Symptoms characteristic of the acute period of myocardial infarction. Manifestations of small focal lesions

Myocardial infarction is acute ischemic necrosis of the heart muscle due to a discrepancy between the coronary circulation and the needs of the myocardium due to prolonged spasm of the coronary arteries or their blockage (thrombosis).

There are large focal, transmural (with a Q wave, Q-myocardial infarction) and small focal (without a Q wave, non-Q-myocardial infarction) myocardial infarction.

Localization of myocardial infarction: anterior, lateral, posterior wall of the left ventricle, interventricular septum and, relatively rarely, the right ventricle.

Classification of clinical types of onset of myocardial infarction(Tetelbaum, 1960):

1. Retrosternal pain (classic status anginosus) type; 50%

2. Peripheral type; 25%

3. Abdominal type; 5%

4. Cerebral type; 10%

5. Painless type; 10%

6. Arrhythmic type.

7. Asthmatic type.

8. Combined type

Forms of the peripheral type according to the localization of pain: left-scapular, left-handed, upper vertebral, mandibular, laryngeal-pharyngeal.

The abdominal type is clinically similar to: an acute abdominal catastrophe such as a perforated ulcer, gastric bleeding, intestinal obstruction; on the picture of the inflammatory process in the abdominal cavity (cholecystitis, pancreatitis, appendicitis); esophageal disease.

Cerebral type - the onset of myocardial infarction in the form of fainting, hypertensive crisis, hemiplegia (stroke), toxic infection.

Painless type - the onset of myocardial infarction, total heart failure, collapse.

Arrhythmic type - in the absence of pain, transient arrhythmias appear.

Asthmatic type - the onset of myocardial infarction with acute left ventricular failure (pulmonary edema).

Periods of myocardial infarction:

1) pre-infarction (from several days to 1-3 weeks),

2) acute,

3) spicy,

4) subacute.

1. The pre-infarction period is characterized by a clinical picture of progressive, unstable angina. The intensity, duration, and frequency of attacks increase; they occur with less physical activity and pass more slowly under the influence of rest or nitroglycerin. Between attacks of angina, there is a dull pain or feeling of tightness in the chest (pressure). The appearance of angina at rest in a patient with exertional angina is characteristic.

Negative ECG dynamics are noted: ischemic changes in the ST segment and T wave (“acute coronary” T - pointed, symmetrical). There are no changes in general and biochemical blood tests.

2. The most acute period of myocardial infarction is the time from the appearance of the first clinical electrocardiographic signs of acute myocardial ischemia to the beginning of the formation of a focus of necrosis (about 2–3 hours). Characterized by extremely intense, sharp, “dagger” pain, radiating under left shoulder blade, in the left hand. The pain is wave-like in nature, can last for several hours or even days, is not relieved by taking nitroglycerin, and is accompanied by a feeling of fear and excitement.

Upon examination, pallor of the skin and mucous membranes and acrocyanosis are revealed.

Palpation of the heart area reveals a displacement of the apical impulse outward and downward, it becomes low, unresistant and diffuse. The pulse is low tension and full, frequent, and may be arrhythmic. Blood pressure during pain attack may rise, then decline.

Percussion reveals an outward displacement of the left border of relative dullness and an expansion of the diameter of the heart. On auscultation, weakening of the first tone, dullness of tones, gallop rhythm, systolic murmur at the apex of the heart and aorta are observed, different kinds rhythm disturbances (extrasystole, paroxysmal tachycardia, atrial fibrillation).

When examining the respiratory organs, tachypnea is revealed. With the development of acute left ventricular failure over the lungs, there is dull tympanitis in the posteroinferior sections, there is weakening of vesicular breathing and, successively, crepitus, small-, medium- and large-bubble moist rales, spreading to the upper sections. With the development of pulmonary edema - bubbling breathing with the release of pinkish foamy sputum.

3. The acute period of myocardial infarction is characterized by the disappearance of pain and lasts 7-10 days. Previous symptoms of acute heart failure and arterial hypotension may persist and even increase. The objective research data remains the same.

In the acute period of myocardial infarction, signs of resorption of necrotic masses and aseptic inflammation in the tissues adjacent to the necrosis zone are revealed - fever occurs.

4. Subacute period of myocardial infarction – formation of a connective tissue scar at the site of necrosis, remodeling of the left ventricle. The duration of the subacute period is 4 - 6 weeks.

Features of manifestation different forms myocardial infarction.

A clear division of the periods of myocardial infarction and clinical signs are characteristic of myocardial infarction with Q wave(transmural).

Main clinical manifestation myocardial infarction without Q wave(non-transmural) - pain syndrome in the form of prolonged attacks of resting angina (lasting more than 20–30 minutes), poorly controlled by nitroglycerin. The intensity of pain is less than with myocardial infarction with a Q wave (transmural). Substernal pain may be accompanied by general symptoms: increasing weakness, sweating, shortness of breath, transient rhythm and conduction disturbances, decreased blood pressure.

Myocardial infarction without a Q wave can manifest as mild but frequent attacks of exertional angina.

Objective examination does not provide specific signs to confirm the diagnosis. During auscultation, a weakening of the first tone and additional tones (III or IV) may appear. Transient disturbances in heart rhythm and changes in blood pressure are possible.

Only targeted laboratory and instrumental research can confirm or refute the presence of myocardial infarction without a Q wave.

The prognosis of the course of the disease and the likelihood of mortality in acute myocardial infarction is determined by the main clinical signs (degree of heart failure, arrhythmia), localization of the infarction (worse with anterior infarction).

Clinical Killip myocardial infarction severity classification(Killip) is based on assessing the severity of heart failure and is prognostic:

Class I – without signs of circulatory failure; mortality rate up to 5%.

Class II – signs of circulatory failure are moderately expressed, there are signs of right ventricular failure (a gallop rhythm is heard, moist rales are heard in the lower parts of the lungs, signs of venous stasis are hepatomegaly, edema); mortality rate 10-20%.

Class III – acute left ventricular failure (pulmonary edema); mortality rate is 30-40%.

Class IV – cardiogenic shock (blood pressure less than 90 mm Hg, constriction of peripheral vessels, sweating, impaired consciousness, oliguria); mortality rate is more than 50%.

Laboratory and instrumental diagnostics.

General blood test: in the first days, neutrophilic leukocytosis appears (up to 10-12 10 9 / l), which normalizes by the tenth day. By the eighth to tenth day, ESR increases and can persist for several weeks.

Biochemical blood test: increased activity of the MB fraction of creatine phosphokinase, the first fraction of lactate dehydrogenase, AST and ALT, increased myoglobin, troponin. Nonspecific changes: increased urea, CRP, fibrinogen, seromucoid, sialic acids, glucose.

Coagulogram: increase in APTT, prothrombin index.

ECG: changes depend on the stage of myocardial infarction (ischemic, damage, acute, subacute, cicatricial).

The focus of myocardial damage during a heart attack consists of a zone of necrosis, an adjacent zone of damage, which passes into the ischemia zone.

The ischemic stage lasts only 15-30 minutes and is characterized by the formation of a “coronary” T wave. This stage cannot always be recorded.

The stage of damage lasts from several hours to several days, is characterized by an arched rise or depression of the ST segment, which turns into the “coronary” T wave and merges with it. The R wave is reduced or a pathological Q wave has appeared: the ventricular complex QR or Qr in non-transmural infarction and QS in transmural infarction.

The acute stage lasts up to 2-3 weeks, is characterized by an increase in the depth of the Q wave. The ST segment approaches the isoline, a negative, symmetrical “coronal” T wave appears.

The subacute stage is characterized by the absence of a damaged zone (the ST segment returns to the isoline, the “coronal” T wave is negative, symmetrical remains or even increases, the “pathological” Q wave remains (more than 1/4 the size of the R wave). The end of the subacute stage is the absence of wave dynamics T.

The scar stage is characterized by persistent preservation of the “pathological” Q wave. The ST segment is on the isoline, the T wave is positive, smoothed or negative, there are no dynamics of its changes.

Topical diagnosis of myocardial infarction:

Infarction of the anterior wall and apex is characterized by ECG changes in leads I, II, aVL and V 1–4,

For the anterolateral wall - in leads I, II, aVL, V 5–6,

For the anterior part of the interventricular septum in leads V3,

For the posterior diaphragmatic wall III, II, aVF,

For posterolateral –III, II, aVF, V 5–6,

For back wall(common) – III, II, aVF, V 5-7.

Complications of myocardial infarction:

Rhythm disturbances (extrasystole, paroxysmal tachycardia, atrial fibrillation, blockade); acute circulatory failure (fainting, collapse, cardiogenic shock, pulmonary edema, cardiac asthma); pericarditis; thromboendocarditis; cardiac aneurysm; thromboembolism; cardiac tamponade; post-infarction Dressler syndrome (pneumonitis, pleurisy, pericarditis); acute erosive and ulcerative lesions of the gastrointestinal tract; stomach bleeding; paralytic ileus; bladder paresis; chronic circulatory failure.

Treatment uncomplicated myocardial infarction.

Patients with myocardial infarction are transported on a stretcher or gurney to the intensive care cardiology department.

The treatment program includes: relief of a painful attack, restoration of the main coronary blood flow and prevention of further thrombus formation, limiting the size of myocardial infarction, preventing the development of arrhythmias.

The pain syndrome is relieved with narcotic analgesics (morphine) and neuroleptanalgesia.

To restore coronary blood flow, thrombolytic and antithrombotic drugs are used (streptokinase once, anticoagulants 3-5 days 24 hours after administration of strepokinase, acetylsalicylic acid).

In order to limit the size of myocardial infarction, nitrates are used intravenously with a transition to long-acting nitrates and beta-blockers.

Indications: angiotensin-converting enzyme inhibitors, calcium antagonists.

Physical rehabilitation of patients is carried out under the supervision of a physician, taking into account the class of clinical severity of myocardial infarction.

Surgical and interventional treatment of ischemic heart disease. The optimal treatment of stenosing atherosclerosis is the restoration of adequate blood supply in the ischemic area. Currently, coronary artery bypass grafting and various interventional methods are used (percutaneous transluminal angioplasty, stenting, atherectomy, laser angioplasty). The choice of surgical treatment method is determined by clinical and coronary angiography data.

Coronary artery bypass grafting using vascular grafts allows for a long-term effect of eliminating the ischemic zone. However, the method is traumatic (thoracotomy) and requires expensive special equipment (extracorporeal circulation).

Interventional methods of intravascular interventions make it possible to obtain long-term preservation of the result, to repeatedly perform endovascular procedures with a low risk of complications.

When performing stenting coronary arteries in areas of significant narrowing of their lumen, implantation into the coronary artery of a metal stent, a drug-eluting stent (drugs that disrupt cell division), a conductor with a source of radioactivity (antiproliferative effect of ionizing radiation), or a laser conductor is used. Stenting is combined with predilation (expansion with a balloon) of the stenosis. Stenting is performed, among other things, urgently in case of acute myocardial infarction.

Atherectomy - removal of endothelial hyperplasia or atherosclerotic plaque forming stenosis using blades and drills.

The disadvantage of all endovascular methods, including percutaneous transluminal angioplasty (to a greater extent) and stenting, atherectomy and laser angioplasty, is the process of restenosis.

Myocardial infarction is necrosis (death) of a section of the heart muscle as a result of a significant disruption of blood flow to the heart. Myocardial infarction is a form of coronary heart disease.

Mechanism of occurrence

In the vast majority of cases (up to 98%), a heart attack develops in one of two ways:

• One of cholesterol plaques cracks, and the body reacts to the damage that has occurred. Platelets migrate to the site of the destroyed plaque, forming a blood clot in the coronary artery, significantly narrowing or completely blocking the lumen of the vessel. As a result acute failure blood supply to the area of ​​the myocardium that received nutrition with the help of this coronary vessel, experiences oxygen starvation - heart cells, cardiomyocytes die - a heart attack develops.
• With a sharp increase in the load on the heart (excessive physical activity, stress, high blood pressure, etc.), an acute discrepancy develops between the delivery of oxygen through the vessels narrowed by atherosclerosis and the need of heart cells for it. As a result of significant oxygen starvation, part of the heart muscle becomes necrotic.

Classification of myocardial infarction

Doctors have created many classifications depending on the volume and location of the lesion, as well as a classification of acute myocardial infarction by stages.

STAGES OF ACUTE MYOCARDIAL INFARCTION:

• Prodromal period (lasts up to 30 days, may be absent).
• The most acute period (lasts up to 2 hours from the onset of anginal status).
• Acute period (lasts up to 10 days from the onset of myocardial infarction).
• Subacute period (starts from day 10 and lasts up to 1-2 months).
• The scarring period (on average lasts from 2-3 months to six months, sometimes ends only after 2-3 years).

Depending on the volume of the lesion, the infarction is divided into transmural, or otherwise large-focal (with a “Q wave” according to ECG data), when the entire thickness of the heart muscle is damaged, and non-transmural (fine-focal, without a “Q wave”).

Symptoms of acute myocardial infarction.

As can be seen from the classification, myocardial infarction is a long-term disease, therefore, depending on the stage of the disease, its manifestations vary greatly.

PRODROME PERIOD OF MYOCARDIAL INFARCTION

This is the period during which patients develop symptoms: chest pain becomes more frequent, they appear with less physical activity, or even at rest, and are less easily relieved by nitrates; a large dose of nitrates is required for the pain to go away.

It's no coincidence stable angina, acute myocardial infarction and sudden cardiac death are combined by cardiologists into one Acute Coronary Syndrome (ACS). All these conditions, despite the different manifestations, are based on one mechanism. Thus, both during a heart attack and unstable angina, the integrity of one of the cholesterol plaques in the coronary artery is disrupted. The body reacts to the resulting defect by sending platelets to the site and activating the blood coagulation system. As a result, a blood clot forms, blocking the blood flow. Short-term or incomplete closure of the lumen of the vessel leads to the development of symptoms of unstable angina. If the blockage gets worse, a heart attack develops.

This is why patients with unstable angina should be urgently hospitalized: it is better to prevent a catastrophe than to deal with its consequences.

THE ACUTE PERIOD OF MYOCARDIAL INFARCTION

The highest mortality rate from myocardial infarction is observed during this period. At the same time, the most acute period is the most fertile in terms of therapy. Thus, there are drugs that destroy the formed blood clot, thereby restoring the impaired blood flow through the vessel. These medications are effective within the first 12 hours from the onset of a heart attack, and the earlier they are used, the better the result.

In the most acute period, anginal status occurs - very intense pain localized behind the sternum or in the left half chest. Patients describe the pain as stabbing, boring or pressing (“the heart is squeezed in a vice”). The pain often comes in waves, radiates to left shoulder, hand, lower jaw, interscapular region. Sometimes it can spread to the right side of the chest and upper abdomen.

In general, the pain is similar to that during angina attacks, but its intensity is much higher, it does not go away after taking 2-3 tablets of nitroglycerin and lasts, as a rule, 30 minutes or more.

In addition to pain, there is often cold sweat, severe general weakness. Blood pressure more often decreases as a result of a decrease in the force of contractions of the damaged heart, less often it increases, since the body, in response to stress, releases a large amount of adrenaline, which has a stimulating effect on work of cardio-vascular system. Almost always, with myocardial infarction, patients experience severe anxiety and fear of death.

It is important to know that in 20% of patients the acute period of a heart attack is asymptomatic (the so-called painless form of myocardial infarction). Such patients note an unclear heaviness in the chest (“heartbreak”), severe fatigue, malaise, insomnia, and “unreasonable” anxiety.

In some patients, myocardial infarction may manifest itself as the development of rhythm and conduction disturbances. Such patients experience interruptions in the functioning of the heart, possibly a sharp increase in heart rate, or, conversely, a slowdown in heart rate. Dizziness may occur severe weakness, episodes of loss of consciousness.

Sometimes myocardial infarction can manifest as sudden shortness of breath or pulmonary edema.

ACUTE PERIOD OF MYOCARDIAL INFARCTION

During this period sharp pain subsides because the process of destruction of cardiomyocytes (heart cells) is completed, and necrotic (dead) tissue is not sensitive to pain. Most patients may note the preservation of the so-called. residual pain: dull constant pain, usually localized behind the sternum.

On the second day, enzymes from damaged cells and destroyed tissues enter the blood, causing a temperature reaction: fever up to 39°C may appear, as well as malaise, weakness, and sweating.

The effect of stress hormones (adrenaline, norepinephrine, dopamine) subsides, resulting in a decrease in blood pressure, sometimes very significantly.

During this period there may appear dull pain in the chest, worsening with breathing, which is a sign of the development of pleuropericarditis. Some patients have intense pressing pain in the heart can resume - in this case, post-infarction angina or relapse of myocardial infarction is diagnosed.

Since the scar has not yet formed, and part muscle cells heart is destroyed, during this period it is very important to minimize physical activity, stress. If these rules are not followed, a cardiac aneurysm may develop - a saccular protrusion of the heart wall, or death from heart rupture may occur.

SUBACUTE PERIOD OF MYOCARDIAL INFARCTION

During this period, pain is usually absent. Considering the fact that the contractility of the heart is reduced, since a section of the myocardium is “switched off” from work, symptoms may appear: shortness of breath, swelling of the legs. In general, the patient’s condition improves: the temperature normalizes, blood pressure stabilizes, and the risk of developing arrhythmia decreases.

Scarring processes occur in the heart: the body eliminates the resulting defect, replacing destroyed cardiomyocytes with connective tissue.

PERIOD OF SCARING OF MYOCARDIAL INFARCTION

During this period, the formation of a full-fledged scar from coarse fiber continues and ends. connective tissue. The patient’s well-being depends on the size of the lesion and the presence or absence of complications of myocardial infarction.

In general, the condition is returning to normal. There is no pain in the heart, or there is stable angina pectoris of a certain functional class. A person gets used to new living conditions.

Acute myocardial infarction is one of the most dangerous complications of coronary heart disease. The pathology is associated with the occurrence of necrotic processes in the heart muscle due to oxygen starvation of tissues. What kind of condition is this, and how to deal with it, we will understand further.

What it is?

The pathology is accompanied by the death of one or more sections of the heart muscle. This happens due to the fact that coronary circulation stops. Parts of the heart can remain without oxygen for many reasons, but the main one is the presence of a blood clot in the artery that supplies the heart muscle.

In this oxygen-free state, myocardial cells “live” for about half an hour, after which they die. The pathology is accompanied by numerous complications caused by irreversible processes as a result of disruption of the posterior wall of the left ventricle.

This form of heart attack can cause loss of legal capacity and disability!

Causes of development and risk factors

Arrest of coronary circulation can be caused by several reasons. This:

• Atherosclerosis. Chronic illness arteries, which is characterized by the formation dangerous blood clots. If their development is not prevented, they will increase in size and eventually block the artery and blood supply.
• Sharp spasm of the coronary arteries. This can occur from cold or exposure to chemicals (poisons, drugs).
• Embolism. This pathological process, in which particles appear in the lymph or blood that should not be there, which leads to disruption of the local blood supply. The cause of acute myocardial infarction is most often a fat embolism, when droplets of fat enter the blood.
• Advanced anemia. In this condition, there is a sharp decrease in hemoglobin in the blood, therefore, the transport functions of the blood decrease, so oxygen does not flow in the proper amount.
• Cardiomyopathy. Sharp hypertrophy of the heart muscle is characterized by a discrepancy between the level of blood supply and increased needs.
• Surgical interventions . During the operation, the vessel was completely dissected transversely or ligated.

In addition to the main reasons, risk factors can also be identified - pathological conditions which can lead to a heart attack. These include:

• diseases of the cardiovascular system (often ischemic disease hearts);
• diabetes;
• previous myocardial infarction;
• hypertonic disease;
• increased level cholesterol;
• smoking or alcohol abuse;
• obesity;
• poor nutrition(abuse of salt and animal fats);
• increased concentration triglycerides in the blood;
• age over 40 years;
• chronic stress.

Symptoms

Like any other heart disease, acute myocardial infarction is characterized by pain in the heart. Other symptoms include:

• severe squeezing pain in the chest, which is periodic and reminds itself several times a day, and it can be very intense and radiate to other places without being localized in one place;
• unbearable pain in the heart that cannot be relieved with Nitroglycerin;

If after taking Nitroglycerin the pain does not go away, you should take another 300 mg and call urgently ambulance!

• pain in the left arm, shoulder blade, shoulder, neck or jaw;
• acute shortage air, which can be observed due to impaired blood supply;
• dizziness, weakness, increased sweating, nausea and even vomiting (these manifestations often accompany pain);
• abnormal pulse that is irregular or slow.

Stages

The development of acute myocardial infarction can be divided into four:

1. Damage phase. The most acute stage course of the disease. Duration - from 2 hours to a day. It is during this period that the process of dying of the myocardium in the affected area occurs. According to statistics, most people die at this stage, so it is extremely important to diagnose the disease in a timely manner!
2. Acute. Duration - up to 10 days. During this period there is inflammatory process in the heart attack zone. The phase is characterized by .
3. Subacute. Duration - from 10 days to a month or two. At this stage, scar formation occurs.
4. Scarring or chronic phase. Duration - 6 months. Symptoms of a heart attack do not appear in any way, however, the risk of developing heart failure, angina pectoris and recurrent heart attack remains.

What complications can there be?

Acute myocardial ischemia can be further complicated by the following manifestations:

• Heart rhythm disturbances. Ventricular fibrillation progressing to fibrillation can cause death.
• Heart failure. Dangerous condition may cause pulmonary edema and cardiogenic shock.
• Thromboembolism pulmonary artery . May cause pneumonia or pulmonary infarction.
• Cardiac tamponade. This occurs when the heart muscle ruptures in the infarction zone and blood breaks into the pericardial cavity.
• . In this condition, a “protrusion” of a section of scar tissue occurs if there has been extensive damage to the myocardium.
• Post-infarction syndrome. This may include pleurisy, arthralgia.

Diagnostics

Successful is a complex process that consists of several stages:

1. History taking. The doctor finds out whether there were attacks of pain different frequencies and localization in the past. In addition, he conducts a survey to find out whether the patient is at risk and whether blood relatives have had myocardial infarctions.
2. Carrying out laboratory research . In the blood test acute myocardium indicates an increase in the number of white blood cells and an increase in the erythrocyte sedimentation rate (ESR). At the biochemical level, an increase in activity is detected:

• aminotransferase enzymes (ALT, AST);
• lactate dehydrogenase (LDH);
• creatine kinase;
• myoglobin.

1. Usage instrumental techniques research. On an ECG (electrocardiography), a characteristic sign of a heart attack is considered to be a negative T wave and a pathological QRS complex, and on an EchoCG (echocardiography), a local violation of the contractility of the affected ventricle is considered. Coronary angiography reveals narrowing or occlusion of the vessel supplying the myocardium.

Emergency care and treatment

Emergency assistance may include taking Nitroglycerin tablets (up to 3 pieces) and immediately calling an ambulance. Basic measures for the treatment of acute heart attack can only be performed by medical staff.

There are several principles of therapy:

1. Restoration of blood circulation in the coronary arteries. After the patient is admitted to cardio intensive care unit carry out everything necessary research to confirm the diagnosis. After that it gets up urgency rapid restoration of blood circulation in the coronary arteries. One of the main methods is thrombolysis (dissolution of thrombus cells inside the vascular bed). As a rule, thrombolytics dissolve the blood clot within 1.5 hours and restore normal blood circulation. The most popular means are:

• Alteplase;
• Reteplase;
• Anistreplase;
• Streptokinase.

1. Pain relief. To eliminate pain use:

• Sublingual nitroglycerin (0.4 mg), however, nitrates are contraindicated in low blood pressure;
• beta blockers, which eliminate myocardial ischemia and reduce the infarction area (usually prescribed 100 mg of Metoprolol or 50 mg of Atenolol);
• narcotic analgesics - in special cases when Nitroglycerin does not help, morphine is administered intramuscularly to the patient.

1. Surgical intervention. It may be necessary to urgently perform a stent to restore blood flow. A metal structure is passed to the area with the thrombus, which expands and dilates the vessel. Planned operations are performed to reduce the area of ​​necrotic lesions. Also, to reduce the risk of a recurrent heart attack, coronary artery bypass grafting is performed.
2. General events. The first few days the patient is in the intensive care unit. The regime is strict bed rest. It is recommended to exclude visits from relatives in order to protect the patient from worries. During the first week, he can gradually begin to move, but following all the doctor’s recommendations on diet and physical activity. As for the diet, it is necessary to exclude spicy, salty and peppery foods in the first week, and enrich the menu with fruits, vegetables, and pureed dishes.

After discharge, you should be monitored systematically by a specialist and take prescribed cardiac medications. Eliminate smoking and give up alcohol, as well as avoid stress, perform feasible physical activity and monitor your body weight.

Video: educational film about pathology

In a short educational video you can clearly see what a patient looks like with acute myocardial infarction, how diagnosis and treatment are carried out:

So, the prognosis for recovery in acute myocardial infarction depends on the volume of the lesion and the location of the necrosis focus. In addition, they play an important role accompanying illnesses and heredity. In any case, with timely and qualified treatment, the chances of a successful recovery increase. Don't delay your visit to the doctor!

– a focus of ischemic necrosis of the heart muscle, developing as a result of an acute violation of the coronary circulation. Clinically manifested by burning, pressing or squeezing pain behind the sternum, radiating to the left arm, collarbone, scapula, jaw, shortness of breath, a feeling of fear, cold sweat. Developed myocardial infarction is an indication for emergency hospitalization in the cardiac intensive care unit. Failure to provide timely assistance can result in death.

During this period, acute left ventricular failure (cardiac asthma, pulmonary edema) may develop.

Acute period

In the acute period of myocardial infarction, pain syndrome usually disappears. The persistence of pain is caused by a pronounced degree of ischemia of the peri-infarction zone or the addition of pericarditis.

As a result of the processes of necrosis, myomalacia and perifocal inflammation, fever develops (from 3-5 to 10 or more days). The duration and height of the temperature rise during fever depend on the area of ​​necrosis. Arterial hypotension and signs of heart failure persist and increase.

Subacute period

There is no pain, the patient’s condition improves, and body temperature normalizes. Symptoms of acute heart failure become less pronounced. Tachycardia and systolic murmur disappear.

Post-infarction period

In the post-infarction period, there are no clinical manifestations, laboratory and physical data are practically without deviations.

Atypical forms of myocardial infarction

Sometimes there is an atypical course of myocardial infarction with localization of pain in the neck. typical places(in the throat area, fingers of the left hand, in the area of ​​the left shoulder blade or cervicothoracic region spine, in the epigastrium, in the lower jaw) or painless forms, the leading symptoms of which may be coughing and severe suffocation, collapse, swelling, arrhythmias, dizziness and confusion.

Atypical forms of myocardial infarction are more common in elderly patients with pronounced signs cardiosclerosis, circulatory failure, against the background of repeated myocardial infarction.

However, usually only the most acute period occurs atypically, further development myocardial infarction becomes typical.

The erased course of myocardial infarction is painless and is accidentally detected on an ECG.

Complications of myocardial infarction

Often complications arise already in the first hours and days of myocardial infarction, complicating its course. In most patients, in the first three days, various types of arrhythmias are observed: extrasystole, sinus or paroxysmal tachycardia, atrial fibrillation, complete intraventricular block. The most dangerous is ventricular fibrillation, which can turn into fibrillation and lead to the death of the patient.

Left ventricular heart failure is characterized by congestive wheezing, symptoms of cardiac asthma, pulmonary edema and often develops during the acute period of myocardial infarction. An extremely severe degree of left ventricular failure is cardiogenic shock, which develops with a large heart attack and usually leads to death. Signs of cardiogenic shock are a drop in systolic blood pressure below 80 mmHg. Art., impaired consciousness, tachycardia, cyanosis, decreased diuresis.

Gap muscle fibers in the area of ​​necrosis it can cause cardiac tamponade - hemorrhage into the pericardial cavity. In 2-3% of patients, myocardial infarction is complicated by thromboembolism of the pulmonary artery system (can cause pulmonary infarction or sudden death) or great circle blood circulation

Patients with extensive transmural myocardial infarction in the first 10 days may die from ventricular rupture due to acute cessation of blood circulation. With extensive myocardial infarction, failure of scar tissue may occur, its bulging with the development of acute cardiac aneurysm. An acute aneurysm can transform into a chronic one, leading to heart failure.

The deposition of fibrin on the walls of the endocardium leads to the development of parietal thromboendocarditis, which is dangerous due to the possibility of embolism of the vessels of the lungs, brain, and kidneys from detached thrombotic masses. In more late period post-infarction syndrome may develop, manifested by pericarditis, pleurisy, arthralgia, eosinophilia.

Diagnosis of myocardial infarction

Among the diagnostic criteria for myocardial infarction, the most important are the medical history, characteristic changes on the ECG, and indicators of serum enzyme activity. The patient's complaints during myocardial infarction depend on the form (typical or atypical) of the disease and the extent of damage to the heart muscle. Myocardial infarction should be suspected in the event of a severe and prolonged (longer than 30-60 minutes) attack of chest pain, disturbances in cardiac conduction and rhythm, and acute heart failure.

To the characteristic ECG changes include the formation of a negative T wave (with small-focal subendocardial or intramural myocardial infarction), a pathological QRS complex or Q wave (with large-focal transmural myocardial infarction). EchoCG reveals a violation of local contractility of the ventricle and thinning of its wall.

In the first 4-6 hours after a painful attack, an increase in myoglobin, a protein that transports oxygen into cells, is detected in the blood. An increase in the activity of creatine phosphokinase (CPK) in the blood by more than 50% is observed 8-10 hours after the development of myocardial infarction and decreases to normal in two days. CPK levels are determined every 6-8 hours. Myocardial infarction is excluded with three negative results.

To diagnose myocardial infarction for more than later resort to determining the enzyme lactate dehydrogenase (LDH), the activity of which increases later than CPK - 1-2 days after the formation of necrosis and comes to normal values in 7-14 days. Highly specific for myocardial infarction is an increase in the isoforms of the myocardial contractile protein troponin - troponin-T and troponin-1, which also increase in unstable angina. An increase in ESR, leukocytes, activity of aspartate aminotransferase (AsAt) and alanine aminotransferase (AlAt) is determined in the blood.

Coronary angiography (coronary angiography) allows you to establish thrombotic occlusion of the coronary artery and decreased ventricular contractility, as well as assess the possibilities of coronary artery bypass surgery or angioplasty - operations that help restore blood flow to the heart.

Treatment of myocardial infarction

In case of myocardial infarction it is indicated emergency hospitalization to the cardiac intensive care unit. In the acute period, the patient is prescribed bed rest and mental rest, fractional meals limited in volume and calorie content. In the subacute period, the patient is transferred from intensive care to the cardiology department, where treatment of myocardial infarction continues and the regimen is gradually expanded.

Relief of pain syndrome is carried out by a combination of narcotic analgesics (fentanyl) with antipsychotics (droperidol), intravenous administration nitroglycerin.

Therapy for myocardial infarction is aimed at preventing and eliminating arrhythmias, heart failure, and cardiogenic shock. Assign antiarrhythmic drugs(lidocaine), beta-blockers (atenolol), thrombolytics (heparin, acetylsalicylic acid), calcium antagonists (verapamil), magnesia, nitrates, antispasmodics, etc.

In the first 24 hours after the onset of myocardial infarction, perfusion can be restored by thrombolysis or emergency balloon coronary angioplasty.

Prognosis for myocardial infarction

Myocardial infarction is severe, associated with dangerous complications disease. Most of deaths develops in the first days after myocardial infarction. The pumping ability of the heart is related to the location and volume of the infarct area. If more than 50% of the myocardium is damaged, as a rule, the heart cannot function, which causes cardiogenic shock and death of the patient. Even with less extensive damage, the heart does not always cope with the load, resulting in heart failure.

After the acute period, the prognosis for recovery is good. Unfavorable prospects for patients with complicated myocardial infarction.

Prevention of myocardial infarction

Necessary conditions for the prevention of myocardial infarction are maintaining a healthy and active image life, giving up alcohol and smoking, balanced diet, exclusion of physical and nervous overstrain, control blood pressure and blood cholesterol levels.

A few words about the course of myocardial infarction. On this moment V clinical picture Both uncomplicated and complicated myocardial infarction are divided into five periods: prodromal (pre-infarction), acute, acute, subacute, post-infarction immediate and distant.

What are the periods of mycoardial infarction?

1. Pre-infarction period (prodromal)– this period of myocardial infarction is considered as a period of increasing severity coronary insufficiency. It lasts from a few minutes to 1.5 months. Most often during this period, attacks of unstable angina become more frequent and their intensity increases. The area of ​​pain expands and begins to bother the right side of the sternum. The irradiation zone also increases significantly, occupying the interscapular and epigastric regions; some patients note it in the cervical-occipital region. The decrease in tolerance to habitual physical activity progresses. The effectiveness of nitroglycerin taken sublingually is significantly reduced, and sometimes it does not relieve pain. Patients are restless, anxious, and sometimes they have a feeling of fear of death. They show signs cardiovascular failure: cold extremities, sticky sweat, etc. occur various disorders heart rate, drop in blood pressure. Patients may note that the above complaints include a feeling of shortness of breath and dizziness. The signs listed above are most characteristic of the first period - painful, or ischemic. If treatment is started on time, a heart attack can be avoided. We can name the objective symptoms of this period: slight cyanosis of the lips and subungual spaces, an increase in blood pressure (then a decrease); increased heart rate; slight increase in the left border of the heart; on auscultation, sometimes muffled heart sounds are heard; practically unchanged biochemical parameters blood, characteristic features on the ECG. Holter ECG monitoring for a day or more is especially helpful in diagnosis. In this case, a decrease in the 8T interval of the ischemic type, the appearance of a negative “coronary” T wave, an increase in the P wave in some leads, the absence of a pathological O wave, and the appearance of rhythm disturbances are revealed.

2. Course of myocardial infarction. The most acute period (febrile, inflammatory) The course of myocardial infarction is characterized by the occurrence of necrosis at the site of ischemia of the heart muscle. All signs of aseptic inflammation appear, hydrolysis products of necrotic masses begin to be absorbed. The pain usually goes away. The duration varies, according to some data, from 30 minutes to 2-4 hours. The development of this period of myocardial infarction is facilitated by provoking factors: intense exercise stress, psycho-emotional stressful situation, trauma, possibly overeating, surgery, severe cooling or overheating, in patients diabetes mellitus– insulin hyperglycemia, sexual intercourse. These factors significantly increase the myocardial oxygen demand and at the same time increase blood pressure and cause spasm of the coronary arteries. In most patients with myocardial infarction, pain in the heart area becomes excessively intense. The pain is characterized as strong pressing, squeezing, many report intense burning or “dagger” pain. Clinical studies A direct relationship was revealed between the intensity of pain in the heart area, the extent of the infarction and the age of the patient. As a rule, the pain radiates to left hand, there may be a feeling of severe squeezing pain in the wrist area. It can radiate to the left shoulder, left shoulder blade, neck, lower jaw, ear. The pain is characterized by waves. It gradually increases, becomes intense, and then decreases somewhat, but soon resumes with greater force. This wave-like course of myocardial infarction can last up to several hours. The use of nitroglycerin in any form, sublingually or as a spray, does not relieve pain. During an attack of pain, people experience a feeling of fear of death, melancholy, doom, sometimes excited and restless; patients with myocardial infarction may feel a feeling of lack of air. When examining a patient with myocardial infarction during this period of the disease, pallor, often increased skin moisture, cyanosis of the lips, nose, ears, and subungual spaces are revealed. When palpating the heart area in patients with extensive transmural myocardial infarction, presystolic pulsation can be detected, synchronous with the IV sound. Systolic pulsation can also be detected in the III, IV, V intercostal spaces to the left of the sternum. The pulse rate in the uncomplicated course of the disease is normal, but the pulse is sometimes arrhythmic due to extrasystoles. Blood pressure may increase slightly, but then quickly return to normal. But with extensive myocardial infarction, a decrease is observed, mainly systolic. Arterial hypotension often occurs with repeated myocardial infarctions. The borders of the heart only sometimes slightly increase due to the left border. The increase in size may be associated with extensive myocardial infarction. In patients with uncomplicated but extensive myocardial infarction, a muffled 1 tone and a soft systolic murmur at the apex are detected. With extensive transmural myocardial infarction, a gallop rhythm may be heard. In some cases, a systolic “cat purr” is heard. Physical examination of other organs and systems does not reveal any significant changes in patients with uncomplicated myocardial infarction. The ECG clearly shows signs of myocardial damage:

1) in case of penetrating myocardial infarction, when the necrosis zone extends from the pericardium to the endocardium on the ECG, the displacement of the 8T segment is above the isoline, the shape is convex upward, this is the first sign of penetrating myocardial infarction. The fusion of the T wave with the 8T segment occurs on days 1–3; deep and wide wave (5 is one of the main signs; a decrease in the size of the K wave is also characteristic. Discoordinate changes occur - opposite displacements of 8T and T (for example, in standard leads 1 and 2 compared to standard lead 3); on average, with On the 3rd day there is a reverse trend characteristic changes ECG: segment 8T approaches the isoline, a uniform deep T wave appears. The wave ((also undergoes reverse dynamics, but changed (and deep T wave may persist forever;

2) with intramural infarction, a large increase in the wave (does not occur; the displacement of the 8T segment can be not only up, but also down. For a more reliable assessment, a repeat ECG is necessary.

Of course, ECG signs have great importance when making a diagnosis, but all signs of diagnosing myocardial infarction must be taken into account:

1) clinical signs;

2) electrocardiographic signs;

3) biochemical signs indicating damage to heart muscle cells.

In cases of doubt, it is necessary to perform echocardiography (identification of “immobile” zones of the myocardium) and radioisotope research heart (myocardial scintigraphy). In the same way, a retrospective diagnostic assumption about myocardial infarction complicating the course of other diseases or postoperative period.

3. Acute period. During this period, a focus of myocardial necrosis is finally formed, and myomalacia occurs in it. The period lasts from 2 to 10–14 days. Pain disappears in the acute period, but in rare cases, with the expansion of the necrosis zone during progressive myocardial infarction, the pain syndrome may persist. An increased heart rate and a tendency to decrease blood pressure are detected; muffled tones and a quiet systolic murmur at the apex of the heart remain. During this period, on the 2nd, or less often the 3rd, day there is a rise in body temperature to 37.1-37.9°C, in rare cases exceeding 38°C. The increase in temperature lasts about 3–7 days, possibly up to 10 days. The magnitude of the temperature reaction and its duration depend to a certain extent on the extent of necrosis and the age of the patient. The following changes are noted in blood tests: the number of leukocytes increases already on days 2–4 and persists until days 3–7. Usually their number reaches 10–12 X 10 9 /l, with widespread transmural myocardial infarction - up to 15 X 10 9 /l. Leukocytosis is accompanied by a shift leukocyte formula to the left. There is also an increase in ESR from 2–3 days of illness, which reaches a maximum between 8–12 days, and then slowly decreases, normalizing after 3–4 weeks. Longer persistence of an increased ESR indicates the presence of complications. IN biochemical analysis blood levels of fibrinogen, seromucoid, sialic acids, γ-globulin, and C-reactive protein increase. Markers of cardiomyocyte death are determined, such as aspartate aminotransferase, lactate dehydrogenase, creatine phosphokinase, myoglobin, myosin, cardiotropins T and I, glycogen phosphorylase. The ECG also shows changes characteristic of this period of the disease.

4. Subacute period lasts about 8 weeks. During this time, the scar is fully formed and thickened. The duration of this period is influenced by the extent of the necrosis zone, the presence of complications, as well as the reactivity and age of the patient. In prognostic terms, this period is more favorable, since the most life-threatening complications for the patient most often develop in the first days from the onset of the disease. It has been established that with uncomplicated myocardial infarction, the subacute period proceeds most favorably. Upon examination, the patient's condition is satisfactory, there is no pain syndrome. The heart rate has returned to normal, and no systolic murmur is heard at the apex of the heart. Blood pressure is usually normal; if there was arterial hypertension before the development of myocardial infarction, then during this period the blood pressure begins to rise again. In the subacute period, body temperature normalizes, changes in the blood disappear. A pathological O wave is recorded on the ECG.

5. Post-infarction period of myocardial infarction– the period of complete adaptation of the cardiovascular system to new operating conditions, i.e. turning off the contractile function of a section of the myocardium. Considering the presence of connective tissue scar necrosis at the site, this period is also called the period of post-infarction cardiosclerosis. The post-infarction period continues throughout the rest of the patient’s life; this period, in turn, is divided into 2 periods: immediate – 2–6 months and long-term – after 6 months. Pain most often does not bother the patient during this period, but sometimes there are cases of resumption of angina. In the post-infarction period, the patient's condition is satisfactory. The patients are fully adapted in social, everyday and psychological terms. When examining a patient, only signs of atherosclerosis of the thoracic and abdominal aorta can be detected; sometimes a slight expansion of the left border of the heart to the left and muffled first heart sound above the apex of the heart are found. In patients with arterial hypertension, diagnosed before myocardial infarction, an increase in blood pressure is recorded, which requires immediate antihypertensive therapy. The pathological O wave remains on the ECG. When examining other organs and systems pathological changes not detected.

Atypical forms of myocardial infarction

1) peripheral with atypical localization of pain. With this type of pain syndrome varying intensity, localized not behind the sternum or in the pericardial region, but in typical places for the classic form. This form is difficult to diagnose, but by studying blood parameters and ECG data, you can obtain data indicating myocardial infarction;

2) abdominal form (gastralgic). It occurs according to the type of gastrointestinal tract lesion, with characteristic abdominal pain, nausea, vomiting and bloating. Most often, the gastralgic form (abdominal) of myocardial infarction occurs with an infarction of the posterior wall of the left ventricle. Sometimes this variant of the course of a heart attack is mistaken for surgical or infection. In this case, sometimes an erroneous diagnosis of food poisoning is made, the stomach is washed out, and a cleansing enema is given, thereby causing great harm to the patient;

3) asthmatic form: begins with shortness of breath, cardiac asthma and contributes to the development of complications such as pulmonary edema. Pain syndrome may be absent. The asthmatic form is most common in elderly people with cardiosclerosis, as well as with repeated heart attacks or very large heart attacks;

4) brain form (cerebral): symptoms of the disorder are in the foreground cerebral circulation like a stroke with loss of consciousness, patients may complain of headaches, dizziness, and visual disturbances. Paralysis and paresis of the limbs are possible. This form occurs more often in older people who have cerebral vascular sclerosis;

5) the silent or painless form sometimes becomes accidental discovery during medical examination. From the clinical manifestations: suddenly I felt “feeling bad”, there was severe weakness, sticky cold sweat, then everything went away, weakness remained. This course is typical in old age and with repeated myocardial infarctions;

6) the arrhythmic form is the main sign of paroxysmal tachycardia, while pain syndrome may be absent. Patients complain of increased heart rate or, conversely, the heart rate drops sharply and the patient loses consciousness. The latter is a manifestation of complete atrioventricular block;

7) collaptoid form is characterized by the absence of pain in the heart area, sudden development fainting, darkening of the eyes, drop in blood pressure, dizziness. Loss of consciousness is usually not observed. This form often occurs with repeated, extensive or transmural myocardial infarctions;

8) the edematous form is manifested by the rapid appearance of shortness of breath, weakness, palpitations, interruptions in heart rate and edematous syndrome. This option is observed in extensive, transmural, repeated myocardial infarctions leading to the development of total heart failure;

9) combined-atypical. This variant of the course of myocardial infarction combines manifestations of several atypical forms. Myocardial infarction is a very serious disease with big amount lethal outcomes and the risk of complications, especially in the first and second periods.