Acute coronary syndrome without ST segment elevation: symptoms, diagnosis and treatment. Recommendations of the European Society of Cardiology for the appointment of antiplatelet agents in patients with non-ST elevation ACS

Treatment of acute coronary syndrome without persistent ST elevation on ECG

Developed by a committee of experts of the All-Russian Scientific Society of Cardiology

Moscow 2006

All-Russian Scientific Society of Cardiology

Moscow, 2006

© All-Russian Scientific Society of Cardiology Reproduction in any form and reprint of these materials is possible only with the permission of VNOK

Dear colleagues!

These guidelines are based on new data that have become available since the first version was published in 2001. They can be considered a unified standard for the treatment of patients with non-ST elevation acute coronary syndrome, based on the most modern ideas about the pathogenesis, diagnosis and treatment of this group of diseases and, of course, taking into account the specific conditions of Russian healthcare.

The proposed methods of treatment, based on a clear stratification of risk factors, are confirmed by the results of recent international, multicenter studies and have proven their effectiveness in thousands of treated patients.

The All-Russian Scientific Society of Cardiology hopes that Russian Recommendations on the treatment of non-ST elevation acute coronary syndrome will be a guide to action for every cardiologist.

President of VNOK, Academician R.G. Oganov

ACC/AAC - American College of Cardiology/American-

GP IIb/IIIa of platelets – glycoproteins of IIb/IIIa of platelets

HTG - hypertriglyceridemia DBP - diastolic blood pressure

ACE inhibitors - angiotensin-converting enzyme inhibitors

1. Introduction

As a chronic disease, CHD is characterized by periods of stable course and exacerbations. The period of exacerbation of CBS is referred to as ACS. This term includes such clinical conditions as MI, including non-Q-MI, small-focal, micro-, etc.) and NS. NS and MI are different clinical manifestations of a single pathophysiological process - thrombosis of varying severity over atherosclerotic plaque tear or erosion of the coronary endothelium, and subsequent distal thromboembolism.

The term ACS was introduced into clinical practice when it became clear that the question of the use of certain active methods of treatment, in particular TLT, should be decided before the final diagnosis of the presence or absence of large-focal MI.

At the first contact of a doctor with a patient with suspicion of the presence of ACS according to clinical and ECG featured it can be classified into one of its two main forms.

OKSP ST . These are patients with pain or other unpleasant sensations (discomfort) in chest and persistent ST-segment elevations or "new", new onset, or presumably new onset LBBB on the ECG. Persistent ST segment elevations reflect the presence of acute complete occlusion of the CA. The goal of treatment in this situation is the rapid and stable restoration of the lumen of the vessel. For this, in the absence of contraindications, thrombolytic agents or direct angioplasty - PCI are used.

OKSBP ST . Patients with chest pain and ECG changes indicative of acute myocardial ischemia, but PD ST. These patients may have persistent or transient ST depressions, T-wave inversion, flattening, or pseudo-normalization; The ECG on admission may be normal. The management strategy for such patients is to eliminate ischemia and symptoms, follow-up with repeated (serial) ECG recording and determination of markers of myocardial necrosis: STR and CPK MV. In the treatment of such patients, thrombolytic agents are not effective and are not used. Treatment tactics depend on the degree of risk (severity of the condition) of the patient.

1.1. Some definitions ACS is any group of clinical signs

The criteria or symptoms suggestive of acute MI or UA include AMI, ST UTI, ST STEMI, MI diagnosed by enzyme changes, by biomarkers, by late ECG features, and UA. The term appeared in connection with the need to choose medical tactics until the final diagnosis of these conditions. Used to refer to patients on first contact with them and implies the need for treatment as patients with MI or NS.

STEMI is an acute process of myocardial ischemia of sufficient severity and duration to cause myocardial necrosis. There are no ST elevations on initial ECGs. Most patients who begin as STEMI do not develop Q waves and are eventually diagnosed with non-Q MI. IMBP ST differs from NS in the presence (increased levels) of markers of myocardial necrosis, which are absent in NS.

NS is an acute process of myocardial ischemia, the severity and duration of which are insufficient for the development of myocardial necrosis. There is usually no ST elevation on the ECG. There is no release into the bloodstream of biomarkers of myocardial necrosis in quantities sufficient for the diagnosis of MI.

1.1.1. Correlation between the concepts of NS and IBMP ST. NS with elevated STR levels

The concept of IMBP ST appeared in connection with the widespread introduction into clinical practice of the definition of STR. Patients with ST-ACSBP with elevated STR have a worse prognosis (higher risk) and require more active treatment and follow-up. The term ST STEMI is used to “mark” a patient for a short time until it is finally determined whether he has developed a large-focal MI or the process was limited to the occurrence of non-Q-MI. Isolation of ST IMBP without determination of STR based on less sensitive markers of necrosis, in particular CF CF, is possible, but leads to the identification of only a part of patients with necrosis foci in the myocardium and, therefore, a high risk.

Thus, rapid differentiation within ST-ACBP, ST-IMBP, and HC requires determination of STR levels.

NS and IMBP ST– conditions are very similar, having a common pathogenesis and a similar clinical picture, they can differ only in the severity (severity) of symptoms. In Russia, medical institutions use different, both quantitative and qualitative methods for determining STR. Accordingly, depending on the sensitivity of the method for determining necrosis markers, the same condition can be assessed differently: NS or IMBP ST. So far, the attitude to the diagnosis of MI based on the fact of an increase in the content of STR of any degree of severity has not been officially formulated. On the other hand, positive analysis on Tr (elevated levels when quantified) significantly affects the choice of method and place of treatment and should be somehow reflected in the diagnosis. Therefore, it is acceptable to use the wording "NS with an increased level of STR" (T or I) as equivalent to the term ST IMBP. This wording is provided by the classification of HC Hamm CW and Braunwald E - HC class IIIB, Tr positive (table 1).

2. Diagnosis

2.1. Clinical symptoms

Patients with suspected development of ST-ACSBP, whose treatment is considered in these recommendations, when applying for

medical care can be assigned to the following clinical groups:

patients after prolonged >15 min. an attack of anginal pain at rest. Such a condition usually serves as a basis for calling an ambulance or emergency treatment to a medical institution in some other way. It corresponds to HC class III according to the classification of Hamm CW and Braunwald E (Table 1). The patients belonging to this group form the main object of the present recommendations;

patients with a first onset in the previous 28-30 days of severe angina;

patients who have experienced destabilization of pre-existing CV with the appearance of characteristics inherent in at least FC III according to the classification of the Canadian Heart Association (Appendix), and / or attacks of pain at rest (progressive angina pectoris, crescendo angina pectoris).

ACS may manifest atypically, especially in young (25-40 years) and elderly (>75 years) patients, patients with diabetes and women. Atypical manifestations of NS include pain predominantly at rest, epigastric pain, acute indigestion, stabbing chest pain, pleural pain, or worsening dyspnoea. In these

Table 1

Classification NS Hamm CW, Braunwald E.

I - First appearance of severe angina, progressive angina; without rest angina

II - Angina pectoris in the previous month, but not in the next 48 hours; (rest angina, subacute)

III - Angina at rest in the previous 48 hours; (rest angina, acute)

Note: * Circulation 2000; 102:118.

cases of correct diagnosis are facilitated by indications of a more or less long-term existence of coronary heart disease.

2.2. Physical examination

The objectives of the examination are: to exclude non-cardiac causes of pain, non-ischemic heart disease (pericarditis, valvular disease), as well as non-cardiac causes that potentially contribute to increased ischemia (anemia); identification of cardiac causes that increase (or cause) myocardial ischemia (CH, AH).

Resting ECG is the main method for evaluating patients with ACS. An ECG should be provided when symptoms are present and compared with an ECG taken after symptoms have disappeared. It is desirable to compare the recorded ECG with the "old" ones obtained before the current exacerbation, especially in the presence of LVH or previous MI. Q waves indicating MI scarring are highly specific for severe coronary atherosclerosis but do not indicate instability at the moment.

ECG signs of unstable CAD - ST segment displacement and T wave changes. The likelihood of NS is especially high when the corresponding clinical picture is combined with ST segment depression > 1 mm in two or more adjacent leads, as well as T wave inversion > 1 mm in leads with a predominant wave R; the last sign is less specific. Deep symmetrical T-wave inversions in the anterior chest leads often indicate severe proximal stenosis of the anterior descending branch of the LCA; non-specific shifts of the ST segment and changes in the T wave, in amplitude ≤1 mm, are less informative.

Fully normal ECG in patients with symptoms suggestive of ACS does not rule out its presence. However, if a normal ECG is recorded during severe pain, one should more persistently look for other possible causes of the patient's complaints.

ST-segment elevation indicates transmural myocardial ischemia due to coronary artery occlusion. Persistent ST segment elevation is characteristic of developing MI. Preho-

Dramatic ST-segment elevation may be associated with Prinzmetal's angina (vasospastic angina).

2.4. Biochemical markers of myocardial damage

In AKSBP ST STR T and I as markers of myocardial necrosis due to their greater specificity and reliability are preferable to traditionally determined CPK and its MB fraction. Elevated levels of CTP T or I reflect necrosis of myocardial cells. In the presence of other signs of myocardial ischemia - retrosternal pain, changes in the ST segment, such an increase should be called MI.

The determination of STR makes it possible to detect myocardial damage in about a third of patients without an increase in CPK MV. Repeat blood draws and measurements are needed to confirm or rule out myocardial injury within 6–12 hours of admission and after any episode of severe chest pain.

The change in the content of various markers of myocardial necrosis over time in relation to the pain attack is shown in Figure 1. Myoglobin is a relatively early marker, while an increase in CPK MV and STR appears later. STR may remain elevated for 1–2 weeks, making it difficult to diagnose recurrent necrosis in patients with recent MI (Table 6 in the Appendix).

2.5. Risk assessment

At in patients diagnosed with ST ACSBP in each case, the choice of treatment strategy depends on the risk of developing MI or death.

The risk of death and MI increases with age. Male gender and previous manifestations of CAD, such as severe and long-term angina pectoris or previous MI, are associated with an increased risk of coronary complications. Signs of increased risk include LV dysfunction, congestive heart failure, and hypertension and diabetes. Most of the well-known CVD risk factors are also signs of poor prognosis in ACS.

* vertical axis- the content of the marker in the blood in relation to the level sufficient for the diagnosis of AMI (diagnostic level for MI), taken as a unit.

Rice. 1 Biochemical markers of myocardial necrosis and changes in their content in the blood after a pain attack.

2.5.1.1. Clinical Data

Prognostically important are the time elapsed since the last episode of ischemia, the presence of rest angina and the response to drug treatment. These signs, along with the concentration of STR, are taken into account in the classification of Hamm CW and Braunwald E. (Table 1).

ECG data are decisive for the diagnosis of ACS and the assessment of prognosis. Patients with ST-segment depression have a higher risk of subsequent complications than patients whose only change is T-wave inversion. In turn, the latter have a greater risk of complications compared to patients with a normal ECG.

Painless ("silent") episodes of myocardial ischemia cannot be determined using a conventional ECG. Therefore, Holter monitoring of the ECG is advisable, although its capabilities are limited to recording only

two or three leads and getting the result no less than a few hours after the recording*.

2.5.1.3. Markers of myocardial damage - STR

Patients with elevated FR have poorer short-term and long-term prognosis compared with patients without such an increase. The risk of new coronary events correlates with the degree of increase in Tr. The increased risk associated with high FR levels is independent of other RFs, including ECG changes at rest or on long-term monitoring. Identification of patients with elevated levels of STR is important for choosing a treatment method.

2.5.1.4. echocardiography

Echocardiography allows assessing the state of LV systolic function, which has an important prognostic value. During myocardial ischemia, local

* A promising technique is continuous 12-lead ECG monitoring with continuous analysis of the results using a computer. Continuous ST segment monitoring is also useful for evaluating the effect of treatment on ischemia.

hypokinesia or akinesia of the LV wall, and after the disappearance of ischemia - the restoration of normal contractility. To assess the prognosis and choose the tactics of managing patients, it is important to diagnose conditions such as aortic stenosis or hypertrophic cardiomyopathy.

2.5.1.5. Stress tests before discharge

A stress test performed after stabilization of the patient's condition and before discharge is useful for confirming the diagnosis of CAD and for assessing the risk of its complications. A significant proportion of patients fail to perform exercise tests, and this in itself is associated with a poor prognosis. The addition of imaging modalities to detect myocardial ischemia, such as echocardiography, provides a further increase in the sensitivity and specificity of prognosis. However, there are no large, long-term, predictive studies using stress echocardiography in patients after an episode of ST-ACSBP.

This research method provides information about the presence of stenosing changes in the coronary artery and their severity. Patients with multivessel disease and patients with LCA stenosis have a higher risk of serious complications. CAG assessment of the extent and location of the stenosis that caused deterioration and other stenoses is necessary if PCI is planned. The greatest risk is associated with the presence of filling defects indicating an intracoronary thrombus.

3. Methods of treatment

3.1. Anti-ischemic drugs

These drugs reduce myocardial oxygen consumption, lowering heart rate, blood pressure, suppressing LV contractility, or causing vasodilation.

evidence that a particular BAB is more effective. Therapy may be initiated with metoprolol, propranolol, or atenolol. In cases where, in the opinion of the doctor, a very rapid termination of the action of the BAB is necessary, it is advisable to use esmolol.

With the shortest active drugs treatment should be started if there are comorbidities, such as lung disease or LV dysfunction. Parenteral administration of β-blockers requires careful monitoring of blood pressure, preferably continuous ECG monitoring. The goal of the subsequent intake of BAB per os should be to achieve a heart rate of 50-60 beats / min. BAB should not be used in patients with severe AV conduction disorders (1st degree AV block with PQ>0.24 sec, II or III degrees) without a working artificial pacemaker, a history of bronchial asthma, severe acute LV dysfunction with signs of heart failure*.

Particular care should be taken in patients with chronic obstructive pulmonary disease, starting treatment with a relatively short-acting, cardioselective β-blocker, such as metoprolol in reduced doses.

3.1.2. Nitrates

It should be borne in mind that the use of nitrates in NS is based on pathophysiological prerequisites and clinical experience. Data from controlled studies that would prove the optimal dosage and duration of use are not available.

In patients with persistent episodes of myocardial ischemia (and / or coronary pain), it is advisable to prescribe intravenous nitrates. The dose should be gradually increased (“titrated”) until symptoms disappear or side effects: headache, hypotension. It should be remembered that long-term use of nitrates can be addictive.

As symptoms are controlled, intravenous nitrates should be replaced with non-parenteral forms, while maintaining a certain nitrate-free interval.

* For the use of BBs after the elimination of acute myocardial ischemia in patients with chronic HF, see the relevant recommendations of the VNOK.

10 Supplement to the journal "Cardiovascular Therapy and Prevention"

In order to improve the efficiency of providing medical care in emergencies, evidence-based methods of diagnosis and treatment, presented in clinical guidelines, are widely introduced into practice.

This approach allows not only to improve the quality of care, but also to ensure continuity at individual stages of patient treatment - from first aid to the implementation of high-tech methods of treatment.

One of the first documents regulating the conduct of therapeutic measures from the first contact with the patient to specialized inpatient treatment was the American Heart Association standards for caring for a victim with cardiac arrest. These algorithms are well known in our country, thanks to the inclusion of the basics of resuscitation in university and postgraduate education programs.

Currently, algorithms for providing care to patients with acute coronary syndrome have acquired particular relevance. This article presents a number of guidelines for prescribing oral antiplatelet agents in the management of patients with non-ST-segment elevation ACS, in accordance with the clinical guidelines of the European Society of Cardiology revised in 2011.

Acetylsalicylic acid(aspirin) is indicated for all patients with ACS without ST segment elevation. The initial (first) dose of aspirin is 150-300 mg, followed by 75-100 mg of the drug per day indefinitely in the absence of contraindications (class I recommendations, degree of evidence A).

It is emphasized that the concomitant chronic use of aspirin with non-steroidal anti-inflammatory drugs (selective cyclooxygenase-2 inhibitors and non-selective non-steroidal anti-inflammatory drugs) is not recommended (class III recommendation, grade C).

Against the background of treatment with aspirin, therapy with drugs that affect other mechanisms of platelet activation and aggregation is indicated. The drugs recommended for taking as a "second" antiplatelet agent include inhibitors of P2Y12 platelet receptors (adenosine diphosphate antagonists).

These drugs interfere with the formation of adenosine diphosphate (ADP) binding to platelet receptors belonging to the P2Y12 class. The current clinical guidelines include three drugs from this group: clopidogrel, ticagrelor, prasugrel.

In patients with ACS, ADP antagonists should be given as early as possible in combination therapy with aspirin (dual antiplatelet therapy) for up to 12 months, unless there are contraindications, in particular, high risk development of bleeding (class of recommendations I, the degree of scientific evidence A).

Often, when prescribing dual therapy with antiplatelet agents, there is a need for therapy with proton pump inhibitors in order to reduce the risk of developing gastrointestinal bleeding. However, ex vivo evaluation of clopidogrel has shown that proton pump inhibitors, especially omeprazole, reduce the ability of clopidogrel to inhibit platelet aggregation.

However, it has been proven that the appointment of omeprazole reduces the risk of gastrointestinal bleeding in patients taking antiplatelet agents. In this regard, all patients with gastrointestinal bleeding and peptic ulcer patients on dual antiplatelet therapy are advised to use proton pump inhibitors, and omeprazole should be avoided (Recommendation Class I, Evidence A).

The appointment of proton pump inhibitors is also advisable for patients with other risk factors for bleeding: infection Helicobacter pylori, age over 65 years, with the simultaneous appointment of anticoagulants and steroids.

Reception of dual therapy with antiplatelet agents should be continuous. It has been established that discontinuation of dual antiplatelet therapy shortly after percutaneous coronary intervention can lead to subacute stent stenosis and significantly worsen the prognosis with an increase in the risk of death up to 15-45% within a month.

Thus, according to clinical guidelines, if it is necessary to revise ongoing treatment during the period of taking dual antiplatelet therapy (the first 12 months from the onset of ACS), long-term or complete withdrawal of P2Y12 inhibitors is highly undesirable, unless there are clear clinical indications for discontinuation of treatment (recommendation class I, grade scientific evidence C).

It is emphasized that when planning coronary artery bypass grafting, it is recommended to cancel the drug 5-7 days before surgery. However, discontinuation of drugs in patients belonging to the high ischemic risk group (for example, with prolonged episodes of anginal pain, with stenosis of the common trunk of the left coronary artery or severe proximal multivessel lesion) can lead to a significant deterioration in the prognosis, therefore, in some cases, cancel dual antiplatelet therapy should not be, but during surgery, the fact of taking antiplatelet agents should be taken into account.

When treating such patients, it is also important to take into account the risk of bleeding, if it is very high - drug withdrawal is still indicated, but 3-5 days before surgical treatment.

Thus, before elective major surgery (including coronary intervention), it is recommended to consider the expediency of discontinuing ticagrelor/clopidogrel 5 days before surgery, and prasugrel 7 days, except for cases with a high risk of developing complications of myocardial ischemia (class IIa, degree of evidence C).

The management of patients on dual antiplatelet therapy requiring surgical treatment should be carried out with the joint participation of cardiologists, anesthesiologists, hematologists and surgeons to more accurately and individually determine the risk of bleeding, assess ischemic risk and analyze the need for urgent surgical treatment.

Ticagrelor(brilinta). The mechanism of action of ticagrelor is based on the formation of a reversible bond with the platelet receptor P2Y12 To adenosine diphosphate. Unlike prasugrel and clopidogrel, the severity of suppression of platelet aggregation by ticagrelor depends to a greater extent on the level of ticagrelor itself in the blood plasma and, to a lesser extent, on the concentration of its metabolite.

The effect of the drug occurs faster (after 30 minutes from the moment of taking the drug) than the effect of clopidogrel (after 2-4 hours from the start of therapy), while cases of genetically determined "resistance" to the drug have not been registered. The duration of action of ticagrelor is 3-4 days, as opposed to 3-10 days with clopidogrel.

According to the results of the PLATO randomized controlled trial, it was shown that ticagrelor is significantly more effective than clopidogrel in reducing the risk of death from cardiovascular causes (4.0% of cases in the ticagrelor group, in contrast to the group of patients treated with clopidogrel - 5.1%) and the risk of overt stent thrombosis (1.3% of cases in the ticagrelor group versus 1.9% in the clopidogrel group).

The study included patients with non-ST elevation ACS, who belonged to the group of medium and high risk of developing complications of myocardial ischemia, regardless of what treatment tactics were planned (surgical revascularization or conservative treatment).

The results of the PLATO study confirm the clinical safety profile derived from previous studies of ticagrelor. There was no difference between ticagrelor and clopidogrel in major bleeding as measured by PLATO, the primary safety endpoint. However, in the ticagrelor-treated group, the risk of major non-coronary bypass bleeding and the risk of minor bleeding were significantly higher, while the risk of fatal bleeding complications did not differ.

It is emphasized that quite often against the background of treatment with ticagrelor, side effects develop that are not typical for other drugs belonging to this group. Approximately 14% of patients experienced shortness of breath during the first week of treatment, usually not requiring discontinuation of the drug.

In a number of cases, during daily ECG monitoring, an increase in the number of pauses in heart contractions was recorded. In this regard, patients with an increased risk of bradycardia (for example, patients with sick sinus syndrome without a pacemaker, with II-III degree AV block, syncope associated with bradycardia) should be prescribed with caution. In some patients, an asymptomatic increase in the level of uric acid was detected.

Clinical guidelines recommend that ticagrelor (180 mg as a starting loading dose followed by 90 mg twice daily) is recommended for all patients with moderate to high ischemic risk (eg, elevated troponin levels), regardless of initial treatment strategy. If the patient is taking clopidogrel, discontinuation of the drug and administration of ticagrelor is indicated (recommendation grade I, evidence grade B).

Prasugrel(effient) in comparison with clopidogrel also suppresses platelet aggregation much faster, the effect occurs 30 minutes after the start of therapy and lasts 5-10 days. The action of prasugrel does not depend on a number of genetic features responsible for the inter-individual variability in the effectiveness of clopidogrel. In this regard, the effect of prasugrel is more predictable.

According to the randomized controlled trial TRITON-TIMI, prasugrel is significantly more effective than clopidogrel in reducing the risk of acute myocardial infarction (AMI) - in the prasugrel group, 7.1% of patients suffered an AMI, and in the clopidogrel group - 9.2%. The risk of stent thrombosis is also lower in the prasugrel-treated group than in the clopidogrel-treated group (1.1% vs. 2.4%).

The study included patients with ACS of medium and high ischemic risk who were scheduled for percutaneous coronary intervention.

However, in the prasugrel group, an increased risk of life-threatening bleeding (1.4% compared with 0.9% in the clopidogrel group) and fatal bleeding (0.4% in the prasugrel group versus 0.1% in the clopidogrel group) was found.

A comparative analysis of the effectiveness of the drug in subgroups of patients with various concomitant diseases showed that in patients with diabetes mellitus treatment with prasugrel has clear advantages.

However, the appointment of the drug to patients who have undergone an acute violation cerebral circulation(stroke), and persons aged 75 years and older, as well as patients weighing less than 60 kg, is associated with an increased risk of bleeding. Among the side effects of prasugrel, cases of thrombocytopenia and neutropenia were noted.

Clinical guidelines (Class I, Level of Evidence B) recommend that prasugrel (at a loading dose of 60 mg followed by 10 mg daily) be used in patients who have not previously taken other P2Y12 platelet receptor inhibitors (especially those with diabetes mellitus) who have features of the anatomical structure of the coronary arteries have already been studied and are planned for percutaneous coronary intervention.

The drug is not prescribed in cases where the risk of developing life-threatening bleeding is regarded as high, or there are other contraindications.

Clopidogrel(Plavix) at a loading dose of 300 mg followed by 75 mg daily, according to the current recommendations of the European Society of Cardiology, is indicated only in cases where prasugrel and ticagrelor are not possible (recommendation grade I, level of evidence A).

This is due to the fact that a fairly large amount of scientific data obtained indicates the existence of genetically determined resistance to treatment with clopidogrel, which is quite widespread.

In some cases, genotyping and / or analysis of the degree of suppression of the ability of platelets to aggregate during treatment with this drug is advisable to correct clopidogrel therapy (recommendation grade IIb, level of evidence B).

In order to evaluate the effectiveness of clopidogrel, the drug was also prescribed in an increased dose (600 mg - loading dose, then 150 mg during the week and 75 mg thereafter). Coronary angiography to determine the indications for percutaneous coronary intervention was performed during the first 72 hours.

In the subgroup of patients who underwent the intervention, the efficacy of clopidogrel at an increased dose was higher than in the group of patients taking clopidogrel at the standard dose. According to the results of the assessment of the total risk of death from cardiovascular causes, the development of a heart attack or stroke when using clopidogrel at an increased dose, it was 3.9% versus 4.5% in patients receiving clopidogrel at a standard dose (p = 0.039).

Therefore, clopidogrel 600 mg (or an additional 300 mg during percutaneous coronary intervention after receiving initial therapy with clopidogrel 300 mg) is recommended in cases where surgical myocardial revascularization is planned, and ticagrelor or prasugrel cannot be prescribed. (class of recommendation I, level of evidence B).

Routine escalation of the maintenance dose of clopidogrel is not recommended, but may be considered in selected cases (recommendation class IIb, grade B). A higher maintenance dose of clopidogrel (150 mg daily) for the first 7 days followed by the usual dose (75 mg daily) is recommended in patients undergoing PCI, provided there is no increased risk of bleeding (Recommendation Class IIa, Grade of Evidence B) .

Thus, more intensive treatment with antiplatelet agents is currently recommended in the management of patients with non-ST elevation ACS. Continuous combination therapy with aspirin and P2Y12 inhibitors (ticagrelor or prasugrel is preferred) for up to 12 months is contemplated. If it is necessary to revise therapy during this period, the timing of the withdrawal of antiplatelet agents should be considered on an individual basis.

E.V. Frolova, T.A. Dubikaitys

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 distally located areas of the vascular channels. In this regard, unstable angina and developing myocardial infarction are currently combined 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, it is of great importance to develop 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 the appointment of invasive interventions. In the course of creating such criteria, all acute coronary syndromes were divided into those accompanied and not accompanied by persistent ST segment elevation. Currently, the optimal therapeutic interventions, the effectiveness of which is based on the results of well-designed randomized clinical trials, have already been largely developed. So, in acute coronary syndrome with persistent ST segment elevation (or first-time complete blockade of the left bundle branch block), reflecting acute total occlusion of one or more coronary arteries, the goal of treatment is the rapid, complete and persistent restoration of the lumen of the coronary artery using thrombolysis (if it is not contraindicated) or primary coronary angioplasty (if it is technically feasible). The effectiveness of these therapeutic measures has been proven in a number of studies.

Non-ST elevation acute coronary syndrome refers to patients with chest pain and ECG changes suggestive of acute ischemia (but not necessarily necrosis) of the myocardium.

These patients often present with persistent or transient ST-segment depression, as well as T-wave inversion, flattening, or ｫpseudo-normalizationｻ. In addition, non-ST-elevation ACS ECG changes may be nonspecific or 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) can be included in this category of patients.

In contrast to situations with persistent ST-segment elevation, previous proposals for treatment tactics for non-ST-segment elevation acute coronary syndrome were less clear-cut. Recommendations were published only in 2000 working group European Society of Cardiology for the treatment of non-ST elevation acute coronary syndrome. Relevant recommendations will soon be developed for Russian doctors as well.

This article only considers the management of patients with suspected acute coronary syndrome who do not have persistent ST elevation. At the same time, the main attention is paid directly to the diagnosis and the choice of therapeutic tactics.

But beforehand 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 tests were performed on specially selected groups of patients and, accordingly, do not reflect all the conditions encountered in clinical practice.

Secondly, it should be taken into account that cardiology is developing rapidly. Accordingly, these guidelines should be reviewed regularly as new clinical trial results accumulate.

The degree of persuasiveness of conclusions about the effectiveness of various methods of diagnosis and treatment depends on the data on the basis of 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 in several randomized clinical research or meta-analyses.

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

Level C. The conclusions are based on the consensus opinion of the experts.

In the following discussion, after each item, the level of its validity will be indicated.

Tactics of managing patients with acute coronary syndrome

Initial assessment of the patient's condition

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

1. Careful history taking . Classical characteristics of anginal pain, as well as typical CAD exacerbations (protracted [> 20 minutes] anginal pain at rest, first-onset severe [not lower than Canadian Cardiovascular Society (CCS) Class III] angina pectoris, recent worsening of stable angina pectoris of at least up to III FC according to CCS) are well known. However, it should be noted that ACS can also present with atypical symptoms, including chest pain at rest, epigastric pain, sudden onset dyspepsia, stabbing chest pain, ｫpleuralｻ pain, and increased dyspnoea. 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 was fully reproduced on palpation. Especially often, atypical manifestations of ACS are observed in young (25-40 years old) and senile (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, data on auscultation of the heart, as well as indicators of heart rate and blood pressure are usually within the normal range. The purpose of the physical examination is primarily 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 detect heart disease not associated with coronary artery disease (pericarditis, heart defects), as well as assess the stability of hemodynamics and the severity of circulatory failure.

3. ECG . Resting ECG recording is a key diagnostic tool for ACS. Ideally, an ECG should be recorded during a pain attack and compared with an electrocardiogram recorded after the pain disappeared.

With recurring pain, multi-channel 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 probability of having ACS is greatest if the corresponding clinical picture associated with ST segment depression greater than 1 mm in two or more contiguous leads. A slightly less specific sign of ACS is T-wave inversion greater than 1 mm in R-wave-dominant leads. Deep negative, symmetrical T waves in the anterior chest 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, an ECG at rest should be recorded and long-term multichannel monitoring of the ST segment should be started. If monitoring is not feasible for any reason, then frequent ECG recording is necessary (level of evidence: C).

Hospitalization

Patients with suspected non-ST-elevation ACS should be immediately admitted to a specialized cardiology emergency/intensive care unit (LE) (Level of Evidence: C).

Study of biochemical markers of myocardial damage

ｫTraditionalｻ cardiac enzymes, namely creatine phosphokinase (CPK) and its CPK MB isoenzyme, are less specific (in particular, false positive results are possible in skeletal muscle injury). In addition, there is significant overlap between normal and abnormal serum concentrations of these enzymes. The most specific and reliable markers of myocardial necrosis are cardiac troponins T and I. . Troponin T and I concentrations should be determined 612 hours after admission to the hospital, and also after each episode of intense chest pain.

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

It should also be taken into account that after necrosis of the heart muscle, 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, while the concentrations of CPK MB 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 with a recent 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 pain attack. Myoglobin and/or CK MV should be measured in 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 Therapy in Patients with Suspected Non-ST Elevation ACS

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

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

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

3. bblockers (level of evidence: B);

4. For persistent or recurrent chest pain, oral or intravenous nitrates (level of evidence: C);

5. In the presence of contraindications or intolerance to b-blockers, calcium antagonists (level of evidence: B and C).

Dynamic Surveillance

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

Recurrent chest pain. During each pain attack, it is necessary to record an ECG, and after it, re-examine the level of troponins in the blood serum. It is highly advisable to conduct continuous multichannel ECG monitoring to detect signs of myocardial ischemia, as well as disorders heart rate.

Signs of hemodynamic instability (arterial hypotension, congestive rales in the lungs, etc.)

Assessing the risk of myocardial infarction or death

Patients with acute coronary syndrome represent a highly heterogeneous group of patients that differ in the prevalence and/or severity of atherosclerotic coronary artery disease, as well as in the degree of ｫthromboticｻ risk (i.e.

risk of 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 assigned to one of the two categories below.

1. Patients at high risk of myocardial infarction or death

repeated episodes of myocardial ischemia (either recurring chest pain or ST segment dynamics, especially depression or transient ST segment elevations);

an increase in the concentration of troponin T and / or troponin I in the blood;

episodes of hemodynamic instability during the observation period;

life-threatening cardiac arrhythmias (repeated paroxysms of ventricular tachycardia, ventricular fibrillation);

the occurrence of ACS without ST segment elevation in the early postinfarction period.

2. Patients at low risk of myocardial infarction or death

no recurrence of chest pain;

there was no increase in the level of troponins or other biochemical markers of myocardial necrosis;

there were no ST depressions or elevations associated with inverted T waves, flattened T waves, or 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 heparin sodium according to the scheme (Table 2) or low molecular weight heparins (level of evidence: B).

In modern practice, the following are widely used low molecular weight heparins : adreparin, dalteparin, nadroparin, tinzaparin and enoxaparin. Let us take a closer look at nadroparine as an example. Nadroparin is a low molecular weight heparin obtained from standard heparin by depolymerization.

The drug is characterized by a 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 s / c 2 times a day in combination with acetylsalicylic acid (up to 325 mg / day). The initial dose is determined at the rate of 86 units / kg, and it should be administered as an intravenous 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 soon as possible. In preparation for CAG, the administration of heparin should be continued. In the presence of atherosclerotic damage, allowing for 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 a stent 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 justification: A.

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

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

2. Cancellation of low molecular weight heparins in the event that during the dynamic observation there were no changes in the ECG and the level of troponin did not increase (level of evidence: C).

3. Stress test to confirm or establish the 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 CAG followed by revascularization. If standard tests are not informative, stress echocardiography or exercise myocardial perfusion scintigraphy may be useful.

Management of patients with non-ST elevation ACS after discharge from the hospital

1. The introduction of low molecular weight heparins in the event that repeated episodes of myocardial ischemia occur and it is impossible to perform revascularization (level of evidence: C).

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

3. Widespread impact on risk factors. First of all, smoking cessation and normalization of 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 capacity to carry out the above-mentioned diagnostic and therapeutic measures (determination of the level of troponins T and I, myoglobin; emergency coronary angiography, the use of IIb / IIIa receptor blockers, etc.). We can expect, however, their ever wider inclusion in medical practice in our country in the near future.

The use of nitrates in unstable angina is based on pathophysiological considerations and clinical experience. Data from controlled studies indicating the optimal dosage and duration of their use are not available.

Acute coronary syndrome ( OKS) - this is one of the options for a preliminary diagnosis, which is used in cases where it is not possible to accurately determine the nature of the disease ( make a definitive diagnosis). As a rule, this term is used in relation to acute clinical manifestations. ischemic heart disease ( ischemic heart disease) . Ischemic disease, in turn, is a lack of oxygen supply to the heart muscle. This is usually associated with problems at the level of the vessels that feed the heart. IHD can develop for years without leading to serious disorders of the heart. As soon as the lack of oxygen becomes more pronounced, and there is a threat of myocardial infarction, the disease is diagnosed as an acute coronary syndrome.

The term ACS is commonly used in relation to three main pathologies that share a common mechanism of development and a common cause:

• unstable angina;
• non-ST elevation myocardial infarction ( sign on electrocardiogram);
• myocardial infarction with ST segment elevation.

Anatomy of the heart

In the structure of the heart, take into account the following anatomical departments:

• heart chambers;
• walls of the heart;
• conducting system of the heart;
• coronary vessels;
• heart valves.

chambers of the heart

The heart contains the following chambers:

• Right atrium. This is where venous blood comes from great circle circulation ( vessels of all internal organs and tissues other than pulmonary vessels). The walls of the atrium are quite thin, they do not normally perform serious work, but only distill blood in portions into the ventricles. From the right atrium, venous blood enters the right ventricle.
• Right ventricle. This department pumps the incoming venous blood into the pulmonary circulation. From the right ventricle, it enters the pulmonary artery. In the small circle, gas exchange occurs, and the blood from the venous turns into arterial.
• Left atrium. This chamber receives already arterial blood from a small circle. Here it enters through the pulmonary veins. When the left atrium contracts, blood flows into the left ventricle.
• left ventricle. It is the largest chamber of the heart. It receives arterial blood and ejects it under great pressure into the aorta. This pressure is necessary to pump blood throughout the vasculature of the systemic circulation. When the left ventricle cannot cope with this function, heart failure sets in, and the organs begin to suffer from a lack of oxygen. The walls of the left ventricle are the thickest. They have developed muscle tissue, which is necessary for strong contractions. It is in the muscle cells of the left ventricle that a heart attack most often occurs, since oxygen requirements are greatest here.

Walls of the heart

The walls of the heart in any department consist of three main layers:

• Endocardium. It is the inner lining of the heart. Its thickness usually does not exceed 0.5 - 0.6 mm. The main function is the regulation of normal blood flow ( no turbulence in the flow that can cause blood clots).
• Myocardium. The muscularis is the thickest part of the heart wall. It consists of individual fibers that intertwine and form a complex network. The functional unit of the myocardium is a special cell - the cardiomyocyte. These cells have not only a high potential for contraction, but also a special ability to carry out bio electrical impulse. Due to these features, myocardial fibers are almost simultaneously covered by excitation and contract. It is the work of the muscle layer that determines the two main phases of the cardiac cycle - systole and diastole. Systole is the period of contraction of the fibers, and diastole is their relaxation. Normally, atrial systole and diastole begin somewhat earlier than the corresponding phases of the ventricles.
• epicardium. It is the most superficial layer of the heart wall. It is tightly fused with the myocardium and covers not only the heart, but also partially large vessels that bring blood. Wrapping back, the epicardium passes into the visceral layer of the pericardium and forms the heart sac. Sometimes the epicardium is also called the parietal leaf of the pericardium. The pericardium separates the heart from neighboring organs of the chest cavity and ensures its normal contraction.

conduction system of the heart

The conduction system consists of the following departments:

• sinoatrial node. This node is the main pacemaker of the heart. Cells in this area receive signals nervous system, coming from the brain, and generate an impulse, which then propagates along the conducting paths. The sinoatrial node is located at the confluence of the vena cava ( top and bottom) into the right atrium.
• Interatrial Bachmann bundle. Responsible for the transmission of impulses to the myocardium of the left atrium. Thanks to him, the walls of this chamber are reduced.
• Internodal conductive fibers. This is the name of the pathways connecting the sinoatrial and atrioventricular nodes. As the impulse passes through them, the muscles of the right atrium contract.
• atrioventricular node. It is located in the thickness of the septum on the border of all four chambers of the heart, between the tricuspid and mitral valves. Here there is some deceleration in the propagation of the impulse. This is necessary in order to allow the atria to fully contract and eject all the blood volume into the ventricles.
• Bundle of His. This is the name of the set of conductive fibers, which ensures the propagation of the impulse to the myocardium of the ventricles and contributes to their simultaneous reduction. The bundle of His consists of three branches - right leg, left leg and left posterior branch.

coronary vessels

There are two main coronary arteries in the heart:

• Arteria coronaria dextra. The branches of this artery feed the right wall of the right ventricle, the posterior wall of the heart, and partially the interventricular septum. The diameter of the artery itself is quite large. With thrombosis or spasm of one of its branches, ischemia occurs ( lack of oxygen) in the area of ​​the myocardium that it nourishes.
• Arteria coronaria sinistra. The branches of this artery supply blood to the left sections of the myocardium, almost the entire anterior wall of the heart, most of the interventricular septum, and the region of the apex of the heart.

Heart valves

There are 4 valves in the heart:

• Tricuspid valve. It is located in the opening between the right atrium and the ventricle. Prevents blood from flowing back into the atrium during ventricular contraction. During atrial systole, blood flows freely through the open valve leaflets.
• Pulmonary valve. It is located at the outlet of the right ventricle. During diastole, the ventricle expands again from a contracted state. The valve prevents blood from being sucked back from the pulmonary artery.
• mitral valve. Located between the left atrium and ventricle. The mechanism of operation is similar to that of a tricuspid valve.
• aortic valve. It is located at the base of the aorta, at the site of its exit from the left ventricle. The mechanism of operation is similar to that of the pulmonary valve.

What is coronary syndrome?

Unstable angina

Unstable angina is diagnosed when:

• progressive angina ( crescendo) . With this form, attacks of pain are repeated more and more often. Their intensity also increases. The patient complains that it is increasingly difficult for him to perform the usual physical activity, as it provokes a new attack of angina pectoris. With each attack, an increasing dose of drugs is required ( usually sublingual nitroglycerin) to dock ( eliminate) attack.
• New onset angina pectoris de novo) . It is diagnosed if the patient says that the characteristic pains appeared no more than a month ago. As a rule, this form is also progressive, but not as pronounced as crescendo angina. Due to the recent onset of pain, it is difficult for doctors to tell what the true severity of the patient's condition is and to give a reliable prognosis. That is why this form is classified as ACS.
• Early postinfarction angina. This form diagnosed after a myocardial infarction, if the pain appeared in the first 1 to 30 days. According to some classifications, this period can be reduced to 10 - 14 days. The bottom line is that the appearance of pain may indicate insufficient restoration of blood flow after treatment and the threat of a new heart attack.
• Angina after angioplasty. It is diagnosed if a patient with coronary artery disease has undergone surgery to replace a portion of a coronary vessel. Theoretically, this is done in order to eliminate the narrowing and restore normal blood flow. However, sometimes angina pectoris recurs even after surgery. This form is diagnosed if the pain appeared 1 to 6 months after angioplasty.
• Angina pectoris after coronary artery bypass grafting. The diagnostic criteria in this case are the same as for angioplasty. The only difference is that the narrowed section of the coronary artery is not removed, but rather a new vessel is sutured ( shunt) around the site of injury.
• Prinzmetal's angina. This form is also called variant angina. It is distinguished by severe pain during attacks, as well as a high frequency of the attacks themselves. It is believed that this form may appear not so much due to blockage of the coronary arteries with plaques, but due to spasm ( narrowing of the lumen caused by smooth muscle) vessels. Most often, attacks occur at night or in the morning. Usually patients complain of 2 - 6 severe attacks of pain behind the sternum, the interval between which is no more than 10 minutes. With Prinzmetal's angina, even an ST segment elevation on the electrocardiogram can be observed.

Non-ST elevation myocardial infarction

Without an ST segment, the diagnosis is based on the rise in the level of specific markers and the patient's characteristic complaints. Later, typical manifestations on the ECG may also join. As a rule, if the infarction is not manifested by ST segment elevation, then the area of ​​ischemia captures a small area of ​​the heart muscle ( small focal infarction). Previously, another classification was used, based on the increase in the Q wave. In this case, this wave will always be absent.

Since the ST segment can also rise in some forms of unstable angina, it is very difficult to draw a clear line. That is why the signs of exacerbation of coronary artery disease on the ECG are not sufficient confirmation of the diagnosis. All these forms are combined into a collective term - ACS, which is diagnosed at the first stages of the disease ( emergency physicians, when a patient is admitted to a hospital). Only after conducting other examinations, in addition to the ECG, can we talk about the differentiation of clinical forms within the very concept of ACS.

ST elevation myocardial infarction

A more severe option is myocardial infarction with the appearance of a pathological Q wave. It indicates an extensive area of ​​necrosis ( macrofocal infarction), which affects both the superficial and internal layers of the heart wall.

In general, myocardial infarction is the most severe form of coronary artery disease, in which myocardial cell death occurs. Currently, quite a lot of classifications of this pathology have been proposed, which reflect its course and other features.

According to the prevalence of the necrosis zone, all heart attacks are divided into two types:

• Large focal infarction. There is a rise in the ST segment, the formation of a Q wave. Usually, the zone of necrosis is localized in the wall of the left ventricle. Such a heart attack is usually transmural, that is, it covers all layers of the heart wall, from the epicardium to the endocardium.
• Small focal infarction. In this case, there may be no ST segment elevation, and the Q wave, as a rule, is not formed. We are talking about superficial necrosis, not transmural. It is classified as subendocardial ( if a certain number of cardiomyocytes have died directly near the endocardium) or as intramural ( if the zone of necrosis does not border either the epicardium or the endocardium, but is located strictly in the thickness of the myocardium).

• Left ventricular wall infarction. It can be anterior, septal, apical, lateral, posterior. Other localizations are also possible for example, anterolateral, etc.). This species is the most common.
• right ventricular wall infarction. It occurs much less frequently, usually with hypertrophy of this department ( cor pulmonale and etc.). Normally, the right ventricle does not do such hard work that there is a serious lack of oxygen.
• Atrial myocardial infarction. Also very rare.

Causes of coronary syndrome

The flow of blood to the myocardium can be caused by the following pathological changes:

• Narrowing of the vessel lumen. The most common cause of CAD and ACS is atherosclerosis. This is a pathology in which the arteries of the elastic and muscular-elastic type are predominantly affected. The lesion consists in the deposition of so-called lipoproteins on the walls of the vessels. This is a class of proteins that transport lipids ( fats) in the human body. There are 5 classes of lipoproteins that differ from each other in size and function. With regard to the development of atherosclerosis, the most dangerous are low-density lipoproteins responsible for the transfer of cholesterol. They are able to penetrate the vascular wall and linger there, causing a local tissue reaction. This reaction consists in the production of pro-inflammatory substances and, after a while, connective tissue. Thus, the lumen of the artery is narrowed, the elasticity of the wall decreases, and the former volume of blood can no longer pass through the vessel. If this process affects the coronary arteries, coronary artery disease gradually develops, which threatens the appearance of ACS in the future.
• Plaque formation. The actual deposition of lipoproteins and cholesterol in the wall of an artery is called an atherosclerotic plaque. It can be of various shapes, but most often resembles a small cone-shaped elevation protruding into the lumen of the vessel and interfering with the flow of blood. On the surface of the plaque, a dense capsule is formed, called a tire. Atherosclerotic plaques are dangerous not only by the progressive narrowing of the lumen of the vessel. Under certain conditions ( infection, hormonal imbalance and other factors) the tire is damaged and an intense inflammatory process develops. In this case, the blood flow in this place may stop completely, or a fragment of the plaque will come off. Such a detached plaque becomes a thrombus, which moves with the blood and gets stuck in a vessel of a smaller caliber.
• Inflammation of the vessel wall. Inflammation in the wall of a coronary artery is relatively rare. In most cases, it is associated precisely with the atherosclerotic process. However, there are other reasons as well. For example, the entry of certain microbes and viruses into the blood can be an impetus for the development of inflammation. Also, the walls of the arteries can become inflamed under the influence of autoantibodies ( antibodies that attack the body's own cells). This process is observed in some autoimmune diseases.
• Vascular spasm. The coronary arteries contain some smooth muscle cells. These cells are able to contract under the influence of nerve impulses or certain substances in the blood. A vasospasm is a contraction of these cells, in which the lumen of the vessel narrows, and the volume of incoming blood decreases. Usually the spasm does not last long and does not cause serious consequences. However, if the arteries have already been affected by the atherosclerotic process, the lumen of the vessel may close completely, and cardiomyocytes will begin to die from a lack of oxygen.
• Blockage of a vessel by a thrombus. As mentioned above, a thrombus often forms due to the detachment of an atherosclerotic plaque. However, it may also have other origins. For example, if the heart is damaged by an infectious process ( bacterial endocarditis) or bleeding disorders, blood clots also form. Once in the coronary arteries, they get stuck at a certain level, completely blocking the blood flow.
• Increased need for oxygen. By itself, this mechanism is not capable of causing ACS. Normally, the vessels themselves adapt to the needs of the heart and expand if it works in an enhanced mode. However, when coronary vessels are affected by atherosclerosis, their elasticity is reduced and they are not able to expand if necessary. Thus, the increased myocardial oxygen demand is not compensated and hypoxia occurs ( acute lack of oxygen). This mechanism can cause ACS if a person performs heavy physical work or experiences strong emotions. This increases the heart rate and increases the muscle's need for oxygen.
• Lack of oxygen in the blood. This reason is also quite rare. The fact is that in some diseases or pathological conditions, the amount of oxygen in the blood decreases. Together with a weakened blood flow in the coronary arteries, this exacerbates the oxygen starvation of tissues and increases the risk of developing ACS.

Atherosclerotic lesions of the coronary arteries are considered the classical cause of the development of coronary artery disease and subsequent ACS. According to various sources, it is observed in 70 - 95% of all patients. The mechanism of development of atherosclerosis itself is very complex. Despite the importance of this problem for medicine, today there is no single theory that would explain this pathological process. However, statistically and experimentally, it was possible to identify a number of predisposing factors that play a role in the development of atherosclerosis. Through it, they also strongly influence the risk of developing acute coronary syndrome.

Factors predisposing to the appearance of atherosclerosis of the coronary arteries are:

• An imbalance between various fats in the blood ( dyslipidemia) . This factor is one of the most important, since it increased amount cholesterol in the blood leads to its deposition in the walls of the arteries. The influence of this indicator on the incidence of IHD and ACS has been proved statistically and experimentally. When assessing the risk in a particular patient, two main indicators are taken into account. It is believed that the risk increases greatly if total blood cholesterol exceeds 6.2 mmol/l ( norm up to 5.2 mmol/l). The second indicator is an increase in cholesterol in the composition of low-density lipoproteins ( LDL cholesterol) above 4.9 mmol/l ( norm up to 2.6 mmol/l). In this case, critical levels are indicated, at which the likelihood of developing arterial atherosclerosis and the occurrence of ACS is very high. The gap between the norm and this critical mark is regarded as an increased risk.
• Smoking. According to statistics, smokers are 2 to 3 times more likely to develop ACS than non-smokers. From a medical point of view, this is due to the fact that substances contained in tobacco smoke can increase blood pressure, disrupt endothelial cells ( cells that make up the walls of arteries), cause vasospasm. It also increases blood clotting and increases the risk of blood clots.
• High blood pressure. According to statistics, an increase in pressure by 7 mm Hg. Art. increases the risk of developing atherosclerosis by 30%. Thus, people with a systolic blood pressure of 140 mm Hg. Art. ( norm - 120) suffer from coronary artery disease and ACS almost twice as often as people with normal pressure. This is due to impaired blood circulation and damage to the vascular walls under conditions of high pressure. That is why hypertensive patients ( patients with high blood pressure) you need to take antihypertensive drugs regularly.
• Obesity. Obesity is considered as a separate risk factor, although in itself it does not affect the occurrence of atherosclerosis or coronary artery disease. However, obese people are more likely to have metabolic problems. They usually suffer from dyslipidemia, high blood pressure, diabetes mellitus. Weight loss objectively leads to the disappearance of these factors or to a decrease in their influence. The most common in assessing the risk of ACS is the Quetelet index ( body mass index). It is calculated by dividing body weight ( in kilograms) by the squared growth ( in meters, with hundredths). The normal result of division in healthy people will be 20 - 25 points. If the Quetelet index exceeds 25, they speak of various stages of obesity and an increased risk of heart disease.
• "Passive lifestyle. Physical inactivity, or a sedentary lifestyle, is considered by many experts as a separate predisposing factor. moderate exercise ( regular walks at a brisk pace, gymnastics several times a week) help maintain the tone of the heart muscle and coronary arteries. This prevents the deposition of atherosclerotic plaques and reduces the likelihood of ACS. With a sedentary lifestyle, people are more likely to suffer from obesity and other problems associated with it.
• Alcoholism. There are studies that indicate that alcohol in small doses may be useful for the prevention of atherosclerosis, as it stimulates the processes of "cleansing" of the coronary arteries. But many experts question this benefit. But chronic alcoholism, disrupting liver function, unequivocally leads to metabolic disorders and dyslipidemia.
• Diabetes. At diabetes in patients, many metabolic processes in the body are disturbed. In particular, we are talking about an increase in the level of low-density lipoproteins and “dangerous” cholesterol. Because of this, in patients with diabetes, atherosclerosis of the coronary arteries occurs 3 to 5 times more often than in other patients. The likelihood of developing ACS, respectively, also increases.
• hereditary factors. There are quite a few hereditary forms of dyslipidemia. In this case, the patient in one of the DNA chains has a defect in the gene responsible for metabolic processes related to fats. Each gene codes for a specific enzyme. The severity of violations depends on which enzymes are absent in the body. Therefore, when assessing the risk of developing atherosclerosis and ACS in the future, the patient must be asked about the cases of these diseases in the family.
• Stress. In stressful situations, a certain amount of special hormones are released in the body. Normally, they contribute to a kind of "protection" in an unfavorable situation. However, the frequent release of these substances can affect metabolic processes and play a role in the development of atherosclerosis.
• Increased blood clotting. Platelets and blood clotting factors play a role in the formation of atherosclerotic plaque and its cap. In this regard, some scientists consider clotting disorders as a possible cause of atherosclerosis.

In addition to the classical atherosclerotic causes of ACS, there are others. In medical practice, they are much less common and are called secondary. The fact is that in these cases, coronary artery disease develops rather as a complication of other diseases. That is, acute coronary syndrome is not preceded by coronary heart disease, as it happens in the classical version. Most often, non-atherosclerotic causes of ACS lead to the development of acute myocardial infarction. As a result, they are considered more dangerous. Neither the patient nor the doctor often can predict the damage to the heart in advance. Other pathologies are considered here as causes.

Non-atherosclerotic causes of ACS may include:

• inflammation of the coronary arteries ( arteritis);
• deformation of the coronary arteries;
• congenital anomalies;
• trauma;
• irradiation of the heart;
• embolism of the coronary arteries;
• thyrotoxicosis;
• increased blood clotting.

Arteritis

Diseases that can cause myocardial infarction against the background of arteritis are:

• syphilis ( the pathogen spreads with the blood stream and is fixed in the coronary arteries);
• Takayasu's disease;
• Kawasaki disease;
• arterial disease in SLE systemic lupus erythematosus);
• damage to the arteries in other rheumatic diseases.

Deformation of the coronary arteries

Deformation of the coronary arteries can be detected in the following diseases:

• mucopolysaccharidosis;
• Fabry disease;
• fibrosis after radiotherapy;
• idiopathic ( reason is unclear) calcium deposition in the wall of the artery ( more common in children).

congenital anomalies

Injuries

Irradiation of the heart

Embolism of the coronary arteries

Embolism of the coronary arteries can occur in the following diseases:

• bacterial endocarditis;
• thromboendocarditis ( a thrombus formed in the cavity of the heart without the participation of microbes);
• malformations of the heart valves ( normal blood flow is disturbed, eddies and blood clots form);
• blood clots formed in the inserted catheters ( in medical procedures);
• blood clots after cardiac surgery.

Thyrotoxicosis

Increased blood clotting

Thus, acute coronary syndrome can have many different causes. Most often it is associated with atherosclerosis and coronary heart disease, but there is also a secondary lesion of the coronary arteries. The mechanism of development of angina pectoris and heart attack can also be different. Unites all these pathologies common clinical manifestations, similar tactics of diagnosis and treatment. That is why, from a practical point of view, it was convenient to combine such diverse forms into the collective concept of ACS.

Symptoms of coronary syndrome

Typical symptoms of ACS are:

• pain;
• sweating;
• skin pallor;
• fear of death;

pain

In typical angina pectoris or myocardial infarction, pain has the following characteristics:

• Paroxysmal character. Most often, the attack can be provoked by physical activity ( sometimes even insignificant), but can also occur at rest. If angina occurs even at rest or at night, the prognosis is worse. The pain appears due to the relative lack of oxygen. That is, there is a narrowing in the lumen of the vessel ( usually atherosclerotic plaque), which restricts the supply of oxygen. At the time of exercise, the heart begins to beat faster, consumes more oxygen, but blood flow to it does not increase. Then there is an attack of pain. Sometimes it can also be triggered by emotional experiences. Then the coronary arteries narrow due to irritation of the nerve fibers ( spasm). Again, blood flow is interrupted and pain occurs.
• Description of pain. Usually patients, describing the nature of pain, define it as cutting, stabbing or squeezing. Often they take their hand on the left side of the chest, as if showing that the heart cannot beat.
• pain intensity. With angina pectoris, the intensity of pain can be moderate. However, with myocardial infarction, the pain is often very severe. The patient freezes in place, afraid to move, so as not to provoke a new attack. Such pain, unlike an attack of angina pectoris, may not be relieved by nitroglycerin and disappear only with the introduction of narcotic painkillers. Often, with severe anginal pain, the patient cannot find a comfortable position, is in a state of excitement.
• Attack duration. With angina pectoris, several attacks usually follow with a short interval. The duration of each most often does not exceed 5 - 10 minutes, and the total duration is about an hour. With a myocardial infarction, the pain can stably last for an hour or more, causing unbearable suffering to the patient. The protracted nature of the pain is an indication for immediate hospitalization.
• Pain localization. Most often, the pain is localized behind the sternum or slightly to the left of it. Sometimes it covers the entire anterior wall of the chest as a whole and the patient cannot accurately indicate the place where the pain is most severe. Also, with myocardial infarction, irradiation is characteristic ( Spread) pain in adjacent anatomical areas. Most often, the pain gives to the left arm, neck, lower jaw or ear. much less frequently ( usually with extensive posterior wall infarcts) the pain radiates down to the lumbar region and groin. Sometimes patients even complain of pain between the shoulder blades.

sweating

Dyspnea

Pale skin

Fear of death

fainting

Cough

A different picture may be observed with the following atypical forms ah myocardial infarction:

• abdominal;
• asthmatic;
• painless;
• cerebral;
• collaptoid;
• edematous;
• arrhythmic.

Abdominal shape

Typical symptoms in the abdominal form of myocardial infarction are:

• bout of hiccups;
• pain in the abdomen, right or left hypochondrium;
• tension of the abdominal wall;

Asthmatic form

Painless form

cerebral form

Typical symptoms in the cerebral form of myocardial infarction are:

• severe sudden dizziness;
• severe headaches;
• an attack of nausea;
• recurring fainting;
• blurred vision and temporary visual disturbances.

Collaptoid form

edematous form

Arrhythmic form

Thus, ACS can have a variety of clinical forms. The relatively small number of symptoms leads to the fact that atypical manifestations of a heart attack are often confused with other diseases that are not of a cardiac nature. Only if the patient has already had episodes of angina pectoris and is aware of the presence of coronary artery disease, it becomes easier to suspect the correct diagnosis. At the same time, most heart attacks occur with classic manifestations. And in this case, the presence of cardiac pathology can be judged even by the nature of the pain.

Diagnosis of coronary syndrome

In the diagnosis of acute coronary syndrome, the following methods are used:

• general examination and analysis of complaints;
• determination of biomarkers of necrosis;
• electrocardiography;
• echocardiography;
• myocardial scintigraphy;
• coronary angiography;
• pulse oximetry.

General examination and analysis of complaints

In addition to measuring temperature, the doctor may resort to the following standard methods physical examination:

• Palpation. During palpation, the doctor probes the area of ​​​​the heart. In the case of ACS, there may be a slight displacement of the apex beat.
• Percussion. Percussion is the tapping of the heart area with fingers in order to determine the boundaries of the organ. In ACS, the boundaries are usually not much changed. A moderate expansion of the left border of the heart is characteristic, as well as an expansion of vascular dullness in the II intercostal space on the left.
• Auscultation. Auscultation is listening to heart sounds with a stethophonendoscope. Here you can hear pathological murmurs and heart sounds that occur due to disturbances in blood flow inside the cavities. Characterized by the appearance of systolic murmur in the apex of the heart, the appearance of a pathological third tone, and sometimes the gallop rhythm.
• Blood pressure measurement. Arterial hypertension is an important criterion for unstable angina. If the patient's blood pressure is elevated, appropriate medications should be prescribed. This will reduce the chance of a heart attack. Immediately after a heart attack, blood pressure may be low.

General blood analysis

Another important indicator of resorption-necrotic syndrome is leukocytosis ( increased levels of leukocytes). These cells are engaged in "cleansing" the blood and tissues from foreign elements. In the case of necrosis, such elements are dead myocardial tissue. Leukocytosis is recorded already 3-4 hours after a heart attack and reaches a maximum on 2-3 days. The level of leukocytes usually remains elevated for about a week. Normally, the content of these cells is 4.0 - 8.0x10 9

/ l. At the same time, changes are observed in the leukocyte formula itself. Proportional increase in the number of stab neutrophils ( shift of the leukocyte formula to the left).

Blood chemistry

The following indicators are of greatest importance in the diagnosis of myocardial infarction:

• Seromucoid. It can be determined on the very first day after myocardial infarction. Its concentration remains elevated for another 1-2 weeks. Normally, it is found in the blood at a concentration of 0.22 - 0.28 g / l.
• Sialic acids. Like seromucoid, they increase already on the first day, but the maximum concentration is recorded on days 2-3 after a heart attack. They remain elevated for another 1-2 months, but their concentration gradually decreases during this period. The physiological norm of the content of sialic acids is 0.13 - 0.2 conventional units ( identical 2.0 – 2.33 mmol/l).
• Haptoglobin. Appears in the blood only on the second day after the attack, reaching a maximum approximately on the third day. In general, the analysis can be informative for another 1-2 weeks. The norm of haptoglobin in the blood of a healthy person is 0.28 - 1.9 g / l.
• fibrinogen. It is an important indicator of blood clotting. It can increase on 2-3 days after a heart attack, reaching a maximum in the period from 3 to 5 days. The analysis is informative for 2 weeks. The norm of fibrinogen content in the blood is 2 - 4 g / l.
• C-reactive protein. This indicator is of great importance in the prognosis of the course of the disease in patients with unstable angina. It has been shown that when the content of C-reactive protein is more than 1.55 mg in combination with fast positive reaction for troponin ( necrosis biomarker) almost 10% of patients die within 2 weeks. If the content of C-reactive protein is less and the reaction to troponin is negative, the survival rate is as much as 99.5%. These indicators are relevant for unstable angina and non-Q wave myocardial infarction.

With unstable angina, all of the above changes in the biochemical blood test are usually absent, but this study is still prescribed. It is necessary to indirectly confirm the presence of atherosclerosis in a patient. To do this, measure the level of cholesterol in the blood, triglycerides and lipoproteins ( low and high density). If these indicators are increased, it is highly likely that coronary artery disease has developed against the background of atherosclerosis of the coronary arteries.

Coagulogram

To obtain accurate coagulogram results, you should donate blood on an empty stomach. Food intake is stopped at least 8 hours before the test is taken.

The coagulogram measures the following indicators:

• prothrombin time ( norm - 11 - 16 seconds or 0.85 - 1.35 in the international normalized ratio);
• thrombin time ( the norm is 11 - 18 seconds);
• fibrinogen content ( norm - 2 - 4 g / l).

Determination of biomarkers of necrosis

Myocardial necrosis markers are:

• Troponin-T. It is determined in the blood in the first 3-4 hours after a heart attack and increases within 12-72 hours. After that, it gradually decreases, but can be detected during the analysis for another 10-15 days. The norm of this marker in the blood is 0 - 0.1 ng / ml.
• Troponin-I. Appears in the blood after 4 - 6 hours. The peak concentration of this marker is a day ( 24 hours) after necrosis of myocardial cells. The analysis turns out to be positive for another 5 to 10 days. The norm of Troponin-I in the blood is 0 - 0.5 ng / ml.
• myoglobin. It is determined in the blood within 2 - 3 hours after a heart attack. The maximum content falls on 6 - 10 hours after the attack. The marker can be detected for another 24 - 32 hours. The norm in the blood is 50 - 85 ng / ml.
• Creatine phosphokinase ( KFK) . Appears in the blood after 3-8 hours and increases for another 24-36 hours. The marker remains elevated for another 3-6 days. Its normal concentration is 10 - 195 IU / l.
• Creatine phosphokinase MB fraction ( KFK-MV) . It is determined in the blood, starting from 4 to 8 hours after a heart attack. The peak concentration occurs at 12 - 24 hours. It is advisable to do an analysis for the MB fraction only in the first three days after a heart attack. Normally, its concentration is less than 0.24 IU / l ( or less than 65% of the total concentration of CPK).
• Isoforms of CPK-MB. Appear 1-4 hours after the attack. The maximum concentration falls on a period of 4-8 hours, and a day after a heart attack, this analysis is no longer carried out. Normally, the proportion between fractions MB2 and MB1 is greater than 1.5 ( 3/2 ).
• lactate dehydrogenase ( LDH) . It is determined in the blood 8-10 hours after necrosis. The maximum concentration is recorded after 1 - 3 days. This indicator can be determined within 10 - 12 days after a heart attack. It remains above 4 mmol/h per liter ( at a body temperature of 37 degrees). When determined using an optical test, the norm is 240 - 480 IU / l.
• LDH-1 ( lactate dehydrogenase isoform) . It also appears 8 to 10 hours after a heart attack. The maximum falls on the second - third day. In the blood, this isoform of LDH remains elevated for two weeks. Normally, it is 15 - 25% of the total concentration of LDH.
• Aspartate aminotransferase ( AST) . Increases in 6 - 8 hours after a heart attack. The maximum falls on 24 - 36 hours. The analysis remains positive 5 - 6 days after the attack. Normally, the concentration of AST in the blood is 0.1 - 0.45 µmol / h x ml. Also, AST can increase with the death of liver cells.

Electrocardiography

When conducting an ECG, the patient takes a recumbent or semi-recumbent ( for severe patients) position. Before the procedure, the patient should not perform heavy physical activity smoking, drinking alcohol, or taking medications that affect the functioning of the heart. All this can cause changes in the electrocardiogram and lead to an incorrect diagnosis. It is best to start the procedure 5-10 minutes after the patient has taken a comfortable position. The fact is that in a number of patients, the work of the heart can be disturbed even with a rapid change in body position. Another important condition is the removal of all metal objects and turning off powerful electrical appliances in the room. They can affect the operation of the device, and small fluctuations will appear on the cardiogram, which will make it difficult to make a diagnosis. The places where the electrodes are applied are wetted with a special solution or simply with water. This improves metal-to-skin contact and provides more accurate data.

The electrodes are applied to the body as follows:

• red - on the right wrist;
• yellow - on the left wrist;
• green - on the lower part of the left leg;
• black - on the lower part of the right shin;
• chest electrodes ( 6 items) - on the anterior part of the chest.

Typically, an ECG is taken in the following 12 leads:

• I- left hand- positive electrode, right - negative;
• II - right hand - negative, left leg - positive;
• III - left arm - negative, left leg - positive;
• aVR - enhanced abduction from right hand (relative to the average potential of the remaining electrodes);
• aVL - enhanced abduction from the left hand;
• aVF - enhanced abduction from the left leg;
• V 1 - V 6 - leads from the chest electrodes ( from right to left).

On a standard ECG, the following intervals can be distinguished:

• Isoline. Talk about lack of momentum. Also, no deviations can be observed if the pulse propagates strictly perpendicular to the measurement axis. Then the vector projection on the axis will be equal to zero and there will be no changes on the ECG.
• Wave R. Reflects the propagation of the impulse through the atrial myocardium and atrial contraction.
• PQ segment. Registers the delay of the wave of excitation at the level of the atrioventricular node. This ensures complete pumping of blood from the atria to the ventricles and closure of the valves.
• QRS complex. Displays the propagation of the impulse through the myocardium of the ventricles and their contraction.
• ST segment. Usually located on the isoline. Its rise is the most important diagnostic criterion for myocardial infarction.
• Wave T. Displays the so-called repolarization of the ventricles, when muscle cells relax and return to a resting state. After the T wave, a new cardiac cycle begins.

The main electrocardiological signs of ACS are:

• An increase in the ST segment of at least 1 mV in two or more adjacent leads. It speaks of severe oxygen starvation of the heart muscle, usually when a coronary vessel is blocked by a thrombus.
• Elevation of the ST segment in leads V 1 - V 6 , I, aVL, plus signs of bundle branch block. Speaks of extensive infarction of the anterior wall ( left ventricle). Mortality reaches 25.5%.
• Elevation of the ST segment in leads V 1 - V 6 , I, aVL without blockade of the bundle branch. He speaks of a large area of ​​infarction in the anterior wall. Mortality is about 12.5%.
• Elevation of the ST segment in leads V 1 - V 4 or I, aVL and V 5 - V 6. Talks about anterolateral or anterolateral myocardial infarction. Mortality is approximately 10.5%.
• A sign of a large inferior myocardial infarction is the elevation of the ST segment in leads II, III, aVF. When the wall of the right ventricle is damaged, the rise in lead V 1, V 3 r, V 4 r joins. With lower lateral infarction - in leads V 5 - V 6. With a posterior wall infarction, the R wave is larger than the S wave in leads V 1 - V 2. Mortality in these cases is approximately 8.5%.
• An isolated ST segment elevation in leads II, III, aVF indicates a small inferior myocardial infarction, in which mortality does not exceed 7%.

echocardiography

The echocardiographic features of ACS are:

• Changes in the functioning of the heart valves (tricuspid - with right ventricular infarction and mitral - with left ventricular infarction). They are due to hemodynamic disturbances. The damaged heart muscle cannot cope with the incoming blood volume, the chamber is stretched, and the fibrous ring of the valve is also stretched with it.
• Expansion of the chamber of the heart. In this case, the chamber in the wall of which the infarction occurred usually expands.
• Swirls in the blood stream. Occur due to uneven contraction of the muscle walls.
• Wall bulge. Formed with large-focal myocardial infarction and can transform into an aneurysm. The fact is that the area of ​​necrosis is replaced by connective tissue, which is not as elastic as a healthy myocardium. Due to constant movement during heart contractions) this tissue does not have time to gain sufficient strength. The damaged area swells under the action of internal pressure ( especially in the left ventricle).
• Expansion of the inferior vena cava. It is observed in myocardial infarction of the right ventricle. As the right side of the heart can no longer keep up with the blood flow, this blood pools in the large veins that lead to the heart. The inferior vena cava expands earlier and stronger than the superior one, since under the action of gravity a larger volume of blood accumulates in it.

Myocardial scintigraphy

The procedure proceeds as follows. Special reagents are injected into the patient's vein. The most commonly used isotope of technetium with a molecular weight of 99 ( 99 mTc-pyrophosphate). It has a special property to accumulate only in the zone of myocardial necrosis. This is due to the accumulation of excess calcium in the dead cells, which interacts with the isotope. This analysis will indicate the area of ​​necrosis if the mass of dead tissue is more than a few grams. Thus, the procedure is not prescribed for microinfarctions. Technetium will accumulate as early as 12 hours after a heart attack, but the most informative result is obtained between 24 and 48 hours. A weaker accumulation is noted for another 1 to 2 weeks.

Another option with a similar execution technology is the thallium isotope - 201 Tl. On the contrary, it is retained only by viable cardiomyocytes. Thus, the places where the isotope does not accumulate will be the areas of necrosis. True, accumulation defects can also be detected in some forms of angina pectoris, when necrosis has not yet occurred. The study is informative only in the first 6 hours after an attack of pain.

The disadvantage of these methods is the strict time frame in which you can get a reliable result. Also, the study does not give a clear answer, what is the cause of necrosis. Accumulation defects can also be detected in cardiosclerosis of other origin ( not after a heart attack).

coronary angiography

For this study, an incision is made in the femoral artery, and a special catheter is brought through it to the heart. Through it near aortic valve contrast agent is injected. Most of it enters the coronary arteries. If the cause of coronary artery disease is atherosclerosis, then coronary angiography will reveal places of vasoconstriction and the presence of plaques that pose a threat in the future. If any of the branches of the contrast did not spread at all, this indicates the presence of thrombosis ( a detached plaque or thrombus of another origin has completely blocked the lumen of the vessel and blood does not flow through it).

Coronary angiography is performed more often as a preventive measure to understand the nature of angina pectoris. With a heart attack and other acute conditions, its appointment is dangerous. In addition, there is a certain risk of complications ( arrhythmias or infection). Coronary angiography is definitely indicated before surgery, bypass or angioplasty. In these cases, surgeons need to know exactly at what level the clot or narrowing is located.

Magnetic resonance imaging

For the diagnosis of ACS, MRI is used relatively rarely due to its high cost. It is prescribed before surgical treatment to clarify the localization of the thrombus. With the help of this study, you can also find out the condition of the so-called fibrous cover ( evaluate the chance of detachment of an atherosclerotic plaque), to detect calcium deposits in the thickness of the plaque. All this supplements information about the patient's condition and allows more accurate diagnosis.

Pulse oximetry

Of the above diagnostic procedures, only a general examination of the patient, an ECG, and the determination of markers of myocardial necrosis are mandatory for suspected ACS. All other studies are prescribed as needed, depending on the characteristics of the course of the disease in a particular patient.

Separately, it is necessary to highlight the diagnosis of unstable angina pectoris. This pathological condition sometimes it is very difficult to recognize. Its diagnosis is based on the principles of the so-called evidence-based medicine. According to them, the diagnosis can be made only according to certain criteria. If, after carrying out all the necessary procedures, these criteria are met, then the diagnosis is considered confirmed.

Diagnostic criteria for unstable angina are:

• In patients with previously diagnosed angina pectoris, attention is paid to changes in the nature of pain. During the last month before going to the doctor, the duration of the attacks increased ( more than 15 minutes). Along with them, attacks of suffocation, arrhythmias, and sudden inexplicable weakness began to appear.
• Sudden attacks of pain or shortness of breath after activities that were previously tolerated normally.
• angina attacks at rest without visible provoking factors) within the last 2 days before going to the doctor.
• Decreased effect of sublingual nitroglycerin ( the need to increase the dose, the slow retreat of pain).
• An attack of angina pectoris during the first 2 weeks after an already suffered myocardial infarction ( regarded as unstable angina, threatening re-infarction).
• The first attack of angina pectoris in my life.
• Shift of the ST interval on the ECG by more than 1 mm upwards from the isoline simultaneously in 2 or more leads, or the presence of arrhythmia attacks on the ECG. However, there are no reliable signs of myocardial infarction.
• The disappearance of signs of oxygen starvation of the heart on the ECG simultaneously with the disappearance of pain ( in a heart attack, changes remain).
• The absence in the patient's analyzes of signs of resorption-necrotic syndrome, which would indicate the death of cardiomyocytes.

Treatment of coronary syndrome

• A preliminary diagnosis is made on the spot and basic measures are taken to provide assistance. At this stage, treatment is carried out by emergency doctors.
• Patients with confirmed myocardial infarction and signs of circulatory disorders are hospitalized immediately in the intensive care unit.
• Patients with suspected heart attack and signs of circulatory disorders are also hospitalized immediately in the intensive care unit.
• Hemodynamically stable patients ( no signs of circulatory disorders) with a confirmed infarction can be placed both in the intensive care unit and in a regular cardiological hospital.
• Hemodynamically stable patients with suspected myocardial infarction or with unstable angina should also be hospitalized. In the emergency room, they should be examined by a cardiologist within the first hour after admission. Based on the results of the examination, the doctor decides whether further outpatient treatment is possible ( at home) or hospitalization is required for a more accurate diagnosis.

Treatment of ACS is carried out in the following areas:

• drug treatment;
• prevention of exacerbations;
• treatment with folk remedies.

Medical treatment

First aid for suspected ACS is of great importance. As mentioned above, the process of myocardial ischemia in this case goes through several stages. It is very important at the first symptoms to do everything to restore normal blood flow to the heart muscle.

Drugs used as part of first aid for ACS

Beta-blockers used in the treatment of ACS

As noted above, one of the main manifestations of ACS is pain in the region of the heart, which can be very severe. In this regard, painkillers are an important component of treatment. They not only improve the patient's condition, but also relieve such unwanted symptoms as anxiety, fear of death.

Drugs for pain relief in ACS

The following drugs can be used as a thrombolytic agent:

• streptokinase;
• urokinase;
• alteplase;
• tenecteplase.

Prevention of exacerbations

The main preventive measures are:

• Exclusion of risk factors for atherosclerosis. The most important thing in this case is to stop drinking alcohol and smoking. Patients with diabetes should regularly check their blood sugar levels to prevent long-term rises. A complete list of factors contributing to the development of atherosclerosis is given in the Causes of ACS section.
• Body weight control. People suffering from excess weight should consult a nutritionist to normalize the Quetelet index. This will reduce the chance of ACS if you have heart problems.
• Moderate physical activity. Healthy people need to avoid a sedentary lifestyle and, if possible, play sports or do basic exercises to keep fit. For people who have had a heart attack, as well as those suffering from angina pectoris, the load may be contraindicated. This point should be clarified with the attending physician. If necessary, a special test is done with an ECG during exercise ( treadmill test, bicycle ergometry). It allows you to understand what load is critical for the patient.
• Dieting. With atherosclerosis, the proportion of animal fats in the diet should be reduced. Also limit salt intake to reduce the risk of hypertension. The energy value practically unlimited if the patient does not have problems with being overweight or severe hemodynamic disorders. In the future, the subtleties of the diet should be discussed with the attending cardiologist or nutritionist.
• Regular observation. All patients who have had a myocardial infarction or suffering from angina pectoris are at risk of developing ACS. For this reason, regular at least once every six months) visiting the attending physician and carrying out the necessary diagnostic procedures. In certain cases, more frequent monitoring may be required.

Treatment with folk remedies

To improve the nutrition of the heart muscle, the following folk remedies are recommended:

• Infusion of grains of oats. Grains are poured in a ratio of 1 to 10 ( for 1 cup of oats 10 cups of boiling water). Infusion lasts at least a day ( preferably 24-36 hours). Infusion drink half a cup 2 - 3 times a day before meals. It should be taken for several days until the periodic pain in the heart disappears.
• Nettle decoction. Nettles are harvested before flowering and dried. For 5 tablespoons of chopped herbs, 500 ml of boiling water is needed. After that, the resulting mixture is boiled for another 5 minutes over low heat. When the decoction has cooled down, it is taken 50 - 100 ml 3 - 4 times a day. For taste, you can add a little sugar or honey.
• Centaury infusion. For 1 tablespoon of dry grass, you need 2 - 3 cups of boiling water. Infusion lasts 1 - 2 hours in a dark place. The resulting infusion is divided into 3 equal portions and consumed during the day half an hour before meals. The course of treatment lasts several weeks.
• Decoction of eryngium. The grass is harvested during flowering and carefully dried in the sun for several days. For 1 tablespoon of chopped herbs, 1 cup of boiling water is needed. The agent is boiled over low heat for 5 to 7 minutes. Take it 4 - 5 times a day, 1 tablespoon.

Operations for the treatment of coronary syndrome

Bypass coronary arteries

This operation has the following advantages:

• provides a reliable supply of arterial blood to the myocardium;
• risk of infection or autoimmune reactions ( rejection) is extremely small, since the patient's own tissues are used as a shunt;
• there is almost no risk of complications associated with blood stasis in the lower leg, since the vascular network is well developed in this area ( other veins will take over the outflow of blood instead of the removed site);
• vein walls have a different cellular structure than arteries, so the risk of atherosclerosis damage to the shunt is very small.

Most patients tolerate coronary artery bypass surgery well. The postoperative period lasts several weeks, during which it is necessary to regularly treat the incision sites on the lower legs and chest in order to avoid infection. It takes several months for the sternum, which is dissected during the operation, to heal ( up to six months). The patient will have to be regularly observed by a cardiologist and undergo a preventive examination ( ECG, echocardiography, etc.). This will allow you to evaluate the efficiency of blood supply through the shunt.

Many points relating to the course of the operation are determined individually. This is due to various causes of ACS, different localization of the problem, and the general condition of the patient. Any coronary bypass surgery is performed under general anesthesia. The choice of drugs may be affected by the age of the patient, the severity of the disease, the presence of allergies to certain medications.

Stenting of the coronary arteries

The main advantages of stenting are:

• the use of a heart-lung machine is not required, which reduces the risk of complications and reduces the time of the operation ( on average, the installation of a stent requires 30-40 minutes);
• after the operation, only one small scar remains;
• rehabilitation after surgery requires less time;
• the metal used to make the stent does not cause allergic reactions;
• statistically shows a high and long-term survival of patients after this operation;
• low risk of serious complications, since the chest cavity is not opened.

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

Acute Coronary Syndrome A term for any group of clinical signs or symptoms suggestive of AMI or unstable angina. Includes AMI, STEMI, STEMI ECG, MI diagnosed by enzyme changes, by other biomarkers, by late ECG signs, and unstable angina.

The term “ACS” was introduced into clinical practice when it became clear that the use of certain active therapies, in particular thrombolytic therapy, must 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 shifted upward (ST elevation), coronary angioplasty is the method of choice for restoring coronary blood flow, but if it is impossible to perform it at the appropriate time, it is effective and, accordingly, thrombolytic therapy is indicated. Restoration of coronary blood flow in ACS-ST 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 expedient at the first contact of a doctor with a patient who has a suspicion of the development of ACS, the use of the following diagnostic terms (identification of the following forms of ACS ): “OKSpST” and “OKSbpST”.

ACS with ST-segment elevation and ACS without ST-segment elevation

ST-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) LBBB on the ECG. Typically, patients who begin as ACS-ST later develop signs of myocardial necrosis—elevated biomarker levels and ECG changes, including Q wave formation.

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

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

About correlation of diagnostic terms "ACS" and "MI"

The term “ACS” is used when diagnostic information is still insufficient for a final judgment on 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 result in signs of myocardial necrosis) are retained for use in formulating the final diagnosis.

If signs of myocardial necrosis are found in a patient with ACS who has persistent ST elevations on the initial ECG, this condition is referred to as STEMI. Further, depending on the ECG picture, the maximum level of cardiac troponin or enzyme activity and imaging data, the diagnosis is specified: MI can be large-focal, small-focal, with Q waves, without Q waves, etc.