Myocardial infarction (MI ) is a focal necrosis (necrosis) of the heart muscle (myocardium), caused by a more or less prolonged cessation of blood access to the myocardium. The basis of this process is impaired patency of one of the coronary (coronary) arteries of the heart affected by atherosclerosis, which leads to coronary heart failure . Atherosclerosis is a long process that gradually leads to vasoconstriction and a slowdown in blood flow. A heart attack is the most severe manifestation of coronary heart disease. Violation of patency of the coronary arteries can occur as a result of blockage of the artery with a rhombus or because of its sharp narrowing – spasm. Most often, both of these factors are simultaneously involved in the origin of myocardial infarction. The prolonged and severe spasm of the coronary artery resulting from nervous influences (overfatigue, excitement, mental trauma, etc. ), slows down the blood flow in it and forms a blood clot as a result. The mechanism of occurrence of a heart attack is very important for clotting process: an increase in the blood prothrombin and other substances povyshayushih blood clotting, which creates conditions for the formation of a blood clot in an artery. In myocardial infarction, in favorable cases, after the melting of the dead tissue, it is resorbed and replaced with young connective tissue (scarring). A durable scar forms within 1.5 to 6 months. Less often, in an unfavorable, severe course of a heart attack, when the heart muscle has died to a great depth, it will sharply thin out, and under the influence of intracardiac pressure, a section of the heart muscle, an aneurysm of the heart, will bulge in this place. There may be a gap at this point, which can lead to immediate death, but this happens quite rarely.
Causes of a heart attack.
- Thrombosis, thromboembolism + atherosclerosis.
- Atherosclerosis + neuropsychic stress, physical activity.
As a result of stress, catecholamines are released, which strengthen and speed up heart contractions, causing vasoconstriction, resulting in chronic hypoxia of tissues and organs.
- Alcohol abuse.
A heart attack often occurs in men aged 40-60 years, and sometimes in younger ones. People with a sedentary lifestyle, prone to atherosclerosis , hypertension , obesity, diabetes and other metabolic disorders, are more likely to get sick . About half of cases of myocardial infarction occur against the background of angina pectoris, and vice versa – in many patients, angina pectoris occurs after a heart attack. Angina pectoris and myocardial infarction are different manifestations of the same disease process.
Types of myocardial infarction.
Heart attacks most often develop in the anterior wall of the left ventricle, the posterior wall of the left ventricle, the interventricular septum, and the lateral wall of the left ventricle. Right ventricular infarction is very rare.
By localized necrosis : 1. Myocardial infarction left ventricular (front, side, bottom, rear) 2. Isolated myocardial infarction cardiac apex, 3. Myocardial infarction ventricular septal 4. Myocardial infarction right zheludochoka , 5. Co-localization: postero – anterior, anterolateral, inferolateral, etc. The width of the lesion is determined by ECG: 1. Large-focal (extensive) myocardial infarction (Q-infarction), 2. Small-focal myocardial infarction. In depth (depending on which layer of the heart is covered): 1. Subendocardial, 2. Subepicardial , 3. Intramural 4. Transmural (covers all layers of the heart). With the course: 1. Monocyclic myocardial infarction 2. Long-term myocardial infarction 3. Recurrent myocardial infarction (a new focus of necrosis develops within 3-7 days) 4. Repeated myocardial infarction (a new focus develops after 1 month)
Electrically silent zones on an ECG are a heart attack. On an ECG, transmural infarction, anterior wall infarction is better diagnosed . It is difficult to determine the infarction from the ECG, which is combined with arrhythmia, paroxysmal tachycardia, blockade and ECG-negative forms. By ECG, a heart attack is determined in 80% of cases.
Stages of development of a heart attack.
- The period of the precursors, prodromal (from several hours to several days). It manifests itself as short-term pain in the region of the heart or behind the sternum. During this period, the blood supply to the heart decreases.
- Acute period , pain attack (from a few hours to 1 day).
- The acute period, febrile (8-10 days). In the 2nd and 3rd periods, necrosis and softening of the affected area of the myocardium occur.
- Subacute period (from 10 days to 4-8 weeks). The recovery period begins.
- Scarring period (from 1.5-2 months to 6 months ).
The clinic includes 2 syndromes: 1. Pain syndrome (conditionally) 2. Resorption necrotic syndrome (conditionally).
- Pain syndrome is a clinical manifestation of a developing focus of necrosis. (1st stage of necrosis).
This is pain in the region of the heart, burning, pressing, radiating wider than with angina pectoris in the left hand, right, jaw. There is no position to soothe pain. The pain is increasing, the patient pale appearance of sticky cold sweat, the color of skin covers gray-pale, then waxy may be puffy face, arrhythmia. Systolic pressure drops, diastolic pressure remains at the same level or rises. A decrease in the distance of blood pressure between systolic and diastolic is a sign of a heart attack. The pulse is weak, threadlike. The tones are deaf.
- Atypical pain cm.
1st group — Gastralgic pain , heartburn, weakness, vomiting 5-10 minutes after eating, as a rule, accompanied by impaired stool, bloating. 2nd group — Painless syndrome, as an attack of cardiac asthma ( status astmaticus ), suffocation, bubbling breathing. But it is impossible to enter aminophylline in case of a heart attack, acute left ventricular failure . Arrhythmic form – until the arrhythmia is stopped, the patient must be treated like a heart attack. Transient brain disorders.
- Asymptomatic form – no complaints .
Resection necrotic syndrome is a clinical manifestation of an already developed focus of necrosis that has developed in the focus of aseptic inflammation. (2nd stage of a heart attack).
- Resection- necrotic syndrome – this is already towards the end of the first day and by the beginning of the second the temperature rises to 37.5-38.5 C. The temperature should normalize within 7 days. But if it lasts more than 7 days , then complications have appeared .
By the end of the first day , leukocytosis appears – 10-12000 (moderately neutrophilic ), stess – up to 20,000 leukocytes. The urine protein appears, the urine is colored red ( myoglobinuria , myoglobin in). Myoglobin comes out with muscle injuries , in a large amount it can clog renal filters and lead to kidney failure. Acceleration of ESR occurs at the end of the first day. And after 3-4 weeks it normalizes.
By the end of the first day, fibrinogen A rises . Pathological fibrinogen B appears in the blood (up to ++++). Fibrinogen B should normalize for 3-4 days. Fibrinogen B increases if fibrinolytic substances are administered to the patient . C-reactive protein appears in the acute stage of inflammation. An increase in intracellular transaminases in heart attack was described by Vrublevsky. Transaminases are catalytic enzymes in cells. Cells age, collapse, transaminases enter the bloodstream. When many cells die, transaminases in large quantities are washed off by the blood, the myocardium works more actively – metabolic hypertrophy. With a heart attack , the number of transaminases ALAT, ACAT, creatine phosphatase , creatine phosphogenase , lactate dehydrogenase increases . Enlarged enzymes are a good diagnostic method , but only in the acute phase. Echocardiogram – determines the foci at any stage, but does not determine the time of development of a heart attack.