Diagnostics and treatment of postinfarction cardiosclerosis

Definition

Postinfarction cardiosclerosis is the presence of areas of the heart that have died as a result of myocardial infarction and have been replaced by connective tissue. The transformation of the heart muscle begins 3-4 days after the vascular accident and ends by the end of 2-4 months. At an earlier date, the diagnosis is not possible. Mortality from pathology, according to personal observations, is about 20% in the first few hours after an attack and about 30-40% in the long-term period (1-5 years).

The volume and density of scarring foci directly depend on the area of ​​myocardial damage and are a determining factor in the prognosis of the disease.

Etiology

Postinfarction cardiosclerosis has only one reason. This is myocardial infarction - an acute violation of the supply of blood to the heart as a result of obstruction of the coronary arteries.

The following can lead to blockage of blood vessels:

• migratory blood clots (usually from the veins of the lower extremities);
• the imposition of thrombotic masses on ulcerated atherosclerotic plaques;
• functional disorders of the central nervous system, leading to a pronounced spasm of the arteries of the coronary bed;
• anatomical defects of the vascular wall due to the prolonged course of hypertension, diabetes mellitus, etc.

As a result, individual segments of the muscular organ cease to receive oxygen-enriched blood, and after 4-6 hours they begin to die off.

Under the action of enzymes, myocytes are absorbed and replaced by a scar, the existence of which entails many problems in the future:

• rhythm and conduction disturbances;
• decrease in cardiac output and cardiac output;
• cardiomyopathy (hypertrophy or dilatation of the organ chambers).

Cicatricial changes can affect the valves (most often the mitral valve), leading to valve failure. My professional experience shows that in 100% of cases myocardial infarction does not go unnoticed. Complications progress and shorten life expectancy significantly.

The following risk factors significantly increase the incidence of heart attack:

• male gender;
• age over 45;
• arterial hypertension;
• smoking;
• obesity (BMI over 30);
• diabetes;
• low physical activity (WHO recommends walking a distance of 8,000 steps daily);
• alcohol abuse (more than 20 g of pure ethanol per day for women and 40 g for men).

Read more about risk factors here.

In most cases, myocardial infarction develops against the background of a long course of coronary heart disease, although we had to meet in our practice young patients (25-30 years old) with a similar disease, leading an unhealthy lifestyle (overweight, alcohol abuse, drugs and smoking).

Clinical picture

The symptomatology of pathology is extremely diverse. At the initial stages (the first six months), the following can be detected:

1. Conduction disturbances (AV blockade, slowing down of conduction along the Purkinje fibers and His bundles). The phenomena are caused by damage to the conducting system, when nerve fibers are transformed into connective tissue. Manifested by sensations of interruptions in work or prolonged cardiac arrest, periodic fainting and dizziness.
2. Tachyatrhythmias... Atrial fibrillation or ventricular fibrillation is common, in which the frequency of contractions of individual fibers reaches 350-800 per minute. The patient feels an attack of heartbeat, weakness, episodes of loss of consciousness are possible due to impaired tissue oxygenation.

When a scar hardens, it can compress other coronary vessels, provoking or exacerbating the manifestations of coronary artery disease (angina pectoris):

• pain and shortness of breath with minor physical activity;
• general weakness, fatigue.

After 6-12 months, the heart is trying to compensate for its previous functional activity. Hypertrophic changes and dilatation of the organ chambers occur. Such phenomena contribute to the growth of signs of heart failure.

With a predominant lesion of the left half of the heart, pulmonary edema is observed with symptoms such as:

• chest discomfort (tightness, compression);
• shortness of breath (up to 40-60 respiratory movements per minute) at rest or with low physical exertion;
• pallor of the skin;
• acrocyanosis (bluish color of the limbs, nasolabial triangle).

All symptoms are relieved in the "orthopedic" position (sitting on a chair with the legs lowered), making the patient feel better.

Insufficiency of the right sections of the muscular organ is manifested by stagnation of blood in the systemic circulation:

1. Edematous syndrome. Fluid retention can be observed from the lower extremities, liver (enlarged, painful on palpation), less often - body cavities (hydrothorax, hydropericardium, ascites).
2. Dyspnea... It is caused by tissue hypoxia.

In the future, all types of metabolism are significantly disrupted, acidosis and irreversible changes in organs (dystrophy and sclerosis) develop, which is manifested by their insufficiency.

With cardiosclerosis, changes in the heart are irreversible and manifestations of circulatory disorders will steadily increase. I have seen patients who were practically bedridden and could not exist without oxygen support.

Fatal complications

Typical disorders on the part of the body have already been described above, however, a number of pathologies are distinguished that pose a direct threat to life and cause death, including sudden death. These include:

1. Aneurysm... The wall of the organ becomes thinner and stretched, at any time a rupture with cardiac tamponade can occur.
2. Blockade... The impulse is not transmitted to individual parts of the heart, which stop contracting.
3. Atrial fibrillation or extrasystole - inconsistent work of different departments of the organ. With a severe course of fibrillation and failure to provide emergency care, the complication can be fatal.
4. Acute heart failure - the final stage of chronic, when the organ is no longer able to provide adequate blood flow. The cause of death is ischemia.

Diagnostics

All patients who have had myocardial infarction require dispensary observation, within the framework of which the following types of laboratory and instrumental studies are carried out:

1. General blood analysis (identification of possible changes: leukocytosis, increased ESR).
2. Electrocardiogram... The ECG shows all conduction pathologies, episodes of overload against the background of postinfarction cardiosclerosis, hypertrophic changes.
3. Echo-KG Is a key way of recognizing a deviation, which allows visualizing the volume of involved muscle tissue, the degree of loss of functional activity, and concomitant disorders of the valve apparatus.
4. Plain chest x-ray... The parts of the heart are usually enlarged, the cardiothoracic index exceeds 50%.
5. Coronography... The method allows assessing the diameter of the lumen of the coronary arteries and, if necessary, referring patients to surgical treatment.
6. INR... The study is important for the appointment of anticoagulant and antiplatelet therapy, which is a key step in secondary prevention.

If there are signs of heart failure (they are in 80% of cases), a thorough assessment of the biochemical blood test is shown.

Indicators such as:

1. Lipid profile (total cholesterol, HDL, LDL, TAG, atherogenic index). The values ​​characterize the risk of recurrent myocardial infarction.
2. Liver necrosis markers. Against the background of congestive right ventricular failure, the level of ALT and AST, bilirubin (direct and indirect) often increases, which indicate the death of hepatocytes.
3. Renal complex (urea, creatinine, electrolytes). Rise signals CKD.

In the presence of signs of damage to various organs, enhanced diagnostics are carried out, as well as algorithms for subsequent compensation of conditions are developed.

Treatment

It should be understood that cardiosclerosis is an irreversible pathology and all therapy is aimed exclusively at slowing the progression of heart failure and correcting rhythm disturbances. Often, patients do not realize this and quickly return to their usual incorrect lifestyle, not realizing that they will soon find themselves on the border with death. Judging by the experience of working in the admission department, such persons are encountered quite often (approximately every 5th). Why is this happening? It remains a mystery to me.

Non-drug

Treatment of a pathology such as postinfarction cardiosclerosis involves a complete change in lifestyle. All patients are recommended to exercise feasible (remedial gymnastics, aerobic exercise, walks in parks, etc.). It is advisable to train daily.

The second condition is giving up bad habits (drinking and smoking) and correcting the diet. Fatty, spicy, fried foods are completely excluded, table salt is limited to 2 g / day. The basis of the diet is fresh vegetables and fruits, seafood (fish, squid, shrimp), vegetable oils, whole grain bakery products.

Drug therapy

Treatment of postinfarction cardiosclerosis in the presence or progression of signs of myocardial ischemia involves the appointment of nitrates. Their use is justified, both on an ongoing basis and during seizures. Recommended long-acting nitro-drugs ("Nitrolong", "Isosorbidadinitrate") and symptomatic (with pain in the chest). For the relief of a seizure, "Nitrospray" and the usual "Nitroglycerin" are shown.

The presence of arterial hypertension is an indication for antihypertensive therapy, which includes at least 2 groups of drugs from the main ones:

1. ACE inhibitors and AAF ("Enalapril", "Valsartan", "Captopril"). They act at the level of the renin-angiotensin-aldosterone system, quickly and permanently reduce blood pressure, and prevent myocardial remodeling.
2. Diuretics - reduce pressure by removing fluid from the body, are indicated for edema. Usually used thiazide ("Indapamide") and loop ("Furosemide", "Torasemide").
3. Beta blockers ("Bisoprolol", "Atenolol", "Metoprolol", "Nebivalol", "Carvedilol") - reduce the total peripheral resistance of the vascular bed, decrease heart rate and weaken the force of contractions of the heart muscle, contributing to relaxation and rest of the myocardium. They are a means of preventing tachyarrhythmias.
4. Calcium antagonists - relax the muscular wall of the arteries, have a mild diuretic effect. Most often, dihydroperidine drugs are prescribed ("Nifedepine", "Corinfar", "Lacidipine").

To reduce the severity of oxygen starvation and increase the functionality of organs, antihypoxants are used. The only remedy with a proven effect is Preductal. As early as 3-5 days, my patients notice an improvement in thought and associative processes, activation of memory, and an increase in mood. In neurology, Mexidol has proven itself well.

Atherosclerosis occurring in the postinfarction period should be the reason for the appointment of statins ("Rosuvastatin"). Less commonly used fibrates and blockers of absorption of cholesterol in the intestine ("Ezetrol").

With severe heart failure, glycosides are used. Medicines of this pharmacological group increase the activity of myocytes, slightly reduce the frequency of contractions.

Glycosides make the heart work at the expense of its own condition. For a while, heart failure stabilizes, and then the myocardium is completely depleted, circulatory disorders increase and death from cardiogenic shock may occur. Consequently, such medicines are used in exceptional cases, or in extremely small doses.

All patients undergo prophylaxis of thromboembolic complications. Anticoagulants are used ("Heparin", "Ksarelto").

Surgical correction

In severe rhythm disturbances, when the hollow muscular organ is not able to cope with the load on its own, an electrostimulator or cardioverter is installed. They are activated in case of extrasystole, cardiac arrest, tachyarrhythmias and quickly normalize myocardial function.

The formation of an aneurysm is an indication for resection of a thinned area. The operation requires wide access and lengthy manipulations. Not usually done in the elderly.