serious reason to see a doctor.
If you have at least once had a pressure of 180/100, consult a doctor, even if nothing else bothers or hurts. To get started, go to an appointment with a therapist who will send you for blood and urine tests, an ECG, a consultation with other specialists (oculist, cardiologist, neuropathologist, endocrinologist), if necessary, for additional examinations (MRI, ultrasound of the heart and blood vessels, daily monitoring of blood pressure and other).
Based on all the examinations, the doctor will make a conclusion about the cause of high blood pressure and select the best treatment option. The main recommendations that are given to all hypertensive patients are as follows:
- Healthy lifestyle (restriction of salt, fats, refusal of caffeine, smoking and alcohol, weight loss, light physical activity, walks in the fresh air);
- Constant control of pressure twice a day using a home tonometer;
- If necessary, medications are prescribed, which should be taken strictly in the prescribed dosage and canceled only with the permission of the attending physician.
Watch your health, learn to hear the alarm signals of your body - this will allow you to avoid many serious problems.
Angina pectoris: tension and rest, stable and unstable - signs, treatment
One of the most common clinical manifestations of IHD (ischemic heart disease) is angina pectoris. It is also called "angina pectoris", although this definition of the disease has recently been used very rarely.
Symptoms
The name is associated with the signs of the disease, which are manifested in a feeling of pressure or compression (narrow - stenos from Greek), a burning sensation in the region of the heart (kardia), behind the sternum, turning into pain.
In most cases, the pain comes on suddenly. In some people, the symptoms of angina pectoris are pronounced in stressful situations, in others - during overexertion during heavy physical work or sports exercises. In still others, seizures cause them to wake up in the middle of the night. Most often, this is due to stuffiness in the room or too low ambient temperature, high blood pressure. In some cases, an attack occurs when overeating (especially at night).
The duration of pain is no more than 15 minutes. But they can give in the forearm, under the shoulder blades, neck and even jaw. Often an attack of angina pectoris is manifested by unpleasant sensations in the epigastric region, for example, heaviness in the stomach, stomach cramps, nausea, heartburn. In most cases, pain disappears as soon as a person’s emotional arousal is removed, if he stops while walking, takes a break from work. But sometimes, to stop the attack, you need to take drugs from the nitrate group, which have a short effect (nitroglycerin tablet under the tongue).
There are many cases when the symptoms of an angina attack appear only in the form of discomfort in the stomach or headaches. In this case, the diagnosis of the disease causes certain difficulties. It is also necessary to distinguish painful attacks of angina pectoris from symptoms of myocardial infarction. They are short-term, and are easily removed by taking nitroglycerin or nidefilin. While the pain of a heart attack with this drug is not stopped. In addition, with angina pectoris, there is no congestion in the lungs and shortness of breath, the body temperature remains normal, the patient does not experience excitation during an attack.
Often this disease is accompanied by cardiac arrhythmia. External signs of angina pectoris and cardiac arrhythmias are manifested in the following:
- Paleness of the skin of the face (in atypical cases, redness is observed);
- Beads of cold sweat on the forehead;
- On the face - an expression of suffering;
- Hands - cold, with loss of sensation in the fingers;
- Breathing - superficial, rare;
- The pulse at the beginning of the attack is frequent, towards the end of its frequency decreases.
Etiology (causes of occurrence)
The most common causes of this disease are atherosclerosis of the coronary vessels and hypertension. Angina is thought to be caused by a decrease in oxygen supply to the coronary vessels and heart muscle, which occurs when blood flow to the heart does not meet its needs. This causes myocardial ischemia, which, in turn, contributes to the disruption of the oxidation processes occurring in it and the appearance of an excess of metabolic products. Often, the heart muscle requires an increased amount of oxygen with severe left ventricular hypertrophy. The reason for this are diseases such as dilated or hypertrophic cardiomyopathy, aortic regurgitation, aortic valve stenosis.
Very rarely (but such cases have been noted), angina pectoris occurs against the background of infectious and allergic diseases.
Course of the disease and prognosis
This disease is characterized by a chronic course. Seizures may recur when performing heavy work. Often they occur when a person is just starting to move (walking), especially in cold and humid weather, on sweltering summer days. Subject to angina attacks are emotional, mentally unbalanced people who are subject to frequent stress. There have been cases when the first attack of angina led to death. In general, with the right method of treatment, following the recommendations of doctors, the prognosis is favorable.
Treatment
To eliminate angina attacks are used:
- Conservative methods of treatment, including drug (drug) and non-drug therapy;
- Surgery.
Treatment of angina pectoris with drugs is carried out by a cardiologist. It includes the following:
| 1 | ACE and f-channel inhibitors, b-blockers | Maintaining normal blood pressure, reducing heart rate and myocardial oxygen consumption, increasing the degree of exercise tolerance |
| 2 | Lipid-lowering drugs: Omega-3 polyunsaturated fatty acids, fibrates, statites | Slowdown and stabilization of the formation of atherosclerotic plaques |
| 3 | Antiplatelet agents (antithrombotics) | Prevention of thrombus formation in coronary vessels |
| 4 | calcium antagonists | Prevention of coronary spasms in vasospastic angina |
| 5 | Short-acting nitrates (nitroglycerin, etc.) | Relief of an attack |
| 6 | Long acting nitrates | They are prescribed as a prophylactic before an increased and prolonged load or a possible surge of emotions. |
Non-drug treatments include:
- The use of diets aimed at lowering cholesterol levels in the blood;
- Bringing body weight in line with its growth index;
- Development of individual loads;
- Treatment by means of alternative medicine;
- Elimination of bad habits: smoking, drinking alcohol, etc.
Surgical treatment includes atherotomy, rotoblation, coronary angioplasty, in particular with stenting, as well as a complex operation - coronary artery bypass grafting. The method of treatment is selected depending on the type of angina pectoris and the severity of the course of the disease.
Classification of angina pectoris
The following classification of the disease is accepted:
- Due to occurrence:
- Angina pectoris that occurs under the influence of physical activity;
- Rest angina, the attacks of which overtake the patient during night sleep, and during the day, when he is in the supine position, without obvious prerequisites.
- According to the nature of the course: Prinzmetal's angina pectoris is distinguished as a separate type.
- stable. Attacks of the disease appear with a certain, predictable frequency (for example, every other day or two, several times a month, etc.). It is divided into functional classes (FC) from I to IV.
- Unstable. First emerging (VVS), progressive (PS), postoperative (early pre-infarction), spontaneous (variant, vasospastic).
Each species and subspecies has its own characteristics and features of the course of the disease. Let's consider each of them.
Stable exertional angina
The Academy of Medical Sciences conducted studies on what types of physical work people with diseases of the cardiovascular system can do without experiencing discomfort and seizures in the form of heaviness and pain in the chest. At the same time, stable exertional angina was divided into four functional classes.
I functional class
It is called latent (hidden) angina pectoris. It is characterized by the fact that the patient can perform almost all types of work. He easily overcomes long distances on foot, easily climbs the stairs. But only if all this is done measuredly and for a certain time. With the acceleration of movement, or an increase in the duration and pace of work, an angina attack occurs. Most often, such attacks appear during extreme stress for a healthy person, for example, when resuming sports, after a long break, performing excessive physical activity, etc.
Most people suffering from angina pectoris of this FC consider themselves healthy people and do not seek medical help. However, coronary angiography shows that they have moderate individual vessel lesions. Carrying out a bicycle ergometric test also gives a positive result.
II functional class
People with angina of this functional class often experience attacks at certain hours, for example, in the morning after waking up and getting out of bed abruptly. In some, they appear after climbing the stairs of a certain floor, in others - while moving in bad weather. Reducing the number of seizures, contributes to the proper organization of work and the distribution of physical activity. Doing them at the right time.
III functional class
Angina pectoris of this type is inherent in people with strong psycho-emotional arousal, in whom attacks appear when moving at a normal pace. And overcoming the stairs to their floor turns into a real test for them. These people often experience rest angina. They are the most frequent patients in hospitals diagnosed with coronary artery disease.
IV functional class
In patients with angina pectoris of this functional class, any kind of physical activity, even minor, causes an attack. Some are not even able to move around the apartment, without pain in the chest. Among them, the largest percentage of patients in whom pain occurs at rest.
Unstable angina
Angina pectoris, the number of attacks of which can either increase or decrease; their intensity and duration at the same time also changes, is called unstable or progressive. Unstable angina (UA) is distinguished by the following features:
- The nature and severity of the occurrence:
- Class I. The initial stage of chronic angina. The first signs of the onset of the disease were noted shortly before going to the doctor. In this case, the exacerbation of coronary artery disease is less than two months.
- Class II. Subacute flow. Pain syndromes were noted during the entire month preceding the date of the visit to the doctor. But for the last two days they have been absent.
- Class III. The current is sharp. Attacks of stenocardia were observed at rest during the last two days.
- Occurrence conditions:
- Group A. Unstable, secondary angina pectoris. The cause of its development are factors provoking coronary artery disease (hypotension, tachyarrhythmia, uncontrolled hypertension, infectious diseases accompanied by fever, anemia, etc.)
- Group B. Unstable, primary angina. It develops in the absence of factors that increase the course of IHD.
- Group C. Early postinfarction angina pectoris. Occurs in the coming weeks, after suffering an acute myocardial infarction.
- Against the background of ongoing therapeutic treatment:
- It develops with a minimum of medical procedures (or not carrying them out).
- With a course of medication.
- Development continues with intensive treatment.
rest angina
Patients diagnosed with functional class IV stable angina almost always complain of pain at night and early in the morning when they just woke up and are in bed. The examination of the cardiological and hemodynamic processes of such patients, through continuous daily monitoring, proves that the harbinger of each attack is an increase in blood pressure (diastolic and systolic) and an increase in heart rate. In some people, the pressure was high in the pulmonary artery.
Resting angina is a more severe course of exertional angina. Most often, the onset of an attack is preceded by a psycho-emotional load that causes an increase in blood pressure.
It is much more difficult to stop them, since the elimination of the cause of their occurrence is fraught with certain difficulties. After all, any occasion can serve as a psycho-emotional load - a conversation with a doctor, a family conflict, troubles at work, etc.
When an attack of this type of angina occurs for the first time, many people experience a feeling of panic fear. They are afraid to move. After the pain passes, the person experiences a feeling of excessive fatigue. Beads of cold sweat break out on his forehead. The frequency of seizures is different for everyone. In some, they can manifest themselves only in critical situations. Other attacks are visited more than 50 times a day.
One type of rest angina is vasospastic angina. The main cause of seizures is a spasm of the coronary vessels that occurs suddenly. Sometimes this occurs even in the absence of atherosclerotic plaques.
Many older people have spontaneous angina that occurs in the early morning hours, at rest, or when they change position. At the same time, there are no visible prerequisites for seizures. In most cases, their occurrence is associated with nightmares, a subconscious fear of death. Such an attack can last a little longer than other types. Often it is not stopped by nitroglycerin. All this is angina pectoris, the signs of which are very similar to the symptoms of myocardial infarction. If you make a cardiogram, it will be seen that the myocardium is in the stage of dystrophy, but there are no clear signs of a heart attack and enzyme activity indicating it.
Prinzmetal's angina
Prinzmetal's angina is a special, atypical and very rare type of coronary heart disease. She received this name in honor of the American cardiologist who first discovered it. A feature of this type of disease is the cyclical occurrence of seizures that follow one after another, with a certain interval of time. Usually they make up a series of attacks (from two to five) that always occur at the same time - in the early morning. Their duration can be from 15 to 45 minutes. Often this type of angina is accompanied by severe arrhythmia.
It is believed that this type of angina pectoris is a disease of young people (up to 40 years old). It rarely causes a heart attack, but it can contribute to the development of life-threatening arrhythmias, such as ventricular tachycardia.
The nature of pain in angina pectoris
Most people with angina pectoris complain of chest pain. Some characterize it as pressing or cutting, in others it is felt as constricting the throat or burning the heart. But there are many patients who cannot accurately convey the nature of the pain, as it radiates to various parts of the body. The fact that this is angina pectoris is often indicated by a characteristic gesture - a clenched fist (one or both palms) attached to the chest.
Pain in angina pectoris usually follows one after another, gradually intensifying and growing. Having reached a certain intensity, they almost immediately disappear. Angina pectoris is characterized by the onset of pain at the moment of exercise. Pain in the chest, which appears at the end of the working day, after the completion of physical work, has nothing to do with coronary heart disease. Do not worry if the pain lasts only a few seconds, and disappears with a deep breath or a change in position.
Video: Lecture on angina pectoris and coronary artery disease at St. Petersburg State University
At-risk groups
There are features that can provoke the occurrence of various types of angina pectoris. They are called risk groups (factors). There are the following risk groups:
- Unmodified - factors that a person cannot influence (eliminate). These include:
- Heredity (genetic predisposition). If someone in the male family died before the age of 55 from heart disease, then the son is at risk of angina pectoris. In the female line, the risk of disease occurs if death is frowning from heart disease before the age of 65.
- Racial affiliation. It has been noted that residents of the European continent, in particular northern countries, have angina pectoris much more often than residents of southern countries. And the lowest percentage of the disease is in representatives of the Negroid race.
- Gender and age. Before the age of 55, angina is more common in men than in women. This is due to the high production of estrogens (female sex hormones) during this period. They are a reliable protection of the heart from various diseases. However, during menopause, the picture changes and the risk of angina in both sexes becomes equal.
- Modified - a risk group in which a person can influence the causes of the development of the disease. It includes the following factors:
- Overweight (obesity). With weight loss, the level of cholesterol in the blood decreases, blood pressure decreases, which invariably reduces the risk of angina pectoris.
- Diabetes. By keeping blood sugar levels close to normal, the frequency of CHD attacks can be controlled.
- Emotional loads. You can try to avoid many stressful situations, which means reducing the number of angina attacks.
- High blood pressure (hypertension).
- Low physical activity (hypodynamia).
- Bad habits, in particular smoking.
Emergency care for angina pectoris
People diagnosed with progressive angina (and other types) are at risk for sudden death and myocardial infarction. Therefore, it is important to know how to quickly cope with the main symptoms of the disease on your own, and when the intervention of medical professionals is required.
In most cases, this disease is manifested by the occurrence of sharp pain in the chest area. This happens due to the fact that the myocardium experiences oxygen starvation due to a reduced supply of blood during exercise. First aid during an attack should be aimed at restoring blood flow.
Therefore, every angina patient should carry a fast-acting vasodilator, such as nitroglycerin, with them. At the same time, doctors recommend taking it shortly before the alleged onset of an attack. This is especially true if an emotional outburst is foreseen or hard work is to be done.
If you notice a walking person on the street who suddenly froze, turned very pale and involuntarily touches his chest with his palm or clenched fist, this means that he was overtaken by an attack of coronary heart disease and urgent care is required for angina pectoris.
In order to provide it, you need to do the following:
- If possible, seat a person (if there is no bench nearby, then directly on the ground).
- Open his chest by undoing the button.
- Look for a saving pill of nitroglycerin (valocordin or validol) from him and put it under his tongue.
- Keep track of the time, if within one or two minutes he does not feel better, then you need to call an ambulance. At the same time, before the arrival of the doctors, it is advisable to stay close to him, trying to involve him in a conversation on abstract topics.
- After the arrival of the doctors, try to clearly explain to the doctors the picture of what is happening, since the onset of the attack.
Today, fast-acting nitrates come in a variety of forms that work instantly and are much more effective than tablets. These are aerosols called Nitro poppy, Isotket, Nitrospray.
The way to use them is as follows:
- Shake the bottle
- Direct the spraying device into the patient's oral cavity,
- Make him hold his breath, inject one dose of aerosol, trying to get under the tongue.
In some cases, it may be necessary to inject the medicine again.
Similar assistance should be provided to the patient at home. It will relieve an acute attack and may turn out to be saving, preventing myocardial infarction from developing.
Diagnostics
After providing the first necessary aid, the patient must definitely see a doctor who will clarify the diagnosis and select the optimal treatment. For this, a diagnostic examination is carried out, consisting of the following:
- A medical history is compiled from the words of the patient. Based on the patient's complaints, the doctor establishes the preliminary causes of the disease. After checking blood pressure and pulse, measuring heart rate, the patient is sent for laboratory diagnostics.
- Blood samples are analyzed in the laboratory. Important is the analysis for the presence of cholesterol plaques, which are prerequisites for the occurrence of atherosclerosis.
- Instrumental diagnostics is carried out:
- Holter monitoring, during which the patient wears a portable recorder during the day, which records the ECG and transfers all the information received to the computer. Thanks to this, all violations in the work of the heart are detected.
- Stress tests to study the reaction of the heart to various types of stress. According to them, classes of stable angina pectoris are determined. Testing is carried out on a treadmill (treadmill) or bicycle ergometer.
- To clarify the diagnosis for pain, which is not a fundamental factor in angina pectoris, but is also inherent in other diseases, computed multislice tomography is performed.
- Choosing the optimal method of treatment (between conservative and operative), the doctor can refer the patient to coronary angiography.
- If necessary, to determine the severity of damage to the heart vessels, an EchoCG (endovascular echocardiography) is performed.
Video: Diagnosis of elusive angina
Drugs for the treatment of angina pectoris
Medicines are needed to reduce the frequency of attacks, reduce their duration and prevent the development of myocardial infarction. They are recommended for anyone who suffers from any kind of angina pectoris. The exception is the presence of contraindications to taking a particular drug. A cardiologist selects a medicine for each individual patient.
Video: Opinion of a specialist on the treatment of angina pectoris with an analysis of a clinical case
Alternative medicine in the treatment of angina pectoris
Today, many people are trying to treat various diseases with alternative medicine methods. Some are addicted to them, sometimes reaching fanaticism. However, we must pay tribute to the fact that many traditional medicines help to cope with angina attacks, without the side effects inherent in some drugs. If treatment with folk remedies is carried out in combination with drug therapy, then the number of seizures that occur can be significantly reduced. Many medicinal plants have a calming and vasodilating effect. And you can use them instead of regular tea.
One of the most effective remedies that strengthen the heart muscle and reduce the risk of heart and vascular disease is a mixture that includes lemons (6 pieces), garlic (head) and honey (1 kg). Lemons and garlic are crushed and poured with honey. The mixture is infused for two weeks in a dark place. Take a teaspoon in the morning (on an empty stomach) and in the evening (before going to bed).
You can read more about this and other methods of cleansing and strengthening blood vessels here.
Breathing exercises according to the Buteyko method give no less healing effect. She teaches how to breathe correctly. Many patients who mastered the technique of breathing exercises got rid of blood pressure surges and learned to tame angina attacks, regaining the opportunity to live a normal life, play sports and physical labor.
Prevention of angina pectoris
Everyone knows that the best treatment for a disease is its prevention. To always be in good shape, and not grab your heart at the slightest increase in load, you must:
- Watch your weight, trying to prevent obesity;
- Forever forget about smoking and other bad habits;
- Timely treat concomitant diseases that can become a prerequisite for the development of angina pectoris;
- With a genetic predisposition to heart disease, devote more time to strengthening the heart muscle and increasing the elasticity of blood vessels by visiting the physiotherapy room and strictly following all the advice of the attending physician;
- Lead an active lifestyle, because physical inactivity is one of the risk factors in the development of angina pectoris and other diseases of the heart and blood vessels.
Today, almost all clinics have exercise therapy rooms, the purpose of which is the prevention of various diseases and rehabilitation after complex treatment. They are equipped with special simulators and devices that control the work of the heart and other systems. The doctor who conducts classes in this office selects a set of exercises and a load that is suitable for a particular patient, taking into account the severity of the disease and other features. By visiting it, you can significantly improve your health.
Video: Angina - how to protect your heart?
Discirculatory encephalopathy of the brain
Clinic of the disease
Dyscirculatory encephalopathy of the brain is a polymorphic disease, involving the emotional, cognitive and motor spheres in the pathological process.
Depending on the severity of clinical symptoms, the following stages are distinguished:
I - moderately severe encephalopathy. There is a complex of symptoms known as "cerebrosthenia". In this period, there is a slight decrease in memory for current events and dates, while memory for the past is preserved. The patient is concerned about frequent headaches, slight disturbance of gait and coordination of movements, increased fatigue, sleep disturbance, weakening of libido. Emotional lability, increased irritability and tearfulness can be observed.
II - severe encephalopathy. Memory deteriorates significantly - patients gradually cease to cope with professional activities. Changes in the personal-emotional sphere are growing: patients become "viscous", selfish, often conflict over trifles. Focal symptoms become more distinct: reflexes of oral automatism are revived, tendon intensifies and pathological reflexes appear. At the same time, the patients' criticism of their condition decreases - they stop making complaints, they believe that their condition has stabilized. Violation of the extrapyramidal system is especially characteristic: gait with small steps, quiet speech, akinesia. Psychological examination reveals some intellectual impairments.
III - pronounced encephalopathy. The main difference from stage II is that not one syndrome dominates in the clinical picture, but several. Amyostatic, parkinsonian, pyramidal, discoordinate syndromes, significant cerebellar disorders reach great severity. Paroxysmal conditions are often observed: fainting, falls, epileptic seizures. The mnestic and emotional sphere suffers significantly - a psycho-organic syndrome develops. Cognitive disorders can reach the degree of severe dementia. Criticism of patients to their condition is almost completely absent, although complaints of heaviness in the head, poor sleep, and gait disturbance may persist. Patients are socially and professionally maladjusted, often losing the ability to self-service. 
Diagnostics
The diagnosis of dyscirculatory encephalopathy of the brain usually does not cause difficulties and is based on the results of laboratory and instrumental diagnostics.
Laboratory methods include a clinical blood test, a study of the rheological properties of blood, and the lipid composition of the blood.
The main task of instrumental methods is to clarify the degree and extent of brain damage, as well as to identify underlying diseases. This is achieved using Doppler scanning of cerebral vessels, EEG, ECG, ophthalmoscopy, computed and magnetic resonance imaging.
Treatment of the disease
Treatment of dyscirculatory encephalopathy of the brain is complex, its goal is to slow the progression of cerebral ischemia, prevent strokes and treat the underlying disease.
Medical therapy includes:
- Antihypertensive therapy
- Fight against atherosclerosis and ischemia
- Improving the rheological properties of blood
- Antioxidant and metabolic therapy
Depends on the stage of the disease. At stage I, patients retain full or partial ability to work. II and III stages give the right to receive a disability group.
Angina pectoris is a form of coronary heart disease. This disease is manifested by sudden bouts of chest pain. In this case, there is a burning sensation and squeezing of the sternum.
In another way, angina pectoris is called angina pectoris. In men, this pathology occurs much more often than in women. Angina pectoris usually develops in people after 40 years of age, but there are cases when angina pectoris affects younger people.
Angina pectoris and its etiology
The etiology of angina pectoris is associated with stenosis of the heart vessels. Most often, this phenomenon occurs against the background of any serious diseases. One of the most common pathologies that causes angina pectoris is atherosclerosis. Elevated cholesterol causes the appearance of atherosclerotic plaques, which are gradually deposited on the walls of blood vessels. With the development of atherosclerotic deposits, the lumen of the vessels becomes narrower. There may also be other diseases and pathological conditions that cause angina pectoris:
- spasm of the arteries;
- blockage of the coronary arteries as a result of thrombosis;
- coronary heart disease;
- acute and chronic inflammatory processes in the coronary arteries;
- arterial injury;
- fast heartbeat (tachycardia) or increased diastolic blood pressure;
- myocardial infarction;
- diabetes;
- stress and nervous strain;
- obesity;
- valvular heart disease;
- shock state;
- systolic dysfunction.
There may be other prerequisites for the occurrence of angina pectoris. Bad habits, an inactive sedentary lifestyle, various infections and viruses in the body, taking hormonal drugs for a long period of time, genetic predisposition, male gender, menopause in a woman - all this can also be attributed to risk factors for the formation of angina pectoris in humans. Cases of conditioned reflex angina pectoris are also known.
Pathogenesis of angina pectoris
The pathogenesis of angina pectoris is associated with acute myocardial ischemia. There is a violation of blood circulation and metabolism. The metabolic products remaining in the myocardium irritate the receptors of the myocardium, as a result of which a person has an attack, he feels pain in the sternum.
In this case, the state of the central nervous system is of importance, the activity of which can be disturbed by psycho-emotional stresses and nervous tensions. Under stressful conditions, the body releases catecholamines (adrenal hormones adrenaline and norepinephrine). Violation of the functioning of the central nervous system affects the parasympathetic part of the autonomic nervous system, as a result of which the arteries narrow, causing an attack of angina pectoris.
Clinical picture
The etiology and pathogenesis of angina causes the following symptoms:
- the patient has pain in the sternum after emotional stress or physical exertion;
- the pain is accompanied by a feeling of pressure and burning in the chest;
- pain sensations radiate under the shoulder blade, to the side, to the neck, lower jaw, to the arm;
- after taking the medicine for heart pain, the attack passes.
At rest, seizures usually do not occur, but with a certain course of the disease, a person is also affected at night.
Treatment
If symptoms of the disease occur, the patient is given Corvalol, nitroglycerin, or another medicine for heart pain. It is better to immediately contact the clinic. After diagnosing the disease, the patient will be prescribed medication.
angina pectoris
angina pectoris
Angina pectoris is a form of coronary artery disease characterized by paroxysmal pain in the region of the heart due to acute insufficiency of blood supply to the myocardium. There are angina pectoris that occurs during physical or emotional stress, and rest angina that occurs outside of physical effort, more often at night. In addition to pain behind the sternum, it is manifested by a feeling of suffocation, pallor of the skin, fluctuations in the pulse rate, sensations of interruptions in the work of the heart. May cause heart failure and myocardial infarction.
As a manifestation of ischemic disease, angina pectoris occurs in almost 50% of patients, being the most common form of coronary artery disease. The prevalence of angina pectoris is higher among men - 5-20% (against 1-15% among women), with age its frequency increases sharply. Angina pectoris, due to its specific symptoms, is also known as "angina pectoris" or coronary heart disease.
The development of angina pectoris is provoked by acute insufficiency of coronary blood flow, as a result of which an imbalance develops between the need of cardiomyocytes for oxygen supply and its satisfaction. Violation of perfusion of the heart muscle leads to its ischemia. As a result of ischemia, oxidative processes in the myocardium are disturbed: there is an excessive accumulation of underoxidized metabolites (lactic, carbonic, pyruvic, phosphoric and other acids), ionic equilibrium is disturbed, and ATP synthesis decreases. These processes first cause diastolic and then systolic dysfunction of the myocardium, electrophysiological disturbances (changes in the ST segment and T wave on the ECG) and, ultimately, the development of a pain reaction. The sequence of changes occurring in the myocardium is called the "ischemic cascade", which is based on a violation of perfusion and a change in metabolism in the heart muscle, and the final stage is the development of angina pectoris.
Oxygen deficiency is especially acutely felt by the myocardium during emotional or physical stress: for this reason, angina attacks often occur with increased heart function (during physical activity, stress). Unlike acute myocardial infarction, in which irreversible changes develop in the heart muscle, with angina pectoris, the disorder of the coronary circulation is transient. However, if myocardial hypoxia exceeds the threshold of its survival, then angina pectoris can develop into myocardial infarction.
Causes and risk factors for angina pectoris
The leading cause of angina pectoris, as well as coronary heart disease, is the narrowing of the coronary vessels caused by atherosclerosis. Attacks of angina pectoris develop when the lumen of the coronary arteries is narrowed by 50-70%. The more pronounced atherosclerotic stenosis, the more severe angina pectoris. The severity of angina pectoris also depends on the extent and localization of stenosis, on the number of affected arteries. The pathogenesis of angina pectoris is often mixed, and along with atherosclerotic obstruction, thrombus formation and spasm of the coronary arteries may occur.
Sometimes angina pectoris develops only as a result of angiospasm without atherosclerosis of the arteries. In a number of pathologies of the gastrointestinal tract (diaphragmatic hernia, cholelithiasis, etc.), as well as infectious and allergic diseases, syphilitic and rheumatoid vascular lesions (aortitis, periarteritis, vasculitis, endarteritis), reflex cardiospasm may develop, caused by a violation of the higher nervous regulation of the coronary arteries of the heart - the so-called reflex angina.
Modifiable (removable) and non-modifiable (non-removable) risk factors influence the development, progression and manifestation of angina pectoris.
Non-modifiable risk factors for angina include gender, age, and heredity. It has already been noted that men are most at risk of angina pectoris. This trend prevails until the onset of menopausal changes in the female body, when the production of estrogens, the female sex hormones that “protect” the heart and coronary vessels, decreases. After 55 years, angina pectoris occurs in both sexes with approximately equal frequency. Often angina pectoris is observed in direct relatives of patients suffering from coronary artery disease or who have had a myocardial infarction.
Modifiable risk factors for angina pectoris can be influenced or eliminated from your life. Often these factors are closely interrelated, and reducing the negative impact of one eliminates the other. So, reducing fat in the food consumed leads to a decrease in cholesterol, body weight and blood pressure. Avoidable risk factors for angina include:
In 96% of patients with angina pectoris, an increase in cholesterol and other lipid fractions with an atherogenic effect (triglycerides, low-density lipoproteins) is found, which leads to the deposition of cholesterol in the arteries that feed the myocardium. An increase in the lipid spectrum, in turn, enhances the processes of thrombosis in the vessels.
It usually occurs in people who consume high-calorie foods with an excessive content of animal fats, cholesterol and carbohydrates. Patients with angina pectoris need to limit cholesterol in the diet to 300 mg, salt - up to 5 g, and increase the intake of dietary fiber - more than 30 g.
Insufficient physical activity predisposes to the development of obesity and lipid metabolism disorders. The impact of several factors simultaneously (hypercholesterolemia, obesity, physical inactivity) plays a decisive role in the occurrence of angina pectoris and its progression.
Cigarette smoking increases the concentration of carboxyhemoglobin in the blood - a compound of carbon monoxide and hemoglobin that causes oxygen starvation of cells, primarily cardiomyocytes, arterial spasm, and an increase in blood pressure. In the presence of atherosclerosis, smoking contributes to the early manifestation of angina pectoris and increases the risk of developing acute myocardial infarction.
Often accompanies the course of coronary artery disease and contributes to the progression of angina pectoris. With arterial hypertension, due to an increase in systolic blood pressure, myocardial tension increases and its need for oxygen increases.
These conditions are accompanied by a decrease in oxygen delivery to the heart muscle and provoke angina attacks, both against the background of coronary atherosclerosis and in its absence.
In the presence of diabetes, the risk of coronary artery disease and angina pectoris increases by 2 times. Diabetics with a 10-year history of the disease suffer from severe atherosclerosis and have a worse prognosis in case of angina pectoris and myocardial infarction.
Promotes the processes of thrombosis at the site of atherosclerotic plaque development, increases the risk of coronary artery thrombosis and the development of dangerous complications of coronary artery disease and angina pectoris.
The heart under stress works under conditions of increased load: angiospasm develops, blood pressure increases, the supply of myocardium with oxygen and nutrients worsens. Therefore, stress is a powerful factor provoking angina pectoris, myocardial infarction, and sudden coronary death.
Other risk factors for angina include immune responses, endothelial dysfunction, increased heart rate, premature menopause, and hormonal contraceptive use in women, among others.
The combination of 2 or more factors, even moderately expressed, increases the overall risk of developing angina pectoris. The presence of risk factors should be taken into account when determining treatment tactics and secondary prevention of angina pectoris.
Classification of angina pectoris
According to the international classification adopted by WHO (1979) and the All-Union Cardiological Scientific Center (VKSC) of the USSR Academy of Medical Sciences (1984), the following types of angina pectoris are distinguished:
1. Angina pectoris - occurs in the form of transient attacks of retrosternal pain caused by emotional or physical stress that increases the metabolic needs of the myocardium (tachycardia, increased blood pressure). Usually the pain disappears at rest or is stopped by taking nitroglycerin. Strenuous angina includes:
First-time angina pectoris - lasting up to 1 month. from the first manifestation. It may have a different course and prognosis: regress, go into stable or progressive angina pectoris.
Stable angina - lasting more than 1 month. According to the patient's ability to endure physical activity, it is divided into functional classes:
- Class I - good tolerance to ordinary physical activity; the development of angina attacks is caused by excessive loads performed for a long time and intensively;
- Class II - ordinary physical activity is somewhat limited; the occurrence of angina attacks is provoked by walking on a flat area for more than 500 m, climbing stairs more than 1 floor. The development of an angina attack is influenced by cold weather, wind, emotional arousal, and the first hours after sleep.
- Class III - ordinary physical activity is sharply limited; angina pectoris attacks are caused by walking at the usual pace on flat ground, climbing stairs to the 1st floor.
- Class IV - angina pectoris develops with minimal physical exertion, walking less than 100 m, in the middle of sleep, at rest.
Progressive (unstable) angina - an increase in the severity, duration and frequency of attacks in response to the patient's usual load.
2. Spontaneous (special, vasospastic) angina - caused by a sudden spasm of the coronary arteries. Attacks of stenocardia develop only at rest, at night or early in the morning. Spontaneous angina accompanied by ST-segment elevation is called variant or Prinzmetal's angina.
Progressive, as well as some variants of spontaneous and first-time angina pectoris, are combined into the concept of "unstable angina".
Symptoms of angina pectoris
A typical symptom of angina pectoris is pain behind the sternum, less often to the left of the sternum (in the projection of the heart). Pain sensations can be squeezing, pressing, burning, sometimes cutting, pulling, drilling. Pain intensity can be from tolerable to very pronounced, forcing patients to moan and scream, to experience fear of imminent death.
Pain radiates mainly to the left arm and shoulder, lower jaw, under the left shoulder blade, to the epigastric region; in atypical cases - in the right half of the trunk, legs. The irradiation of pain in angina pectoris is due to its spread from the heart to the VII cervical and I-V thoracic segments of the spinal cord and further along the centrifugal nerves to the innervated zones.
Pain in angina pectoris often occurs at the time of walking, climbing stairs, effort, stress, and may occur at night. The attack of pain lasts from 1 dominut. Factors facilitating an attack of angina are taking nitroglycerin, standing or sitting.
During an attack, the patient experiences a lack of air, tries to stop and freeze, presses his hand to his chest, turns pale; the face takes on a pained expression, the upper limbs become cold and numb. At first, the pulse quickens, then slows down, arrhythmias may develop, more often extrasystole, and blood pressure rises.
A prolonged attack of angina pectoris can develop into a myocardial infarction. Long-term complications of angina pectoris are cardiosclerosis and chronic heart failure.
Diagnosis of angina pectoris
When recognizing angina pectoris, the patient's complaints, the nature, location, irradiation, duration of pain, the conditions for their occurrence and the factors for stopping the attack are taken into account. Laboratory diagnostics includes a study in the blood of total cholesterol, AST and ALT, high and low density lipoproteins, triglycerides, lactate dehydrogenase, creatine kinase, glucose, coagulogram and blood electrolytes. Of particular diagnostic significance is the determination of cardiac troponins I and T - markers indicating myocardial damage. The detection of these myocardial proteins indicates a microinfarction or myocardial infarction that has occurred and can prevent the development of postinfarction angina pectoris.
An ECG taken at the height of an angina attack reveals a decrease in the ST interval, the presence of a negative T wave in the chest leads, conduction and rhythm disturbances. Daily ECG monitoring allows you to record ischemic changes or their absence with each attack of angina pectoris, heart rate, arrhythmias. Increasing heart rate before an attack allows you to think about angina pectoris, normal heart rate - about spontaneous angina. Echocardiography in angina pectoris reveals local ischemic changes and impaired myocardial contractility.
Velgoergometry (VEM) is a test that shows what maximum load a patient can endure without the threat of ischemia. The load is set using an exercise bike until submaximal heart rate is reached with simultaneous ECG recording. With a negative test, submaximal heart rate is achieved after min. in the absence of clinical and ECG manifestations of ischemia. A test is considered positive if it is accompanied by an attack of angina pectoris or a displacement of the ST-segment by 1 or more millimeters at the time of exercise. Detection of angina pectoris is also possible by inducing controlled transient myocardial ischemia using functional (transesophageal atrial stimulation) or pharmacological (isoproterenol, dipyridamole tests) exercise tests.
Myocardial scintigraphy is performed to visualize the perfusion of the heart muscle and detect focal changes in it. The radioactive drug thallium is actively absorbed by viable cardiomyocytes, and in angina pectoris accompanied by coronary sclerosis, focal zones of myocardial perfusion disturbance are detected. Diagnostic coronary angiography is performed to assess the localization, extent and extent of damage to the arteries of the heart, which allows you to decide on the choice of treatment method (conservative or surgical).
Treatment of angina pectoris
It is aimed at stopping, as well as preventing attacks and complications of angina pectoris. The first aid drug for an attack of angina pectoris is nitroglycerin (keep a piece of sugar in your mouth until completely absorbed). Pain relief usually occurs within 1-2 minutes. If the attack is not stopped, nitroglycerin can be used repeatedly with an interval of 3 minutes. and no more than 3 times (due to the danger of a sharp drop in blood pressure).
Planned drug therapy for angina pectoris includes taking antianginal (anti-ischemic) drugs that reduce the oxygen demand of the heart muscle: long-acting nitrates (pentaerythrityl tetranitrate, Isosorbide dinitrate, etc.), b-blockers (anaprilin, oxprenolol, etc.), molsidomine, calcium channel blockers (verapamil, nifedipine), trimetazidine, etc.;
In the treatment of angina pectoris, it is advisable to use antisclerotic drugs (groups of statins - lovastatin, simvastatin), antioxidants (tocopherol), antiplatelet agents (acetylsalicylic acid). According to indications, prevention and treatment of conduction and rhythm disturbances is carried out; in high-functional angina pectoris, surgical myocardial revascularization is performed: balloon angioplasty, coronary artery bypass grafting.
Forecast and prevention of angina pectoris
Angina pectoris is a chronic disabling pathology of the heart. With the progression of angina pectoris, the risk of developing myocardial infarction or death is high. Systematic treatment and secondary prevention help control the course of angina pectoris, improve prognosis and maintain working capacity while limiting physical and emotional stress.
For effective prevention of angina pectoris, it is necessary to exclude risk factors: reducing excess weight, controlling blood pressure, optimizing diet and lifestyle, etc. prevention of atherosclerosis, treatment of concomitant pathologies (diabetes mellitus, gastrointestinal diseases). Exact adherence to the recommendations for the treatment of angina pectoris, taking prolonged nitrates and dispensary control by a cardiologist can achieve a state of long-term remission.
Angina pectoris - treatment in Moscow
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Etiology of angina pectoris
ANGINA (Greek stenos narrow, tight + kardia heart; synonym: angina pectoris) is a symptom of acute myocardial ischemia, which is expressed by an attack of pain behind the sternum. In a wedge, practice there was an attitude to S. as to an independent wedge, a syndrome requiring urgent therapy, which was facilitated, in particular, by the possibility of an unfavorable outcome of an attack (myocardial infarction, ventricular fibrillation), as well as a frequent combination of pain sensations with emotions of fear, impaired autonomic functions (cold sweat, changes in blood pressure, etc.).
On the recommendation of WHO experts (1979), S. refers to manifestations of coronary heart disease (see). Allocate S. of tension, to-ruyu subdivide on for the first time arisen, stable and progressing; S. rest (spontaneous S.); a special form of S., often referred to as Prinzmetal's angina. Based on the frequency of occurrence of seizures and their dependence on physical activity, S. is divided into several forms: a mild form (attacks rarely occur, with excessive physical or psycho-emotional stress for this patient); moderate form, when the development of seizures is associated with everyday professional or domestic stress and is rarely observed at rest; a severe form with frequent daily or repeated attacks during the day at the slightest physical exertion and at rest.
A detailed description of the wedge, pictures of S. was first given by W. Heberden in 1768: , seem to take life if they only increase or continue, but as soon as they stop, this stiffness disappears. In all other respects, patients at the onset of this disease feel well and, as a rule, there is no shortened breathing, from which this condition is completely different. It was already known to Geberden that S.'s attacks can occur during defecation, during unrest, and also at rest, in the supine position, that in winter the disease is more severe than in summer, which is more common in overweight men over 50 years of age. He described the irradiation of pain in the left arm, cases of sudden death during an attack. Parry (SN Parry, 1799) suggested that pain in angina pectoris is caused by a decrease in the supply of oxygen to the heart. Leytham (R. M. Latham, 1876) believed that spasm of the coronary (coronary, T.) arteries can be the cause of S.. At the same time, there were views on S. as a disease of the nervous system. R. Laennec (1826) called S. neuralgia of the heart. It was clinically important to establish S.'s connection with the pathology of the coronary arteries and S.'s differentiation with myocardial infarction (see) during its lifetime diagnosis. In 1918, G. Bousfield published data on ECG changes with S. In 1959, M. Prinzmetal described a special form of S. In the 60s. 20th century ideas about the pathogenesis of S. expanded by studying the effect on the heart of the sympathetic-adrenal system and catecholamines, to-rye, according to W. Raab, can cause the onset of S., increasing myocardial oxygen demand. In the same years, information about the mechanisms of self-regulation of the tone of the coronary arteries expanded, the role of their spasm in the development of an attack in certain forms of S. was proved, and the possibilities of differential diagnosis of S. and similar pain attacks that were not related to manifestations of coronary insufficiency (so called cardialgia).
Being a rather specific symptom of coronary heart disease (CHD), S. is observed, however, not in all cases of this disease. At one-stage eggidemiol. In a survey of one of the districts of Moscow, conducted among men aged 50-59 years, coronary artery disease was detected in 18.8% of the examined, and S. tension - in 11.4%. Observation for 4.52-5 years of randomly selected individuals among the population of New York (4% of 110 thousand inhabitants) aged 35 - 64 years showed that the incidence of S. tension was 2.03 in men and 2.03 in women 0.92 per 1000 examined per year. In rare cases, S. is associated with coronary insufficiency (see), caused not by coronary artery disease, but by damage to the coronary arteries in other diseases, in particular vasculitis in rheumatism, nodular periarteritis, syphilitic mesaortitis. The cause of S. may be disturbances in coronary blood flow with a significant decrease in diastolic blood pressure in the aorta, in particular with aortic valve insufficiency, a significant decrease in cardiac output (eg, with aortic stenosis, heart failure). S.'s development is facilitated by a violation of the transport function of the blood (anemia, carbon monoxide poisoning), an increase in blood viscosity (erythremia), hypoxemia associated with lung disease or a decrease in the oxygen content in the inhaled air.
Pathogenesis
S.'s attack formation is connected with irritation of nervous receptors in a zone of myocardial ischemia by products of the broken metabolism. The likelihood of S.'s occurrence is the higher, the more pronounced ischemia, i.e., the greater the discrepancy between blood flow to the myocardium and its metabolic needs. To a large extent, the degree of ischemia is determined by the severity of atherosclerosis of the coronary arteries. Under experimental conditions, the blood flow in the coronary artery remains normal until its cross section is reduced by 85%, which corresponds to a decrease in the lumen area by about 75%. This is provided by the expansion of arterioles located distal to the stenosis. The data of coronary angiography and the results of studies obtained during coronary artery bypass surgery indicate that arterial stenosis, reaching 50% of its lumen, is rarely accompanied by S.; with a narrowing of the lumen by 75% S. occurs often; with more pronounced stenosis (90-100% of the lumen), S. develops even at rest. The occurrence of myocardial ischemia and S.'s attack is directly related to the magnitude of the work of the heart (determining metabolic needs), the edge increases with physical exertion and emotional stress, accompanied by increased heart rate and increased blood pressure. When carrying out a functional stress test on a bicycle ergometer (see Electrocardiography), S. occurs when a certain value of the product of the number of heartbeats and mean blood pressure is reached, which is constant for this patient. The state of intracardiac and general hemodynamics also affects the magnitude of the work of the heart. An increase in the end-diastolic pressure and diastolic volume of the left ventricle increases the tension developed by it and, consequently, the need for oxygen; in addition, under these conditions, the blood supply to the subendocardial layers of the myocardium worsens. The load on a bicycle ergometer is worse tolerated in a horizontal position, when venous flow to the heart is increased, diastolic volume and end-diastolic pressure in the left ventricle increase. Due to the existing mechanisms of regulation of coronary blood flow, an increase in myocardial oxygen demand in healthy individuals leads to expansion of the coronary arteries and an adequate increase in blood flow to the myocardium. In patients with atherosclerosis of the coronary arteries, the same expansion of unaffected arterial branches can lead to a redistribution of blood flow: mainly blood enters the areas supplied by non-sclerotic arteries, and its flow through stenotic branches is sharply reduced (the phenomenon of intercoronary "stealing"). Dilated vessels located distal to the stenosis, losing their tone, acquire the properties of passive tubes and are easily compressed with increased cardiac activity and systolic tension of the myocardium, with an increase in end-diastolic volume and pressure in the left ventricle. This exacerbates ischemia of the myocardial region supplied by sclerosed arteries.
The cause of transient ischemia of the myocardium and S. may be a spasm of the coronary arteries due to a violation of the regulation of their tone, in particular, the excitation of alpha-adrenergic receptors in the walls of large branches of the coronary arteries during activation of the sympathoadrenal system (during stress, hypothalamic dysfunction, when α-agonists are administered to patients) or a change in reactivity of the walls of the arteries due to their atherosclerotic lesions. The role of spasm of the coronary arteries is shown, for example, in Prinzmetal's angina pectoris. Spasm of the coronary artery, accompanied by an attack of S., the rise of the S T segment on the ECG, can be provoked by intracoronary administration of the ergot alkaloid ergometrine to the patient during coronary angiography. Ergometrine spasm occurs in places of hypersensitivity of the smooth muscles of the coronary artery, which does not always coincide with the localization of the ischemia zone caused in the same patient by exercise on a bicycle ergometer (when ischemia usually develops in areas corresponding to the greatest organic narrowing of the coronary artery). Therefore existence of two forms of S. at one patient, differing on the pathogenetic mechanism is possible.
Hyperactivation of the sympathoadrenal system during stress contributes to the development of myocardial and S. hypoxia not only through a-adrenergic mechanisms. Increased release of catecholamines (see) and stimulation of p-adrenergic receptors of the heart increase its work and oxygen demand with insufficient relaxation of the myocardium during diastole. In addition, there is an increase in blood clotting with increased adhesion of platelets (in this case, blood viscosity increases and resistance to blood flow in the vessels increases) and the release of thromboxane, which has a vasoconstrictor effect; the same effect is exerted by prostaglandin F2a, the release of which is possible due to the activation of the kinin-kallikrein system during stress. Myocardial metabolism in the ischemic zone is sharply disturbed; for the occurrence of pain, i.e., S. proper, the accumulation of lactic acid in the hypoxic area of the myocardium, an increase in the concentration of hydrogen ions, extracellular potassium, and polypeptides matter.
The heart has undifferentiated sympathetic receptor endings located between cells. They connect with non-myelinated fibers, which pass perivascularly to the cardiac plexus. It is supposed that S.'s attack is caused by irritation of nervous terminations by polypeptides, in particular kinins (see), to-rye are released in the conditions of ischemia when the cellular environment becomes more sour or the content of potassium ions increases. Impulses along the sensory fibers of the sympathetic nerves of the heart are sent to the ganglia between Sup and ThIV, then they enter the spinal cord (connection with the somatic nerves), ascend to the thalamus and the perception zones of the cerebral cortex. The severity of pain depends on the degree of metabolic changes in the myocardium (proportional to the degree of ischemia) and on the state of the nerve endings; pain attacks can disappear after myocardial infarction, when destruction of nerve endings occurs in the affected area. Localization of the pain felt at S. usually corresponds to zones of an innervation from upper chest segments, but in some cases there is a pain of atypical localization.
pathological anatomy
In overwhelming majority of cases morfol. the basis of S. is atherosclerosis of the coronary arteries of the heart. The microscopic picture and ultrastructure of the myocardium in S. have not been studied enough due to the short duration of ischemia. In the experiment, signs of myocardial ischemia can be detected a few minutes after its onset. Intracellular glycogen disappears and myofibrils relax. These changes are reversible if ischemia lasts no more than 30 minutes. According to the puncture biopsy of the myocardium (see Heart), dystrophic changes in the organelles of myocytes, mainly in the membrane systems of the cell, and to a lesser extent in the myofibrillar apparatus, were revealed in patients with IHD. Along with dystrophy in nek-ry myocytes signs of intracellular regeneration come to light (presence of kernels and euchromatin in kernels, free ribosomes, the policy and a granular reticulum in a sarcoplasm).
Clinical picture and course
In typical cases, S. is characterized by an attack of pain of a compressive or pressing character, localized more often in the region of the upper part of the sternum, sometimes to the left of it. Pain can radiate to the left arm, to the left half of the neck and face, to the lower jaw, left ear, to the region of the left shoulder blade, sometimes to the right shoulder or both shoulders and both arms, back. Less often, the pain spreads to the left side of the abdomen and lower back, to the legs. The onset of pain is rarely sudden, usually it gradually increases and lasts for several minutes. then disappears. Rapid (within 2-3 minutes) relief of pain with nitroglycerin is characteristic. The intensity of pain sensation depends on the individual characteristics of the patient. Many patients complain not of pain, but of a feeling of heaviness, compression or tightness behind the sternum, lack of air. S.'s attack may be accompanied by a feeling of fear, sometimes general weakness, sweating, tremor, and occasionally a feeling of lightheadedness, fainting, dizziness, urge to urinate and profuse diuresis. When examining a patient, sometimes no deviations from the norm are found. At the time of the attack, pallor of the skin may be observed. In some cases, hypersensitivity of the skin in places of pain irradiation is revealed.
Medical examination of the patient during S.'s attack does not reveal significant dynamics in the activity of the heart. The size of the heart is not changed; at auscultation only sometimes a slight weakening of heart sounds, pathological III tone, systolic murmur can be recorded, to-rye disappear after an attack. An attack may be accompanied by a slight tachycardia (see) or bradycardia (see), occasionally extrasystole (see), the latter being especially characteristic of Prinzmetal's angina, an increase in blood pressure.
S. tension is characterized by the appearance of pain during physical exertion, in particular when walking; the patient is forced to stop, after which the pain after 2-3 minutes. stops. Particularly bad patients tolerate walking against the wind, in cold weather. The act of defecation can provoke an attack of S., its occurrence is facilitated by abundant food, bloating. S. tension can also occur during emotional stress that increases myocardial oxygen demand due to the release of catecholamines, increased heart function due to increased blood pressure and increased heart rate.
S. of rest is characterized by the occurrence of seizures without any apparent connection with physical or emotional stress. Typically, the development of an attack at night during sleep. The patient wakes up from a feeling of pressure behind the sternum or suffocation, sits up in bed. Often, S.'s attacks of rest proceed longer and more severely than S.'s attacks of tension. In most cases S. of rest develops at patients with sharply expressed, often stenosing, atherosclerosis of coronary arteries. At such patients S. of rest is combined with S. of tension. In some patients with a diagnosis of S. at rest, during the observation, a connection between seizures and exercise is revealed - an increase in blood pressure and an increase in the number of heartbeats at night (during REM sleep), an increase in the volume of circulating blood at night in patients with latent or overt heart failure. These forms have the same pathogenesis as S. of tension, but exercise tolerance is sharply reduced. Sometimes an angina attack occurs at the time of the patient's transition to a horizontal position (angina decubitus), which is explained by an increase in venous return (preload).
A certain role in S.'s emergence of rest can be played by patol. reflexes from interoreceptors of various organs. They speak of reflex S. proper in cases where attacks are undoubtedly associated with reflex effects: inhalation of cold air (a reflex from the respiratory tract), cooling of the skin (the so-called S. of cold sheets), exacerbation of cholelithiasis (cholecystocoronary reflex) etc.
Typical S. of stress and rest is called classic angina pectoris. Along with it, a special form of S. is distinguished, usually referred to as Prinzmetal's angina pectoris; it is caused by a periodic spasm of one of the large coronary arteries without an increase in the metabolic needs of the myocardium before an attack. This form occurs in 2-3% of patients with C. The appearance of pain is not associated with physical or emotional stress, but they can be provoked by cooling, drinking cold water, overeating, smoking, hyperventilation. Individual cyclicality in the development of seizures is characteristic, to-rye often occur at night or in the morning. As in classical S., the pains are localized behind the sternum, but their duration can reach 20-30 minutes. Often the attack is accompanied by profuse sweating, sometimes nausea, vomiting. Some patients may have several attacks in a row with an interval between them from 2-3 to 10-15 minutes. Prinzmetal's angina can occur both in patients with unchanged coronary arteries and in the presence of coronary atherosclerosis. In the latter case, it can be combined with S. tension. Possible complication of Prinzmetal's angina pectoris with various disorders of rhythm and conduction; ventricular extrasystoles, complete and incomplete atrioventricular block (see Heart block). Severe cardiac arrhythmias can be the cause of sudden death of the patient.
At a part of patients S. proceeds atypically. The pain is sometimes localized not behind the sternum, but in the left or right arm, shoulder, epigastric region, lower jaw, i.e., in places where retrosternal pain often radiates with typical S. In such cases, S. should be thought of, if the pain of atypical localization occurs when walking and disappears when the load is stopped.
In some cases, acute coronary insufficiency is manifested not by attacks of pain, but by other symptoms equivalent to C. Equivalent to C., especially in long-term ill people or after a myocardial infarction, there may be a feeling of lack of air or difficulty breathing while walking in the absence of obvious signs of cardiac insufficiency; with pronounced cardiosclerosis, acute coronary insufficiency in some cases is manifested not by typical S.'s attacks, but in the form of cardiac asthma (see) - the asthmatic equivalent of S. - or pulmonary edema (see). Sometimes S.'s equivalent can be a paroxysm of atrial fibrillation (see), the occurrence of frequent ventricular extrasystoles, paroxysmal tachycardia (S.'s arrhythmic equivalent).
Flow
The severity of S. is determined by the frequency, severity and duration of pain attacks; the less the load that provokes S., the greater the degree of coronary insufficiency. S.'s current can be stable when attacks arise under the same circumstances, and their frequency depends on a way of life and loads of the patient. Progressive, or unstable, S. is characterized by an increase in the severity and duration of attacks (the number of nitroglycerin tablets taken by the patient per day usually increases, sometimes nitroglycerin becomes ineffective); sometimes S. of rest join S. of tension. Unstable S. also includes S. for the first time (prescription up to 1 month, later on it can take a stable course or precede the development of myocardial infarction), as well as a long (up to 15-30 minutes) anginal attack that is not stopped by nitroglycerin , with ECG changes such as focal dystrophy, but without laboratory data characteristic of myocardial infarction (see), and Prinzmetal's angina pectoris in the acute phase, if the last attack was no later than 1 month. ago. If unstable S.'s course comes to the end with development of a myocardial infarction, retrospectively speak about a preinfarction condition.
Diagnosis
In S.'s diagnosis the major role is played by carefully collected anamnesis and detailing of complaints of the patient. The most significant paroxysmal and short-term pain, its relationship with physical stress, localization behind the sternum (in typical cases), the rapid effect of nitroglycerin. Laboratory data during an attack do not change. Electrocardiographic and vectorcardiographic changes during attacks are detected in 50-70% of patients. The most characteristic changes on the ECG are depression of the ST segment and a decrease in amplitude, flattening or inversion of the T wave; often it becomes negative or biphasic (Fig., c, d and e), sometimes it increases to a giant pointed tooth. Transient arrhythmias and conduction disturbances may be recorded. Outside of an attack, the ECG may not be changed. For Prinzmetal's angina, ST-segment elevation during an attack is typical, which indicates transmural myocardial ischemia. With incomplete vasoconstriction or partial compensation of blood flow, ST segment depression is possible. Repeated attacks of Prinzmetal's angina usually occur with the same ECG changes in the same leads. With long-term monitoring of patients suffering from this form of S., episodes of a painless increase in the ST segment are observed, which is also due to spasm of the coronary arteries. On the vectorcardiogram (see Vectorcardiography), during an attack of S., the T loop most often changes, it deviates and goes beyond the QRS loop, forming an angle of up to 60-100 ° with it, and with severe hypoxia - up to 100-150 °, while there is a non-closure of the QRS loop.
Since ECG registration during S.'s attack is not always possible, functional stress tests are used to detect coronary insufficiency. These include dosed physical activity on a bicycle ergometer or treadmill (see Ergography), electrical stimulation of the atria and pharmacol. samples with isoprenaline or dipyridomole (see Electrocardiography). Samples are used both for the diagnosis of coronary artery disease and for determining exercise tolerance. Contraindications for these tests are myocardial infarction in the acute period, frequent S.'s attacks, heart failure, high blood pressure, cardiac arrhythmias, aortic stenosis. Relative contraindication - severe obesity, emphysema, pulmonary heart failure. Positive, i.e., indicating myocardial hypoxia, consider the following changes during exercise: 1) the onset of S.'s attack with simultaneous changes in the ECG or without them; 2) the appearance of severe shortness of breath or suffocation; 3) decrease in blood pressure; 4) ECG signs: horizontal or arcuate displacement of the S T segment up or down by 1 - 2 mm, the appearance of a negative T wave, especially with a simultaneous decrease in the height of the R wave; oblique upward shift of the S T segment down, a cut also occurs in healthy individuals (Fig., b), but is regarded as a sign of coronary insufficiency if the duration of the decrease in the S T segment is more than 0.08 seconds. with a displacement depth of at least 1.5 mm; 5) the occurrence of frequent polytopic and especially early ventricular extrasystoles or disorders of atrioventricular conduction. When one of these signs appears or with a significant increase in blood pressure, the load is stopped. The basis for the termination of the load is also the achievement of a heart rate corresponding to the level of submaximal load. Such a pulse rate, according to WHO criteria (1971), at the age of 20-29 years is 170 beats per minute, at the age of 30-39 years - 160, at the age of 40-49 years - 150, at the age of 50-59 years - 140, 60 years and older - 130 beats per 1 min. If the achievement of a submaximal heart rate is not accompanied by clinical or electrocardiographic signs of myocardial ischemia, the test is considered negative, which, however, does not refute the diagnosis of IHD, although it makes it doubtful.
False-positive results occur in patients with heart defects, with arterial hypertension and left ventricular hypertrophy, with vegetative-vascular dysfunction, when taking cardiac glycosides, diuretics, estrogens. The load on a bicycle ergometer also allows you to evaluate the power and amount of work performed. Electrical stimulation of the atria makes it possible to bring the number of heartbeats to a submaximal level without increasing blood pressure and without the participation of peripheral factors. As the method is invasive, it is seldom used in a wedge, practice.
The same electrocardiographic and clinical criteria are used with the rarely performed, but with a number of advantages (the possibility of an immediate cessation of tachycardia), the method of frequent electrical atrial stimulation.
Pharmacol use. tests with isoprenaline and dipyridamole is based on the fact that the β-agonist isoprenaline increases myocardial oxygen demand and increases heart function, and dipyridamole causes ischemia of the myocardium supplied by sclerosed arteries due to the expansion of unaffected arteries (the "steal" phenomenon). The introduction of these drugs to patients with coronary atherosclerosis causes the appearance of signs of ischemia on the ECG. Erg alkaloid ergometrine is used to detect spasm of the coronary arteries. At the same time, in patients suffering from Prinzmetal's angina, an increase in the ST segment is recorded on the ECG, sometimes a pain attack occurs, while in patients with classical S., depression of the ST segment or an attack of pain without ECG changes is possible, which indicates the involvement of the spastic component in the genesis of C attacks. Coronary angiography is used to diagnose atherosclerotic narrowing of the coronary arteries (see). Indications for its implementation are the proposed surgical intervention or significant diagnostic difficulties.
X-ray contrast or radionuclide ventriculography makes it possible to detect areas of hypokinesia, akinesia or dysknesia of the ischemic myocardium. Local violations of myocardial contractility due to its ischemia are detected using echocardiography (see). After taking nitroglycerin, the zone of hypokinesia may decrease or disappear. Ischemia of a site of a myocardium is found also by means of a scintigraphy (see) with thallium-201, absorption to-rogo myocardial tissue in the ischemic zone is reduced. Technetium-99 pyrophosphate or technetium-99-tetracycline, on the contrary, accumulate in the foci of myocardial ischemia or necrosis, which is used for diagnosis.
The differential diagnosis is carried out between S.'s attack and myocardial infarction (see), as well as between S. and pains in the region of the heart of non-coronary origin - the so-called. cardialgia. It is necessary to think of a myocardial infarction if S.'s attack proceeds more than 30 min. and is characterized by intense pain if S. is accompanied by a decrease in blood pressure, cardiac asthma, pronounced dynamics of heart tones. In such cases, the diagnosis is clarified with the help of electrocardiography. Cardialgia can occur in diseases of the myocardium, pericardium or pleura, have a psychogenic origin, may be due to the pathology of the musculoskeletal system or the peripheral nervous system, went. - kish. tract, diaphragm. As a rule, with cardialgia, unlike S., there is no clear paroxysmal pain, they can last for hours and days, they are often aching, aching, piercing. Pain is localized not behind the sternum, but in the region of the apex of the heart, there is no clear connection with physical activity, walking, the effect of nitroglycerin. In inflammatory diseases (myocarditis, pericarditis), corresponding changes in laboratory data are detected, with pericarditis (see), pericardial friction noise is heard. At diseases of the musculoskeletal device and neuralgia characteristic painful points come to light, sometimes rentgenol. changes, pains are often provoked by sharp movements of the left hand, an uncomfortable posture, they are stopped by analgesics. At diseases went. - kish. path should pay attention to the relationship of pain with food, their appearance in a horizontal position after eating (with hiatal hernia). Help in diagnosis special endoscopic and rentgenol. research methods. In middle-aged and elderly people, cardialgia due to osteochondrosis of the spine, endocrine disorders, etc. can be combined with IHD and C.
Treatment
Nitroglycerin is used to stop S.'s attack (tablets of 0.0005 g under the tongue or 1% alcohol solution, 1-3 drops for sugar). Nitroglycerin relieves spasm of the coronary arteries, lowers their resistance and thus has a coronary dilating effect. Under its influence, the blood flow through the collaterals and the number of functioning branches increase, the intraventricular pressure and the volume of the ventricles of the heart decrease, which reduces the tension of the myocardial walls and their pressure on the arteries and collaterals in the ischemic zone. In addition, nitroglycerin reduces peripheral arterial resistance and causes venous dilatation, which leads to hemodynamic unloading of the left ventricle and a decrease in myocardial oxygen consumption. The action of nitroglycerin appears after 1 - 2 minutes. and lasts 20-30 minutes. Side effects of nitroglycerin - a throbbing headache, sometimes a decrease in blood pressure. These phenomena can be eliminated by reducing the dose of the drug or using it as part of Votchal drops (9 hours 5% menthol alcohol and 1 hour 1% nitroglycerin). At the prolonged attacks apply narcotic and non-narcotic analgesics, to-rye enter parenterally. Angiospastic angina, or Prinzmetal's angina, is most clearly stopped by sublingual administration of nifedipine (Corinfar). The use of mustard plasters on the heart area, immersion of hands in hot water also contributes to S.'s relief (reflex effect from skin receptors on coronary vessels). Patients with unstable S. should be hospitalized, preferably in an intensive care unit.
With persistent S., the issue of surgical intervention is resolved, the goal of which is to eliminate pain attacks that reduce the patient's ability to work, increase heart productivity and prevent myocardial infarction in patients with severe S. of rest and tension, not amenable to drug therapy. To do this, myocardial revascularization is performed, which is considered absolutely indicated for patients with unstable (pre-infarction) S., who have atherosclerotic lesions of the trunk of the left coronary artery, proximally located critical stenoses (more than 75% of the lumen) of the anterior interventricular artery, lesions of the three main arteries of the heart with a passable distal bed.
Surgical intervention performed under cardiopulmonary bypass (see) and Cold cardioplegia (see), consists in shunting the affected area of the coronary artery using aortocoronary autovenous shunts (see Atherosclerosis, surgical treatment of occlusive lesions; Myocardial infarction, surgical treatment) or internal thoracic arteries (see Arterialization of the myocardium). The latter operation is performed less frequently due to the advantages of multiple bypass surgery (see Blood Vessel Bypass). In this case, one "jumping" autovenous shunt with successive anastomoses with several coronary arteries is often used. Single shunting is shown by hl. arr. with an isolated lesion of the anterior interventricular artery; in this case, endovascular dilation of a limited area of stenosis is also successfully performed without open surgery on the heart (see X-ray endovascular surgery). In case of repeated operations or in the absence of a high-quality autogenous graft, synthetic (core-tex) allogeneic or xenogenic vascular bioprostheses are used.
The most formidable complication of operations is an intraoperative myocardial infarction (see) with the development of cardiogenic shock in the postoperative period (see). Prevention of this complication consists in carrying out high-quality protection of the myocardium from anoxic damage during the main stage of the operation on a stopped heart (see Cardioplegia).
Immediate and long-term results are directly dependent on the initial state of the contractile function of the myocardium, the completeness of its revascularization, the amount of volumetric blood flow through the bypass shunt (blood flow less than 40-50 ml/min is unfavorable prognostically due to the risk of shunt thrombosis). After direct myocardial revascularization, S.'s attacks almost completely disappear in 80-95% of patients or the need for specific drug therapy is significantly reduced, exercise tolerance increases, and working capacity is completely restored or improved.
Prevention of angina pectoris
Primary prevention (see Primary prevention). the vast majority of cases of angina is reduced to measures aimed at preventing the development of atherosclerosis (see) and coronary heart disease (see). If other diseases are the cause of angina pectoris (eg, rheumatic heart disease, syphilitic mesoaortitis, anomalies in the development of the cardiovascular system, severe anemia), the prevention of angina pectoris is the treatment of appropriate diseases (see Coronary insufficiency, Congenital heart defects, Acquired heart defects, Rheumatism, Syphilis). Secondary prevention includes continuous drug treatment and a system of physiotherapy measures used to improve coronary collateral circulation, as well as measures to combat the progression of diseases underlying angina pectoris.
Long-acting nitroglycerin preparations (sustak, nitrong, trinitrolong, and especially nitrosorbide) are widely used to prevent S.'s attacks in individually determined doses, as well as other long-acting nitrates (erinite, nitrosorbide). An important place in the prevention of S.'s attacks is occupied by beta-blockers (propranolol, trazikor, etc.), which reduce the frequency, strength and speed of heart contractions, cardiac output, blood pressure and, as a result, reduce myocardial oxygen demand. Their possible side effects are bronchospasm, increased heart failure, hypoglycemia in diabetic patients receiving hypoglycemic drugs. They are contraindicated in bronchial asthma, severe bradycardia, atrioventricular blockade. In heart failure, these drugs are used in combination with cardiac glycosides or use cardioselective beta-blockers (eg, cordanum).
If spasm is the basis of S.'s attack, calcium antagonists are shown, for example, nifedipine (Corinfar). Nifedipine does not affect atrioventricular conduction, the number of heart contractions under the influence of nifedipine increases and therefore it can be prescribed in combination with beta-blockers. Verapamil (Isoptin) has a similar mechanism, but less pronounced coronary dilating effect; it reduces the number of heartbeats, can slow down atrioventricular conduction, so it is not combined with beta-blockers.
Isoptin is characterized by antiarrhythmic action. It can be used for the prevention of S.'s attacks in case of its non-severe course with S.'s combination and extrasystole. Derivatives of isoquinoline - papaverine and no-shpa - have a direct relaxing effect on the vascular wall. They are used orally to prevent seizures or parenterally to relieve prolonged seizures in combination with analgesics. Preparations are shown at the accompanying spastic conditions of bilious ways, intestines, hron. gastritis.
Carbochromen (Intensain, Intecordin) increases coronary blood flow and, with prolonged use, promotes the development of collaterals. It is used mainly in localized coronary atherosclerosis, since there is evidence that in patients with widespread stenosing atherosclerosis, carbochromene preparations can cause (especially when administered parenterally) increased pain. Dipyridamole (persantin, chimes) also increases collateral blood flow due to an increase in the concentration of adenosine in the myocardium and reduces platelet aggregation. However, in high doses, dipyridamole can worsen the blood supply to the ischemic area in the area of arterial stenosis due to the distribution of blood into dilated vessels (the "steal" phenomenon).
The wedge, application is also found by p-adrenergic activators - oxyphedrin (ildamen, myofedrin), nonahlazin, to-rye have a positive ino-tropic effect, increase coronary blood flow. However, they can increase myocardial oxygen demand, so they are used only in patients with mild forms of S. without severe coronary atherosclerosis with concomitant arterial hypotension and bradycardia.
Contribute to the reduction of S.'s attacks peripheral vasodilators, in particular mole and dominoes (kor-vaton), to-ry increases the capacity of the venous system, reduces venous blood flow to the heart, reducing the load on the heart and oxygen consumption; the drug also inhibits platelet aggregation.
To reduce myocardial oxygen demand, pyridoxinyl-glyoxylate (glio-6, gliosis) is used, which activates anaerobic and inhibits aerobic processes, providing a protective effect on myocardial ultrastructure during hypoxia.
Quite often there is a need for appointment to sick S. psihofar-makol. drugs (sedatives, hypnotics, tranquilizers, antidepressants).
The emergence of a large number of effective antianginal agents, primarily long-acting nitrates and p-blockers, has reduced the importance of prophylactic use of papaverine, no-shpy, and antithyroid drugs in S.. The treatment plan and the selection of drugs are determined by the clinic and the severity of the course of coronary artery disease, depending on the phase of the disease, the presence of complications and comorbidities.
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E. I. Sokolov, I. E. Sofieva; S. L. Dzemeshkevich (hir.).
ANGINA (THE ANGINA)- attacks of sudden pain in the chest due to an acute lack of blood supply to the myocardium - a clinical form of coronary heart disease. · Etiology of angina pectoris: Spasm of blood vessels and arteries; Inflammatory processes in the coronary arteries; Tachycardia; arterial injury; myocardial infarction; Blockage of the coronary arteries by a thrombus; Obesity; Diabetes; Heart disease; Shock, stress or nervous strain; Also, the prerequisites for the occurrence of angina pectoris can be: 1. Addictions. Smoking, alcohol in large quantities, drug use, lead to the destruction of the walls of blood vessels. 2. Male sex. Men, as the main breadwinners in the family, spend more time at work, so their heart is more prone to stress and physical exertion, besides, women produce a hormone - estrogen, which perfectly protects the heart. 3. A sedentary lifestyle. A sedentary or sedentary lifestyle often leads to a problem such as obesity, which adversely affects the walls of blood vessels, the functioning of the heart muscle and the quality of the blood, since oxygen does not fill it properly. 6. Genetic factor. If someone in the male family died of heart failure before the age of 50, then the child is at risk and has a high chance of earning angina pectoris. 7. Race. It is noted that people of the African race practically do not suffer from heart disease, while Europeans, especially northern countries, are at risk. Pathogenesis of angina pectoris: During physical exertion, the myocardium requires more oxygen, but there is no opportunity to fully provide blood that contains it in the vessels, since the walls of the coronary arteries are narrowed. Thus, myocardial ischemia occurs, which disrupts the contractile functions of sections of the heart muscle. With ischemia, not only physical changes in the heart muscle are recorded, but also failures of all biochemical and electrical processes inside the heart. Moreover, at the initial stage, all changes can be returned to their previous course, but with a long course, the process is irreversible. The pathogenesis of angina is directly related to myocardial ischemia. The metabolic processes of blood and nutrients are disturbed, and the metabolic products that remain in the myocardium irritate its receptors, which leads to an attack. All this is reflected in a person with an attack of pain in the sternum. Clinic: an attack of retrosternal pain after physical and psycho-emotional stress, the pain is short-lived (up to 15 minutes), stops after 1-2 minutes. after stopping the load or taking nitroglycerin (any drug containing menthol). Localized behind the sternum, with irradiation to the lower jaw, left arm, shoulder, shoulder blade. By nature, it is compressive, pressing. A symptom of a “clenched fist” is characteristic (the patient puts his fist on the region of the heart). During an attack, the patient feels the fear of death, freezes, tries not to move. Clinical forms of angina pectoris: - Stable exertional angina- this is angina pectoris that occurs on physical activity, characteristic of each patient. - Unstable angina- an acute process of myocardial ischemia, the severity and duration of which are insufficient for the development of myocardial necrosis. - Spontaneous angina occurs at rest without previous physical or emotional stress. An attack of angina pectoris usually occurs at night or early in the morning, a series of attacks with an interval of 10-15 minutes is also possible, they may be accompanied by arrhythmia, a decrease in blood pressure. - Microvascular angina(syndrome X) - angina attacks occur in patients in the absence of stenosing atherosclerosis of the coronary arteries, the cause is damage to the arteries of medium and small caliber. Emergency help during an attack:- complete physical and mental rest; - access to fresh (but not cold, because it can increase the pain symptom) air; - unbutton tight clothing; - lay down, raising the head end of the bed high or seated in bed (armchair, on the couch) with legs down; - Determine the pulse, evaluate its rhythm, measure blood pressure; - distracting procedures: mustard plasters on the heart area, hot hand baths, put a towel moistened with hot water on the interscapular area, talking with the patient; - Validol (under the tongue), and after 15 minutes. - give nitroglycerin in tablets 0.5 mg sublingually (if necessary, again after 5-10 minutes), or in the form of an aerosol, 1-2 doses are injected under the tongue; 13) Myocardial infarction. Etiology. Pathogenesis. Clinical forms of myocardial infarction. First aid for an attack of pain in the heart. myocardial infarction - an acute disease caused by the occurrence of one or more foci of ischemic necrosis in the heart muscle due to absolute or relative insufficiency of the coronary circulation. Etiology and pathogenesis The most common cause of impaired coronary blood flow is atherosclerosis of the coronary arteries. Atherosclerotic plaques are formed on the intima of the vessels, protruding into its lumen. Growing to a significant size, the plaques cause narrowing of the lumen of the vessel. Naturally, the area of the myocardium that receives blood through this vessel is ischemic. When the lumen of the vessel is completely closed, the blood supply to the corresponding part of the myocardium stops - necrosis (infarction) of the myocardium develops. It should be noted that the lumen of the coronary artery can be obturated both by the atherosclerotic plaque itself and by a thrombus formed on the surface of the vessel ulcerated by the plaque. The cause of myocardial infarction can be some diseases, for example, septic endocarditis, in which embolism and closure of the lumen of the coronary artery with thrombotic masses are possible; systemic vascular lesions with involvement in the process of the arteries of the heart and some other diseases. Depending on the size of necrosis, small-focal and large-focal myocardial infarction is distinguished. According to the prevalence of necrosis to the depth of the heart muscle, the following forms of myocardial infarction are distinguished: subendocardial (necrosis in the myocardial layer adjacent to the endocardium), subepicardial (damage to the myocardial layers adjacent to the epicardium), intramural (necrosis develops inside the walls, not reaching the endocardium and epicardium) and transmural (damage extends to the entire thickness of the myocardium). Clinical picture The most striking and constant symptom of acute myocardial infarction is an attack of intense pain. Most often, the pain is localized behind the sternum in the region of the heart and can radiate to the left arm, shoulder, neck and lower jaw, to the back (into the interscapular space). Pain in the retrosternal region is more often observed with an infarction of the anterior wall; localization of pain in the epigastric region is more often observed with myocardial infarction of the posterior wall. However, the exact localization of a heart attack can only be determined on the basis of ECG data. The pain is compressive, bursting or pressing. The duration of a painful attack in acute myocardial infarction is from 20-30 minutes to several hours. The duration of the pain attack and the lack of effect from taking nitroglycerin distinguish acute myocardial infarction from an angina attack. The severity of the pain syndrome does not always correspond to the magnitude of myocardial damage, but in most cases a prolonged and intense pain attack is observed with extensive myocardial infarction. The pain is often accompanied by a feeling of fear of death, lack of air. Patients are agitated, restless, groaning in pain. In the future, a sharp weakness usually develops. First aid: 1. The patient must be carefully laid on his back and given the most comfortable position (semi-sitting or a cushion under the back of the head). 2. Ensure the flow of fresh air and the most comfortable temperature conditions. Remove clothing that prevents free breathing (tie, belt, etc.). 3. Convince the patient to remain calm (especially if the patient has signs of motor arousal). 4. Give the patient a Nitroglycerin tablet under the tongue and a sedative (Corvalol, motherwort tincture or valerian). 5. Measure blood pressure. If the pressure is not more than 130 mm. rt. Art., then repeated intake of Nitroglycerin should be carried out every five minutes. Before the arrival of doctors, you can give 2-3 tablets of this drug. If the first dose of Nitroglycerin caused a severe throbbing headache, then the dosage should be reduced to ½ tablet. 6. Give the patient a crushed Aspirin tablet (to thin the blood). 7. You can put a mustard plaster on the area of pain localization (do not forget to follow it so that there is no burn). 14) Acute cardiovascular failure: syncope. Causes, clinical picture. First aid.
