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Myocardial infarction

Myocardial infarction is the focus of ischemic necrosis of the cardiac muscle, which develops as a result of acute coronary artery disease. Clinically manifested burning, pressing or compressive pain behind the breastbone, giving to the left arm, clavicle, scapula, jaw, shortness of breath, a sense of fear, a cold sweat. Developed myocardial infarction serves as an indication for emergency hospitalization in cardiac resuscitation. If you do not provide timely assistance, a fatal outcome is possible.

At the age of 40-60 years myocardial infarction is 3-5 times more common in men due to earlier (10 years earlier than women) development of atherosclerosis. After 55-60 years, the incidence among people of both sexes is approximately the same. The mortality rate for myocardial infarction is 30-35%. Statistically, 15-20% of sudden deaths are due to myocardial infarction.

Infringement of a blood supply of a myocardium for 15-20 and more minutes leads to development of irreversible changes in a cardiac muscle and frustration of cardiac activity. Acute ischemia causes death of a part of functional muscle cells (necrosis) and their subsequent replacement by fibers of connective tissue, i.e., the formation of postinfarction cicatrix.

In the clinical course of myocardial infarction, five periods are distinguished:

1 period - pre-infarction (prodromal): increased frequency and intensity of angina attacks, can last several hours, days, weeks;
2 period - the most acute: from the development of ischemia to the onset of myocardial necrosis, lasts from 20 minutes to 2 hours;
3 period - acute: from the formation of necrosis to myomalation (enzymatic melting of necrotic muscle tissue), duration from 2 to 14 days;
4 period - subacute: initial processes of scar organization, development of granulation tissue in place of necrotic, duration 4-8 weeks;
5 period - postinfarction: maturation of the scar, adaptation of the myocardium to new conditions of functioning.

Causes of myocardial infarction

Myocardial infarction is an acute form of ischemic heart disease. In 97-98% of cases for the development of myocardial infarction is the atherosclerotic lesion of the coronary arteries, which causes the narrowing of their lumen. Often atherosclerosis of the arteries is accompanied by acute thrombosis of the affected area of ​​the vessel, causing complete or partial cessation of blood supply to the corresponding area of ​​the heart muscle. The thrombus formation is promoted by the raised viscosity of a blood observed at patients with an ischemic heart disease. In such cases, myocardial infarction occurs against a background of spasm of the branches of the coronary arteries.

The development of myocardial infarction is promoted by diabetes mellitus, hypertension, obesity, neuropsychic stress, alcohol addiction, smoking. A sharp physical or emotional strain on the background of ischemic heart disease and angina may provoke the development of myocardial infarction. Myocardial infarction of the left ventricle often develops.

Classification of myocardial infarction

In accordance with the size of the focal lesion of the heart muscle, myocardial infarction is distinguished:

  • large-focal
  • small-focal

The share of small-focal myocardial infarctions accounts for about 20% of clinical cases, but often small foci of necrosis in the heart muscle can be transformed into large-focal myocardial infarction (in 30% of patients). Unlike large-focal, with small-focal infarctions, there is no aneurysm and rupture of the heart, the latter is less often complicated by heart failure, ventricular fibrillation, thromboembolism.

Depending on the depth of necrotic lesion of the heart muscle, myocardial infarction is distinguished:

  • transmural - with necrosis of the entire thickness of the muscular wall of the heart (often large-focal)
  • Intramural - with necrosis in the thickness of the myocardium
  • subendocardial - with myocardial necrosis in the area of ​​attachment to the endocardium
  • subepicardial - with myocardial necrosis in the epicardial attachment zone

On the changes fixed on the ECG, distinguish:

  • "Q-infarct" - with the formation of a pathological Q wave, sometimes the ventricular complex QS (more often large-scale transmural myocardial infarction)
  • "Not Q-infarction" - is not accompanied by the appearance of a Q wave, is manifested by negative T-teeth (usually small-focal myocardial infarction)

According to the topography and depending on the lesion of certain branches of the coronary arteries, the myocardial infarction is divided into:

  • right ventricular
  • left ventricular: anterior, lateral and posterior walls, interventricular septum

By the multiplicity of occurrence, myocardial infarction is distinguished:

  • primary
  • recurrent (develops within 8 weeks after primary)
  • repeated (developing 8 weeks after the previous one)

On the development of complications, myocardial infarction is divided into:

  • complicated
  • uncomplicated
  • By the presence and localization of pain syndrome

identify forms of myocardial infarction:

  • typical - with localization of pain behind the sternum or in the precordial region
  • atypical - with atypical painful manifestations:
  • peripheral: left-handed, left-handed, laryngeal, pharyngeal, vertebrate, gastralgic (abdominal)
  • painless: collaptoid, asthmatic, edematic, arrhythmic, cerebral
  • malosymptomatic (erased)
  • combined

In accordance with the period and the dynamics of myocardial infarction, there are:

  • stage of ischemia (acute period)
  • stage of necrosis (acute period)
  • stage of organization (subacute period)
  • stage scarring (post-infarction period)

Symptoms of myocardial infarction

Pre-infarction (prodromal) period

About 43% of patients notice a sudden development of myocardial infarction, while the greater part of patients have a different period of unstable progressive angina pectoris.

The sharpest period

Typical cases of myocardial infarction are characterized by extremely intense pain syndrome with localization of pain in the chest and irradiation to the left shoulder, neck, teeth, ear, collarbone, lower jaw, interscapular zone. The nature of pain can be constrictive, burgeoning, burning, pressing, sharp ("dagger"). The more the zone of myocardial damage, the more pronounced the pain.

The painful attack proceeds wavyly (then increasing, then weakening), lasts from 30 minutes to several hours, and sometimes even days, is not stopped by repeated intake of nitroglycerin. Pain is associated with a sharp weakness, excitement, a sense of fear, shortness of breath.

Perhaps the atypical course of the acute period of myocardial infarction.

Patients noted a sharp pallor of the skin, sticky cold sweat, acrocyanosis, anxiety. Arterial pressure during the attack is increased, then moderately or sharply decreases in comparison with the initial (systolic <80 Hg, pulse <30 mm Hg), tachycardia, arrhythmia.

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

Acute period

In the acute period of myocardial infarction, the pain syndrome, as a rule, disappears. Preservation of pains is caused by a pronounced degree of ischemia of the near infarction zone or by the attachment of pericarditis.

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

Subacute Period

Painful sensations are absent, the patient's condition improves, the body temperature is normalized. Symptoms of acute heart failure become less pronounced. Disappears tachycardia, systolic murmur.

Post-infarction period

In the post-infarction period, clinical manifestations are absent, laboratory and physical data are practically without deviations.

Atypical forms of myocardial infarction

Sometimes there is an atypical course of myocardial infarction with the localization of pain in atypical places (in the throat, fingers of the left hand, in the zone of the left scapula or cervico-thoracic spine, in the epigastrium, in the lower jaw) or painless forms, the leading symptoms of which can be cough and severe suffocation, collapse, swelling, arrhythmias, dizziness and dizziness.

Atypical forms of myocardial infarction are more common in elderly patients with marked signs of cardiosclerosis, circulatory failure, against a background of repeated myocardial infarction.However, atypical usually only an acute period, the further development of myocardial infarction becomes typical.The erased course of myocardial infarction is painless and is accidentally detected on the ECG.

Complications of myocardial infarction

Often complications occur already in the first hours and days of myocardial infarction, weighting its course. Most patients have different kinds of arrhythmia in the first three days: extrasystole, sinus or paroxysmal tachycardia, ciliary arrhythmia, complete intraventricular blockade. The most dangerous is the fibrillation of the ventricles, which can go into fibrillation and lead to the death of the patient.

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

The rupture of muscle fibers in the necrosis zone can cause a cardiac tamponade - a hemorrhage into the pericardial cavity. In 2-3% of patients, myocardial infarction is complicated by thromboembolism of the pulmonary artery system (may cause a pulmonary infarction or sudden death) or a large circulation.

Patients with extensive transmural myocardial infarction in the first 10 days may die from rupture of the ventricle due to acute cessation of circulation. With extensive myocardial infarction, there may be an inconsistency of scar tissue, its swelling with the development of acute heart aneurysm. Acute aneurysm can be transformed into a chronic aneurysm, leading to heart failure.

The deposition of fibrin on the walls of the endocardium leads to the development of parietal thromboendocarditis, a dangerous possibility of embolism of the vessels of the lungs, the brain, and the kidneys with detached thrombotic masses. In a later period, postinfarction syndrome, manifested by pericarditis, pleurisy, arthralgia, eosinophilia, may develop.

Diagnosis of myocardial infarction

Among the diagnostic criteria for myocardial infarction, the most important are the history of the disease, the characteristic changes on the ECG, the enzyme activity indices of serum. Complaints of the patient with 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 severe and prolonged (longer than 30-60 minutes) an attack of chest pains, conduction and heart rhythm disturbances, acute heart failure.

Characteristic changes in the ECG include the formation of a negative T wave (with a small-focal subendocardial or intramural myocardial infarction), a QRS pathological complex, or a Q wave (with large-focal transmural myocardial infarction). With echocardiography, there is a violation of locally contracting the ventricle, thinning its walls.

In the first 4-6 hours after a painful attack in the blood, the increase in myoglobin, the protein that carries oxygen into the cells, is determined. The increase in the activity of creatine phosphokinase (CK) 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. The determination of the level of CK is carried out every 6-8 hours. Myocardial infarction is excluded with three negative results.

To diagnose myocardial infarction at a later date, the enzyme lactate dehydrogenase (LDH) is used, the activity of which increases later CPC - 1-2 days after the formation of necrosis and comes to normal values ​​after 7-14 days. Highly specific for myocardial infarction is an increase in isoforms of myocardial contractile protein troponin-troponin-T and troponin-1, which also increase with unstable angina. In the blood, the increase in ESR, leukocytes, activity of aspartate aminotransferase (AcAt) and alanine aminotransferase (AlAt) is determined.

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

Treatment of myocardial infarction

With myocardial infarction, an emergency hospitalization in cardiac resuscitation is indicated. In an acute period, the patient is prescribed a bed rest and mental rest, a fractional meal, limited in volume and caloric content. In the subacute period, the patient is transferred from the intensive care unit to the cardiology department, where the treatment of myocardial infarction continues and the regime is gradually expanded.

Pain relief is combined with a combination of narcotic analgesics (fentanyl) with neuroleptics (droperidol), intravenous nitroglycerin.

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

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

Prognosis with myocardial infarction

Myocardial infarction is a serious, associated with dangerous complications of the disease. Most of the lethal outcomes develop in the first day after myocardial infarction. Pumping ability of the heart is associated with the localization and volume of the infarction zone. If more than 50% of the myocardium is damaged, the heart can not normally 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.

At the end of the acute period, the prognosis for recovery is good. Unfavorable perspectives in patients with complicated course of myocardial infarction.

Prevention of myocardial infarction

The necessary conditions for the prevention of myocardial infarction are the maintenance of a healthy and active lifestyle, the refusal of alcohol and smoking, a balanced diet, the exclusion of physical and nervous overstrain, control of blood pressure and blood cholesterol.