TO clinical manifestations coronary disease heart disease are stable angina, silent myocardial ischemia, unstable angina, myocardial infarction, heart failure and sudden death. For many years, unstable angina was considered as an independent syndrome, occupying an intermediate position between chronic stable angina and acute myocardial infarction. However, in recent years it has been shown that unstable angina and myocardial infarction, despite differences in their clinical manifestations, are consequences of the same pathophysiological process, namely rupture or erosion of an atherosclerotic plaque in combination with associated thrombosis and embolization of more distal areas of the vascular beds. In this regard, unstable angina and developing myocardial infarction are currently united by the term acute coronary syndrome (ACS) .

Acute coronary syndrome is a preliminary diagnosis that allows the doctor to determine urgent therapeutic and organizational measures. Accordingly, the development of clinical criteria that allow the doctor to make timely decisions and choose optimal treatment, which is based on an assessment of the risk of complications and a targeted approach to prescribing invasive interventions. During the creation of such criteria, all acute coronary syndromes were divided into those accompanied and those not accompanied by persistent ST segment elevation. Currently, optimal treatment interventions, the effectiveness of which is based on the results of well-designed randomized clinical trials, have largely been developed. Thus, in acute coronary syndrome with persistent ST segment elevation (or new complete blockade of the left bundle branch), reflecting acute total occlusion of one or more coronary arteries, the goal of treatment is rapid, complete and durable restoration of the lumen of the coronary artery using thrombolysis (if not contraindicated) or primary coronary angioplasty (if technically feasible). The effectiveness of these therapeutic measures proven in a number of studies.

In acute coronary syndrome without ST segment elevation, we are talking about patients with pain in the chest and ECG changes indicating acute ischemia (but not necessarily necrosis) of the myocardium. Such patients often exhibit persistent or transient ST segment depression, as well as inversion, flattening, or “pseudonormalization” of T waves. In addition, ECG changes in acute coronary syndrome without ST segment elevation may be nonspecific or completely absent. Finally, some patients with the above changes on the electrocardiogram, but without subjective symptoms (i.e., cases of painless “silent” ischemia and even myocardial infarction) may also be included in this category of patients.

In contrast to situations with persistent ST-segment elevation, previous treatment proposals for acute coronary syndrome without ST-segment elevation were less clear. It was not until 2000 that guidelines were published Working group European Society of Cardiology on the treatment of non-ST segment elevation acute coronary syndrome. Soon, corresponding recommendations will be developed for Russian doctors.

This article discusses only the management of patients with suspected acute coronary syndrome who do not have persistent ST segment elevation. In this case, the main attention is paid directly to diagnosis and the choice of therapeutic tactics.

But first we consider it necessary to make two remarks:

First, the recommendations below are based on the results of a number of clinical trials. However, these trials were performed on specially selected groups of patients and, accordingly, do not reflect all conditions encountered in clinical practice.
Secondly, it should be borne in mind that cardiology is developing rapidly. Accordingly, these recommendations should be reviewed regularly as new clinical trial results accumulate.

The degree of persuasiveness of conclusions about effectiveness various methods diagnosis and treatment depends on the data on which they were made. In accordance with generally accepted recommendations, the following are distinguished: three levels of validity (“proof”) of conclusions:

Level A: Conclusions are based on data that were obtained from several randomized clinical trials or meta-analyses.

Level B: Conclusions are based on data that have been obtained from single randomized trials or non-randomized studies.

Level C. Conclusions are based on consensus expert opinion.

In the following presentation, after each point the level of its validity will be indicated.

Tactics for managing patients with acute coronary syndrome

Initial assessment of the patient's condition

The initial assessment of a patient complaining of chest pain or other symptoms suggestive of ACS includes:

1. Careful history taking . Classic characteristics of anginal pain, as well as typical exacerbations of coronary artery disease (prolonged [> 20 minutes] anginal pain at rest, new-onset severe [at least class III according to the Canadian Cardiovascular Society (CCS) classification] angina pectoris, recent worsening stable angina at least up to FC III according to CCS) are well known. However, it should be noted that ACS can also manifest itself with atypical symptoms, including chest pain at rest, epigastric pain, sudden dyspepsia, stabbing chest pain, “pleural” pain, and increased shortness of breath. Moreover, the frequency of these manifestations of ACS is quite high. Thus, according to the Multicenter Chest Pain Study (Lee T. et al., 1985), acute myocardial ischemia was diagnosed in 22% of patients with acute and stabbing pain in the chest, as well as in 13% of patients with pain characteristic of pleural lesions , and in 7% of patients in whom painful sensations were completely reproduced by palpation. Atypical manifestations of ACS are especially often observed in young (25-40 years old) and old (over 75 years old) patients, as well as in women and patients with diabetes mellitus.

2. Physical examination . The results of examination and palpation of the chest, cardiac auscultation data, as well as heart rate and blood pressure are usually within normal limits. The purpose of the physical examination is primarily to exclude noncardiac causes of chest pain (pleurisy, pneumothorax, myositis, inflammatory diseases musculoskeletal system, chest trauma, etc.). In addition, physical examination should identify heart diseases not associated with coronary artery disease (pericarditis, heart defects), as well as assess hemodynamic stability and the severity of circulatory failure.

3. ECG . Recording an ECG at rest is a key method for diagnosing ACS. Ideally, you should record an ECG during a painful attack and compare it with an electrocardiogram recorded after the pain has disappeared. For recurring pain, multichannel ECG monitoring can be used for this. It is also very useful to compare the ECG with “old” films (if available), especially if there are signs of left ventricular hypertrophy or previous myocardial infarction.

The most reliable electrocardiographic signs of ACS are the dynamics of the ST segment and changes in the T wave. The likelihood of ACS is greatest if the corresponding clinical picture is combined with depression of the ST segment with a depth of more than 1 mm in two or more adjacent leads. A somewhat less specific sign of ACS is T wave inversion, the amplitude of which exceeds 1 mm, in leads with a predominant R wave. Deep negative symmetrical T waves in the anterior precordial leads often indicate severe proximal stenosis of the anterior descending branch of the left coronary artery. Finally, shallow (less than 1 mm) ST segment depression and slight T wave inversion are the least informative.

It should be remembered that completely normal ECG in patients with characteristic symptoms does not exclude the diagnosis of ACS.

Thus, in patients with suspected ACS, a resting ECG should be recorded and long-term multichannel ST segment monitoring should be initiated. If monitoring is not feasible for any reason, then frequent ECG recording is necessary (level of evidence: C).

Hospitalization

Patients with suspected non-ST segment elevation ACS should be immediately hospitalized in specialized emergency cardiology departments/departments intensive care and cardiac resuscitation (Level of Evidence: C).

Study of biochemical markers of myocardial damage

“Traditional” cardiac enzymes, namely creatine phosphokinase (CPK) and its isoenzyme MB CPK are less specific (in particular, possible false positive results with skeletal muscle injury). In addition, there is significant overlap between normal and pathological serum concentrations of these enzymes. The most specific and reliable markers of myocardial necrosis are cardiac troponins T and I . The concentration of troponins T and I should be determined 6-12 hours after admission to the hospital, as well as after each episode of intense chest pain.

If a patient with suspected non-ST segment elevation ACS has elevated levels of troponin T and/or troponin I, then this condition should be regarded as myocardial infarction and appropriate medical and/or invasive treatment should be provided.

It should also be taken into account that after cardiac muscle necrosis, the increase in the concentration of various markers in the blood serum does not occur simultaneously. Thus, the earliest marker of myocardial necrosis is myoglobin, and the concentrations of CPK and troponin increase somewhat later. In addition, troponins remain elevated for one to two weeks, making it difficult to diagnose recurrent myocardial necrosis in patients who have recently suffered a myocardial infarction.

Accordingly, if ACS is suspected, troponins T and I should be determined at the time of admission to the hospital and re-measured after 6-12 hours of observation, as well as after each painful attack. Myoglobin and/or MB CPK should be determined at recent (less than six hours) onset of symptoms and in patients with a recent (less than two weeks ago) myocardial infarction (Level of Evidence: C).

Initial treatment of patients with suspected non-ST segment elevation ACS

For non-ST segment elevation ACS, the initial therapy should be:

1. Acetylsalicylic acid (level of evidence: A);

2. Sodium heparin and low molecular weight heparins (level of evidence: A and B);

3. b-blockers (level of evidence: B);

4. For persistent or recurrent chest pain - nitrates orally or intravenously (level of evidence: C);

5. If there are contraindications or intolerance to b-blockers, calcium antagonists (level of evidence: B and C).

Dynamic observation

During the first 8-12 hours, it is necessary to carefully monitor the patient's condition. Subject special attention must be:

Recurrent chest pain. During each painful attack, it is necessary to record an ECG, and after it, re-examine the level of troponins in the blood serum. Continuous multichannel ECG monitoring is highly advisable to identify signs of myocardial ischemia, as well as disorders heart rate.
Signs of hemodynamic instability (arterial hypotension, congestive wheezing in the lungs, etc.)

Assessing the risk of myocardial infarction or death

Patients with acute coronary syndrome represent a very heterogeneous group of patients who differ in the extent and/or severity of atherosclerotic lesions of the coronary arteries, as well as in the degree of “thrombotic” risk (i.e., the risk of developing myocardial infarction in the coming hours/days). The main risk factors are presented in Table 1.

Based on follow-up data, ECG and biochemical studies, each patient should be classified into one of the two categories below.

1. Patients at high risk of myocardial infarction or death

repeated episodes of myocardial ischemia (either recurrent chest pain or ST segment dynamics, especially depression or transient ST segment elevations);
increased concentration of troponin T and/or troponin I in the blood;
episodes of hemodynamic instability during the observation period;
life-threatening heart rhythm disturbances (repeated paroxysms ventricular tachycardia, ventricular fibrillation);
the occurrence of ACS without ST segment elevation in the early post-infarction period.

2. Patients at low risk of myocardial infarction or death

chest pain did not recur;
there was no increase in the level of troponins or other biochemical markers of myocardial necrosis;
there were no ST segment depressions or elevations in the presence of inverted T waves, flattened T waves, or a normal ECG.

Differentiated therapy depending on the risk of myocardial infarction or death

For patients at high risk of these events, the following treatment tactics may be recommended:

1. Administration of IIb/IIIa receptor blockers: abciximab, tirofiban or eptifibatide (level of evidence: A).

2. If it is impossible to use IIb/IIIa receptor blockers, intravenous administration of sodium heparin according to the scheme (Table 2) or low molecular weight heparins (level of evidence: B).

The following are widely used in modern practice: low molecular weight heparins : adreparin, dalteparin, nadroparin, tinzaparin and enoxaparin. As an example, let’s take a closer look at nadroparin. Nadroparin is a low molecular weight heparin obtained from standard heparin by depolymerization. The drug is characterized by pronounced activity against factor Xa and weak activity against factor IIa. The anti-Xa activity of nadroparin is more pronounced than its effect on aPTT, which distinguishes it from sodium heparin. For the treatment of ACS, nadroparin is administered subcutaneously 2 times a day in combination with acetylsalicylic acid (up to 325 mg/day). The initial dose is determined at 86 units/kg and should be administered as an IV bolus. Then the same dose is administered subcutaneously. The duration of further treatment is 6 days, in doses determined depending on body weight (Table 3).

3. In patients with life-threatening cardiac arrhythmias, hemodynamic instability, development of ACS soon after myocardial infarction, and/or a history of CABG, coronary angiography (CAG) should be performed as quickly as possible. In preparation for coronary angiography, heparin administration should be continued. If there is an atherosclerotic lesion that allows revascularization, the type of intervention is chosen taking into account the characteristics of the damage and its extent. The principles for choosing a revascularization procedure in ACS are similar general recommendations for this type of treatment. If percutaneous transluminal coronary angioplasty (PTCA) with or without stent placement is chosen, it can be performed immediately after angiography. In this case, the administration of IIb/IIIa receptor blockers should be continued for 12 hours (for abciximab) or 24 hours (for tirofiban and eptifibatide). Level of validity: A.

In patients at low risk of myocardial infarction or death, the following strategies may be recommended:

1. Ingestion acetylsalicylic acid, b-blockers, possibly nitrates and/or calcium antagonists (level of evidence: B and C).

2. Discontinuation of low-molecular-weight heparins if during follow-up there were no changes in the ECG and the troponin level did not increase (level of evidence: C).

3. Stress test to confirm or establish a diagnosis of coronary artery disease and assess the risk of adverse events. Patients with severe ischemia during standard load test(bicycle ergometry or treadmill), CAG should be performed followed by revascularization. If standard tests are uninformative, stress echocardiography or stress myocardial perfusion scintigraphy may be useful.

Management of patients with ACS without ST segment elevation after discharge from hospital

1. Administration of low molecular weight heparins if there are repeated episodes of myocardial ischemia and revascularization cannot be performed (level of evidence: C).

2. Taking b-blockers (level of evidence: A).

3. Broad impact on risk factors. First of all - smoking cessation and normalization lipid profile(level of evidence: A).

4. Reception ACE inhibitors(level of evidence: A).

Conclusion

Currently many medical institutions in Russia they do not have the capabilities to carry out the above-mentioned diagnostic and therapeutic measures (determining the level of troponins T and I, myoglobin; emergency coronary angiography, use of IIb/IIIa receptor blockers, etc.). One can expect, however, their increasingly wider inclusion in medical practice in our country in the near future.

The use of nitrates for unstable angina is based on pathophysiological reasons and clinical experience. There are no data from controlled studies indicating optimal dosages and duration of use.

Acute coronary syndrome (ACS) without ST segment elevation is a type of myocardial infarction with less severe damage to the heart muscle compared to myocardial infarction with ST segment elevation, which is more common.

Differences between ACS without ST segment elevation and ACS with ST segment elevation

Each contraction of the heart muscle is displayed on the electrocardiogram (ECG) in the form of a curve. Despite the fact that clinically ACS without ST elevation and ACS with ST elevation look the same, on the cardiogram the curves for these types of ACS are very different.

Signs of ACS without ST elevation on ECG:

Decreased ST or T wave inversion

No Q wave changes

Incomplete closure of the coronary artery

Signs of ACS with ST elevation:

ST segment elevation

Q wave changes

Complete occlusion of the coronary artery

Risk factors for ACS without ST segment elevation:

Smoking

Inactive lifestyle

Increased blood pressure or high level cholesterol

Diabetes

Overweight or obesity

Family history of heart disease or stroke

Symptoms:

Feeling of tightness or discomfort in the chest

Pain or discomfort in the jaw, neck, back, or stomach

Dizziness

Sharp weakness

Nausea

Sweating

The appearance of such symptoms should be taken very seriously and urgently call emergency help. When it comes to chest pain, it is better not to take risks and play it safe, since in the event of a heart attack, every minute counts.

Diagnosis of ACS without ST elevation

Diagnosis is carried out using a blood test and ECG.

Blood tests reveal increased levels of cardiac creatine kinase, troponins I and T. These markers indicate possible damage cardiac muscle cells and, in comparison with ACS without ST elevation, their level increases moderately. A blood test alone cannot diagnose a myocardial infarction. On the ECG you can see how the ST segment “behaves” and, based on this, judge both the presence of a heart attack and its type.

Treatment

Tactics depend on the degree of blockage of blood flow and the severity of the disease. The GRACE score determines low, moderate, or high risk of death due to ACS. The following parameters are used for risk stratification:

Age

Heart rate

Systolic blood pressure

Class by Killip

Serum creatinine level

Cardiac arrest upon patient admission

Changes in the ST segment on the ECG

Increased levels of cardiac markers

In patients with ACS without ST elevation at low risk, drug therapy is used. These may be anticoagulants, antiplatelet agents, beta blockers, nitrates, statins, ACE inhibitors or blockers.

In patients at average or high risk, percutaneous coronary artery grafting or coronary artery bypass surgery is performed.

Prevention

Prevention measures involve reducing risk factors. Highest value has a lifestyle change:

Healthy balanced diet (fruits, vegetables, whole grains, healthy fats)

Limit your intake of saturated and trans fats

Minimum 30 minutes physical activity 5 days a week

Stress management practices: yoga, deep breathing, walks

To give up smoking

Fighting excess weight

In addition, measures should be taken to reduce blood pressure or cholesterol levels, and properly control diabetes.

If you have previously had a heart attack or are at risk, plan what you will do in the event of a heart attack. emergency. Always keep your doctor's phone number, a list of your medications, and a list of medications to which you are allergic.

Acute coronary syndrome without segment elevation ST (unstable angina and small focal myocardial infarction).

- with incomplete obstruction of the coronary artery.

It is characterized by anginal attacks and the absence of ST segment elevation on the ECG. ACS without ST segment elevation includes unstable angina and small focal MI.

The typical clinical manifestation is a feeling of pressure or heaviness in the chest (angina pectoris) radiating to the left arm, neck or jaw, which may be transient or permanent.

Traditionally, the following clinical manifestations are distinguished:

* Prolonged (more than 20 minutes) anginal pain at rest;

* New-onset angina II or III functional class;

* Recent worsening of previously stable angina, according to at least up to functional class III - progressive angina;

* Post-infarction angina.

Diagnostics.

ECG— a first-line method for examining patients with suspected ACS without ST-segment elevation. It should be done immediately after the first contact with the patient. Depression of the ST segment below the isoline and changes in the T wave are characteristic, but not obligatory.

Primary ECG data are also risk predictors. The number of leads with ST depression and the magnitude of depression indicate the degree and severity of ischemia and correlate with prognosis. Deep symmetrical T wave inversion in the anterior precordial leads is often associated with significant stenosis of the proximal left anterior descending coronary artery or the main trunk of the left coronary artery.

A normal ECG does not exclude the presence of non-ST segment elevation ACS.

Biochemical markers. During myocardial necrosis, the contents of the dead cell enter the general bloodstream and can be determined in blood samples. Cardiac troponins play a major role in diagnosis and risk stratification, and also help distinguish between non-ST segment elevation ACS and unstable angina. The test is capable of excluding and confirming ACS with a high probability. In order to differentiate a chronic increase in troponin from an acute one, the dynamics of changes in troponin levels compared to the initial value is of great importance.

It is necessary to remember about possible non-coronary causes of increased troponin levels. These include: pulmonary embolism, myocarditis, stroke, aortic aneurysm dissection, cardioversion, sepsis, and extensive burns.

Any increase in troponin in ACS is associated with a poor prognosis.

There is no fundamental difference between troponin T and troponin I. Cardiac troponins increase after 2.5-3 hours and reach a maximum after 8-10 hours. Their levels return to normal after 10-14 days.

- CPK MB increases after 3 hours, reaching a maximum after 12 hours.

- Myoglobin increases after 0.5 hours, reaching a maximum after 6-12 hours.

Markers of inflammation. Currently, much attention is paid to inflammation as one of the main causes of destabilization of atherosclerotic plaque.

In this regard, so-called inflammatory markers, in particular C-reactive protein, are widely studied. Patients with the absence of biochemical markers of myocardial necrosis, but with increased level CRP is also considered to be at high risk for coronary complications.

Echocardiography necessary for all patients with ACS to assess local and global LV function and conduct differential diagnosis. To determine treatment tactics for patients with non-ST segment elevation ACS, stratification models for determining the risk of MI or death are currently widely used in practice: the Grace and TIMI scales.

TIMI risk:

7 independent predictors

Age 65 years (1 point)
Three risk factors for IHD (cholesterol, family history of IHD, hypertension, diabetes, smoking) (1 point)
Previously known CAD (1 point) (stenoses > 50% on coronary angiography)
Aspirin in the next 7 days (!)
Two episodes of pain (24 hours) - 1
ST displacements (1 point)
Presence of cardiac markers (CK-MB or troponin) (1 point)

Risk of MI or death according to TIMI:

– low – (0-2 points) – up to 8.3%

– average – (3-4 points) – up to 19.9%

– high – (5-7 points) – up to 40.9%

Risk assessment according to the GRACE scale

Age
Systolic blood pressure
Creatinine content
SN class according to Killip
ST segment deviation
Heart failure
Increased markers of myocardial necrosis

Treatment

Etiotropic therapy

— the use of statins has been proven to be highly effective in stabilizing the cap of an unstable fibrous plaque. The statin dose should be higher than typical and titrated further to achieve a target LDL cholesterol level of 2.5 mmol/L. Initial doses of statins are rosuvastatin 40 mg per day, atorvastatin 40 mg per day, simvastatin 60 mg per day.

The effects of statins that determine their use in ACS:

- impact on endothelial dysfunction

- decreased platelet aggregation

- anti-inflammatory properties

- decreased blood viscosity

- plaque stabilization

- suppression of the formation of oxidized LDL.

AAC/ACC (2010): Statins should be prescribed within the first 24 hours of hospitalization

regardless of cholesterol level.

EKO (2009): Lipid-lowering therapy should be prescribed without delay.

Pathogenetic therapy has two goals:

1) The effect is aimed at preventing and inhibiting the development of increasing parietal thrombosis of the coronary arteries - anticoagulant and disaggregant therapy.

2) Traditional coronary therapy - beta-blockers and nitrates.__

Antiplatelet agents

Platelet activation and aggregation play a dominant role in the formation of arterial thrombosis. Platelets can be inhibited by three classes of drugs: aspirin, P2Y12 inhibitors and glycoprotein Ilb/IIIa inhibitors.

1) Acetylsalicylic acid. The mechanism of action is due to the inhibition of COX in tissues and platelets, which causes a blockade of the formation of thromboxane A2, one of the main inducers of platelet aggregation. Blockade of platelet cyclooxygenase is irreversible and persists throughout life.

Aspirin in patients with ACS without ST elevation is considered as a first-line drug, since the direct substrate of the disease is the activation of the vascular-platelet and plasma coagulation cascades. That is why the effect of aspirin in this category of patients is even more pronounced than in patients with stable angina.

2) P2Y12 inhibitors: Clopidogrel, Prasugrel, Ticagrelor, Thienopyridine, Thienopyridine, Triazolopyrimidine.

Inhibitor P2Y12 should be added to aspirin as soon as possible and continued for 12 months, provided there is no risk of increased bleeding.

Clopidogrel(Plavike, Zilt, Plagryl) - a representative of the thienopyridine group, is a powerful antiplatelet agent, the mechanism of action of which is associated with the inhibition of ADP-induced platelet activation due to the blockade of purine receptors P2Y12. Pleiotropic effects of the drug were revealed - anti-inflammatory due to inhibition of the production of platelet cytokines and cell adhesion molecules (CD40L, P-selectin), which is manifested by a decrease in the level of

SRB. The advantages of clopidogrel over aspirin have been proven for long-term use in patients with high and very high risk coronary artery disease - with myocardial infarction, a history of stroke, and diabetes.

Recommended doses. The first dose of the drug (as early as possible!) is 300 mg (4 tablets) orally once (loading dose), then the daily maintenance dose is 75 mg (1 tablet) once a day, regardless of food intake, for 1 to 9 months . The antiplatelet effect develops 2 hours after taking a loading dose of the drug (reduction of aggregation by 40%). Maximum effect(60% suppression of aggregation) is observed on days 4-7 of continuous administration of a maintenance dose of the drug and persists for 7-10 days (platelet life period). Contraindications: individual intolerance; active bleeding; erosive and ulcerative processes in the gastrointestinal tract; heavy liver failure; age less than 18 years.

3) Abciximab- antagonist of glycoprotein Ilb/IIIa platelet receptors.

As a result of platelet activation, the configuration of these receptors changes, which increases their ability to fix fibrinogen and other adhesive proteins. The binding of fibrinogen molecules to the Ilb/IIIa receptors of various platelets leads to the connection of the plates with each other - aggregation. This process does not depend on the type of activator and is the final and only mechanism of platelet aggregation

For ACS: intravenous bolus (10-60 minutes before PCI) at a dose of 0.25 mg/kg, then 0.125 mcg/kg/min. (maximum 10 mcg/min.) for 12-24 hours.

At intravenous administration The steady-state concentration of abciximab is maintained only by continuous infusion and, after its cessation, decreases within

6 hours quickly, and then slowly (over 10-14 days) due to the platelet-bound fraction of the drug.

Anticoagulants

They are able to inhibit the thrombin system and/or its activity, thereby reducing the likelihood of complications associated with thrombosis. There is evidence that anticoagulants are effective in addition to inhibiting platelet aggregation and that the combination is more effective than treatment with one drug alone (Class I, Level A).

The drug with the most favorable profile efficiency - safety is fondaparinux (2.5 mg SC daily) (Class I, Level A).

If fondaparinux or enoxaparin are not available, unfractionated heparin with a target APTT of 50–70 sec or other low molecular weight heparins at specific recommended doses is indicated (Class I, Level C).

Unfractionated heparin (UFH).

When using heparin, it is necessary to measure the activated partial thromboplastin time (aPTT) and maintain it in the therapeutic range - prolongation of the aPTT by 1.5-2.5 times higher than the control. The reference (normal) APTT value depends on the sensitivity of the reagent used in a given laboratory (usually 40 seconds). Determination of APTT should be carried out every 6 hours after each change in the dose of heparin and once every 24 hours when the desired APTT is maintained in two consecutive analyses. Currently, it is still recommended to administer heparin intravenously using a dispenser - around the clock, along with aspirin under careful monitoring of the platelet count in the blood serum. Discontinuation of treatment - stabilization of angina (no angina attacks).

Basic by-effect- bleeding. Possible allergic reactions, with long-term use - thrombocytopenia.

They reduce myocardial oxygen demand (by reducing heart rate, blood pressure, preload and myocardial contractility) and increase myocardial oxygen supply through stimulation of coronary vasodilation.

Anti-ischemic drugs include nitrates, beta blockers and calcium antagonists.

Acute coronary syndrome with ST segment elevation (myocardial infarction).

Myocardial infarction is an acute disease caused by the occurrence of foci of ischemic necrosis in the heart muscle due to absolute insufficiency coronary blood flow caused by coronary artery thrombosis.
Reason: rupture of a “soft” atherosclerotic plaque triggers a cascade of blood clotting reactions, which leads to acute thrombotic occlusion of the coronary artery. If restoration of blood perfusion through the artery does not occur, then myocardial necrosis develops (starting from the subendocardial sections). Depending on the duration of ischemia, the condition of the coronary vessels and accompanying circumstances (the so-called premorbid background), both reversible damage to cardiomyocytes and their irreversible necrosis can occur.

Classification.

In the most acute stage of myocardial infarction, which is based on the processes ischemic damage, it is recommended to use the term acute coronary syndrome with ST elevation (as an intermediate diagnosis). When infarct changes form on the ECG (the appearance of a pathological Q or QS wave), it is necessary to diagnose acute myocardial infarction of one location or another.
Myocardial infarction without a pathological Q wave (in our country it is more often referred to as small-focal myocardial infarction). It is also based on thrombosis of the coronary artery, but unlike large-focal MI, it does not completely occlude the lumen of the vessel. Accordingly, this is not accompanied by changes in the QRS complex and ST segment elevation on the ECG. Currently with unstable angina included in the category ACS without ST elevation.

Clinic.

1. Pain syndrome - intense chest pain lasting more than 15 minutes, which does not go away after taking nitroglycerin, usually accompanied by
shortness of breath. The vast majority of patients simultaneously develop signs of activation of the autonomic nervous system(pallor, cold sweat), which is very typical for anginal pain.
2. Acute left ventricular failure syndrome - suffocation (feeling of lack of air at rest). Develops in 100% of acute myocardial infarction, in parallel
with pain syndrome. With repeated and recurrent myocardial infarctions, the leading one in the clinic (with mild or even absence of pain) is the asthmatic variant of myocardial infarction.
3. Electrocardiographic syndrome. Even in the early stages of myocardial infarction, ECG parameters rarely remain normal.
- Small focal myocardial infarction (myocardial infarction without a Q wave) - characterized by the appearance on the ECG of a coronary T wave (negative, pointed
and isosceles).
— Large-focal myocardial infarction — characterized by the appearance of a pathological Q wave in at least two leads:
— Transmural myocardial infarction is determined by the appearance of a pathological QS wave (no R wave):

4. Resorption-necrotic syndrome is caused by the resorption of necrotic masses and the development of aseptic inflammation of the myocardium. The most important signs:
Increased body temperature lasting up to 10 days, with a body temperature of no more than 38 degrees
Leukocytosis up to 10-12 000 from the first days
Acceleration of ESR by 5-6 days
The appearance of biochemical signs of inflammation - increased levels of fibrinogen, seromucoid, haptoglobin, sialic acids, a2-globulin, Y-globulin, C-reactive protein.
The appearance of biochemical markers of myocardial death - aspartate aminotransferase, lactate dehydrogenase, creatine phosphokinase, glycogen phosphorylase, myoglobin, myosin, cardiotroponins T, I.
5. Arrhythmic syndrome - with myocardial infarction, heart rhythm disturbances are recorded in 100% of cases (in the vast majority of cases ventricular),
which in the most acute and acute stages of myocardial infarction often determine the prognosis of patients due to the high risk of developing arrhythmic death as a result of ventricular fibrillation against their background.
6. Cardiogenic shock syndrome occurs in 3 variants - painful (reflex shock as a result of intense chest pain), arrhythmic - significant
increase (more than 180 beats/min) or decrease (less than 40 beats/min) in the number of heart contractions with the natural development of hemodynamic disorders as a result of a fall cardiac output. The third option is the most unfavorable - true cardiogenic shock (it is based on the death of a significant part of the left ventricular myocardium).
Clinical options:
1. Anginal - the classic version, the main clinical manifestation is severe chest pain, accompanied by a feeling of lack of air and severe sweating.
2. Asthmatic variant - the syndrome of acute left ventricular failure dominates. Occurs often, especially with repeated and recurrent myocardial infarctions, in elderly and old age, especially against the background of previous CHF. Anginal pain may not be very intense or may be completely absent, and an attack of cardiac asthma or pulmonary edema is the first and only clinical symptom of MI.
3. Gastralgic - very often the cause of diagnostic errors. More often observed with diaphragmatic MI. It is characterized by pain in the upper abdomen, dyspeptic symptoms - nausea, vomiting, flatulence, and in some cases paresis gastrointestinal tract. There may be tension when palpating the abdomen abdominal wall. In the abdominal form of MI, the clinical picture resembles an acute disease digestive tract. An incorrect diagnosis can lead to erroneous treatment tactics. There are cases when such patients undergo gastric lavage and even undergo surgery. Therefore, every patient with suspected “ acute stomach» It is necessary to register an ECG.
4. Arrhythmic variant - debuts with paroxysmal disturbances of heart rhythm, syncope. In the arrhythmic form of myocardial infarction, pain may be absent or mildly expressed. If severe violations rhythm occur against the background of a typical anginal attack or simultaneously with it, they are not talking about atypical form MI, but its complicated course, although the conventions of such a division are obvious.

5. The cerebral variant is characterized by intense headaches, loss of consciousness, nausea, vomiting, and may be accompanied by transient focal symptoms, which greatly complicates diagnosis. Diagnosis of MI is possible only with timely and dynamic ECG recording. This option MI most often occurs in patients with initially stenotic extracranial and intracranial arteries, often with disorders cerebral circulation in past.
6. “Asymptomatic” option - very often diagnosed by the presence of scar changes on the ECG.

Diagnostics

EchoCG. The main symptom of MI is an area of impaired myocardial contractility.
Using this research method, it is possible to determine the localization of MI, which is especially important if there are no diagnostic signs of the disease on the ECG. EchoCG is the main method for diagnosing a number of complications of MI: rupture of the interventricular septum, rupture of the free wall or the formation of an LV aneurysm, intravenous
Lost thrombosis.
Coronary angiography. Detection of acute coronary artery occlusion along with clinical symptoms allows for an accurate diagnosis.

Treatment

When fibrinolytic therapy is carried out in the first hours of the disease, it is possible to save an additional 50-60 lives per 1000 patients and, in many more, to avoid the development of heart failure and other complications of myocardial infarction or to reduce their severity. The essence of the treatment is the enzymatic destruction of the fibrin threads that form the basis of the occluding coronary thrombus, with the restoration of adequate coronary circulation.
Indications for fibrinolytic therapy are clinical symptoms + ST segment elevation or acute left bundle branch block. The exception is patients with true cardiogenic shock, in which the time from the onset of the disease is not taken into account.

Goals of treatment of acute MI with thrombolytics:

— Rapid recanalization of an occluded coronary artery
— Relief of chest pain
— Limiting the size of acute MI and preventing its spread
— Preservation of LV function due to maximum preservation of its muscle mass in the affected area.
Contraindications to thrombolytic therapy:
1) stroke;
2) lack of consciousness;
3) major trauma or surgery suffered within the last 3 weeks;
4) gastrointestinal bleeding during the last month;
4) hemorrhagic diathesis;
5) dissecting aortic aneurysm;
6) arterial hypertension more than 160 mm Hg. Art.
In our country, the optimal treatment for MI is currently the use of tissue plasminogen activator, alteplase (actilyse). After intravenous administration, alteplase binds to fibrin, is activated and causes the conversion of plasminogen to plasmin, which leads to the dissolution of fibrin in the thrombus. As a result of clinical studies, actilise has been proven to be much more effective in recanalizing coronary arteries - in comparison with other thrombolytics, in particular streptokinase. The continued use of streptokinase to date is determined only by the relative “cheapness” of the drug in comparison with actilise.

Indicators of successful thrombolysis:
1. Resolution of anginal pain;
2. ECG dynamics: | ST by 70% of the initial value in case of infarction of posteroinferior localization and by 50% in case of anterior infarction;
3. t level of isoenzymes (MP-CPK, Tnl, TpT) 60-90 minutes from the start of thrombolysis;
4. Reperfusion arrhythmias ( ventricular extrasystole, accelerated idioventricular rhythm)

2) Direct anticoagulants.

Simultaneously with the administration of actilise, heparin should be started for a period of 24 hours or more (heparin is contraindicated when using streptokinase). Heparin is administered intravenously at a rate of 1000 units per hour. The dose of heparin should be adjusted depending on the results of repeated determination of activated partial thromboplastin time (aPTT) - the values of this indicator should exceed the initial level by 1.5-2.0 times, but no more (threat of bleeding). An alternative to this method of treatment is the use of low molecular weight heparins - enoxaparin (Clexane) 1 mg per kg of patient's body weight, subcutaneously 2 times a day. With proven identical clinical effectiveness— this type of use of anticoagulant therapy is determined by the ease of use and the absence of the need for careful laboratory testing
control.
3. The effectiveness of thrombolytic and anticoagulant therapy increases significantly if it is combined with aspirin in a therapeutic dose of 325 mg.
4. Clopidogrel (Plavike, Zilt, Plagril) is indicated for all patients with ACS with ST segment elevation. The loading dose is 300 mg orally, the maintenance dose is 75 mg per day. The use of this drug is indicated throughout the entire period of hospitalization.
5. Statins. Indicated from the first day of treatment for acute MI.
6. Nitrates (nitroglycerin, isoket, perlinganite) - administered intravenously, improve myocardial perfusion, reduce pre- and afterload on the LV, determining
decreased myocardial oxygen demand.
Clinical indications for which the administration of nitrates is necessary:
- anginal attack
- signs of heart failure
- uncontrolled hypertension.
Contraindications for nitrates:
GARDEN< 90 мм рт. ст. или его снижение более чем на 30 мм рт. ст. от исходного
Heart rate<50 уд/мин
Heart rate >100 beats/min
Right ventricular MI
7. Beta-blockers - by reducing myocardial oxygen demand, improve perfusion in the ischemic zone, providing antiarrhythmic, antifibrillatory effects, provide a reduction in mortality not only in the long term, but also in early dates from the onset of myocardial infarction. It is recommended to use highly selective
drugs that do not have their own sympathomimetic effect. Preference is given to metoprolol, bisoprolol and betaxolol.
8. Calcium antagonists are not recommended in the early stages of myocardial infarction.

9. ACE inhibitors.

Acute coronary syndrome is a pathological process in which the natural blood supply to the myocardium through the coronary arteries is disrupted or completely stopped. In this case, oxygen does not reach the heart muscle in a certain area, which can lead not only to a heart attack, but also to death.

The term "ACS" is used by clinicians to refer to certain heart diseases, including unstable heart disease. This is due to the fact that the etiology of these diseases lies. In this condition, the patient requires emergency medical care. In this case, we are talking not only about the development of complications, but also a high risk of death.

Etiology

The main cause of acute coronary syndrome is damage to the coronary arteries by atherosclerosis.

In addition, there are such possible factors development of this process:

strong, nervous overstrain;
narrowing of the lumen of the vessel;
mechanical damage to the organ;
complications after surgery;
coronary arteries;
inflammation of the coronary artery;
congenital pathologies of the cardiovascular system.

Separately, it is necessary to highlight factors that predispose to the development of this syndrome:

overweight, ;
smoking, drug use;
almost complete lack of physical activity;
imbalance of fats in the blood;
alcoholism;
genetic predisposition to cardiovascular pathologies;
increased blood clotting;
frequent stress, constant nervous tension;
taking certain medications which lead to a decrease in pressure in the coronary arteries (coronary steal syndrome).

ACS is one of the most life-threatening conditions for humans. In this case, not only emergency medical care is required, but also urgent resuscitation measures. The slightest delay or incorrect first aid actions can lead to death.

Pathogenesis

Due to thrombosis of the coronary vessels, which is provoked by a certain etiological factor, from platelets begin to be released biologically active substances- thromboxane, histamine, thromboglobulin. These compounds have a vasoconstrictor effect, which leads to a deterioration or complete cessation of blood supply to the myocardium. This pathological process can be aggravated by adrenaline and calcium electrolytes. At the same time, the anticoagulant system is blocked, which leads to the production of enzymes that destroy cells in the necrosis zone. If the development of the pathological process is not stopped at this stage, then the affected tissue will transform into a scar, which will not take part in the contraction of the heart.

The mechanisms of development of acute coronary syndrome will depend on the degree of thrombus or plaque occlusion of the coronary artery. The following stages are distinguished:

with a partial decrease in blood supply, attacks of angina may occur periodically;
with complete overlap, areas of dystrophy appear, which later transform into necrosis, which will lead to;
sudden pathological changes- lead to ventricular fibrillation and, as a consequence, clinical death.

It is also necessary to understand that a high risk of death is present at any stage of the development of ACS.

Classification

Based modern classification, the following clinical forms of ACS are distinguished:

acute coronary syndrome with ST segment elevation - the patient has typical ischemic pain in the chest, reperfusion therapy is required;
acute coronary syndrome without ST segment elevation – changes typical for coronary disease, attacks of angina, are noted. Thrombolysis is not required;
myocardial infarction diagnosed by changes in enzymes;
unstable angina.

Forms of acute coronary syndrome are used only for diagnostic purposes.

Symptoms

First and most characteristic feature disease is sharp pain in the chest. The pain syndrome can be paroxysmal in nature and radiate to the shoulder or arm. With angina pectoris, the pain will be squeezing or burning in nature and short-lived. In case of myocardial infarction, the intensity of manifestation of this symptom can lead to painful shock, so immediate hospitalization is required.

In addition, in clinical picture The following symptoms may be present:

cold sweating;
unstable blood pressure;
excited state;
confusion;
panic fear of death;
fainting;
pale skin;
the patient feels a lack of oxygen.

In some cases, symptoms may be accompanied by nausea and vomiting.

With such a clinical picture, the patient needs to urgently provide first aid and call an emergency room. medical care. Under no circumstances should the patient be left alone, especially if there is nausea with vomiting and loss of consciousness.

Diagnostics

The main method for diagnosing acute coronary syndrome is electrocardiography, which must be done in as soon as possible from the onset of a painful attack.

A full diagnostic program is carried out only after the patient’s condition has been stabilized. Be sure to notify the doctor about what medications were given to the patient as first aid.

The standard program of laboratory and instrumental examinations includes the following:

general blood and urine analysis;
biochemical blood test - the level of cholesterol, sugar and triglycerides is determined;
coagulogram - to determine the level of blood clotting;
ECG is a mandatory method instrumental diagnostics with ACS;
echocardiography;
coronary angiography - to determine the location and degree of narrowing of the coronary artery.

Treatment

The therapy program for patients with acute coronary syndrome is selected individually, depending on the severity of the pathological process; hospitalization and strict bed rest are required.

The patient’s condition may require measures to provide emergency first aid, which include the following:

provide the patient with complete rest and access to fresh air;
put a nitroglycerin tablet under your tongue;
Call emergency medical services and report your symptoms.

Treatment of acute coronary syndrome in a hospital may include the following therapeutic measures:

oxygen inhalation;
administration of medications.

Within drug therapy, the doctor may prescribe the following medications:

narcotic or non-narcotic painkillers;
anti-ischemic;
beta blockers;
calcium antagonists;
nitrates;
disaggregants;
statins;
fibrinolytics.

In some cases conservative treatment it turns out to be insufficient or not at all appropriate. In such cases, the following surgical intervention is performed:

stenting of the coronary arteries - a special catheter is passed to the site of narrowing, after which the lumen is expanded using a special balloon, and a stent is installed at the site of narrowing;
coronary artery bypass grafting - the affected areas of the coronary arteries are replaced with shunts.

Such medical measures make it possible to prevent the development of myocardial infarction from ACS.

In addition, the patient must follow general recommendations:

strict bed rest until steady improvement conditions;
complete elimination of stress, strong emotional experiences, nervous tension;
exclusion of physical activity;
as the condition improves, daily walks in the fresh air;
exclusion from the diet of fatty, spicy, too salty and other heavy foods;
complete exclusion of alcoholic beverages and smoking.

You need to understand that acute coronary syndrome, if the doctor’s recommendations are not followed, can lead to serious complications, and the risk of death during relapse always remains.

Separately, diet therapy for ACS should be highlighted, which implies the following:

limiting the consumption of animal products;
the amount of salt should be limited to 6 grams per day;
exclusion of overly spicy, seasoned dishes.

It should be noted that compliance with this diet is necessary constantly, both during the treatment period and as a preventive measure.

Possible complications

Acute syndrome coronary insufficiency may lead to the following:

heart rhythm disturbance in any form;
acute development, which can lead to death;
inflammation of the pericardium;

It should also be understood that even with timely medical measures, there remains a high risk of developing the above complications. Therefore, such a patient should be systematically examined by a cardiologist and strictly follow all his recommendations.

Prevention

Prevent development cardiovascular diseases It is possible if you follow the following doctor’s recommendations in practice:

complete cessation of smoking, moderate consumption of alcoholic beverages;
proper nutrition;
moderate physical activity;
daily walks in the fresh air;
elimination of psycho-emotional stress;
control of blood pressure indicators;
control blood cholesterol levels.

In addition, we should not forget about the importance of preventive examination by specialized medical specialists, following all doctor’s recommendations regarding the prevention of diseases that can lead to acute coronary insufficiency syndrome.

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