Division according to the anatomy of the lesion. What is a major myocardial infarction?

3. 1. Large focal (transmural). Q infarction.

3. 2. Finely focal. Not Q heart attack.

4. Post-infarction cardiosclerosis.

The diagnosis is made no earlier than 2 months after the onset of myocardial infarction. The diagnosis indicates the presence of a chronic cardiac aneurysm, internal myocardial ruptures, dysfunction of the papillary muscles of the heart, intracardiac thrombosis, the nature of conduction disorders and heart rate, form and stages of heart failure. If the ECG shows no signs of a previous myocardial infarction, the diagnosis can be made according to typical ECG changes or enzyme changes in history (based on medical documentation).

5. Heart rhythm disturbances (indicating the form).

Typically, conduction and heart rhythm disturbances complicate other forms of coronary artery disease, but sometimes they can be the only manifestation of the disease. In these cases, the diagnosis of IHD requires clarification using functional stress tests and selective coronary angiography.

6. Heart failure.

Heart failure can complicate any form of coronary artery disease. If patients with heart failure do not have clinical or electrocardiographic evidence of CAD (current or history), the diagnosis of CAD becomes questionable.

Note: in case of successful resuscitation of a patient with coronary artery disease, it is better to use the term “SCA - sudden (primary) circulatory arrest,” and in case of “biological” death, you can use the term “sudden coronary death”

Functional severity classes of stable angina pectoris according to the Canadian Heart Association classification

I fk. – Normal daily physical activity (walking or climbing stairs) does not cause angina attacks. An attack of angina occurs when performing very fast or prolonged physical work.

II fk. – Slight limitation of usual physical activity – the occurrence of angina as a result of fast walking or quickly climbing stairs, after eating, in the cold in windy weather, under the influence of emotional stress, in the first few hours after getting out of bed, while walking more than 200 meters (two blocks) on level ground or while climbing more than one flight of stairs at a normal pace under normal conditions.

III fk. – Marked limitation of usual physical activity – an attack of angina occurs as a result of walking one to two blocks (100-200 m) on level ground or when climbing one flight of stairs at a normal pace under normal conditions.

IV fk. – Inability to perform any type of physical work without discomfort – an attack of angina can occur at rest

CLASSIFICATION OF UNSTABLE ANGINA (National Guidelines for Cardiology, 2007)

Clinical forms of unstable angina

-New-onset angina– the occurrence of angina attacks during the last two months

- Progressive angina– an increase in the frequency and/or duration of anginal attacks, a decrease in exercise tolerance, the appearance of attacks at rest, as well as a decrease in the effectiveness of antianginal drugs.

-Angina at rest– attacks at rest lasting more than 20 minutes for 2 months.

Classification of unstable angina(S. W. Hamm, E. Braunwald, 2000)

CLASSIFICATION OF ACUTE CORONARY SYNDROME (National Guidelines on Cardiology, 2007)

Acute coronary syndrome- acute phase of ischemic heart disease. Acute coronary syndrome is a temporary “working” diagnosis, which is necessary for initial assessment, risk stratification, and choice of treatment tactics in patients with exacerbation of coronary artery disease. From the point of view of the peculiarities of the development of the process, the possibility of rapid diagnosis, and the development of treatment tactics, acute coronary syndrome is conveniently divided into 2 groups depending on changes in the initial ECG:

Acute coronary syndrome with segment elevation ST;

ST.

In acute coronary syndrome with ST segment elevation, in most cases, large focal MI subsequently develops. In patients with acute coronary syndrome without segment elevation ST Usually the diagnosis is unstable angina or small focal MI. With the widespread introduction into clinical practice of the determination of cardiac troponins (markers of myocardial damage) in patients with acute coronary syndrome, the division of acute coronary syndrome without segment elevation ST for unstable angina and small focal MI has become widespread.

Acute coronary syndrome without segment elevation ST

DEFINITIONS

Acute coronary syndrome without segment elevation ST characterized by anginal attacks and the absence of segment elevation on the ECG ST. To acute coronary syndrome without segment elevation ST include unstable angina and non-elevation myocardial infarction ST.

Unstable angina is a worsening of the course of angina, expressed in an increase in the frequency and duration of attacks, a decrease in exercise tolerance, and a decrease in the effectiveness of antianginal therapy.

Unstable angina includes any variants of new-onset angina (last 2 months), worsening of existing angina (transition from class I-II to class III or IV), and the appearance of angina attacks at night. The severity and duration of an attack with unstable angina are insufficient for the development of myocardial necrosis. Usually there are no elevations on the ECG ST. There is no release of biomarkers of myocardial necrosis into the bloodstream in quantities sufficient to diagnose MI.

Myocardial infarction without segment elevation ST- acute myocardial ischemia, leading to necrotic damage. There are no segment elevations on the initial ECG ST. In the majority of patients whose disease begins as non-elevation myocardial infarction ST, Q_waves do not appear and, as a result, small focal MI without Q waves is diagnosed. MI without ST segment elevation differs from unstable angina by the appearance or increase in the levels of markers of myocardial necrosis, which are absent in unstable angina.

CLASSIFICATION OF MYOCARDIAL INFARCTION (National Guidelines for Cardiology, 2007)

Initial changes on the ECG:

MI with ST segment elevation (this group also includes acute blockade of the left His bundle branch);

Non-ST segment elevation MI

Subsequent changes on the ECG:

MI with the formation of pathological Q waves (usually MI with ST segment elevation corresponds to developing large-focal MI with the subsequent formation of pathological Q waves);

MI without the formation of pathological Q waves.

Dimensions of the necrosis focus:

large-focal (transmural) MI;

small focal MI.

Localization of the necrosis focus:

MI of the anterior wall of the left ventricle (anterior MI)

MI of the lateral wall of the left ventricle (lateral MI)

isolated apex myocardial infarction

MI of the inferior wall of the left ventricle (inferior MI)

THEM back wall left ventricle

MI of the interventricular septum

Right ventricular MI

Atrial MI

Combined localizations are possible: posteroinferior, anterolateral, etc.

History of MI:

primary MI;

recurrent MI;

recurrent MI.

MI period:

the most acute period: from the onset of a painful attack until the formation of a focus of necrosis (the first 4-6 hours);

acute period: final formation of a necrosis focus (up to 2 weeks);

subacute period: scar formation (up to 2 months)

post-infarction period: complete scarring and scar consolidation (after 2 months)

CLASSIFICATION OF CLINICAL FORMS AND COURSE OF MYOCARDIAL INFARCTION ACCORDING TO THEODORI M.I. WITH ADDENDUMS

“Classic” (retrosternal pain)

With a typical onset in the form of an acute, prolonged painful attack and a cyclic course with clearly defined three periods: acute, subacute and functional-restorative

Erased (reduced) forms

With typical, but mildly expressed symptoms or only with individual symptoms characteristic of myocardial infarction.

Atypical forms:

a) peripheral

With the occurrence or primary localization of pain not in the heart area, but on the periphery: left-scapular, left-hand, upper vertebral, mandibular and ear, laryngeal-pharyngeal.

b) abdominal

With a picture of an acute abdominal catastrophe: perforated gastric ulcer, gastric bleeding, intestinal obstruction.

c) painless

“Asthmatic” - with cardiac asthma syndrome, sometimes with the development of pulmonary edema. With acute development of heart failure (right ventricular or biventricular).

"Collaptoid"

“Arrhythmic” with a picture of severe disturbances in heart rhythm and conduction (in the presence of complete atrioventricular block - often with Morgagni-Adams-Stokes syndrome).

“Asymptomatic” - without pronounced clinical manifestations, detected only by electrocardiographic examination.

d) cerebral

With a picture acute disorder cerebral circulation:

fainting form;

the onset of clinical myocardial infarction masked by a hypertensive crisis;

hemiplegic form

e) combined

When combined, for example, pulmonary edema and cardiogenic shock;

retrosternal pain form and acute cerebrovascular accident, etc.

By localization

Anterior, anterolateral, anteroseptal, posterior, posterolateral, posteroseptal, septal, anteroposterior, involving the papillary muscles, involving the atria (if there are clinical data for damage to the papillary muscles or electrocardiographic data for damage to the atria) .

According to the depth of the lesion Transmural, subepicardial, subendocardial, intramural

By prevalence Widespread (extensive), limited.

According to the number of myocardial infarctions suffered Primary, repeated (indicating, if possible, which one).

Note: repeated (as opposed to recurrent) myocardial infarction should be understood as one that developed at different times after the previous one, but always after completion of the repair processes from the previous lesion

Flow:

a) typical

With pronounced periods - acute, subacute and functional-restorative, the terms of which do not deviate from the usual ones.

b) recurrent

With repeated infarctions of the heart muscle, occurring at different periods of the disease, but always before the completion of the repair processes from the previous infarction.

c) protracted

With a slow pace of development of reparative processes and prolongation of certain periods of the disease.

d) latent (subclinical)

Without any pronounced clinical symptoms, but with typical electrocardiographic dynamics.

According to the presence of complications:

a) uncomplicated

b) complicated

Acute vascular insufficiency - cardiogenic shock-collapse (true cardiogenic collapse; reflex-type collapse; arrhythmic-type collapse; collapse due to rupture of the heart muscle).

Acute heart failure (left ventricular, right ventricular, biventricular).

Rhythm and conduction disturbances (extrasystole, paroxysmal tachycardia, atrial fibrillation and flutter, blockades (intraventricular and atrioventricular), ventricular fibrillation.

Diffuse fibrinous or effusion pericarditis. Acute cardiac aneurysm. Heartbreak. Rupture of the interventricular septum. Avulsion of the papillary muscle. Acute dilatation of the stomach. Intestinal paresis. Gastric bleeding (due to acute ulcer or erosive gastritis).

Acute diabetic syndrome with hyperosmotic or acidotic coma.

Acute renal failure. Thromboendocarditis (usually parietal, aseptic or septic).

Thromboembolic complications:

a) early (from loose parietal thrombi in the ventricles of the heart);

b) late (venous thrombosis with pulmonary embolism, thromboembolism in the arterial system).

Post-infarction syndrome.

Myocardial abscess (purulent melting of a necrotic focus with the development purulent pericarditis or rupture of an abscess into the pericardium and hemotamponade).

Chronic cardiac aneurysm.

Progressive chronic heart failure.

Examples of diagnosis formulation

IHD. New onset angina pectoris. CHF 0 st -FC 0

IHD. Stable angina pectoris functional class III. CHF I stage – FC I

IHD. Stable angina pectoris IIfk, post-infarction (large focal) cardiosclerosis (AMI in 1991) CHF IIa. –FC III

IHD. Spontaneous angina. CHF I stage - FC II.

IHD. Unstable angina IV. HSNIst.-FKI.

IHD. Unstable angina IIС. HSNIst. – FKI.

IHD. transmural myocardial infarction of the anteroseptal region with transition to the apex, the most acute period. Ventricular extrasystole, class II according to Lown, OSNIIIst. by Killip.

IHD. Paroxysm of atrial fibrillation, tachysystolic form, cholesterol level H 1 - FC I.

IHD. Complete atrioventricular block. Adams-Stokes-Morgagni attacks, II degree of severity, CHF IIb - FC III

Classification of hyperlipoproteinemia

CLASSIFICATION OF ARTERIAL HYPERTENSION (HYPERTENSION) (Russian recommendations, 2008)

Classification of blood pressure levels

Threshold blood pressure levels (mmHg) for diagnosing arterial hypertension according to various measurement methods

In addition, classification according to the stages of the disease is used

Stage I hypertension - absence of target organ damage.

Stage II hypertension - the presence of changes in one or more target organs.

Hypertonic disease Stage III- presence of associated clinical conditions.

Of great importance is the assessment of overall cardiovascular risk, the degree of which depends on concomitant risk factors, target organ damage and associated clinical conditions.

Risk stratification criteria

Risk factors

▪ pulse blood pressure value (in the elderly)

men over 55 years old;

women over 65 years of age;

• dyslipidemia (total cholesterol >5.0 mmol/l (>190 mg/dl) or LDL cholesterol >3.0 mmol/l (>115 mg/dl) or HDL cholesterol<1,0 ммоль/л (40 мг/дл) для мужчин и <1,2 ммоль/л (46 мг/дл) для женщин; или ТГ >1.7 mmol/l(150 mg/dl)

  fasting plasma glucose 5.6 – 6.9 mmol/l (102-125 mg/dl)

  Impaired glucose tolerance

  family history of early cardiovascular disease (women under 65 years of age, men under 55 years of age);

  abdominal obesity (waist circumference > 102 cm for men or > 88 cm for women) in the absence of metabolic syndrome;

Target organ damage

LV hypertrophy:

ECG: Sokolov-Lyon sign >38 mm; Cornell product >2440 mm-ms;

EchoCG: LV myocardial mass index >125 g/m2 for men and >110 g/m2 for women.

Vessels

▪Ultrasound signs of atherosclerotic plaques or thickening of the artery wall(thickness of the intima-media layer carotid artery>0.9 mm) or atherosclerotic plaques of the great vessels.

▪pulse wave speed from the carotid to the femoral artery > 12 m/s

▪ ankle/brachial index< 0,9

Kidneys

▪ Small increase in serum creatinine 115-133 µmol/L (1.3-1.5 mg/dL) for men or 107-124 µmol/L (1.2-1.4 mg/dL) for women.

▪ Low GFR< 60 мл/ мин/1,73 м2 (MDRD формула) или низкий клиренс креатинина < 60 мл/ мин (формула Кокрофта-Гаулта)

▪ Microalbuminuria: 30-300 mg/day;

▪ urine albumin/creatinine ratio ≥22 mg/g (2.5 mg/mmol) for men and ≥31 mg/g (3.5 mg/mmol) for women.

Associated (related) clinical conditions

Cerebrovascular diseases:

ischemic stroke;

hemorrhagic stroke;

transient ischemic attack.

Heart diseases:

myocardial infarction;

angina pectoris;

coronary revascularization;

chronic heart failure.

Kidney diseases:

diabetic nephropathy;

renal failure (serum creatinine >133 µmol/L (>1.5 mg/dL) for men or >124 µmol/L (>1.4 mg/dL) for women);

proteinuria (>300 mg/day).

Peripheral arterial diseases:

dissecting aortic aneurysm;

symptomatic damage to peripheral arteries.

Hypertensive retinopathy (hemorrhages or exudates, papilledema).

Diabetes : fasting plasma glucose ≥7 mmol/L (126 mg/dL) with repeated measurements;

blood plasma glucose after a meal or 2 hours after taking 75 g of glucose ≥11 mmol/l (198 mg/dl).

Metabolic syndrome

The main criterion is AO (OT > 94 cm for men and > 80 cm for women)

Additional criteria: blood pressure≥ 140 and 90 mmHg.

LDL cholesterol > 3.0 mmol/l, HDL cholesterol< 1,0 ммоль/л для мужчин или < 1,2 ммоль/л для женщин, ТГ >1.7 mmol/l, fasting hyperglycemia≥ 6.1 mmolk, IGT – plasma glucose 2 hours after taking 75 g of glucose≥ 7.8 and≤ 11.1 mmol/l

▪ The combination of the main and 2 of the additional criteria indicates the presence of MS

Depending on the degree of increase in blood pressure, the presence of risk factors, target organ damage and associated clinical conditions, all patients with hypertension can be classified into one of four risk groups:

Low risk;

Moderate level of risk;

High level of risk;

Very high level of risk.

The European SCORE system evaluates the risk of death from diseases associated with atherosclerosis within 10 years in patients who do not have proven coronary heart disease: low risk corresponds to a value of less than 5%; moderate - 5-9%; high - 10-14% and very high - more than 15%.

Risk stratification in patients with hypertension*

Note* the accuracy of determining the overall cardiovascular risk directly depends on how completely the clinical, instrumental and biochemical examination of the patient is carried out. Without cardiac and vascular ultrasound data to diagnose LVH and carotid artery wall thickening (or plaque), up to 50% of hypertensive patients may be erroneously classified as low or moderate risk instead of high or very high; ** add. – additional risk.

High and very high risk patients

SBP ≥ 180 mmHg. and/or DBP ≥110 mmHg

SBP > 160 mmHg with low DBP (<70 мм.рт.ст.)

Diabetes

Metabolic syndrome

≥3 risk factors

Target organ damage

LVH according to ECG or EchoCG

Ultrasound signs of carotid artery wall thickening (IMT >0.9) mm or atherosclerotic plaques

Increased arterial wall stiffness

Moderate increase in serum creatinine

Decreased GFR or creatinine clearance

Microalbuminuria or proteinuria

Associated clinical conditions.

Formulation of diagnosis

When formulating a diagnosis, the presence of risk factors, target organ damage, associated clinical conditions, and cardiovascular risk should be reflected as fully as possible. The degree of increase in blood pressure is necessarily indicated in patients with newly diagnosed arterial hypertension; in other patients, the achieved degree of arterial hypertension is written. It is also necessary to indicate the stage of the disease.

Examples of diagnostic reports

Stage I hypertension. Degree of hypertension 2. Dyslipidemia. Risk 2 (medium)

Stage II hypertension. Degree of hypertension 3. Dyslipidemia. LVH. Risk 4 (very high).

Stage III hypertension. Degree AG2.. IHD. Angina pectoris II FC. Risk 4 (very high).

Stage III hypertension. Achieved degree of hypertension 1. Obliterating vascular atherosclerosis lower limbs. Intermittent claudication. Risk 4 (very high).

Stage I hypertension. Degree of hypertension 1. Diabetes mellitus type 2. Risk 3 (high).

IHD. Post-infarction (large focal) cardiosclerosis. Stage III hypertension. The achieved degree of hypertension is 1. Risk 4 (very high).

Obesity I degree. Impaired glucose tolerance. Stage 3 hypertension.. Risk 4 (very high).

Pheochromocytoma of the right adrenal gland. AH 3 degrees. LVH. Risk 4 (very high)...

CLASSIFICATION OF HYPERTENSIVE CRISES

International recommendations suggest clinical classification, based on the severity of clinical symptoms and the risk of developing severe (even fatal) life-threatening complications. These conditions are divided into complicated (emergency) and uncomplicated GC (urgency).

A complicated hypertensive crisis (critical, emergency, life-threatening, emergency) is accompanied by the development of acute clinically significant and potentially fatal damage to target organs, which requires emergency hospitalization (usually in a block). intensive care) and immediate reduction of blood pressure using parenteral antihypertensive drugs.

An uncomplicated hypertensive crisis (non-critical, urgent, urgency) occurs with minimal subjective and objective symptoms against the background of a significant increase in blood pressure. It is not accompanied by acute development of target organ damage. Requires a decrease in blood pressure within several hours. Does not require emergency hospitalization.

Classification of hypertensive crises (Russian recommendations, 2008)

Classification of arterial hypertension according to etiology (National Guidelines for Cardiology, 2007).

Symptomatic renal hypertension

♦ Hypertension in chronic kidney diseases:

chronic glomerulonephritis, chronic pyelonephritis, diabetic nephropathy (glomerulosclerosis), chronic urate tubulointerstitial nephritis, analgesic nephropathy, polycystic kidney disease, kidney damage due to systemic vasculitis, renal amyloidosis, renal tuberculosis, kidney tumors and injuries, nephropathy of pregnancy (primary and secondary), congenital anomalies number/location, shape of the kidneys (hypoplasia, duplication, dystopia of the kidneys, hydronephrosis, horseshoe kidney)

● Vasorenal hypertension: atherosclerosis, fibromuscular dysplasia, nonspecific aortoarteritis, hematomas and tumors compressing the renal arteries, congenital pathology (atresia and hypoplasia of the renal arteries, angiomas and arteriovenous fistulas, aneurysms).

Endocrine hypertension:

♦ hypersecretion of mineralcorticoids (primary and idiopathic aldosteronism, familial form of hyperaldosteronism type I);

♦ hypersecretion of glucocorticoids (Itsenko-Cushing syndrome);

♦ damage to the adrenal medulla: hypersecretion of catecholamines (pheochromocytoma);

♦ dysfunction thyroid gland: hyperthyroidism, hypothyroidism; hyperparathyroidism;

♦ damage to the pituitary gland: Itsenko-Cushing’s disease; acromegaly.

● Hypertension caused by damage to large arterial vessels: atherosclerosis of the aorta; coarctation of the aorta; stenosing lesions of the aorta and brachiocephalic arteries in nonspecific aortoarteritis.

Centrogenic hypertension:

♦ with organic lesions of the central nervous system;

♦ with increased intracranial pressure (tumors, injuries, encephalitis, poliomyelitis, focal ischemic lesions), with the syndrome sleep apnea, lead intoxication, acute porphyria.

● Medicines and exogenous substances that can cause hypertension: hormonal contraceptives, corticosteroids, sympathomimetics, mineralcorticoids, cocaine, foods containing tyramine or monoamine oxidase inhibitors, NSAIDs, cyclosporine, erythropoietin.

Examples of diagnosis formulation

Atherosclerosis of the right renal artery. Vasorenal hypertension, stage III hypertension. LVH.Risk 4 (very high).

Atherosclerosis of the left carotid artery, stage II hypertension. LVH. Risk 3 (high).

Chronic pyelonephritis, phase of latent inflammation. AH II degree. LVH. Risk 3 (high). CKD stage 2 – CRF 1 st.

CLASSIFICATION CARDIOGENIC SHOKA (CHAZOV E.I. 1971.

Reflex shock is caused mainly by reflex disorders due to changes in vascular tone, which lead to shifts in the adequate regulation of general and regional blood circulation.

True cardiogenic shock - in its development main role plays a sharp drop in the propulsive function of the left ventricle, which leads to a significant decrease in cardiac output and a decrease in blood pressure.

Arrhythmic shock develops in connection with the occurrence of rhythm disturbances, predominantly ventricular paroxysmal tachycardia or complete transverse block.

Areactive shock can be diagnosed if, within 15-20 minutes, the administration of increasing doses of norepinephrine or hypertensin does not cause an increase in blood pressure.

CLASSIFICATION OF DEGREES OF SEVERITY OF CARDIOGENIC SHOCK, V. N. Vinogradov, V. G. Popov, A. S. Smetnev, 1961.

I degree : 3-5 hours, blood pressure within 90 and 50 mm Hg. Art. - 60 and 40 mm Hg. Art., pulse pressure 40-25 mm Hg. Art. Symptoms of heart failure are mild. Rapid sustained pressor reaction (30-60 minutes after a set of measures). Mortality 6.9%.

II degree : duration from 5 to 10 hours, blood pressure within 80 and 50 mm Hg. Art. - 40 and 20 mm Hg. Art., pulse pressure 30-15 mm Hg. Art. Peripheral signs of shock are expressed, in most cases - symptoms of acute heart failure (shortness of breath at rest, acrocyanosis, congestive wheezing in the lungs). The pressor response to treatment is slow and unstable.

III degree : extremely severe and prolonged course against the background of steadily progressing peripheral signs and sharp fall blood pressure, pulse pressure below 15 mm Hg. Art. Acute heart failure, 70% have alveolar pulmonary edema. There is no pressor response to adrenomimetics or this reaction is unstable and short-term. Mortality - 91%.

CLASSIFICATION OF FUNCTIONAL DISEASES OF THE CARDIOVASCULAR SYSTEM according to N. N. Savitsky, 1952

Some people who have had a heart attack die immediately or almost immediately, others suffer three, four, or even five heart attacks. Why does this happen and how do people live after a heart attack? Let's talk about this on the pages of our website.

Why do people have multiple heart attacks?

And, perhaps, luck. More strong body A person who leads a predominantly healthy lifestyle can survive several heart attacks. While a person with poor health, a weakened psyche, weak nerves and a diseased cardiovascular system may not be able to withstand even one heart attack.

The more you eat, the more likely you are to have another heart attack. concomitant diseases and predisposing conditions. , hereditary predisposition, unhealthy diet, overweight body, as well as psycho-emotional and physical overload - all this affects the condition of the diseased core. And there is no point in hoping that he might be lucky and be able to suffer three more heart attacks - the risk is very high. Moreover, men are more vulnerable to repeated heart attacks than women.

How should a person who has had a heart attack behave?

A patient who has had a myocardial infarction is at risk, so he must adhere to some unshakable rules if he does not want to have another heart attack.

First of all, you should give up bad habits, quitting smoking is a categorical requirement. A heart attack patient who persistently continues to smoke may consider himself suicidal. The fact is that the fat content in a smoker’s blood is much higher than in the blood of a non-smoker, and this is a direct threat to atherosclerosis. When smoking, the clotting time accelerates, which leads to the formation of blood clots and to another attack.

The second most important risk factor is obesity. There is only one recommendation here, long known to everyone - eat less and move more. Concerning physical activity, then no matter how hard it is for a heart attack patient, he needs to move as much as possible.

Atherosclerosis is treated with physical exercise. 30 minutes three times a week is enough to improve general state blood according to fat indicators, decreased, developed circulatory system, nourishing the myocardium, cholesterol normalized, fatty plaques resolved. All this can be proven using angiography of the heart vessels. Moreover, the sooner a heart attack patient begins to load the heart after a heart attack, the better. But the loads should increase gradually.

Patients should not refuse medications prescribed by their doctor. After all, we are talking about, and therefore about life and death. Many do not follow the recommendations at all, do not receive treatment, or are treated sporadically. If you want to avoid a heart attack, follow your doctor's advice.

Due to high blood pressure, the load on the heart increases, resulting in the myocardium requiring more oxygen. Therefore, a hypertensive crisis during myocardial infarction can contribute to an increase in signs of ischemia of the heart muscle and worsening of the infarction. Therefore, it is important to lower blood pressure as quickly as possible to prevent further development of myocardial infarction.

Hypertensive crisis

Cardiology considers a hypertensive crisis as an emergency condition of the body associated with a sharp rise in blood pressure to critical level. In 50% of cases it occurs due to hypertension. Otherwise, a hypertensive crisis can occur as a result of excessive alcohol consumption, strong stressful situation or when sharp changes atmospheric pressure. As a result of a hypertensive crisis, damage occurs to the heart, kidneys, blood vessels, as well as the cardiovascular or central nervous system. In the worst case, the outcome is fatal.

Symptoms of the disease

The attack is accompanied by throbbing pain at the temples.

A hypertensive crisis lasts a relatively short time - on average about 3 hours. The severity of the condition increases gradually - this can last several days. It is accompanied by symptoms such as:

• headache in the back of the head or temples;
• dizziness;
• chest pain;
• dry mouth;
• pulse surges;
• nausea;
• increased sweating;
• dyspnea;
• blurred vision;
• chills;
• agitation or lethargy;
• clouding of consciousness.

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Classification of the disease

The determining factor in the classification of a crisis is damage to target organs. There are 2 types of hypertensive crises:

• A crisis of the first type (uncomplicated) is characteristic of the 2nd stage of hypertension. It happens suddenly and lasts from a few minutes to a couple of hours. It is characterized by a pronounced jump in blood pressure without dysfunction of target organs. Sometimes it goes away without symptoms. Complications are extremely rare, so treatment often takes place at home. It is necessary to lower the pressure to normal limits slowly over several hours.
• A crisis of the second type (severe) is typical for the 3rd stage of hypertension. Progresses gradually, lasts quite a long time - from 2 hours to 5 days. Accompanied by damage to vital organs due to a sharp jump in blood pressure. It must be lowered as quickly as possible, since untimely provision of assistance can lead to failure of important vital organs.

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The patient feels a sharp pressing pain in the heart area.

Myocardial infarction is the death of a small muscle portion of the heart as a result of poor blood supply and oxygen starvation. As a result of pressure surges, blood vessels often become tense and gradually lose their elasticity and become thicker in the walls. Lipids pass through such a dense wall less easily, which causes gradual clogging and smooth narrowing of the openings with lipid plaques. This causes blood clots to form.

Symptoms of the disease

The main symptom of myocardial infarction is a prolonged attack of pain behind the sternum or in the heart area. It is very sharp, burning, pressing, cutting and quite long lasting. This causes the patient to become anxious and restless. He freezes in place, trying not to move, so as not to increase the pain syndrome, which radiates strongly to the left side of the upper body: to the arm, shoulder, neck and head.

Classification of the disease

Myocardial infarction is classified according to several criteria:

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Features of the treatment of hypertensive crisis and myocardial infarction

In order not to cause harm when providing first aid, you need to carefully study the symptoms.

When the pressure jumps to high values, it is important not to confuse a hypertensive crisis with a heart attack. The main thing is to know the symptoms. During a crisis, the pain is moderate and aching in nature, and during a heart attack, the pain is very sharp and squeezing. During a heart attack, a person begins to sweat a lot. In any case, you need to provide first aid and call an ambulance.

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First measures and basics of therapy for heart attack

During a heart attack, first aid is important - the faster it is provided, the faster the patient will recover. You need to take one or more Nitroglycerin tablets to relieve pain; go to bed, try to relax, overcome panic, restore your breathing and wait for the doctor. The patient is hospitalized in the cardiac intensive care unit, where he is constantly monitored and kept at rest. He is then transferred to cardiology. Treatment is aimed at eliminating pain and restoring blood circulation with the help of narcotic analgesics, antiarrhythmic drugs, antispasmodics, and thrombolytics.

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Providing assistance during a crisis

The first task of a patient with a hypertensive crisis is to take a drug that helps smoothly lower blood pressure, for example, Diazoxide or Captopril. Hospitalized when diagnosed with the second type of crisis. Otherwise, the patient is prescribed bed rest and a strict diet. Therapy includes vasodilators, inhibitors, adrenergic blockers. Further treatment includes cardiac glucosides, anticonvulsants, antiarrhythmics.

A comment

Nickname

1. Compound
2. Release form
3. Therapeutic effect
4. Indications
5. Instructions for use
6. Use during pregnancy and lactation
7. Use for children
8. Use in old age
9. Contraindications
10. Side effects
11. Overdose symptoms
12. Drug interactions
13. special instructions
14. Analogues in Russia
15. Reviews

• Active ingredient: nifedipine.
• Pharmacological group: selective calcium channel blockers.
• ATX code: C08CA05.
• Manufacturer: Farmak (Ukraine).
• Price: from 75 rubles.

Compound

In terms of 100% dry matter, 1 ml of solution contains 20 mg of nifedipine (30 drops). In addition, the medicine contains two auxiliary components - polyethylene glycol 400 and 96% ethanol alcohol.

Release form

The drug is in the form liquid solution Contained in a 5 ml brown glass bottle, which is sealed with a special plastic cap with tamper evident. 25 ml of solution can be packaged in the same way, or it can be placed in a light-protective glass bottle, which is closed on top with a dropper stopper or a regular screw cap.

Therapeutic effect

Being calcium channel blockers, Farmadipin drops inhibit the transport of calcium ions through the membrane of cardiomyocytes and smooth muscle tissue of blood vessels, which leads to a decrease in the volume of calcium accumulated in cells. As a result, this medicine, according to its pharmacodynamics data, leads to expansion of both peripheral vessels, and coronary arteries. This is the reason that Farmadipine pressure drops (like their nifedipine-based analogues) reduce OPSS and reduce total load on the heart muscle while improving the supply of oxygen to tissues.

At the same time, the myocardium experiences less oxygen demand, and its tolerance to stress increases: in general, this medicine for lowering blood pressure has a protective effect on the heart, preventing its exhaustion. In addition, the drops have a number of other effects:

• reduce blood pressure;
• completely or partially reduce chest pain (caused by hypoxia);
• improve post-stenotic blood pressure (being vasodilators).

The release of the active substance (nifedipine) is prolonged, therefore overall effect the effect of the medicine lasts up to 24 hours - this allows you to take the medicine once a day. When a doctor chooses this dosage form for a course of treatment (usually not practiced), a stable effect of Farmadipin on the heart is achieved on the third or fourth day of treatment, while general normalization of the patient’s condition occurs, on average, by the end of the month of the therapeutic course.

It remains to add that this drug to lower high blood pressure, among other things, is prophylactic against migraines, suppresses spasms of smooth muscles of internal organs.

Indications

The main indication for use of Farmadipin is arterial hypertension(during crises), but experts also prescribe drops for exertional angina or angiospastic angina. In addition, the medicine is effective in combating migraines and can help with renal, intestinal or gallstone colic - that is, with any spasms that require the use of antispasmodics.

Instructions for use

Pharmacists recommend not using nifedipine in the form of a solution for course use, suggesting that a patient with hypertension should resort to the medicine as an emergency treatment ( hypertensive crisis). At sharp deterioration the patient's condition, expressed in a significant increase in blood pressure, the initial dosage should be from 3 to 5 drops once (for elderly patients, the dose should be reduced to 3 drops). Usually medicinal solution drip under the tongue, but a common method is to apply the drops to sugar or a small cracker, which needs to be kept in the mouth for as long as possible.

If the initial doses are ineffective, the instructions for use of Farmadipin allow an increase in a single dose of individual situations up to 10-15 drops, but such dosages should be carefully monitored.

Use during pregnancy and lactation

WHO has not established the safety level of nifedipine drugs for pregnant women and the children they are carrying, therefore it is recommended not to use Farmadipine during this period.

During lactation, the use of the drug should be discontinued, since nifedipine is excreted breast milk, although the US Pediatrics Association has approved the drug for the treatment of nursing patients.

Use for children

Due to clinical trials has not been carried out on children and adolescents under 18 years of age; the use of the solution in relation to this category of patients falls under the section of contraindications.

Use in old age

Physician supervision is necessary, especially at the beginning of therapy, for patients over 65 years of age, which is due to the fact that their metabolism of nifedipine is inhibited, which is why the half-life may be 2 times higher. This difference requires a reduction in dosage and an increase in time intervals between doses of drops. In addition, older patients are at risk of developing peripheral vasodilation, which can lead to decreased cerebral blood flow.

Contraindications

In addition to lactation, childhood and individual sensitivity to the components of Farmadipin, the following contraindications should be taken into account:

• myocardial infarction, cardiogenic shock, mitral/ aortic stenosis, angina pectoris;
• arterial hypotension, heart failure, ventricular tachycardia, SSSS;
• AV block of the second and third degree;
• porphyria, ileostomy;
• taking Rifampicin.

Side effects

Adverse reactions caused by blood pressure-lowering drugs and their analogues can be classified as infrequent or rare, but attention should be paid to disorders of cardio-vascular system. It's about headaches and redness of the facial skin, swelling of the lower extremities, orthostatic hypotension, heart rhythm disturbances and chest discomfort.

From the nervous system, rare dizziness, muscle cramps and fatigue can be noted, while in the gastrointestinal tract, symptoms such as nausea, heartburn, diarrhea and constipation are noted. Allergic reactions– rash, urticaria and itching – are even less common, but if they develop anaphylactic shock you need to be prepared to provide emergency care to the patient.

Overdose symptoms

In addition to obvious arterial hypotension, an overdose of Farmadipine will lead to many disorders of the heart and blood vessels, including tachycardia and bradycardia, arrhythmia, dizziness and weakness. In addition, the patient will suffer from nausea, vomiting, drowsiness, and deviations in his behavior and perception will appear such as lethargy, impaired color vision, convulsions, or even loss of consciousness.

To relieve this set of symptoms, it will be necessary to induce vomiting in the patient (if he is conscious), after which it will be necessary to adhere to symptomatic therapy.

Drug interactions

The enhancement of the effect of Farmadipin against high blood pressure will be more significant when it is combined with the following drugs:

• antihypertensive medications;
• beta blockers;
• diuretics;
• nitroglycerine;
• Isosorbide mononitrate/dinitrate;
• fentanyl;
• cimetidine;
• tricyclic antidepressants;
• Ranitidine.

Diltiazem slows down the elimination of nifedipine from the body, while cardiac glycosides increase theophylline levels. Radiocontrast agents do not affect the action of Farmadipin. When magnesium sulfate is used in pregnant women, muscle cramps are likely to occur.

special instructions

When using Farmadipin, some patients develop arterial hypotension (especially when using beta-blockers), which has a bad effect on their well-being. They may also develop congestive heart failure, all of which require close monitoring by a doctor. The same applies to patients with a recent myocardial infarction due to hypertrophic cardiomyopathy, patients with decompensated angina, diabetes mellitus, pulmonary hypertension and various severe liver pathologies.

The course of coronary heart disease is likely to worsen in patients with acute coronary insufficiency– Farmadipine can provoke reflex tachycardia. One and a half days before the planned anesthesia with fentanyl, it is necessary to stop treatment with nifedipine. This medicine It is not advisable to prescribe to patients with a history of lactose deficiency, galactosemia, or impaired absorption of glucose or galactose.

• take Farmadipin into account when conducting an inhalation test with methacholine;
• avoid drinking alcohol and grapefruit juice(natural);
• if you refuse therapy, reduce the dose of nifedipine gradually;
• Consult a doctor if taking medication causes chest pain.

Analogues in Russia

Farmadipin has many analogues in Russia that are not inferior to it in terms of treatment effectiveness. For example, these are German Adalat drops, Indian drug Depin-E, produced in different forms, Indian Calcegard-retard and many others like Karin-fer, Cordafen, Cordipin, Nicardia, Nifecard and Fenigidin. All of these drugs can be substitutes for Farmadipine, because their main active ingredient is nifedipine.

If we talk about a wider group of analogues belonging to the group of calcium blockers, then in addition to 1,4-dihydropyridines, which include nifedipine, there are such groups of drugs as:

• phenylalkylamines – Verapamil, Gallopamil;
• benzothiazepines – Diltiazem, Clentiazem;
• diphenylpiperazines – Cinnarizine, Flunarizine;
• Diarylaminopropylamines – Bepridil.

Reviews

According to numerous surveys and studies conducted among control groups of patients, Farmadipin has proven to be an effective and convenient medicine for everyday use. With its help, it is possible to achieve stabilization of the patient’s condition, which persists even after discontinuation of the drug.

What is cardiosclerosis atherosclerosis of the aorta of the coronary arteries?

It is quite possible to cure atherosclerosis of any type. To do this, you just have to adhere to healthy image life and take all necessary medications.

A very dangerous type of disease is atherosclerosis of the aorta and coronary arteries. The disease is fraught with myocardial infarction, heart failure, and coronary heart disease.

Coronary circulation can be stabilized by adequate conservative therapy. If the plaque succumbs to calcification or causes thrombosis, then surgical intervention is indicated.

Pathogenesis and causes of the disease

What is atherosclerosis of the aorta and coronary arteries? To understand this issue, let’s remember the school anatomy course. The aorta is a large blood vessel, which originates in the left cardiac ventricle.

The aorta divides into two vessels. The upper branch in medicine is called thoracic aorta, and the lower one is the abdominal aorta. The coronary arteries are a bloodstream that is responsible for supplying the heart and superior branches coronary artery.

That's sorted out. Now let's remember the concept of atherosclerosis. This term hides a disease in which fatty plaques consisting of low-density lipoproteins and esters are deposited on the inside of arteries and vessels.

At the initial stages, atherosclerosis does not manifest itself at all. Initially, a small fatty spot forms on the inside of the vessel or artery, which causes an inflammatory process. Violation of lipid metabolism leads to the fact that the lipid spot gradually increases in size.

At the terminal stage of atherosclerosis, the lipid plaque succumbs to calcification, that is, calcium salts gradually accumulate in it. The plaque becomes denser, increases in size, and further narrows the lumen of the blood vessels. As a result, blood circulation in the area of ​​the valve leaflets, myocardial bundles and ventricles is disrupted.

Why does atherosclerosis of the aorta of the brain and heart vessels develop? The exact causes of the disease are unknown. But doctors say that there are a number of predisposing factors to the development of the disease.

Let's look at them:

• Gout.
• Coronary heart disease, hypertension, other cardiovascular pathologies.
• Diabetes. Atherosclerotic plaques can be the result of both insulin-dependent and non-insulin-dependent forms of the disease.
• Use large quantity fats of animal origin. Also negatively affects lipid metabolism excessive consumption of sweets.
• Hypothyroidism and other thyroid diseases.
• Stress, depression.
• Predisposition (genetic).
• Being male.
• Menopause period.
• Obesity.
• Bad habits. Alcoholism, drug addiction and smoking have an extremely negative impact on the functioning of the cardiovascular system.
• Sedentary lifestyle (hypodynamia).
• Elderly age.

It is worth noting that the disease is multifactorial, that is, it develops in the presence of more than 2-3 predisposing factors.

How does atherosclerosis of the aorta and coronary arteries manifest?

Atherosclerotic lesions of the coronary arteries and aorta are asymptomatic at stage 1. The disease can only occasionally cause paroxysmal pain in the chest area.

Over time, the disease leads to the appearance of angina pectoris. The patient experiences sudden burning pain in the chest area. The pain syndrome radiates to the cervical spine.

Also, when the aorta and coronary arteries are damaged, the patient experiences:

1. Blood pressure surges. Often blood pressure levels exceed 140/90 mmHg. against the background of atherosclerosis, hypertension may well develop.
2. Dyspnea.
3. Increased sweating.
4. If the abdominal aorta is affected, the patient may experience constipation, diarrhea, abdominal pain after eating, nausea, or vomiting.
5. If the aorta of the brain is affected, memory decreases, headaches, dizziness occur, memory and mental performance decrease.
6. Sleep disorders.
7. Tinnitus, decreased hearing acuity.

Symptoms become more pronounced when atherosclerotic plaques succumb to calcification.

Diagnosis of atherosclerosis of the coronary arteries and aorta

When the first symptoms of atherosclerosis appear, you should immediately contact a cardiologist. Initially, a physical examination and oral interview are performed to clarify complaints.

It is mandatory to pass biochemical analysis blood. The analysis will show the level of triglycerides, low lipoproteins and high density, total cholesterol. What indicators are normal are shown in the table.

Also, the diagnosis of atherosclerosis is supplemented by the following studies:

• General blood and urine analysis.
• Coronary angiography.
• Aortography.
• Angiography.

Based on the data obtained, a final diagnosis is made and treatment tactics are selected.

Treatment of atherosclerosis

For atherosclerosis of the aorta and coronary arteries, treatment can be carried out surgically or conservatively. Surgery indicated for the development of calcification or thrombosis. Surgical procedures are also indicated in cases of life-threatening and high probability development of myocardial infarction.

The most commonly used techniques are coronary artery bypass grafting and stenting. also in Lately Endovascular and laser methods are widely used.

In the vast majority of cases, atherosclerosis is treated conservatively. Therapy involves following a number of recommendations. The patient should:

1. Take medications that normalize lipid metabolism and prevent the formation of blood clots. You should take statins, fibrates, bile acid sequesters, nicotinic acid, multivitamin complexes, anticoagulants. For auxiliary purposes, dietary supplements and herbal tinctures (hawthorn, motherwort, valerian) are used.
2. For cerebral disorders, use cerebral protectors (Piracetam, Ceraxon, Semax, Actovegin, Picamilon).
3. Avoid eating fatty and sweet food. A diet for atherosclerosis should be followed for life. Must be consumed unsaturated fats, as they increase the level of high-density lipoproteins (good cholesterol). The best sources of fats are walnuts, pistachios, olive oil and flaxseed oil.
4. Move more, play sports.
5. If you have high blood pressure, take hypotonic medications. The use of diuretics is allowed ACE inhibitors, sartans, beta-blockers, calcium channel blockers.
6. Lead a healthy lifestyle. Cardiologists insist that the patient should not drink alcohol or smoke, otherwise the effect of therapeutic measures will not be.

You still need to go through it regularly preventive diagnostics. It will allow you to monitor the dynamics of the disease and make adjustments if necessary.

Complications and prevention

Untimely treatment of atherosclerosis of the coronary arteries and aorta can cause many complications. The disease is fraught with complications such as cardiosclerosis, aortic stenosis, aortic aneurysm, thrombosis, and myocardial infarction.

It is also impossible to exclude the possibility of such consequences as ischemic or hemorrhagic stroke, coronary heart disease, hypertension, heart or renal failure. If the abdominal aorta is damaged, aneurysm and necrosis may develop.

Prevention of atherosclerosis:

• Compliance with healthy eating rules.
• BMI level tracking. If you are obese, you should take appropriate measures - exercise, follow a low-carbohydrate diet.
• Timely treatment of cardiovascular diseases, endocrine pathologies, diabetes mellitus.
• Maintaining an active and healthy lifestyle.
• Periodic examinations by doctors.

By the way, with the development of atherosclerosis of the aorta and coronary arteries, the patient may be assigned a disability.

Typically, benefits are given to patients who have suffered a stroke or myocardial infarction and have lost their ability to work.

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– 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 left hand, collarbone, shoulder blade, jaw, shortness of breath, feeling of fear, cold sweat. Developed myocardial infarction is an indication for emergency hospitalization in the cardiac intensive care unit. If not provided timely assistance Possible death.

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

Acute period

IN acute period After myocardial infarction, the 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 clinical manifestations absent, 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 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 severe signs of cardiosclerosis, circulatory failure, and secondary 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 the first three days, most patients experience different kinds arrhythmias: 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 (which can cause pulmonary infarction or sudden death) or systemic 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 characteristic changes ECGs 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 returns 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 in unstable angina. Determined in blood increase in ESR, leukocytes, aspartate aminotransferase (AsAt) and alanine aminotransferase (AlAt) activity.

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

Treatment of myocardial infarction

In case of myocardial infarction, emergency hospitalization in a cardiac intensive care unit is indicated. 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 is carried out by a combination of narcotic analgesics (fentanyl) with antipsychotics (droperidol), intravenous administration of 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 a serious disease associated with dangerous complications. 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 lifestyle, giving up alcohol and smoking, balanced diet, exclusion of physical and nervous overstrain, control blood pressure and blood cholesterol levels.

Myocardial infarction is damage to the heart muscle due to disruption of its blood supply. In the part where oxygen starvation has developed, cells die, the first ones die within 20 minutes after the blood flow stops.

Heart attack is one of the top diseases that cause mortality among the population. Every year in Europe alone, 4.3 million people die for this reason.

The classification of myocardial infarction implies four stages of disease development according to time and clinical picture - damage, acute, subacute, cicatricial.

Damage period (initial)

Symptoms occur during from several hours to 3 days. At this stage, transmural damage to fibers is observed as a result of circulatory disorders. The longer the latent phase, the more serious the disease.

Recognize the disease. Potassium ions, leaving the dead cells, form damage currents. Then a pathological Q wave occurs, which is recorded already on the second day.

If necrotic disorders appear in the heart, then ST segment is much higher than the isoline, the convexity is directed upward, repeating the shape of the monophasic curve. At the same time, the fusion of this segment with a positive T-wave is recorded.

The stronger the ST segment elevation above the isoline, the worse the prognosis for myocardial infarction.

It is noteworthy that if there is no Q wave, then all cardiac muscle cells are still alive. This tooth may appear even on the 6th day.

Acute

Duration of the second stage - from 1 day to 3 weeks.

Gradually, potassium ions are washed out from the damaged area, weakening the strength of the currents. In this case, the damaged area decreases, since some part of the fibers dies, and the surviving part tries to recover and goes into ischemia (local decline blood circulation).

The ST segment descends to the isoline, and the negative T wave acquires an expressive contour. However, with infarction of the anterior wall of the left ventricle, ST elevation is likely to persist for some time period.

If extensive has occurred, the ST segment rise lasts the longest, indicating severe clinical picture and a poor prognosis.

If in the first stage there was no Q wave, now it appears as QS for transmural and QR for non-transmural type.

Subacute

The stage lasts about 3 months, sometimes up to a year.

At this stage, deeply damaged fibers move into the necrosis zone, which stabilizes. Other fibers are partially restored and form an ischemic zone. During this period the doctor determines the size of the lesion. In the future, the ischemic zone is reduced, and the fibers in it continue to recover.

The phenomena are reflected on the ECG. Conventionally, the third stage is divided into two phases. In the first, the T wave becomes larger and wider, causing the electrical systole of the ventricles to become longer. QT. In the second phase, the amplitude of the lower T wave decreases.

Cicatricial (final)

Scarring of the fibers lasts the entire life of the patient. At the site of necrosis, the tissues of neighboring healthy areas are connected. The process is accompanied by compensatory hypertrophy of fibers, the affected areas are reduced, and the transmural type sometimes turns into a non-transmural type.

In the final stage the cardiogram does not always show the Q wave, so the ECG does not report past illness. There is no damage zone, the ST segment coincides with the isoline (myocardial infarction occurs without its elevation). Due to the absence of an ischemic zone, the ECG shows a positive T wave, characterized by flattening or less height.

Division by anatomy of the lesion

Based on the anatomy of the lesion, the disease is distinguished:

• transmural;
• intramural;
• subendocardial;
• subepicardial.

Transmural

Transmural infarction occurs ischemic lesion the entire muscle layer of the organ. The disease has many symptoms that are common to other diseases. This makes treatment significantly more difficult.

In terms of symptoms, the disease resembles with the difference that in the latter case ischemia is a temporary phenomenon, and with a heart attack it becomes irreversible.

Intramural

Defeat is concentrated in the thickness of the wall of the left ventricle, does not affect the endocardium or epicardium. The size of the lesion may vary.

In the intramural form there is no pathological Q wave. Transmural ischemia occurs around the damaged area, due to which the repolarization wave changes direction, and a negative symmetrical T wave is recorded, often accompanied by an increase in the QT segment.

Subendocardial

This is the name for a heart attack in the form of a narrow strip near the endocardium of the left ventricle. Then the affected area is surrounded by subendocardial damage, as a result of which the ST segment falls below the isoline.

During the normal course of the disease, excitation rapidly passes through the subendocardial sections of the myocardium. Therefore, the pathological Q wave does not have time to appear above the infarction area. The main sign of the subendocardial form is that over the affected area the ST segment moves horizontally below the electrical line more than 0.2 mV.

Subepicardial

The lesion occurs near the epicardium. On the cardiogram, the subepicardial form is expressed in a reduced amplitude of the R wave, in the leads above the infarction area a pathological Q wave is visible, and the ST segment rises above the isoline. A negative T wave appears in the initial stage.

For more details about determining the disease on an ECG, watch the video:

Volume of affected area

There are large-focal, or Q-myocardial infarction, and small-focal, which is also called non-Q-infarction.

Large-focal

Causes thrombosis or prolonged spasm of the coronary artery. As a rule, it is transmural.

The following symptoms indicate the development of a Q-infarction:

• pain behind the sternum, radiating to the right top part torso, under left shoulder blade, V lower jaw, to other parts of the body - shoulder, arm with right side, epigastric region;
• ineffectiveness of nitroglycerin;
• the duration of pain varies - short-term or more than a day, possibly several attacks;
• weakness;
• depression, fear;
• often - difficulty breathing;
• more low performance blood pressure in patients with hypertension;
• pale skin, cyanosis (blue color) of mucous membranes;
• profuse sweating;
• sometimes -, in some cases turning into tachycardia;
• arrhythmia.

When examining the organ, signs are revealed, an enlargement of the heart in diameter. Above the apex and at Botkin's point, the 1st tone is weakened, sometimes split, the 2nd tone dominates, and systolic murmurs are heard. Both heart sounds become muffled. But if necrosis did not develop against the background of pathological changes in the organ, then the 1st tone prevails.

For large focal infarction Pericardial friction rub is heard, the heart rhythm becomes galloping, which indicates a weakened contraction of the heart muscle.

In patients, body temperature rises on days 2–3 and persists until days 7–10. The level depends on the degree of organ damage.

Laboratory tests detect in the body high level of leukocytes, increased ESR (after 2 days), there is a “scissors” effect in the relationship between these two indicators. The large-focal form is accompanied by other biochemical abnormalities, the main one of which is hyperenzymemia, which occurs in the first hours and days.

With a large-focal form hospitalization is indicated. In the acute period, the patient is prescribed bed rest and mental rest. Meals are fractional, limited in calories.

Purpose drug therapy is to prevent and eliminate complications- heart failure, cardiogenic shock, arrhythmias. To relieve pain, narcotic analgesics, antipsychotics and nitroglycerin (intravenously) are used. The patient is prescribed antispasmodics, thrombolytics, antiarrhythmic drugs, ß-blockers, calcium antagonists, magnesium, etc.

Finely focal

With this form, the patient develops small lesions of the heart muscle. Disease characterized by a milder course compared with large-focal lesions.

Anginal pain does not last long and is not severe. But if the pain is prolonged, this indicates a relapse, which occurs with the formation of new lesions. With strong pain syndrome in some cases shock develops.

The sonority of the tones remains the same, there is no galloping rhythm and pericardial friction noise. The temperature rises to 37.5 degrees, but not higher.

White blood cell count is around 10,000–12,000, high ESR is not always detected; in most cases, eosinophilia and band shift do not occur. Enzymes are activated briefly and insignificantly.

On the electrocardiogram segment RS - T shifts, most often falls below the isoline. Also observed pathological changes T wave: as a rule, it becomes negative, symmetrical and takes on a pointed shape.

Small focal infarction is also a reason for hospitalization of the patient. Treatment is carried out using the same means and methods as for the large-focal form.

The prognosis for this form is favorable, mortality is low – 2–4 cases per 100 patients. Aneurysm, cardiac rupture, heart failure, asystole, thromboembolism and other consequences small focal infarction myocardium are rare, but this focal form of the disease develops into a large-focal form in 30% of patients.

Localization

Depending on the location, myocardial infarction occurs in the following clinical variants:

• left and right ventricle- more often, several walls may be affected at once.
• septal when the interventricular septum suffers;
• apical- necrosis occurs in the apex of the heart;
• basal- damage high departments back wall.

Atypical types of disease

In addition to the above, there are other forms of this disease - atypical. They develop in the presence of chronic diseases and bad habits, due to atherosclerosis.

Atypical forms significantly complicate diagnosis.

There are gastralgic, asthmatic, asymptomatic and many other variations of heart attacks. We talked about it in more detail in another article.

Multiplicity

Based on this criterion, the following types of myocardial infarction are distinguished:

• primary- occurs for the first time;
• recurrent- the lesion is recorded within two months after the previous one, and in the same area;
• continued- the same as recurrent, but the affected area is different;
• repeated- diagnosed after two months or later, any area is affected.

Therefore, which may indicate a heart attack, you should Seek medical help immediately.