Myocardial Infarction - Causes, Symptoms, Diagnosis And Treatment

Myocardial infarction is a focus of ischemic necrosis of the heart muscle, developing as a result of acute coronary circulatory disorders. It is clinically manifested by burning, pressing or squeezing pains behind the sternum, giving to the left arm, collarbone, shoulder blade, jaw, shortness of breath, a feeling of fear, cold sweat. A developed myocardial infarction serves as an indication for emergency hospitalization in cardiological intensive care. If timely assistance is not provided, a fatal outcome is possible.

General information

Myocardial infarction is a focus of ischemic necrosis of the heart muscle, developing as a result of acute coronary circulatory disorders. It is clinically manifested by burning, pressing or squeezing pains behind the sternum, giving to the left arm, collarbone, shoulder blade, jaw, shortness of breath, a feeling of fear, cold sweat. A developed myocardial infarction serves as an indication for emergency hospitalization in cardiological intensive care. If timely assistance is not provided, a fatal outcome is possible.

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

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

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

Period 1 - preinfarction (prodromal): increased frequency and intensification of angina attacks, can last several hours, days, weeks;

Period 2 - the most acute: from the development of ischemia to the appearance of myocardial necrosis, lasts from 20 minutes to 2 hours;

Period 3 - acute: from the formation of necrosis to myomalacia (enzymatic melting of necrotized muscle tissue), duration from 2 to 14 days;

Period 4 - subacute: initial processes of scar organization, development of granulation tissue at the site of necrotic, duration 4-8 weeks;

Period 5 - postinfarction: scar maturation, adaptation of the myocardium to new conditions of functioning.

Causes of myocardial infarction

Myocardial infarction is an acute form of coronary heart disease. In 97-98% of cases, the basis for the development of myocardial infarction is atherosclerotic lesion of the coronary arteries, causing narrowing of their lumen. Often, atherosclerosis of the arteries is joined 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. Thrombosis is promoted by the increased blood viscosity observed in patients with coronary artery disease. In some cases, myocardial infarction occurs against the background of spasm of the branches of the coronary arteries.

The development of myocardial infarction is promoted by diabetes mellitus, hypertension, obesity, neuropsychiatric stress, alcohol addiction, smoking. Sudden physical or emotional stress on the background of coronary heart disease and angina can provoke the development of myocardial infarction. Left ventricular myocardial infarction develops more often.

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 transform into a large-focal myocardial infarction (in 30% of patients). Unlike large-focal, small-focal infarcts do not cause aneurysm and rupture of the heart, the course of the latter is less often complicated by heart failure, ventricular fibrillation, thromboembolism.

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

• transmural - with necrosis of the entire thickness of the muscular wall of the heart (more often large-focal)
• intramural - with necrosis in the thickness of the myocardium
• subendocardial - with myocardial necrosis in the area adjacent to the endocardium
• subepicardial - with myocardial necrosis in the area adjacent to the epicardium

According to the changes recorded on the ECG, there are:

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

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

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

According to the frequency of occurrence, myocardial infarction is distinguished:

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

According to the development of complications of myocardial infarction is divided into:

• complicated
• uncomplicated

According to the presence and localization of pain syndrome , forms of myocardial infarction are distinguished:

1 typical - with localization of pain behind the sternum or in the precardial region

2 atypical - with atypical pain manifestations:

• peripheral: left-handed, left-handed, laryngopharyngeal, mandibular, upper-vertebral, gastralgic (abdominal)
• pain-free: collaptoid, asthmatic, edematous, arrhythmic, cerebral
• low-symptomatic (erased)
• combined

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

• stage of ischemia (acute period)
• stage of necrosis (acute period)
• stage of organization (subacute period)
• stage of scarring (postinfarction period)

Symptoms of myocardial infarction

Preinfarction (prodromal) period

About 43% of patients report the sudden development of myocardial infarction, while the majority of patients have a period of unstable progressive angina that varies in duration.

The most acute 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, and the interscapular zone. The nature of the pain can be compressive, bursting, burning, pressing, sharp ("dagger"). The larger the myocardial lesion area, the more pronounced the pain.

The pain attack proceeds in waves (then intensifying, then weakening), lasts from 30 minutes to several hours, and sometimes days, is not stopped by repeated intake of nitroglycerin. Pain is associated with sharp weakness, excitement, fear, shortness of breath.

An atypical course of the acute period of myocardial infarction is possible.

Patients have a sharp pallor of the skin, sticky cold sweat, acrocyanosis, anxiety. Blood pressure during the attack is increased, then moderately or sharply decreases compared to the baseline (systolic < 80 Hg, pulse < 30 mm Hg), tachycardia, arrhythmia is noted.

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

Acute period

In the acute period of myocardial infarction, the pain syndrome usually disappears. The preservation of pain can be caused by a pronounced degree of ischemia of the near-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 in fever depend on the area of necrosis. Arterial hypotension and signs of heart failure persist and increase.

Subacute period

There are no pain sensations, the patient's condition improves, the body temperature normalizes. Symptoms of acute heart failure become less pronounced. Tachycardia and systolic noise 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 atypical places (in the throat, fingers of the left hand, in the area of the left shoulder blade or cervical-thoracic spine, in the epigastrium, in the lower jaw) or pain-free forms, the leading symptoms of which may be cough and severe suffocation, collapse, swelling, arrhythmias, dizziness and confusion.

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

However, usually only the acute period is atypical, the further development of myocardial infarction becomes typical.

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

Complications

Complications often occur already in the first hours and days of a myocardial infarction, aggravating its course. Most patients have different types of arrhythmias in the first three days: extrasystole, sinus or paroxysmal tachycardia, atrial fibrillation, complete intraventricular blockade. The most dangerous is ventricular flicker, which can turn into fibrillation and lead to the death of the patient.

Left ventricular heart failure is characterized by congestive wheezing, phenomena of cardiac asthma, pulmonary edema and often develops in the acute period of myocardial infarction. An extremely severe degree of left ventricular insufficiency is cardiogenic shock, which develops with an extensive heart attack and usually leads to a fatal outcome. Signs of cardiogenic shock include a drop in systolic blood pressure below 80 mm Hg, impaired consciousness, tachycardia, cyanosis, and decreased diuresis.

Rupture of muscle fibers in the necrosis zone 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 (may cause a lung infarction or sudden death) or a large circulatory circle.

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, the failure of scar tissue may occur, its swelling with the development of an acute heart 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, dangerous by the possibility of embolism of the vessels of the lungs, brain, kidneys by detached thrombotic masses. In a later period, postinfarction syndrome may develop, manifested by pericarditis, pleurisy, arthralgia, eosinophilia.

Diagnosis of myocardial infarction

Among the diagnostic criteria of myocardial infarction, the most important are the anamnesis of the disease, characteristic changes on the ECG, indicators of the activity of serum enzymes. The patient's complaints of myocardial infarction depend on the form (typical or atypical) of the disease and the extent of the lesion of the heart muscle. Myocardial infarction should be suspected with a severe and prolonged (longer than 30-60 minutes) attack of chest pains, impaired conduction and heart rhythm, acute heart failure.

Characteristic ECG changes include the formation of a negative T wave (in small-focal subendocardial or intramural myocardial infarction), a pathological QRS complex or Q wave (in large-focal transmural myocardial infarction). Echocardiography reveals a violation of the local contractility of the ventricle, 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 after 8-10 hours from the development of myocardial infarction and decreases to normal after two days. Determination of the level of CPK is carried out every 6-8 hours. Myocardial infarction is excluded with three negative results.

To diagnose myocardial infarction at a later date, they resort to the determination of 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 after 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 with unstable angina. An increase in ESR, leukocytes, aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT) activity is detected in the blood.

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

Treatment of myocardial infarction

In case of myocardial infarction, emergency hospitalization in cardiological intensive care is indicated. In the acute period, the patient is prescribed bed rest and mental rest, fractional, limited in volume and caloric intake. In the subacute period, the patient is transferred from the intensive care unit to the cardiology department, where treatment of myocardial infarction continues and a gradual expansion of the regime is carried out.

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

Therapy for myocardial infarction is aimed at preventing and eliminating arrhythmias, heart failure, cardiogenic shock. Antiarrhythmic agents (lidocaine), beta-blockers (atenolol), thrombolytics (heparin, acetylsalicylic acid), Ca antagonists (verapamil), magnesia, nitrates, antispasmodics, etc. are prescribed.

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

Prognosis for myocardial infarction

Myocardial infarction is a severe disease associated with dangerous complications. Most of the deaths develop in the first day after a myocardial infarction. The pumping capacity of the heart is associated with the localization and volume of the infarction zone. 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 loads, as a result of which heart failure develops.

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

Prevention of myocardial infarction

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