Acute coronary syndrome without ST segment elevation. Clinic

The clinical manifestations of coronary 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 the optimal treatment, which is based on an assessment of the risk of complications and a targeted approach to prescribing invasive interventions, is of great importance. 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-onset complete block of the left bundle branch), reflecting acute total occlusion of one or more coronary arteries, the goal of treatment is rapid, complete and persistent restoration of the lumen of the coronary artery using thrombolysis (if it is not contraindicated) or primary coronary angioplasty (if technically feasible). The effectiveness of these therapeutic measures has been proven in a number of studies.

Non-ST segment elevation acute coronary syndrome refers to patients with chest pain and ECG changes indicating acute myocardial ischemia (but not necessarily necrosis).

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 the recommendations of the European Society of Cardiology Working Group on the treatment of non-ST segment elevation acute coronary syndrome were published. 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 studies. 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 to which conclusions about the effectiveness of various diagnostic and treatment methods are convincing 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 obtained from several randomized clinical trials or meta-analyses.

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

Level C. Conclusions are based on expert consensus.

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 [not lower than Canadian Cardiovascular Society (CCS) class III] angina, recent worsening of stable angina of at least to III FC 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 pain sensations were completely reproduced upon palpation. Atypical manifestations of ACS are especially often observed in young (2540 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, first of all, to exclude non-cardiac causes of chest pain (pleurisy, pneumothorax, myositis, inflammatory diseases of the 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 ｫoldｻ 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 a 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/intensive care units and cardiac intensive care units (level of evidence: C).

Study of biochemical markers of myocardial damage

ｫTraditionalｻ cardiac enzymes, namely creatine phosphokinase (CPK) and its isoenzyme CK MB are less specific (in particular, false-positive results are possible in case of 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 612 hours after admission to the hospital, as well as after each episode of severe 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 612 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. 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. The subject of special attention should 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 cardiac arrhythmias.

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 are a highly heterogeneous group of patients who vary in the extent and/or severity of atherosclerotic coronary artery disease, as well as in the degree of thrombotic risk (i.e.

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 of 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 for ACS are similar to the 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 of acetylsalicylic acid, 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 a standard exercise test (bicycle ergometry or treadmill) should undergo coronary angiography 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 blockers (level of evidence: A).

3. Broad impact on risk factors. First of all, stopping smoking and normalizing the lipid profile (level of evidence: A).

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

Conclusion

Currently, many medical institutions in Russia do not have the capabilities to carry out the above-mentioned diagnostic and therapeutic measures (determination of the level of troponins T and I, myoglobin; emergency coronary angiography, use of IIb/IIIa receptor blockers, etc.). We 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.

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Non-ST-segment elevation ACS (Figure 1) covers a heterogeneous spectrum of patients with varying levels of risk for mortality, MI, and recurrent MI. A stepwise, standardized strategy based on available scientific information can be applied to most patients in whom non-ST-segment elevation ACS is suspected. It should be noted, however, that certain indicators in individual patients may lead to some deviations from the proposed strategy. For each patient, the physician must make a separate decision, taking into account the medical history (comorbidities, advanced age, etc.), the clinical condition of the patient, the initial study results at the time of first contact, and the available pharmacological and non-pharmacological treatments.

Rice. 1. Decision-making algorithm for the management of patients with ACS without ST-segment elevation.

Initial assessment

Chest pain or discomfort is a symptom that leads the patient to seek medical attention or hospitalization. A patient suspected of having non-ST segment elevation ACS should be tested in the hospital and immediately seen by a competent physician. Specialized departments, including a chest pain diagnostic section, provide better and faster service.

The initial stage is to immediately establish a working diagnosis for the patient, on which the entire treatment strategy will be based. Criteria:

characteristic feature of chest pain and symptom-focused physical examination;
assessment of the likelihood of having IHD according to indicators (for example, old age, risk factors, history of MI, CABG, PTA);
ECG (ST segment deviations or other ECG pathologies).

Depending on these data, which must be obtained within 10 minutes after the first medical contact with the patient, he can be given one of three main working diagnoses:

ACS with ST segment elevation requiring immediate reperfusion;
ACS without ST segment elevation;
ACS is unlikely.

Classification as “unlikely” should be made with caution and only when there is another basis for the diagnosis (eg, trauma). Additional ECG leads (V3R and V4R, V7-V9) should be recorded, especially in patients with persistent chest pain.

A blood test is taken from the patient upon arrival at the hospital, and the results of the test, which will be used in the second stage of the strategy, must be obtained within 60 minutes. The required minimum initial blood tests should include: troponin T or troponin I, creatine kinase (-MB), creatinine, hemoglobin, and white blood cell count.

Diagnosis confirmation

Once the patient is classified as non-ST-segment elevation ACS, IV and oral treatment will be started as per Table. 1. First line of therapy includes nitrates, β-blockers, aspirin, clopidogrel and anticoagulation. Further treatment will be based on additional information/data listed in the table. 2.

Table 1

Scheme of initial treatment of patients with acute coronary syndrome

Oxygen	Insufflation (4-8 L/min) if oxygen saturation is less than 90%
	Sublingual or IV (use caution if systolic pressure is less than 90 mmHg)
	Initial dose 160-325 mg without soluble coating, followed by 75-100 mg/day (IV administration is acceptable)
Clopidogrel	Loading dose of 300 mg (or 600 mg for faster onset of action) followed by 75 mg daily
Anticoagulation	The choice between different options depends on the strategy Unfractionated heparin IV in the form of a bolus of 60-70 units/kg (maximum mum 5000 units) followed by infusion of 12-15 units/kg per hour (maximum 1000 units/hour) with titration to aPTT of 1.5-2.5 control time Fondaparinux sodium s.c. at a dose of 2.5 mg/day Enoxaparin sodium s.c. dose 1 mg/kg 2 times a day Dalteparin sodium s.c. dose 120 units/kg 2 times a day Nadroparin calcium subcutaneously at a dose of 86 units/kg 2 times a day Bivalirudin 0.1 mg/kg bolus followed by 0.25 mg/kg per hour
	3-5 mg IV or SC, depending on the severity of pain
Taking β-adreno blockers inside	Especially if there is tachycardia or arterial hypertension without symptoms of HF
	At a dose of 0.5-1 mg IV if there is bradycardia or vagal reaction

table 2

Diagnosis confirmation

Treatment of each patient is individualized according to the risk of subsequent adverse events and should be assessed early in the initial clinical picture, as well as repeatedly if symptoms persist or recur and after additional information is obtained from biochemical tests or imaging tests. Risk assessment becomes an important component of the decision-making process and is subject to continuous re-evaluation. This concerns the assessment of both ischemic and bleeding risk.

There is significant overlap between the risk factors for bleeding and ischemia, such that patients at high risk for ischemia are also at high risk for bleeding complications. That is why the choice of pharmacological therapy (double or triple antiplatelet therapy, anticoagulants) becomes extremely important, as does the dosage regimen of drugs. In addition, if an invasive strategy is necessary, the choice of vascular access is very important, as radial access has been shown to reduce the risk of bleeding compared with femoral access. In this context, special attention should be paid to chronic renal failure, which has been shown to be particularly common in older patients and among diabetics.

During this step, other diagnoses, such as acute anemia, pulmonary embolism, or aortic aneurysm, can be confirmed or excluded (Table 2).

During this stage, a decision must be made whether the patient needs to undergo cardiac catheterization or not.

Christian W. Hamm, Helge Möllmann, Jean-Pierre Bassand and Frans van de Werf

Acute coronary syndrome

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 the development of acute coronary syndrome is damage to the coronary arteries by atherosclerosis.

In addition, the following possible factors in the development of this process are identified:

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 that 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, biologically active substances begin to be released from platelets - 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 on the 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

The first and most characteristic sign of the disease is acute chest pain. 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 this symptom can lead to painful shock, so immediate hospitalization is required.

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

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 emergency 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 as soon as possible after 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 of instrumental diagnostics for 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.

As part of drug therapy, the doctor may prescribe the following drugs:

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

In some cases, conservative treatment is not enough or is not appropriate at all. 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 stable improvement;
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 at any time, and the risk of death in case of 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 preventative measure.

Possible complications

Acute coronary insufficiency syndrome can 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

You can prevent the development of cardiovascular diseases 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 a preventive examination by specialized medical specialists and compliance with all doctor’s recommendations regarding the prevention of ailments that can lead to acute coronary insufficiency syndrome.

Is everything in the article correct from a medical point of view?

Answer only if you have proven medical knowledge

Term acute coronary syndrome (ACS) used to indicate exacerbation of ischemic heart disease. This term combines such clinical conditions as myocardial infarction (MI) and unstable angina. Experts of the All-Russian Scientific Society of Cardiology adopted the following definition of ACS and unstable angina (2007):

Acute Coronary Syndrome – a term denoting any group of clinical signs or symptoms that suggest AMI or unstable angina. Includes the concepts of AMI, STEMI, NSTEMI ECG, MI diagnosed by enzyme changes, other biomarkers, late ECG signs, and unstable angina.

The term “ACS” was introduced into clinical practice when it became clear that the use of certain active treatment methods, in particular thrombolytic therapy, should be resolved quickly, often before the final diagnosis of MI. It has been established that the nature and urgency of intervention to restore coronary perfusion is largely determined by the position of the ST segment relative to the isoelectric line on the ECG: when the ST segment is displaced upward (ST elevation), the method of choice for restoring coronary blood flow is coronary angioplasty, but if it is impossible to carry it out within the appropriate time frame, it is effective and, accordingly, thrombolytic therapy is indicated. Restoration of coronary blood flow in NSTE-ACS should be carried out without delay. In NSTE-ACS, thrombolytic therapy is not effective, and the timing of coronary angioplasty (in rare cases, coronary bypass surgery) depends on the degree of risk of the disease. If in a patient with a clear exacerbation of coronary artery disease the choice of the main method of treatment depends on the presence or absence of ST elevation, then from a practical point of view it has become advisable, at the first contact of a doctor with a patient who is suspected of developing ACS, to use the following diagnostic terms (identifying the following forms of ACS ): “OKSpST” and “OKSbpST”.

ACS with ST segment elevation and ACS without ST segment elevation

NSTE-ACS is diagnosed in patients with an anginal attack or other unpleasant sensations (discomfort) in the chest and persistent (lasting at least 20 minutes) ST segment elevation or “new” (first-time) LBP blockade on the ECG. Typically, patients whose disease begins as NSTE-ACS later develop signs of myocardial necrosis - increased biomarker levels and ECG changes, including the formation of Q waves.

The appearance of signs of necrosis means that the patient has developed an MI. The term “MI” reflects the death (necrosis) of cardiac muscle cells (cardiomyocytes) as a result of ischemia (Appendix 1).

OKSbpST. These are patients with an anginal attack and, usually, with ECG changes indicating acute myocardial ischemia, but without ST segment elevation. They may experience persistent or transient ST depression, inversion, flattening or pseudo-normalization of T waves. The ECG on admission may be normal. In many cases, non-occlusive (mural) thrombosis of the coronary artery is detected. Subsequently, some patients develop signs of myocardial necrosis, caused (in addition to the initial cause of ACS) by embolism of small myocardial vessels, fragments of a thrombus and material from a ruptured AB. However, the Q wave rarely appears on the ECG, and the developed condition is referred to as “non-ST-segment elevation MI.”

On the relationship between the diagnostic terms "ACS" and "MI"

The term “ACS” is used when diagnostic information is still insufficient to make a final judgment about the presence or absence of foci of necrosis in the myocardium. Accordingly, ACS is a working diagnosis in the first hours, while the concepts of “MI” and “unstable angina” (ACS that did not end with the appearance of signs of myocardial necrosis) are retained for use in formulating the final diagnosis.

If signs of myocardial necrosis are detected in a patient with ACS whose initial ECG shows persistent ST segment elevations, this condition is designated as STEMI. In the future, depending on the ECG picture, the maximum level of cardiac troponin or enzyme activity and data from imaging methods, the diagnosis is clarified: MI may be large-focal, small-focal, with Q waves, without Q waves, etc.