Atypical forms of myocardial infarction and their symptoms. Heart attack symptoms Myocardial infarction asthmatic form help

Peripheral with atypical localization of pain: a) left-handed; b) left-scapular; c) laryngeal-pharyngeal; d) upper vertebral; e) mandibular.
Abdominal (gastralgic).
Asthmatic.
Collaptoid.
Edema.
Arrhythmic.
Cerebral.
Erased (oligosymptomatic).
Combined.

Atypical forms of myocardial infarction are most often observed in elderly people with severe symptoms of cardiosclerosis, circulatory failure, often against the background of recurrent myocardial infarction. However, only the onset of a heart attack is atypical; in the future, as a rule, myocardial infarction becomes typical.

Peripheral type of myocardial infarction with atypical localization of pain characterized by pain of varying intensity, sometimes increasing, not stopped by nitroglycerin, localized not behind the sternum and not in the precordial region, but in atypical places - in the throat (laryngeal-pharyngeal form), in the left hand, the tip of the left little finger, etc. ( left-handed), left shoulder blade (left-scapular), in the region of the cervicothoracic spine (upper vertebral), in the region of the lower jaw (mandibular). In this case, there may be weakness, sweating, acrocyanosis, palpitations, arrhythmias, and a drop in blood pressure. Diagnosis of this form of MI is based on the above symptoms, repeated ECG recording, taking into account the dynamics of its changes, and the detection of resorption-necrotic syndrome.

Abdominal (gastralgic) type of myocardial infarction observed more often with diaphragmatic (posterior) infarction, manifested by intense pain in the epigastrium or in the region of the right hypochondrium, the right half of the abdomen. At the same time, there is vomiting, nausea, bloating, diarrhea, paresis of the gastrointestinal tract with a sharp expansion of the stomach and intestines. On palpation of the abdomen, there is tension and tenderness of the abdominal wall. It is necessary to differentiate this form from pancreatitis, cholecystitis, appendicitis, intestinal obstruction, perforated stomach ulcer, food poisoning. The diagnosis of this form of MI is made on the basis of changes in the cardiovascular system (arrhythmias, a drop in blood pressure, deafness of heart sounds), ECG recordings in dynamics, resorption-necrotic syndrome, taking into account biochemical changes characteristic of the above-mentioned acute diseases of the abdominal organs.

Asthmatic variant of myocardial infarction proceeds according to the type of severe suffocation, cough with foamy pink sputum (cardiac asthma, pulmonary edema) in the absence or low intensity of pain in the region of the heart. In this case, a gallop rhythm, arrhythmias, a drop in blood pressure are observed; as a rule, this variant occurs more often with repeated MI, as well as with MI against the background of severe cardiosclerosis, and almost always with papillary muscle infarction. To diagnose this variant, it is necessary to record an electrocardiogram in dynamics and identify resorption-necrotic syndrome.

Collaptoid variant of myocardial infarction- this is actually a manifestation of cardiogenic shock, characterized by the absence of pain, a sudden drop in blood pressure, dizziness, darkening of the eyes, the appearance of cold sweat.

At edematous form of myocardial infarction the patient develops shortness of breath, weakness, edema and even ascites relatively quickly, the liver enlarges - that is, acute right ventricular failure develops.

Arrhythmic variant of myocardial infarction manifested by a wide variety of arrhythmias (extrasystole, paroxysmal tachycardia or atrial fibrillation) or various degrees of atrioventricular blockade. Paroxysmal tachycardia completely masks the signs of MI on the ECG. The task of the doctor is to urgently stop the attack of paroxysmal tachycardia and record the ECG again.

Cerebral myocardial infarction due to the development of cerebrovascular insufficiency. More often it is dynamic (dizziness, nausea, vomiting, confusion, transient weakness in the limbs), less often there is a stroke form with the development of hemiparesis and speech impairment (simultaneous thrombosis of the coronary and cerebral arteries).

Erased (malosymptomatic) form of myocardial infarction manifested by weakness, sweating, vague chest pains, which the patient often does not attach importance to.

Combined variant of myocardial infarction combines various manifestations of several atypical forms.

To diagnose atypical forms of myocardial infarction, it is necessary to carefully evaluate the clinical manifestations, the dynamics of ECG changes, resorption-necrotic syndrome, and echocardiography data.

A. Chirkin, A. Okorokov, I. Goncharik

Article: "Atypical forms of myocardial infarction, symptoms" from the section

myocardial infarction- an acute disease of the heart muscle, characterized by one or more foci of necrosis as a result of circulatory disorders. This is the most severe form of coronary heart disease. The patient needs bed rest. Diagnosis is based on three clinical features: characteristic severe anginal pain lasting over 30 minutes, not ameliorated by nitroglycerin; ECX data (pathological Q wave or QS complex as a sign of necrosis, ST segment elevation and negative T wave); an increase in the enzyme FC-MB in the blood serum.

It is observed more often in men aged 40-60 years. In men, myocardial infarction is more common than in women, especially at a young age. At the age of 41-50 years, this ratio is 5:1, and in the period of 51-60 years - 2:1. Later, the difference disappears due to an increase in the frequency of heart attacks in women. It is believed that urban residents suffer from myocardial infarction more often than rural residents, but apparently the unequal level of diagnostic capabilities plays a role here. The maximum mortality occurs in the autumn-winter period. Usually, myocardial infarction occurs as a result of damage to the coronary (coronary) arteries of the heart during atherosclerosis, when their lumen narrows. Often, this process is joined by a blockage of the vessel in the affected area, as a result of which the blood completely or partially stops flowing to the corresponding section of the heart muscle, and foci of necrosis (necrosis) form in it.

Risk of myocardial infarction (according to the American Heart Association)

Risk Factor Scores
Smoking
Never smoked or quit smoking 3 years ago or earlier
Never smoked but live or work near smokers
Quit smoking within the last 3 years

Smoke and live or work near smokers
Systolic blood pressure, mm Hg st


unknown


Total blood cholesterol, mg%


unknown

240 and more

High density lipoproteins, mg%


unknown


Body mass
Not above the norm
5-10 kg above the norm
10-15 kg above the norm
15-25 kg above the norm
Above the norm by more than 25 kg
Physical activity

Moderate to High
Moderate
Low to moderate

The risk of myocardial infarction is low - 6-13 points, average - 14-22 points, high - 23 points.

Stroke survivors, diabetics, and those who are genetically predisposed to heart disease have a much higher risk of developing myocardial infarction.

Classification of myocardial infarction

1. By localization (right ventricular, left ventricular, septal, etc.);

2. According to the depth of myocardial necrosis (penetrating, non-penetrating, focal, widespread);

3. According to the stages of myocardial infarction:

sharpest;
spicy;
subacute;
postinfarction.

4. According to the presence of complications:

complicated;
uncomplicated;

5. According to the depth of the lesion: transmural myocardial infarction (the process captures the entire thickness of the heart muscle), intramural (with localization of the focus of necrosis in the thickness of the heart muscle), as well as subepicardial and subendocardial infarction (adjacent to the endocardium or epicardium).

6. Three main zones of changes in the heart muscle during a heart attack: the focus of necrosis, the prenecrotic zone and the zone remote from necrosis. The outcome of muscle necrosis is the formation of a connective tissue scar.

7. Clinical variants of the course of myocardial infarction: typical (or painful) and atypical, including: asthmatic, abdominal, arrhythmic, cerebrovascular and painless (malosymptomatic), as well as with atypical localization of pain.

Most often, a heart attack develops in the anterior wall of the left ventricle, in the blood supply pool of the anterior descending branch of the left coronary artery, which is most often affected by atherosclerosis. The second most common place is occupied by infarction of the posterior wall of the left ventricle. This is followed by lesions of the interventricular septum and papillary muscles.

1. Painful form (typical development)

In a typical course of severe myocardial infarction, five periods are distinguished: prodromal, acute, acute, subacute and post-infarction.

The prodromal period, or the so-called preinfarction state, is observed in more than half of the patients. Clinically, it is characterized by the occurrence or a significant increase in the severity and severity of angina attacks, as well as changes in the general condition (weakness, fatigue, decreased mood, anxiety, sleep disturbance). The effect of conventional painkillers in patients receiving them, as a rule, becomes less effective.

The most acute period (the time from the onset of myocardial ischemia to the first manifestations of its necrosis).

Characteristics of a typical attack of pain in myocardial infarction:

1. Characteristics of pain: suddenly there is pain behind the sternum, very intense, burning with irradiation to the left arm, left shoulder blade, abdomen, back.

2. Duration of pain: the pain syndrome lasts on average more than 30 minutes, sometimes even 1-2 days.

3. Reaction to drugs: pain is not relieved by nitroglycerin or validol, medical assistance is needed for pain relief.

4. Reaction to physical stress: pain intensifies, bed rest and reduction of any physical activity is necessary.

5. Other signs of pain: a pain attack may be accompanied by a feeling of fear, severe weakness, a feeling of lack of air, fear of death, profuse sweat, shortness of breath at rest are usually noted, nausea and vomiting are also common (especially with lower localization of myocardial infarction). Often this happens in patients in a state of strong psycho-emotional stress, alcohol intoxication.

Myocardial infarction occurs at any time of the day, especially often at night, early morning hours. Rarely, there is no pain.

When examining a patient, pallor of the skin and symptoms associated with intense pain (suffering facial expression, motor restlessness or stiffness, cold clammy sweat) are determined. In the first minutes, blood pressure rises, then progressively decreases as a manifestation of developing cardiac and reflex acute vascular insufficiency. A sharp decrease in blood pressure is usually associated with the development of cardiogenic shock.

The acute period begins immediately after the end of the most acute period and lasts about 2 days - until the final demarcation of the focus of necrosis (during this period, one part of the myocytes located in the periinfarction zone dies, the other is restored). With a recurrent course of myocardial infarction, the duration of the acute period can be extended to 10 or more days.

In the first hours of the acute period, anginal pain disappears. Preservation of pain is possible with the development of inflammation of the pericardium, as well as with prolonged or recurrent course of myocardial infarction. Heart failure and arterial hypotension, as a rule, remain and may even progress, and in some cases they occur already after the end of the most acute period. Rhythm and conduction disturbances of the heart are determined in the vast majority.

The resorption syndrome that develops in the acute period of myocardial infarction is characterized by the occurrence of a febrile reaction (while the body temperature only rarely exceeds 38.5 ° C) and an increase in ESR.

The subacute period, corresponding to the time interval from the complete delimitation of the focus of necrosis to its replacement with tender connective tissue, lasts for about 1 month. Clinical symptoms associated with a decrease in the mass of the functioning myocardium (heart failure) and its electrical instability (cardiac arrhythmias) during this period manifest themselves in different ways. The general state of health of patients, as a rule, improves. Shortness of breath at rest, as well as auscultatory and radiographic signs of blood stasis in the lungs, decrease or disappear.

The sonority of heart tones gradually increases, but in most patients it is not completely restored. Systolic blood pressure in most patients gradually increases, although it does not reach the initial value. If myocardial infarction has developed against the background of arterial hypertension, systolic blood pressure remains significantly lower than before myocardial infarction, while diastolic blood pressure does not change significantly ("headless" arterial hypertension).

You need to know that angina attacks may be absent; their disappearance in a patient who suffered from angina pectoris before myocardial infarction indicates a complete blockage of the artery, in the basin of which myocardial ischemia periodically occurred before the infarction.

The post-infarction period following the acute one completes the course of myocardial infarction, since at the end of this period, the final formation of a dense scar in the infarct zone is expected. It is generally accepted that with a typical course of large-focal myocardial infarction, the post-infarction period ends at a time corresponding to approximately 6 months from the onset of the focus of necrosis. During this period, compensatory hypertrophy of the remaining myocardium gradually develops, due to which heart failure, if it occurred in earlier periods of myocardial infarction, can be eliminated in some patients. However, with large lesions of the myocardium, full compensation is not always possible, and signs of heart failure persist or increase.

2. Asthmatic form

Of the atypical forms of myocardial infarction, the most common is the asthmatic variant, which proceeds according to the type of cardiac asthma or pulmonary edema. It is observed with extensive damage to the heart muscle, with repeated heart attacks, against the background of already existing circulatory failure, in the presence of cardiosclerosis. Occurs in 5-10% of patients. In half of the cases, suffocation is combined with retrosternal pain. An acute increase in blood pressure can contribute to the development of cardiac asthma.

The basis of this syndrome is an extreme degree of left ventricular failure and stagnation of blood in the lungs. Suddenly there is a feeling of lack of air, developing into suffocation, and the fear of death associated with it. The patient becomes very restless, "cannot find a place for himself", takes a forced sitting position, leaning his hands on the bed to increase the respiratory movements. The respiratory rate increases to 80-90 per minute. The nature of breathing changes: a short inhalation is followed by an extended exhalation. The expression of the patient's face is suffering, exhausted, the skin is pale, the lips are bluish, cold sweat appears.

Breathing becomes noisy, bubbling, wheezing is heard in the distance. A cough appears, soon a liquid, foamy sputum of a pinkish color or with an admixture of blood begins to separate.

3. Abdominal shape

The abdominal variant of myocardial infarction is observed in 2-3% of patients, mainly with its lower or lower-posterior localization. Pain is concentrated in the epigastric region. Patients are excited, rush about, moan, the skin at the time of increased pain becomes covered with sweat. However, palpation of the abdomen does not cause significant pain, the abdomen remains soft, there are no symptoms of peritoneal irritation.

Pain in the epigastric region may be accompanied by nausea, vomiting, painful hiccups, loose stools. This may lead to erroneous conclusions about food intoxication or gastroenteritis.

4. Cerebral shape

The cerebrovascular form can proceed in the form of a syncope or a stroke. Violation of cerebral circulation is usually transient. There are signs of vascular damage to the brain (speech disorder, cerebral stroke). Along with cerebral strokes in the acute period of myocardial infarction, other neurological disorders are observed: fainting, loss of consciousness.

Cerebral stroke is often a complication of myocardial infarction. A careful examination of the heart, an ECG recording, and biochemical blood tests clarify the situation.

5. Arrhythmic form

The arrhythmic variant begins with various rhythm disturbances - attacks of atrial fibrillation, tachycardia, frequent extrasystoles. Pain is absent or appears after the arrhythmia has arisen. AMI can be manifested by severe tachyarrhythmias with a decrease in blood pressure, sudden clinical death due to ventricular defibrillation (less often asystole).

The diagnosis of myocardial infarction is conclusive when the patient has a clinical picture of an anginal attack, an increase in a number of enzymes (CPK, LDH, etc.) in the blood, and characteristic changes in the ECG.

Complications of myocardial infarction

1. Violation of the conduction rhythm (arrhythmic shock).

Myocardial infarction affects not only myocarditis - muscle cells, but also the conduction system suffers. The heart finds itself in unusual working conditions, for the optimization of which some restructuring is necessary. But this transformation takes time. Therefore, the heart tries to deliver blood to the human organs with the help of more contractions. Arrhythmias that occur with myocardial infarction can be both temporary and permanent. The so-called atrial fibrillation is very dangerous.

2. True cardiogenic shock- the most severe complication of myocardial infarction, which often ends in death. The cause of shock is a rapidly occurring and extensive necrosis of the muscle of the left ventricle (more than half of its muscle mass), which is accompanied by a sharp decrease in the volume of ejected blood. At the same time, the patient does not move, is sharply weakened, does not complain of pain, answers questions with difficulty, often falls into a state of inhibition, there may be loss of consciousness. The face is pale, with blue lips and mucous membranes, the extremities are cold, the skin acquires a "marble" pattern, covered with copious cold sticky sweat.

One of the main signs of cardiogenic shock is a catastrophic drop in blood pressure - below 80 mm Hg. Often systolic pressure is not detected. Pulse weak filling, frequent, more than 100-120 beats per minute. With a decrease in blood pressure below 60/40 mm Hg. the pulse becomes thready, at lower pressure the pulse is not palpable. Breathing is frequent and superficial (25-35 per minute). In the lungs, against the background of a drop in blood pressure, congestion increases, up to edema. Decreased urination, up to the complete absence of urine.

3. Acute heart failure. Weakness of the left ventricle is not always manifested in the form of cardiac asthma and pulmonary edema. In many patients, left ventricular failure is more moderate. The patient feels a slight shortness of breath, he has a rapid heartbeat (more than 100 beats per minute), his lips are cyanotic. Blood pressure is maintained at a normal or slightly reduced level. In the posterior-lower parts of the lungs, a small amount of moist fine bubbling rales is often heard. Extreme forms of left ventricular failure is cardiac asthma.

4. Rupture of the heart. Ruptures of the heart muscle occur in patients with primary transmural myocardial infarction. Repeated heart attacks are rarely complicated by ruptures. Mortality in this case is very high. Most ruptures occur in the first three days of illness, more often on the first day. There are external and internal ruptures of the heart, external are more common. The rupture usually occurs along the anterior wall of the left ventricle, closer to its apex. Most patients die on the first day of myocardial rupture.

5. Aneurysm of the heart. This complication of advanced transmural myocardial infarction presents as a diffuse bulge or sac-like cavity, usually containing a parietal thrombus. Most often, the aneurysm is located in the region of the apex of the left ventricle or close to it. An aneurysm is formed in 10-15% of patients in the first weeks of myocardial infarction. Chronic aneurysm is the result of scarring of the walls of an acute aneurysm.

Acute aneurysm of the heart may be complicated by rupture in the first 3 weeks from the onset of myocardial infarction. About 70% of patients with chronic postinfarction aneurysm die within 3-5 years from heart failure, arrhythmias, or recurrent myocardial infarction.

One of the following criteria is sufficient for the diagnosis of acute myocardial infarction.

A typical increase and gradual decrease (cardiac troponins) or a more rapid increase and decrease (MB CK) of biochemical markers of myocardial necrosis in combination with one of the following:

a) clinical picture of ACS;

b) the appearance of pathological Q waves on the ECG;

c) ECG changes indicating the appearance of myocardial ischemia: the occurrence of ST segment elevation or depression, blockade of LBPH;

d) the appearance of signs of loss of viable myocardium or impaired local contractility when using techniques that allow visualization of the heart.

Diagnostics

The main clinical and laboratory signs of myocardial infarction are:

1. An increase in body temperature (from subfebrile figures to 38.5-39 ° C).

2. Leukocytosis, usually not exceeding 12-15 x x 10 9 /l.

3. Aneosinophilia.

4. A small stab shift of the blood formula to the left.

5. Increased ESR.

Enzyme diagnostics. The level of enzyme activity can be judged on the severity of myocardial infarction. For example, the activity of the MB-fraction of the enzyme CPK (creatinine phosphokinase) usually increases after 8-10 hours from the onset of myocardial infarction and returns to normal after 48 hours. Determination of activity is carried out every 6-8 hours; At least three negative results are required to rule out myocardial infarction. Treatment is started without waiting for an increase in CPK activity. New methods for determining CPK isoenzymes can speed up diagnosis, but they have not yet been widely used. The activity of the 1st isoenzyme LDH (LDH;) becomes higher than the activity of LDH 2 on the 3rd-5th day of myocardial infarction. LDH activity is determined daily for 3 days if the patient arrives 24 hours after the onset of symptoms of myocardial infarction. If LDH activity reaches borderline values or if the patient arrives 3 days or more after the onset of symptoms, myocardial scintigraphy with 99m Tc-pyrophosphate is indicated.

Electrocardiographic study. According to Bayley, coronary circulation disorders in myocardial infarction lead to the formation of three zones of pathological changes: around the area of necrosis there are zones of ischemic damage and ischemia. In the leads, the active electrode of which is located directly above the MI area, each of these zones is involved in the formation of the following ECG changes.

1. Zone of necrosis - pathological Q wave (lasting more than 30 ms) and a sharp decrease in the amplitude of the R wave or the QS complex.

2. Zone of ischemic damage - displacement of the RS-T segment above (with transmural MI) or below the isoline (with subendocardial damage to the heart muscle).

3. Zone of ischemia - "coronary" (equilateral and pointed) T wave (high positive with subendocardial MI and negative with transmural MI).

Echocardiography is one of the mandatory research methods that are used to diagnose acute MI and assess hemodynamic and structural disorders in this disease.

The use of myocardial scintigraphy with technetium is indicated for the verification of myocardial infarction, mainly in cases where there are significant difficulties in interpreting ECG changes due to the presence of bundle branch block, paroxysmal cardiac arrhythmias, or signs of a past myocardial infarction.

When it comes to coronary heart disease, there are four things to keep in mind:

1. Atherosclerosis of the coronary arteries is an anatomical concept that indicates the possibility of polymorphic narrowing of the coronary arteries.

2. Ischemic heart disease reflects such a state of the coronary arteries, when morphological (structural) or functional disorders lead to their insufficiency. Stenosis of the coronary arteries is noted as a result of concentric or eccentric atheromatous changes in the vessel wall and vasospastic coronary artery disease, reflecting not structural, but functional changes (angiospasm). The existence of transitional forms is possible: a combination of stenosis and vasospastic disease of the coronary arteries.

3. Coronary insufficiency is the main pathological mechanism that accompanies coronary artery disease.

Occurs as a result:

1) imbalance between myocardial oxygen demand and delivery in coronary artery stenosis;

2) decrease in coronary blood flow due to vasospasm of the coronary arteries, as evidenced by the technique with thallium-201 or radionuclide ventriculography during a spontaneous attack or caused by ergonovine

3) disturbances in small (intramural) blood vessels of the myocardium. The latter is characteristic of syndrome X (coronary heart disease without proven coronary artery disease).

Thus, there are areas of myocardial ischemia that are supplied by stenotic or vasospasmic coronary arteries. The area of ischemia is a heterogeneous zone, since it is also supplied with blood from other coronary arteries, and therefore it also contains non-ischemic fibers.

4. Coronary heart disease is a clinical syndrome that manifests itself with symptoms and signs of myocardial ischemia. The degree of narrowing of the coronary artery and the functional significance of the coronary artery lesion, proven by arteriography methods, can be studied using electron radiographic technique.

If during a stress test on a bicycle ergometer at a load of 120-150 W for 14 minutes, anginal pain does not appear in the subject (as well as equivalent symptoms and ECG-specific signs of ischemia), then angina pectoris can be excluded with good reason. In cases where doubts remain, it is necessary to resort to coronary angiography. Negative data coronary angiography exclude angina pectoris.

Unlike all other types of chest pain, angina pectoris as a characteristic pain syndrome is also established on the basis of a detailed study of the subjective sensations of the patient (the nature of anginal pain), which provoke various influences, primarily mental and physical stress. Pain in angina quickly disappears after the cessation of exercise or nitroglycerin (usually already within 1 minute). However, it must be borne in mind that anginal pain sometimes manifests itself atypically.

Atypical manifestations of angina include primarily atypical irradiation of anginal pain: right shoulder, jaw, tip of the nose, tip of the tongue, hard palate and throat, eyebrows, neck.

It should also be remembered that shortness of breath of varying severity can be the equivalent of typical anginal pain.

When conducting differential diagnosis, they are especially helpful: detailed questioning, positive dynamics of specific ECG changes (ischemia), a positive test with nitroglycerin (with simultaneous clinical observation and ECG registration).

If there is no positive ECG dynamics, then lingering pains in the left half of the chest indicate either a severe form of coronary heart disease (MI) or the absence of their connection with coronary artery disease.

Angina is usually indicated by positive ECG data in the form of depression (or elevation) of the ST segment more than 2 mm below or above the isoelectric line. Many authors are of the opinion that the appearance of a negative T wave during a stress test has a similar meaning.

An exercise stress test should not be performed in the case of positive ECG data at rest, it is advisable to repeat the exercise test after taking nitroglycerin.

The deterioration of the subjective state of the patient and the dynamics of ECG changes, indicating severe ischemia, indicate an exacerbation of angina pectoris, which in turn requires the adoption of special measures. To this end, it is urgent to prescribe adequate therapy and bed rest to prevent the development of unstable angina or myocardial infarction.

Unstable angina is a transitional clinical form between stable angina and myocardial infarction.

myocardial infarction- the most severe form of coronary artery disease. In the classic clinical picture, among the characteristic signs, acute anginal pain lasting 15 minutes dominates, or a protracted anginal state lasting hours and days, which is stopped only by narcotic drugs. It is characterized by classical ECG changes that develop in accordance with morphological changes (ischemia, damage, necrosis), and laboratory data (accelerated ESR, hyperglycemia, leukocytosis, increased levels of AST, ALT, CPK, etc.) and an increase in body temperature. These biochemical and ECG signs indicate myocardial necrosis in acute myocardial infarction.

In the differential diagnosis of anginal pain and the definition of the clinical form of coronary artery disease in favor of angina pectoris, a good general condition, better than in myocardial infarction, clinical tests, the absence of tachycardia, shortness of breath, hypertension, biochemical disorders, ECG data specific for MI (pathological Q wave, rise ST segment and elevated body temperature).

In contrast, MI, even in the absence of anginal pain, is indicated by the sudden appearance (for no other apparent reason) of heart failure and collapse. However, a more detailed study of the anamnesis suggests the existence of coronary artery disease in a patient. Specific ECG changes and relevant biochemical findings are helpful in establishing a definitive diagnosis suggestive of MI.

Anginal attack can be provoked (in addition to the already mentioned physical and mental stress) both with coronary artery disease and in the absence of atherosclerosis of the coronary arteries: tachycardia (of any cause), bradycardia (especially with atrioventricular block), high body temperature, metabolic disorders (especially with thyrotoxicosis , severe anemia and hypoglycemia), nicotine intoxication, a sharp change in climatic conditions (cold, hot or humid air) and the environment (stay in high mountain areas), drinking large doses of alcohol.

A decrease in perfusion coronary blood flow with concomitant coronary insufficiency syndrome also reduces the stroke volume of the heart, which is especially caused by: severe bradycardia, arterial hypotension, heart failure.

Differential diagnosis between angina pectoris and other cardiovascular diseases is carried out primarily with those diseases in which coronary insufficiency appears.

These include:

- congenital anomalies of the coronary arteries;

- congenital coronary arterial-venous fistulas;

- embolism of the coronary artery (fatty, air, tumor cells, etc.);

- idiopathic dilatation of the mouth of the pulmonary artery with pulmonary hypertension;

- stenosis of the pulmonary artery or its combination with Fallot's tetrad;

- congenital heart defects with left-right shunts;

- transient mitral valve prolapse;

- lesions of the mouth of the aorta (aortic stenosis, aortic insufficiency);

- mitral stenosis (severe form);

- hypertrophic obstructive myocarditis and idiopathic hypertrophic subaortic stenosis;

- dissecting aneurysm of the heart;

- aortitis (including syphilitic aortitis);

- rheumatic heart disease and especially complications of acute endocarditis;

- acute and chronic pericarditis;

- cardiac arrhythmias, primarily paroxysmal supraventricular tachycardia;

- primary and secondary pulmonary hypertension;

- inflammatory-allergic coronaritis;

- panarteritis of the aorta (Takayashi's disease);

- thromboarteritis obliterans (Buerger's disease);

- nodular periarteritis;

- almost all systemic diseases of the connective tissue of collagenosis).

When conducting differential diagnosis, it is important to remember that there are great therapeutic possibilities for correcting coronary insufficiency in the above diseases, primarily by treating the underlying disease.

Among congenital and acquired heart defects, the following diseases are of particular importance in differential diagnosis:

1. Congenital anomalies of the coronary arteries, primarily abnormal bypass of the coronary artery from the pulmonary artery, leading to coronary insufficiency in early childhood. Some authors believe that the unexpected "painful cries" of children indicate a similar defect.

2. Congenital coronary arterial-venous fistulas can be the cause of anginal pain. In differential diagnosis, the identification of a coarse diastolic murmur in the precordial region helps. Surgical correction (ligation) of the fistula leads to the disappearance of coronary symptoms.

3. Acquired heart defects with the appearance of coronary syndrome. According to many authors, various acquired heart defects, especially in the stage of heart failure, may be accompanied by anginal pain, and in some they are the main subjective manifestation of the disease.

4. Intermittent mitral valve prolapse may be accompanied by coronary insufficiency due to spasm of the coronary arteries. This is also supported by the studies of I. K. Shkhvatsabay (1982), who noted that during coronary angiography and ventriculography, as a result of touching the tip of the catheter to the mouth of the coronary arteries, a spasm occurred, causing in turn ischemia of the papillary muscles and mitral valve insufficiency.

In patients with intermittent mitral valve prolapse, anginal pain occurs spontaneously at rest, often accompanied by syncope, dyspnoea, and ECG changes suggestive of ischemia and arrhythmias.

According to numerous studies, including those conducted in Yugoslavia, a favorable therapeutic effect in the treatment of this disease is achieved with the help of calcium antagonists.

Acquired and congenital heart defects, most often leading to an increase in the requirements for coronary blood flow, respectively, to relative (secondary) coronary insufficiency, are as follows:

- mitral stenosis,

- stenosis of the pulmonary artery,

- heart defects with left-right shunts,

- hypertrophic obstructive myocarditis and idiopathic hypertrophic subaortic stenosis,

- Primary and secondary pulmonary hypertension.

With various types of acquired heart defects, anginal pains occur with different frequencies.

- aortic and aortic-mitral defects - 40%,

- mitral stenosis, especially in children, 6.4%.

The greater the severity of heart failure, the more often anginal pain occurs.

According to I. K. Shkhvatsabay (1982), the use of the method of coronary angiography really makes it possible to detect stenosing atherosclerosis of the coronary arteries in various heart defects. In this way, it was found that it is equally represented in patients with aortic (17%) and mitral (20%) heart defects. I. K. Shkhvatsabaya explains these differences by the fact that hemodynamic insufficiency, and not the degree of atherosclerotic changes in the coronary vessels, plays the main role in the pathogenesis of coronary syndrome with acquired heart defects.

In aortic insufficiency, the appearance of anginal chest pain is caused by low diastolic pressure and the "suction" effect on the coronary arteries of reverse blood flow in the hypertrophied myocardium of the left ventricle of the heart.

In aortic stenosis, including subaortic stenosis, anginal pain is more pronounced as a result of a decrease in systolic and minute blood volume in conditions of increased demand for it from the hypertrophied left ventricular myocardium, which causes a decrease in coronary blood flow.

With mitral valve disease, anginal pain is caused by blood stasis in the coronary sinus as a result of increased pressure in the right atrium, as well as a reduced stroke volume and its inadequate increase during exercise.

Pericarditis (acute and chronic) may be accompanied by pain in the left side of the chest, which simulates angina pectoris.

An abrupt onset and constant intense pain of atypical localization in the chest in acute pericarditis can simulate angina pectoris, especially since ECG signs indicate this (ST segment elevation and negative T wave, even the appearance of a Q wave in some cases).

In differential diagnosis, the difficulty is not only the pain syndrome, but also the acceleration of ESR, an increase in the number of leukocytes, which is also characteristic of severe coronary heart disease, myocardial infarction and pericarditis. However, a clear clinical definition of pericarditis, primarily relevant angiographic data (silhouette of the heart in the form of a trapezoid) and the above ECG changes that do not reflect the dynamics, help the differential diagnosis of acute pericarditis.

Chronic pericarditis accompanied by partial atresias or lime deposits may also resemble angina pectoris due to:

- pain in the left side of the chest, which manifests itself in the form of prolonged compression or tingling, and worsens with a change in body position or changes in weather conditions;

- ECG changes that present known difficulties (persistently negative T wave, "correcting" to positive during exercise and immediately after it returning to its original level).

In differential diagnosis, along with the above signs, the corresponding results of angiography (presence of adhesion and lime deposits) also testify in favor of this type of pericarditis.

Embolism of the coronary arteries (fatty, air, tumor cells) leads to coronary insufficiency. Therefore, in the differential diagnosis, it is necessary to remember the etiological factors that lead to such an embolism of the coronary arteries.

Treatment

The current system of treatment of patients with myocardial infarction includes:

specialized cardiological ambulance teams (prehospital stage);
specialized infarction departments with an intensive care unit or a cardio intensive care unit (hospital stage);
specialized rehabilitation centers (hospital departments and cardiological sanatoriums);
cardiological consultative and diagnostic centers and cardiological offices of polyclinics (medical examination of patients who have undergone MI).

Basic therapy, which is carried out in all patients with Q-wave MI, regardless of the presence or absence of certain complications, includes the following measures:

pain relief (analgesia);
thrombolytic therapy (taking into account individual indications and contraindications);
antithrombotic and antiplatelet therapy;
oxygen therapy;
the use of anti-ischemic drugs;
the use of ACE inhibitors and angiotensin II receptor antagonists.

Myocardial infarction is almost the most common cause of death in middle and older age groups.

The high lethality of this disease is due to the fact that it occurs most often suddenly, and its irreversible consequences develop at lightning speed. Plus, the clinical picture does not always correspond to the "classic scenario".

There are a large number of variations of atypical forms of myocardial infarction: consider all the symptoms and signs, diagnosis and distinguishing features of such options as abdominal (gastralgic), arrhythmic, peripheral, collatoid, edematous, erased, cerebral and combined.

Comparison criterion	typical heart attack	Atypical heart attack
Patient category	Can be diagnosed in people of any age	More commonly diagnosed in people: elderly with re-infarction suffering from severe cardiovascular diseases (hypertension, ischemia) with diabetes
Clinical manifestations at various stages of the disease	At the initial stages (in the pre-infarction, acute and acute periods), pain in the heart, a significant deterioration in well-being, sweating, shortness of breath, fear of death, blue skin and mucous membranes are characteristic.	At the initial stages (in the first few hours or days after the onset of a heart attack), there are no characteristic classic symptoms. Pain in the heart is insignificant or may be absent altogether. Clinical manifestations are unconventional and correspond to one or another variant of atypical myocardial infarction. Later (in the acute, subacute and post-infarction periods), the clinic of the disease becomes the same as in a typical heart attack.
Diagnosis and prognosis	The correct diagnosis is made by an experienced doctor without difficulty	It is difficult to make a correct diagnosis. The prognosis is worse than with a typical heart attack.

Development mechanism and statistics

The atypicality of a heart attack manifests itself only at the time of the crisis itself. The development of non-classical forms of pathology occurs due to an excessively sharp blockage of one or another vessel leading to the heart, in conjunction with concomitant diseases that progress against the background of a heart attack.

So, from the asymptomatic and arrhythmic nature of the disease, diabetics or people with existing heart rhythm disorders are more likely to suffer. Pain, pneumonia and other symptoms do not occur due to the reduced susceptibility of the nervous system. Manifestations of the disease are noticeable only on the ECG.

The cerebral appearance develops in people with impaired cerebral circulation. Symptoms resemble the onset of an ischemic stroke, but then change to a more characteristic one. It occurs due to blockage of an artery close to the brain by a blood clot.

The abdominal form is caused by pain in the abdomen, nausea and vomiting. This is due to the fact that part of the nerve endings of the chest are also located in the abdominal cavity. Pathological processes affect them, which provokes such manifestations.

What the numbers say:

0.5% of men and 0.1% of women suffer a heart attack each year. Of these, one in five is in an atypical form.
Every second patient dies even before an ambulance is provided to him - at the pre-hospital stage. Among patients with an atypical form of the disease, this figure is much higher.
Approximately 3% of all deaths per year in Russia died as a result of an acute heart attack.
Most often, the disease develops in the morning hours (between 4 and 8 am), autumn or spring (in November or March). About 25% of all registered heart attacks occur at this time.
Women suffer from a heart attack less often, but as a result, they have a fatal outcome more often - 53% of women with this disease die. For men, this figure is 10% lower.

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Options, symptoms and differences, diagnostic measures

Atypical forms of myocardial infarction include the following varieties:

abdominal- with this form, the symptoms resemble acute pancreatitis, the pain is localized in the upper abdomen and is accompanied by nausea, bloating, hiccups, and sometimes vomiting;
asthmatic- this form resembles the acute stage of bronchial asthma, shortness of breath appears, the severity of the symptom increases;
atypical pain syndrome- a person complains of pain in the lower jaw, iliac fossa, in the arm, shoulder;
asymptomatic- this form is rarely observed, and it mainly affects diabetics, who, due to the characteristics of a chronic disease, have reduced sensitivity;
cerebral- there are neurological symptoms, complaints of dizziness, impaired consciousness.

Peripheral

Peripheral infarction with atypical localization of pain. Symptoms:

weakness;
sweating at rest;
pressure drop;
heart rhythm disturbances;
blue fingers and lips.

The pain is concentrated in the left arm (over the entire limb or only in the fingers), left shoulder blade (prick), lower jaw on the left (aching), in the neck (sharp pain in the upper part of the spine), in the throat and esophagus. At the same time, the classic pain in the heart is much weaker or completely absent.

Diagnosis: ECG in dynamics, constant monitoring.

Abdominal (gastralgic)

Abdominal form of myocardial infarction. Symptoms:

nausea;
vomit;
flatulence and diarrhea;
hiccups
arrhythmia;
pressure drop.

The pain is sharp and strong in the area of the stomach and liver - at the top of the abdomen, under the ribs on the right. Reminds me of an attack of pancreatitis.

Noticeable signs of the gastralgic form of myocardial infarction: the anterior wall of the abdomen is strongly tense, the heart rhythm is changed. Dynamic ECG is required. Gastroenterologist consultation. It often happens in people with atherosclerosis and digestive problems.

Asthmatic

Asthma and its symptoms:

shortness of breath at rest;
asthma attack;
frothy cough with copious sputum;
pressure drop;
strong heartbeat;
fear of death.

The heart does not hurt or hurts not much. Occurs in patients with cardiosclerosis or severe hypertension. It is more common in women of pre-retirement age and older men. An EKG is required.

Collaptoid

Collaptoid variant of an attack, symptoms:

sudden drop in pressure;
dizziness;
profuse sweat;
darkens before the eyes;
pallor and coldness of the skin;
loss of consciousness;
state of prostration;
veins on the limbs become invisible.

Pain is absent. Elderly diabetics are at risk. It runs very hard. Urgent help required. Diagnosed with an ECG.

Hydropic

Edematous myocardial infarction is accompanied by the following symptoms:

dyspnea;
weakness;
swelling of the limbs;
the liver increases sharply and ascites occurs - fluid accumulates in the abdomen.

Pain is absent. It runs very hard. Urgent help required. Diagnosed with an ECG.

arrhythmic

The arrhythmic form has the following symptoms:

an attack of abnormal heartbeat (a sharp increase or decrease in heart rate);
fainting;
arrhythmic shock (drop in pressure, impalpable pulse).

With an arrhythmic form of myocardial infarction, pain in the region of the heart is weak or absent at all. It is more common in patients with pre-existing heart rhythm problems. An emergency EKG is needed.

Cerebral

Cerebral infarction is characterized by the following features:

a sharp drop in pressure;
sudden fainting;
confusion and loss of consciousness (pseudo-stroke) - from mild lethargy to coma;
there may be nausea and vomiting;
speech disorders;
muscle paresis.

There is no pain in the heart. It is more common in older people with cerebrovascular accidents. It is necessary to consult a neurologist, ECG and EEG.

Erased (oligosymptomatic)

The oligosymptomatic form of infarction can be manifested by the following signs:

unmotivated weakness;
sweating;
insomnia;
chest discomfort.

There are no sharp pains in the heart. Atypical painless forms of a heart attack are often found in diabetics or alcoholics.

Combined

In the combined form, various symptoms of atypical forms of a heart attack are combined. The pain in the heart is insignificant and the patient does not pay attention to it. Careful multilateral diagnostics is required in dynamics with the invitation of doctors of other specializations.

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Risk factors

The basic features that increase the chance of developing atypical forms of a heart attack are:

elderly age;
previous heart attack;
excessive use of alcohol and nicotine.

Specific factors are previously transferred or progressive diseases:

diabetes;
cardiosclerosis;
severe forms of hypertension;
atherosclerosis;
pathology of the gastrointestinal tract;
disorders of cerebral circulation;
ailments that cause irregular heartbeats.

Treatment Method

The algorithm for providing care for any form of atypical heart attack is the same:

Urgent hospitalization is required.
Bed rest and complete rest on the first day. In the future, moderate physical activity is necessary.
Diet with restriction of salt and animal fats.
It is necessary to eliminate pain if it is present, since as a result of pain discomfort, cells and tissues receive less oxygen, therefore, the heart muscle lesion increases in size. Before the arrival of doctors, the patient every 5 minutes give nitroglycerin sublingually. In the hospital, morphine and beta-blockers are used intravenously.
The use of an oxygen mask or oxygen therapy is necessary for all heart attacks in the first few hours after an exacerbation of the disease.
Stabilization of the heart rate with Amiodarone or Atropine.
Antiplatelet therapy or the use of blood thinners. In the absence of contraindications, before the arrival of ambulance doctors, the patient can be given acetylsalicylic acid - chew and swallow 1 tablet with water. Plavix, Ticlopidin, Heparin, Bivalirudin have an even more powerful antithrombotic effect. In a hospital, such patients, in order to dissolve an already formed thrombus, are given thrombolytic therapy using Streptokinase, Urokinase, Alteplase.

Surgery carried out strictly according to indications by methods of coronary bypass grafting, endovascular angioplasty. Studies show that angioplasty is most effective if performed within the first few hours after a heart attack.

If time is missed, conservative medical treatment with thrombolytics is preferable. If this does not help, the only thing that can save the heart muscle is coronary artery bypass grafting.

Possible immediate and long-term complications

Acute period

It starts the day after the attack and lasts up to two weeks. It is the most dangerous time, since the body is maximally weakened and susceptible to all kinds of concomitant diseases. Among them:

acute left ventricular failure leading to cardiac asthma or pulmonary edema;
pathology of atrioventricular conduction;
all types of cardiogenic shock;
paresis of the gastrointestinal tract.

Subacute period

It lasts from the second week after the crisis and lasts up to a month. Diseases that manifest themselves during this period occur less frequently, but are difficult to cure. May develop:

internal and external myocardial ruptures;
parietal thrombendocarditis;
pericarditis.

Scarring period

Lasts up to two months. It is dangerous because the complications expressed before that become chronic incurable and are supplemented by more severe symptoms. During the formation of the scar may appear:

heart aneurysms;
postinfarction autoimmune syndrome Dressler;
ventricular fibrillation;
thrombocarditis;
thromboembolic complications.

Postinfarction cardiosclerosis

It comes after the second month from the moment of a heart attack and continues until the body is fully adapted to the consequences of the disease. Appears in:

loss of strength of the contractile function of the heart;
conduction disorder;
heart rhythm disturbances.

Forecast, rehabilitation and preventive measures

Mortality in atypical myocardial infarction exceeds mortality rates in the usual form of the disease precisely because non-classical infarction is difficult to immediately diagnose and recognize. About half of all patients die before going to the doctor or before the ambulance arrives. The first day is decisive - if the patient survives the first 24 hours, then there is a 70-80% chance that he will survive in the future.

Postinfarction rehabilitation includes a set of measures medical and physiotherapy treatment. Such patients are recommended sanatorium-resort rehabilitation.

In order to prevent relapse and prevent complications, it is necessary to take therapeutic doses of antiplatelet agents (aspirin) and beta-blockers, follow a diet and reasonable physical activity.

At the slightest suspicion of a heart attack, a person should be immediately hospitalized is the only way to prevent death. Self-medication or ignoring the symptoms of the disease in this case is unacceptable. Particular attention should be paid to those who fall into the “heart attack” risk group: the elderly, diabetics, patients with cardiovascular and endocrine diseases.

Atypical forms of myocardial infarction are varieties of the disease that are manifested by symptoms that are not characteristic of it. This article will tell you how to recognize such variants of a heart attack, and what needs to be done.

Features and causes of development

The main symptom of any disease is pain, which can have a different course (be acute, aching, pressing, etc.). According to the presence of pain, two types of heart attack are distinguished: typical and atypical heart attack.

A typical (painful form) of a heart attack is characterized by pronounced soreness in the chest area. As for atypical forms of the disease, they manifest themselves as pains of a different localization or their complete absence.

This not only complicates the symptoms, but also significantly complicates the diagnosis, because often the patient himself does not know exactly where it hurts.

Atypical variants of myocardial infarction develop as a result of an acute disruption of the myocardium. It occurs due to a lack of oxygen supply. In most cases, this is observed with clogging of blood clots, vasospasm, and jumps in blood pressure.

In an increased risk group for these forms of heart attack are people with the following abnormalities or diseases:

previous myocardial infarction,
diabetes,
hypertonic disease,
advanced form of heart failure,
cardiosclerosis,
heart ischemia,
atherosclerosis,
diseases of the digestive system,
various neurological disorders.

Classification of atypical forms of infarction

The following table will most intelligibly help to understand the forms of this disease:

Name of the atypical form of the disease	Development features	Characteristic symptoms
Abdominal heart attack	the disease develops with necrosis of the posterior segment of the myocardium	sharp pain in the abdomen, nausea, vomiting, which exhausts the patient. There may also be bloating, indigestion
Cerebralform	such a heart attack leads to a pronounced violation of cerebral circulation	nausea, vomiting, severe weakness, fainting
Asthmatic form	this form of heart attack resembles an attack of bronchial asthma, which makes it difficult to diagnose	the patient develops a severe cough and fear of death due to an asthma attack. The person cannot breathe properly
Arrhythmic form	pain in this type of disease is absent	a person may suffer from severe arrhythmia (chaotic contraction of the myocardium)
edematous form	this type of disease leads to extensive edema, which is accompanied by an increase in the liver	ascites, limb edema, weakness
Collaptoid shape	the disease is accompanied by insufficiency of cerebral circulation against the background of the complete absence of pain	dizziness, fainting, spots before the eyes
peripheral form	accompanied by atypical pain	a person may have pain in the fingers, sharp pains in the shoulder blade, arm, larynx or jaw. Also, pressure often drops, sweating occurs.
oligosymptomatic form	the disease proceeds with a minimum of signs that people usually do not pay attention to	general deterioration, weakness
Combined form	the disease occurs in a combination of various atypical forms	may develop abdominal pain, vomiting, nausea, loss of strength

Diagnostics

Diagnosing an atypical form of a heart attack is quite difficult due to vague symptoms. That is why, during the collection of anamnesis, the doctor takes into account all the complaints of a person.

Detection of a heart attack involves the mandatory performance of an ECG and ultrasound of the heart. Such studies allow assessing the condition of the heart and its structures, as well as determining the location of damage.

If a heart attack is suspected, urgent hospitalization should be carried out. It is impossible to treat a heart attack at home, as this can only worsen the patient's condition.

Treatment

The traditional treatment of atypical forms of infarction is medication.

The course of therapy includes the following groups of drugs:

Analgesics for pain.
Sedative drugs to eliminate stress.
Beta-blockers, which are used to dilate blood vessels.
Calcium antagonists that change the heart rhythm.
ACE inhibitors.
Blood thinners.

The specific drug should be selected by the attending physician for each patient individually. The duration of treatment is usually 1-2 months, after which maintenance therapy is carried out.

During treatment, the patient must completely limit excitement and physical activity. You should also follow a diet low in salt and fat, and stop smoking.
If necessary, the patient can wear an oxygen mask.

Important! It is possible to practice alternative treatment for a heart attack with the help of various tinctures and decoctions only as an adjuvant therapy and only after the permission of a doctor. Self-medication can cause complications.

Surgery

Surgical treatment is carried out in advanced cases, when the disease is diagnosed too late: a blood clot is found in a person or myocardial function has not improved after drug therapy.

In such a case, two types of operations are usually practiced:

coronary angioplasty. During it, a special stent is inserted into the affected human vessel, which maintains its lumen in a normal state.
Coronary artery bypass grafting. This is a complex operation during which a bypass is made from a person's vein for normal blood circulation.

The recovery period of the patient after such operations is quite long and difficult. It requires the implementation of all medical advice.

Possible complications and prognosis

After an atypical form of a heart attack, a person may experience the following complications:

Violation of the heart rhythm, which can subsequently cause cardiac arrest.
Aneurysm.
Acute heart failure.
thrombus formation.
Pericarditis.
Various neurotrophic disorders.
The occurrence of post-infarction syndrome.

The prognosis in such a state depends on the specific form of infarction, the presence of complications, the age of the patient and the timeliness of the treatment started. The most difficult illness is tolerated by elderly patients or people with chronic diseases.

Fact! According to statistics, 10% of patients die within a year after a heart attack from developing complications. In hospitals, deaths are rare, as doctors can control the patient's condition with drugs that improve heart function.

Prevention

Atypical myocardial infarction is a serious disease that can cause severe complications, so in order to reduce the risk of its development, it is important to adhere to the following recommendations of specialists:

Give up bad habits, whether it is smoking or drinking alcohol.
Exercise every day. It can be any sport (running, cycling, yoga, fitness, etc.).
Maintain normal cholesterol levels. With its increase, it is worth following a diet and taking medications prescribed by a doctor.
Normalize the mode of rest and work. Thus, a person should sleep at least 7 hours a day.
Avoid physical stress.
Enrich your diet with fresh fruits and vegetables, nuts and dried fruits. Also good for the heart are fish and lean meats, juices, greens.
Limit consumption of sweets, fatty and fried foods. Moreover, it is necessary to reduce the amount of salt consumed.
In the presence of chronic diseases, it is worth monitoring their course.
Every six months, undergo a preventive examination by doctors.
Avoid nervous overexertion, as strong excitement can worsen myocardial function.

Myocardial infarction (MI) is one of the clinical forms of coronary heart disease that occurs with the development of ischemic necrosis of a portion of the myocardium (heart muscle) due to relative or absolute insufficiency of its blood supply. Thus, MI occurs with a deep and rather long-term imbalance between the need of the heart muscle for oxygen and its delivery to the myocardium. Most often, the death of the heart muscle occurs in the left ventricle (LV).

A predisposing factor to the development of MI is the state of fatigue, physical activity, psycho-emotional stress, hypertensive crisis. 95-97% of all cases of MI are associated with thrombosis of the coronary artery against the background of its atherosclerotic lesion. In rare cases, myocardial infarction can develop as a result of embolism, dissection (dissection) of the wall of the coronary artery, anomalies of the arteries.

Classification

Myocardial infarction is classified according to several criteria. They are the following:

According to the nature of the course of the disease: primary - in the absence of diagnostic signs in the past of myocardial infarction; repeated - when MI occurs within a period exceeding 28 days from the date of the previous MI; recurrent - diagnostic signs of the formation of new foci of necrosis appear in the period from 72 hours to 28 days after the development of MI.
According to the depth of the lesion: macrofocal transmural (with a pathological QS wave); macrofocal non-transmural (with pathological Q wave); small-focal "no Q" (no pathological Q wave).
According to the localization of the infarction: anterior LV wall, posterior LV wall, circular LV MI, right ventricular MI.
According to the period (stage) of the disease: preinfarction, acute (from 2 hours to 2 days from the onset of MI), acute (up to 7-10 days from the onset of MI), subacute (from the 10th day to the end of the 4th week from the onset of MI ), postinfarction or scar period (after the 4th week).
According to the presence and severity of MI complications: early (developing within 7 days from the onset of MI) - rhythm and conduction disturbances, cardiogenic shock, aseptic pericarditis, pulmonary edema, myocardial ruptures, early postinfarction angina pectoris; late (develop within 8-28 days from the onset of MI) - chronic heart failure, Dressler's syndrome, rhythm and conduction disturbances, thromboembolism, acute and chronic heart aneurysm, etc.
According to the severity class of the course of MI.

Sometimes there is a so-called prodromal period (“pre-infarction state”), which to a certain extent corresponds to the concept of unstable angina, complicated by the development of myocardial infarction. Various medical sources indicate: "the duration of the most acute period is up to 12 hours." This is due to the period during which it is still possible to save the area of the damaged heart muscle when providing emergency care to the patient.

Another myocardial infarction is divided into clinical options, which will be presented below.

Clinical options for the onset of myocardial infarction

The following options for the onset of myocardial infarction are possible:

1. Anginal variant (status anginosus) is a classic variant of the disease. Makes up to 80% of all cases.
2. Peripheral variant (with atypical pain syndrome). Pain is localized not behind the sternum, but in the left arm, shoulder, lower jaw, iliac fossa, upper spine, larynx or pharynx. For example, if the pain is localized in the left hand, the form will be called "left-handed". The remaining options will be named similarly.
3. Asthmatic variant (status asthmaticus). Symptoms of a heart attack resemble an attack of bronchial asthma (suffocation, lack of air, increasing shortness of breath).
4. Abdominal variant (status gastralgicus). The pain is localized in the epigastric region. Gastrointestinal dysfunctions are noted: nausea, hiccups, vomiting, bloating (flatulence). Symptoms of a heart attack may resemble those of acute pancreatitis or other pathologies of the gastrointestinal tract.
5. Arrhythmic variant. The clinical picture resembles the symptoms of rhythm and conduction disturbances (feeling of interruptions in the work of the heart, palpitations, dizziness, etc.).
6. Cerebrovascular variant. Symptoms of a heart attack resemble the clinical picture of stroke (acute cerebrovascular accident) and are represented by episodes of dizziness, impaired consciousness, and other neurological symptoms.
7. Painless (low-symptomatic) variant. It occurs more often in elderly patients, with chronic renal failure, with diabetes mellitus, with alcohol intoxication, with the development of myocardial infarction during surgery under general anesthesia.

In some cases, in patients with osteochondrosis of the thoracic spine, there is an attachment to the main pain syndrome in myocardial infarction, characteristic for intercostal neuralgia, girdle pain in the chest, aggravated by bending the back forward, backward, in both directions.

All of the above forms or variants that do not proceed according to the classical type are called atypical. The most common of the atypical forms is the abdominal variant.

The atypical nature of the onset of myocardial infarction makes it difficult to diagnose and may be the cause of incorrect treatment tactics with an unfavorable outcome of the disease. Even pain sensations can be variable: the patient may complain of discomfort in the chest, pain in the abdomen, arm, throat, shoulder blade. As mentioned above, a painless variant of MI is possible.

In 20-30% of cases with macrofocal lesions of the heart muscle, signs of acute heart failure develop. Patients report shortness of breath, cough with sputum that is not expectorated, and profuse sweat. Often there are arrhythmias (atrial fibrillation or ventricular fibrillation, various forms of extrasystoles).

In some cases, the only symptom of MI is sudden cardiac arrest.

Classic Symptoms

In typical cases, the main clinical sign of a developing myocardial infarction is intense pain behind the sternum (the so-called anginal pain or status anginosus).

Characteristics of anginal pain in myocardial infarction are:

localization - behind the sternum or in the epigastric region;
the intensity of pain is much more pronounced than with an attack of angina pectoris, and increases rapidly, often undulating;
irradiation - wide (in the forearm, shoulder, collarbone, neck, left shoulder blade, lower jaw (often on the left), interscapular space);
character - pressing, compressing, burning, bursting, cutting;
duration - from 20-30 minutes to several hours;
feeling of fear, agitation, restlessness and vegetovascular reactions (hypotension, sweating, nausea, vomiting);
is not eliminated by nitroglycerin, and often with the introduction of narcotic analgesics.

Pain zones in myocardial infarction are shown in the figures below:

Dark red is a typical area, light red is other possible areas.

Diagnosis of various forms of myocardial infarction

The clinical picture of the disease is characterized not only by the presence of a characteristic pain syndrome, but also by the resorption-necrotic syndrome and the ECG pattern. Therefore, if the symptoms of the onset of the disease do not correspond to the classical variant (atypical form of myocardial infarction), then an ECG should be performed. In addition, it is necessary to trace the dynamics of changes in the amount of cardiospecific enzymes (troponin T and I, CK, CK-MB) in the blood serum. To evaluate the latter, a biochemical blood test is performed. Similarly to assessing the amount of cardiospecific enzymes, changes in the amount of markers of myocardial necrosis (myoglobin, ASAT, LDH) should be assessed.

Myocardial necrosis is accompanied by the development of a general inflammatory reaction (resorption-necrotic syndrome), the migration of leukocytes into the necrosis zone, which is reflected in the indicators of the general blood test (leukocytosis, an increase in ESR), and the appearance of fever.

In difficult cases, you can resort to other methods of instrumental diagnostics, except for the ECG. Such studies include:

EchoCG. Allows you to detect a local violation of myocardial contractility, ruptures of the heart muscle, true and false aneurysms, blood clots, fluid in the pericardium, LV function.
Tissue Doppler echocardiography. Allows you to quantify the regional speed of myocardial contraction with color highlighting.
Perfusion scintigraphy with technetium-99m (accumulates in the area of MI - "hot" focus) or thallium-201 (accumulates in a viable myocardium - "cold" focus). It is used to assess the blood supply to the heart muscle and determine the zone of the dead myocardium.
MRI. Allows a detailed assessment of the functional state of the heart.
Spiral (multispiral) computed tomography. Allows to exclude coronary pathology, but is not able to assess the degree of narrowing of the artery.
Positron emission computed tomography (PET).

A person with a suspected myocardial infarction must be hospitalized in a hospital (clinic). Only in this case it is possible to save the patient.