home Consultations Acute coronary syndrome without ST segment elevation: symptoms, diagnosis and treatment. Acute coronary syndrome without ST segment elevation on ECG Treatment of coronary syndrome with ST elevation aimed at

Acute coronary syndrome without ST segment elevation: symptoms, diagnosis and treatment. Acute coronary syndrome without ST segment elevation on ECG Treatment of coronary syndrome with ST elevation aimed at

For quotation: Kashtalap V.V., Barbarash O.L. Controversial issues in the management of patients with acute coronary syndrome without ST segment elevation (review of the recommendations of the European Society of Cardiology 2015) // RMZh. 2015. No. 26. pp. 1524-1527

The article discusses controversial issues in the management of patients with acute coronary syndrome without ST-segment elevation based on the recommendations of the European Society of Cardiology 2015.

For citation. Kashtalap V.V., Barbarash O.L. Controversial issues in the management of patients with acute coronary syndrome without ST segment elevation (review of the recommendations of the European Society of Cardiology 2015) // RMZh. 2015. No. 26. pp. 1524–1527.

Currently, the problem of choosing the optimal method of managing a patient with acute coronary syndrome without persistent ST segment elevation on the ECG (ST-ACS) does not lose its relevance for the practitioner. It is known that patients with clinical and electrocardiographic signs of NSTE-ACS are a fairly diverse cohort of patients. It may include patients with clinical manifestations of acute coronary syndrome (ACS) without changes on the ECG and reactions of cardiac-specific markers (unstable angina) and patients with myocardial infarction (MI) without persistent ST-segment elevation on the ECG. Patients without diseases of the cardiovascular system (with exacerbation of osteochondrosis, pathology of the gastrointestinal tract, pneumonia) are often admitted to specialized hospitals with suspicion of NSTE-ACS.
It can be assumed that patients with NSTE-ACS are a more favorable group of patients in terms of the course of an acute coronary event, compared to patients with ST-segment elevation acute coronary syndrome (ST-ACS). However, this is not true: hospital mortality in NSTE-ACS may be 2-3 times higher than that in patients with NSTE-ACS, however, in the long-term (one-year) follow-up period, the incidence of recurrent cardiovascular events in patients with NSTE-ACS who have not undergone hospital revascularization exceeds that in patients with NSTE-ACS.
It should be said that among practicing physicians, the optimal treatment strategy for patients with NSTE-ACS is beyond doubt and has fully justified itself - this is the most complete and early reperfusion of the myocardium by any available method (surgical or medicinal) within the next few hours from the onset of the disease.
Tactics regarding revascularization in patients with NSTE-ACS are individual and depend on the objectification of risk factors for the development of an unfavorable course of ACS in a particular patient. The main problem of managing patients with NSTE-ACS is the correct assessment by the practitioner of the individual risk and, based on this assessment, determining the time to use an invasive strategy (urgently upon admission; up to 24 hours from the onset of the disease (early invasive strategy); up to 72 hours from the onset of the disease ( late invasive strategy) or the choice of conservative tactics for managing a patient with NSTE-ACS.
Due to the existing objective difficulties of practicing physicians regarding the choice of optimal treatment tactics for patients with NSTE-ACS, updated recommendations of the European Society of Cardiology for the management of patients with NSTE-ACS were adopted in August 2015 in London at the next European Congress of Cardiology.
Clinical manifestations of NSTE-ACS may include prolonged (>20 min) anginal pain at rest; new-onset angina pectoris II or III functional class (FC) according to the Canadian classification; progression of manifestations of previously stable angina to FC III–IV; post-infarction angina.
In elderly patients, women, patients with diabetes mellitus (DM), renal failure and dementia, atypical clinical forms of NSTE-ACS are often encountered: abdominal, asthmatic, peripheral, which requires increased attention to these categories of patients.
If there is any suspicion that a patient has ACS, the first-line diagnostic test is to record a 12-lead ECG at rest within 10 minutes of the patient’s first contact with the doctor. In 1/3 of patients with NSTE-ACS there may be no ischemic changes on the ECG, which does not exclude the diagnosis of an acute coronary event. In other patients, the ECG may reveal changes in the ST segment: depression, transient (up to 20 minutes) elevation, changes in the T wave in the form of its inversion. If a patient has an unchanged ECG against the background of persistent ischemic discomfort, then recording additional leads: V7–V9 and right thoracic (V3R–V4R) is useful in this case. In any case, only the absence of persistent ST segment elevation on the ECG classifies the patient into the category of patients with NSTE-ACS. If clinical manifestations of myocardial ischemia persist during treatment, serial recording of an ECG during patient monitoring and comparison with previous results is necessary.
The 2015 European guidelines specifically emphasize that the determination of biomarkers of myocardial necrosis is absolutely mandatory for all patients with NSTE-ACS, since the results of the studies can determine further patient management tactics. And the diagnosis of myocardial infarction itself, according to the latest universal definition of this disease, must be confirmed by positive results of determining biomarkers of myocardial necrosis in a quantitative way. Biomarkers of myocardial damage have proven themselves well, such as the MB fraction of creatine kinase, the total fraction of creatine kinase, and myoglobin. However, currently the leader in cardiac specificity is troponin (types T or I), which is what the authors of the recommendations prefer to determine in patients with NSTE-ACS. Its significant drawback for practical use is the relatively late increase in blood concentration (6–12 hours after the onset of MI), however, when using a highly sensitive troponin test (hsT), its sensitivity to ischemic damage and necrosis appears already in the first hour from the onset of ACS . However, high troponin values can occur not only with MI, but also with myocarditis, sepsis, shock of any etiology, life-threatening arrhythmias, aortic dissection and pulmonary embolism. Positive positive troponin test results should be interpreted with caution in patients with coronary artery disease and severe renal impairment, as they may be due to a decrease in glomerular filtration rate (GFR).
As an alternative to troponin, if it is impossible to determine it, the authors of the 2015 European recommendations suggest the use of the MB fraction of creatine kinase and copeptin. Copeptin is the C-terminal portion of the prohormone vasopressin, which can quantitatively reflect the severity of endogenous stress in various emergency conditions, including MI.
The 2015 European recommendations describe diagnostic algorithms that allow, based on the assessment of clinical, electrocardiographic and laboratory data (serial determination of hsT) in a very short time (within 1 or 3 hours from the patient’s admission to the hospital), to confirm or refute the presence of myocardial necrosis and clarify further tactics for managing a patient with NSTE-ACS or start searching for another cause of chest pain. There are 2 such algorithms: 1-hour (0h/1h) and 3-hour (0h/3h), which are of equal importance for practical use. The first algorithm proposes serial assessment of hsT (T or I) upon patient admission to the intensive care unit and after 1 hour of intensive treatment. Determination of initial hsT concentrations and their dynamic assessment after 1 hour allows us to divide patients into a group with definite NSTE-ACS, a follow-up group, and a group of patients with likely non-cardiac causes of chest pain. This algorithm makes it possible to quickly stratify patients with respect to the risk of complications of the acute period of ACS and apply earlier invasive tactics for the management of these patients. The only drawback of this algorithm is its clear link to the test parameters of a specific test system manufacturer, which are specified in the recommendations (Elecsys, Architect, Dimension Vista). It is for the test systems of these manufacturers that the hsT boundary values are described, which serve to stratify patients depending on the likelihood of the ischemic nature of chest pain.
The 0h/3h algorithm is more accessible for practical use. It also involves assessing hsT in a patient with chest pain and without NSTE-ACS criteria on ECG upon admission to the hospital. If hsT values are below the upper limit of normal, then it is necessary to assess the duration of pain in the chest. If the duration of this in a patient is more than 6 hours, then re-evaluation of hsT is not carried out. The patient should undergo pain management, assess the likelihood of adverse events using the GRACE scale, order stress testing before discharge, and carry out a differential diagnosis for other causes of chest pain. If the pain syndrome lasted less than 6 hours from the patient’s admission to the hospital, then after 3 hours of the patient’s stay in the intensive care unit, it is necessary to re-determine the hsT values. If a difference in 2 hsT values is detected above the upper limit of normal, the patient is considered a candidate for invasive treatment. If there is no difference between the 2 hsT values, the patient is stratified into an observation group with a risk assessment according to the GRACE scale and exercise testing before discharge. If a patient with signs of NSTE-ACS has hsT values above the upper limit of normal upon admission to the hospital, then the following should be done: a patient with abnormally high hsT concentrations (several times higher than the upper limit of normal) is immediately identified as a candidate for invasive treatment. In a situation where hsT values slightly exceed the upper limit of normal, a repeat study after 3 hours is acceptable to determine the difference between the 2 values. If this exceeds the upper limit of the norm, the patient is considered as a candidate for coronary angiography; if it does not exceed, then the patient is indicated for further examination in the general ward and early discharge after stress testing. The above algorithms for rapid risk assessment of a patient with suspected ACS and differential diagnosis are recommended only if hsT is available for routine clinical use.
The above approaches are not entirely familiar to practicing doctors in our country. The main purpose of their implementation, according to European cardiologists, is the ability to quickly stratify patients with suspected ACS depending on the identified risk of an unfavorable outcome in order to determine indications for invasive tactics of patient management, or for early transfer to the outpatient stage of pre-examination after stress testing. The 2015 European Society of Cardiology recommendations for the management of patients with NSTE-ACS make it possible to implement such an approach.
As additional research methods in patients with NSTE-ACS for differential diagnosis with other diseases, the following can be performed: echocardiography at rest and stress test, magnetic resonance imaging of the heart with perfusion, multislice computed tomography of the coronary arteries. Echocardiography is recommended for assessing regional and global contractile function of the left ventricle in a patient with NSTE-ACS, as well as for the differential diagnosis of chest pain. Multispiral computed tomography coronary angiography may be considered as a diagnostic test (instead of invasive coronary angiography) in low- or intermediate-risk patients when ECG and biomarker data are not informative.
Despite the proposed algorithms for rapid stratification of patients with NSTE-ACS upon admission, the authors of European recommendations do not deny the need for individual assessment of the risk of developing an adverse cardiovascular event during the short-term observation period. To do this, it is proposed to use the GRACE scale, known to practical doctors in Russia, its improved analogue GRACE 2.0 or the TIMI scale, which, as the authors of the recommendations admit, is still inferior to the GRACE scales. The GRACE scale allows for fairly objective risk stratification of the patient both upon admission and upon discharge. The use of the improved risk calculator GRACE 2.0 makes it possible to predict hospital mortality and mortality of patients after NSTE-ACS after 6, 12 and 36 months. . The GRACE 2.0 score uses patient age, systolic blood pressure, heart rate, serum creatinine concentration, Killip class of acute heart failure (HF) on admission, cardiac arrest on admission, elevated cardiac markers on admission, and abnormalities. ST segment. If HF class and serum creatinine values are not available, the modified GRACE 2.0 score allows risk assessment based on additional history of chronic kidney disease and diuretic use.
Episodes of major bleeding, even when adequately corrected with blood transfusion, significantly increase the risk of death in patients with NSTE-ACS. Taking into account the active use of endovascular interventions and drugs that affect blood clotting (combinations of disaggregants and anticoagulants) in the treatment of patients with ACS, the authors of European recommendations draw attention to the need to assess the risk of bleeding in patients with invasive management tactics. The ST CRUSADE scale for assessing the risk of bleeding in patients with acute coronary syndrome appears to be preferable for practical use.
All patients with NSTE-ACS require continuous ECG monitoring for 24 hours before undergoing primary risk stratification or before percutaneous coronary intervention (PCI). It is unacceptable for a patient with a preliminary diagnosis of NSTE-ACS to be in the ward without the possibility of ECG monitoring. ECG monitoring in patients with NSTE-ACS for more than 24 hours can be used if there is a high risk of arrhythmic complications.
The drug treatment of patients with NSTE-ACS has not undergone significant changes in the new recommendations. Beta-blockers are prescribed as early as possible for symptoms of ischemia in patients without contraindications (acute HF of Killip classes III–IV). In patients with vasospastic angina, beta-blockers should be excluded from treatment and replaced with calcium antagonists and nitrovasodilators. IV nitrovasodilators are recommended if ischemic discomfort persists, uncontrolled hypertension and pulmonary congestion.
A number of well-known drugs are used as disaggregants in the treatment of patients with NSTE-ACS: acetylsalicylic acid (ASA), clopidogrel, ticagrelor, prasugrel. The recommendations also indicate a new drug with antiplatelet effect via intravenous administration - cangrelor.
During the initial examination of a patient with suspected ACS, ASA is prescribed by a doctor in a loading dose of 150–300 mg in an “uncoated” form, then the patient receives ASA indefinitely at a dosage of 75–100 mg once a day in a “protected” form.
Prescription of platelet P2Y12 receptor inhibitors in addition to ASA is recommended for 12 months, unless the patient has contraindications, such as a high risk of bleeding.
Ticagrelor at a loading dose of 180 mg and a maintenance dose of 90 mg twice a day is recommended for use in the absence of contraindications (history of intracranial hemorrhage or ongoing bleeding) in all patients with intermediate- and high-risk NSTE-ACS (with elevated troponin levels), regardless of the drug chosen initial management tactics, including patients who were previously prescribed clopidogrel at a loading dose. Treatment with clopidogrel should be discontinued if ticagrelor is available. Ticagrelor is highly effective in preventing recurrent cardiovascular events in patients over 12 months. after NSTE-ACS compared with clopidogrel was shown in the PLATO trial.
Prasugrel (not commercially available in Russia) at a loading dose of 60 mg and a maintenance dose of 10 mg is prescribed daily to patients with planned invasive management tactics in the absence of contraindications.
Clopidogrel at a loading dose of 300 or 600 mg and a maintenance dose of 75 mg daily is recommended for patients who cannot take ticagrelor or prasugrel or require additional indirect anticoagulants (atrial fibrillation and ACS).
The authors of the recommendations allow shortening the duration of dual antiplatelet therapy to 3–6 months. after ACS with implanted drug-eluting stents (DES) in patients at high risk of bleeding. However, the same authors suggest discussing the need to prolong dual antiplatelet therapy for more than 12 months. in certain categories of patients after careful assessment of the risk of ischemic events and bleeding.
The place for a new drug - cangrelor in the recommendations is determined to be quite modest - it can be prescribed to provide PCI in patients with NSTE-ACS who have not previously received one of the P2Y12 platelet receptor inhibitors.
Anticoagulant therapy is prescribed to all patients upon diagnosis of ACS. The following drugs can be used as anticoagulants in the acute phase of NSTE-ACS:
– unfractionated heparin (should be administered intravenously only);
– low molecular weight heparin (enoxaparin, intravenous bolus and subcutaneous administration);
– fondaparinux (s.c. administration);
– bivalirudin (should be administered intravenously only).
It is noted that fondaparinux (2.5 mg/day s.c.) is recommended as a drug with an optimal efficacy/safety profile in patients with NSTE-ACS, regardless of the chosen treatment tactics. If it is not possible to prescribe fondaparinux, enoxaparin or unfractionated heparin are alternatives to anticoagulant therapy. It is not allowed to change one prescribed type of heparin to another, as this increases the risk of bleeding.
Bivalirudin is considered as an optimal alternative to unfractionated heparin in combination with IIB/IIIA platelet receptor blockers and can be used in patients with NSTE-ACS when choosing invasive management tactics.
Anticoagulant therapy should be discontinued in patients with NSTE-ACS after PCI, unless there are additional indications for this (prevention of venous thromboembolism, atrial fibrillation). Additionally, it is stipulated that in patients with NSTE-ACS without a history of strokes or transient ischemic attacks, with a high risk of developing recurrent ischemic events and a low risk of bleeding after stopping anticoagulant therapy, additional administration of rivaroxaban at a dosage of 2.5 mg 2 times / day can be considered for 12 months together with ASA and clopidogrel.
The use of statins in patients with NSTE-ACS should be started as early as possible in the hospital at the maximum therapeutic dose and continued for life.
Angiotensin-converting enzyme inhibitors (ACE inhibitors) are prescribed to patients with NSTE-ACS in the hospital during the 1st day of the disease if the patient has a decrease in left ventricular ejection fraction (LVEF)<40%, СН, артериальная гипертензия или СД. Альтернативой иАПФ могут быть сартаны, особенно при непереносимости иАПФ. Назначение осуществляется пожизненно.
Mineralocorticoid receptor antagonists (preferably eplerenone) are prescribed to patients with NSTE-ACS with detected LVEF<35%, клиникой СН или выявленным СД. Однако у пациента не должно быть тяжелых проявлений почечной недостаточности и гиперкалиемии.
Separately, the 2015 recommendations describe an approach to the selection of invasive tactics for the management of patients with NSTE-ACS, based on individual risk stratification. Emergency invasive management tactics (conducting coronary angiography up to 2 hours from the patient’s admission to the hospital) are used when very high-risk signs are identified in patients with NSTE-ACS (hemodynamic instability or cardiogenic shock; persistent ischemic chest pain refractory to drug treatment; cardiac arrest or life-threatening rhythm disturbances; mechanical complications of MI (myocardial ruptures); recurrent dynamic changes in the ST segment on the ECG, especially transient elevations). If such patients are hospitalized without the availability of emergency coronary angiography and PCI, they should be transferred to an appropriate specialized interventional center immediately.
Early invasive tactics for managing a patient with NSTE-ACS involves performing coronary angiography within 24 hours of the patient’s admission to the hospital and is carried out in high-risk patients. These include patients with a typical increase and decrease in markers of myocardial necrosis; dynamic changes in the ECG of the ST segment or T wave (including asymptomatic); with an identified score on the GRACE scale >140. If such patients are in a hospital without the possibility of emergency coronary angiography and PCI, they must be transferred to an appropriate specialized interventional center within 1 day after hospitalization.
Invasive tactics for patient management involve performing coronary angiography up to 72 hours from the patient’s admission to the hospital, if the patient meets the criteria for intermediate risk: has diabetes or renal dysfunction (decreased GFR<60 мл/мин); характеризуется значением ФВЛЖ <40% или наличием признаков застойной СН; с ранней постинфарктной стенокардией, перенесенными ранее ЧКВ или коронарным шунтированием (КШ); при выявленной сумме баллов по шкале GRACE от 109 до 140. Если такие пациенты находятся в стационаре без возможности проведения экстренной коронарографии и ЧКВ, их необходимо перевести в соответствующий специализированный интервенционный центр в период госпитализации.
In low-risk patients, stress tests and coronary angiography are indicated based on their results.
When performing coronary angiography and PCI in patients with NSTE-ACS, preference should be given to the maximum use of radial access and drug-eluting stents.
Up to 10% of patients with NSTE-ACS may require CABG as a method of complete myocardial revascularization in multivessel coronary atherosclerosis. Currently, the decision on the preferred method of myocardial revascularization for NSTE-ACS is made collectively by specialists: cardiologists, cardiac surgeons and anesthesiologists (Heart Team), taking into account many factors and individually. There are no clear recommendations in this regard, since there are no results from randomized clinical trials examining the benefits of PCI or CABG in patients with NSTE-ACS. Emergency CABG is used for NSTE-ACS with hemodynamic instability, recurrent myocardial ischemia and in patients with very high-risk coronary lesions, regardless of the use of dual antiplatelet therapy. In relatively stable patients with NSTE-ACS, the second antiplatelet agent – ticagrelor or clopidogrel – should be discontinued 5 days before CABG, prasugrel – 7 days before. In patients with NSTE-ACS, it is permissible to evaluate platelet function after discontinuation of a platelet receptor P2Y12 inhibitor to reduce the waiting time for CABG. Resumption of dual antiplatelet therapy after CABG is possible within a time frame that seems safe to doctors. It is recommended to continue therapy with low doses of ASA until CABG; moreover, 6–24 hours after CABG it is recommended to resume taking ASA if there is no ongoing postoperative bleeding.
One of the sections of the 2015 European recommendations is a chapter devoted to efforts to change the lifestyle of the patient who has suffered an acute coronary event. Emphasis is placed on the need for special programs to quit smoking and increase the adherence of this category of patients to comply with medical prescriptions.
It should be summarized that not all positions outlined in the new recommendations of our European colleagues for the management of patients with NSTE-ACS can be fully implemented into the actual clinical practice of hospitals in the Russian Federation. It should be taken into account that a clear understanding of the principles of management of this heterogeneous cohort of patients will encourage more active practitioners in relation to risk stratification, stress testing and referral of patients for invasive coronary studies.

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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 final diagnosis). Typically, this term is used in relation to acute clinical manifestations coronary heart disease ( IHD) . Coronary disease, in turn, is a lack of oxygen supply to the heart muscle. This is usually due to problems at the level of the vessels that supply the heart. IHD can develop for years without leading to serious problems with the heart. Once the lack of oxygen becomes more severe and there is a threat of myocardial infarction, the disease is diagnosed as acute coronary syndrome.

The term ACS is usually used to refer to three main pathologies that have a common mechanism of development and a common cause:

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

In general, coronary heart disease is one of the most common pathologies in the world. According to the World Health Organization ( WHO), for example, in 2011, this particular disease claimed the lives of more than 7 million people, becoming the most common cause of death. This figure is quite applicable to ACS, since it is the stage of exacerbation of IHD. Currently, this pathology occurs in men somewhat more often than in women. The ratio is 1 to 1.5 or 1 to 2 ( according to various sources). Many studies are being conducted that are aimed at studying the causes and factors contributing to the development of ACS. The risk of angina and heart attacks increases greatly with age. In children and adolescents in the absence of congenital pathologies, ACS practically does not occur.

Anatomy of the heart

The heart is one of the most structurally complex organs in the human body. It is located in the anterior left part of the chest. It distinguishes between the base - the wider part located at the top, and the apex - the narrower part located at the bottom. In general, a normal heart can be compared to a cone shape. Its longitudinal axis is inclined. The base of the organ is located partly to the right of the sternum, and partly behind it. Most of ( approximately 2/3) is located to the left of the sternum. Large vessels flow into the base of the heart, bringing and carrying away blood. The heart itself performs a pumping function. In an adult, the heart can weigh from 200 to 380 g ( men have more than women). Its length can reach 15 cm, and the width of the base is 11 cm.

In the structure of the heart, consider the following anatomical sections:

chambers of the heart;
walls of the heart;
conduction system of the heart;
coronary vessels;
heart valves.

Chambers of the heart

In humans, the heart has 4 chambers - two atria and two ventricles. The right chambers of the heart are separated from the left by a septum consisting of connective tissue and muscle fibers. It prevents the mixing of venous and arterial blood. Between the atrium and the ventricle on each side there is a valve that prevents the reverse flow of blood.

The heart contains the following chambers:

Right atrium. Venous blood from the systemic circulation enters here ( vessels of all internal organs and tissues except the vessels of the lungs). The walls of the atrium are quite thin; they do not normally perform serious work, but only drive blood in portions into the ventricles. From the right atrium, venous blood enters the right ventricle.
Right ventricle. This section pumps 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 venous turns into arterial.
Left atrium. This chamber already receives arterial blood from the small circle. It enters here through the pulmonary veins. When the left atrium contracts, blood is directed into the left ventricle.
Left ventricle. It is the most voluminous chamber of the heart. It takes arterial blood and releases it under high pressure into the aorta. This pressure is necessary to pump blood throughout the vascular network of the systemic circulation. When the left ventricle fails to cope with this function, heart failure occurs and 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 the oxygen demand is greatest here.

The cameras are positioned relative to each other as follows. The atria occupy the upper part of the heart ( at its base). The ventricles are located below. In this case, the left ventricle occupies the anterior left part of the organ. Almost the entire anterior surface of the heart and its apex are the wall of the left ventricle. The right ventricle is located slightly behind and to the right, on the posterior surface of the heart.

Heart walls

The walls of the heart consist of several layers, each of which has its own functions. The muscle layer has the greatest thickness and greatest importance ( myocardium). The thickness of the walls of the heart is uneven in all chambers. The smallest thickness is in the area of the atria. The walls of the right ventricle and the interventricular septum are somewhat thicker. The thickest walls ( up to 0.8 - 1.2 cm) has a left ventricle.

The walls of the heart in any part 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 to regulate normal blood flow ( without turbulence in the flow, which can cause blood clots).
Myocardium. The muscularis propria 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 not only have a high contraction potential, but also a special ability to conduct a bioelectric impulse. Thanks to these features, the myocardial fibers are almost simultaneously covered by excitation and contracted. 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 fibers, and diastole is their relaxation. Normally, atrial systole and diastole begin slightly earlier than the corresponding ventricular phases.
Epicard. 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 the large vessels that supply blood. Turning back, the epicardium passes into the visceral layer of the pericardium and forms the cardiac sac. Sometimes the epicardium is also called the parietal 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 refers to special nodes and fibers in the heart that are capable of independently producing and quickly conducting a bioelectric impulse. These paths are located in such a way that the impulse propagates at the desired speed and different parts of the myocardium contract in a certain order. The atria should contract first, and only after them the ventricles. Only in this case will blood be pumped normally throughout the body.

The conduction system consists of the following sections:

Sinoatrial node. This node is the main pacemaker of the heart. Cells in this area perceive signals from the nervous system coming from the brain and generate an impulse, which then spreads along the pathways. The sinoatrial node is located at the junction of the vena cava ( top and bottom) into the right atrium.
Interatrial bundle of Bachmann. Responsible for transmitting impulses to the myocardium of the left atrium. Thanks to it, the walls of this chamber shrink.
Internodal conductive fibers. This is the name given to 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 at the border of all four chambers of the heart, between the tricuspid and mitral valves. Here there is some inhibition in the propagation of the impulse. This is necessary in order to allow the atria to contract completely and release the entire volume of blood into the ventricles.
Bundle of His. This is the name of a set of conductive fibers that ensures the propagation of an impulse to the ventricular myocardium and promotes their simultaneous contraction. The bundle of His consists of three branches - the right bundle, the left bundle and the left posterior branch.

During myocardial infarction, when muscle cells die in a certain area of the heart muscle, the transmission of impulses through the conduction system of the heart may be disrupted. This will lead to disharmonious propagation of the contraction wave and disruption of pumping function. In such cases, they speak of a blockade of a branch or at the level of a node.

Coronary vessels

Coronary vessels are the heart's own blood vessels that supply the heart muscle. It is muscle tissue that makes up the bulk of this organ, performs a pumping function and consumes the largest amount of oxygen. The coronary arteries originate from the aorta at its very exit from the left ventricle.

There are two main coronary arteries in the heart:

Arteria coronaria dextra. The branches of this artery supply 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 parts 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.

Coronary arteries have a significant number of anastomoses ( connections). Thanks to this, even if one of the branches narrows, blood continues to flow to the heart muscle from the basin of the other artery ( although to a lesser extent). This is a kind of protection against acute heart attack. Thus, when small branches are blocked, the damage to the heart muscle will be moderate. A severe heart attack occurs only when there is spasm or thrombosis of a more or less large coronary artery, or if the heart works at an increased rate and its oxygen requirements are greatly increased.

Heart valves

The valves are formed by connective tissue. They consist of several valves and a dense ring. The main function of the heart valves is to regulate one-way blood flow. Normally, they prevent blood from returning to the chamber of the heart from where it was ejected. If the valves malfunction, the pressure in the chambers of the heart may increase. This leads to increased work of the myocardium, increases the need of cells for oxygen and creates a threat of the development of ACS.

The heart has 4 valves:

Tricuspid valve. 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. Located at the exit of the right ventricle. During diastole, the ventricle expands again from its 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 the tricuspid valve.
Aortic valve. It is located at the base of the aorta, where it exits the left ventricle. The mechanism of operation is similar to that of the pulmonary valve.

What is coronary syndrome?

As mentioned above, ACS is a kind of exacerbation of coronary heart disease. At the same time, the flow of arterial blood to the heart muscle is further aggravated, and the threat of death of cardiomyocytes is created. All pathologies that appear in this case are, as it were, stages of the same process. The easiest option is unstable angina. If qualified assistance is not provided at this stage, myocardial infarction develops without ST segment elevation, and then with elevation of this segment. In this case, it is difficult to say how long the transition from one stage to another takes. These periods are very individual and largely depend on the causes of the disease.

Unstable angina

This disease is also popularly called “angina pectoris”. This name appeared due to the fact that the main manifestation of angina is pain in the heart and behind the sternum, as well as a feeling of pressure and discomfort in this area. In medical practice, it is customary to distinguish between stable and unstable angina. The first is characterized by relative constancy. The pain with it is of the same type, appearing under the same conditions. Such angina can be easily classified by severity. It is not classified as ACS, since it is believed that the risk of such an attack developing into myocardial infarction is minimal. Unstable angina is much more dangerous. It combines a number of clinical forms in which it is difficult to predict how the patient’s condition will change in the near future. That is why it was included in the concept of ACS as a transitional form to myocardial infarction.

Unstable angina is diagnosed in the following cases:

Non-ST segment elevation myocardial infarction

In fact, ST segment elevation is not the main criterion for the presence or absence of myocardial infarction. However, this group is identified separately in most new classifications. It combines those cases of cardiac muscle necrosis when ST segment elevation does not occur. Most often it is still present, then they talk about the classic version of the flow.

Without the ST segment, diagnosis is based on elevated levels of specific markers and characteristic patient complaints. Later, typical manifestations on the ECG may also appear. As a rule, if the infarction is not manifested by ST segment elevation, then the ischemic area covers 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 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 in the first stages of the disease ( by emergency doctors when admitting a patient to a hospital). Only after carrying out other examinations, in addition to the ECG, can we talk about distinguishing clinical forms within the very concept of ACS.

ST segment elevation myocardial infarction

ST segment elevation usually indicates more severe damage to the heart muscle. The isoline, which should be recorded normally at this interval of the cardiogram, indicates the absence of electrical activity. If the segment rises, we are talking about the appearance of pathological electrical activity in the muscle. In this case, it is of a chemical nature. Against the background of cell ischemia, an imbalance occurs between the potassium concentration inside cardiomyocytes and in the extracellular space. This creates a current that raises the isoline.

A more severe option is myocardial infarction with the appearance of a pathological Q wave. It indicates a large 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 few classifications of this pathology have been proposed, which reflect its course and other features.

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

Large focal infarction. There is an elevation of the ST segment, the formation of a Q wave. Typically, the zone of necrosis is localized in the wall of the left ventricle. Such an infarction 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 died directly near the endocardium) or as intramural ( if the necrosis zone does not border either the epicardium or the endocardium, but is located strictly in the thickness of the myocardium).

Based on the location of the necrosis zone, the following types of infarction can be distinguished:

Left ventricular wall infarction. It can be anterior, septal, apical, lateral, posterior. Other localizations are possible ( for example, anterolateral, etc.). This type is the most common.
Right ventricular wall infarction. It occurs much less frequently, usually with hypertrophy of this section ( pulmonary heart, etc.). Normally, the right ventricle does not work so hard that there is a serious lack of oxygen.
Atrial myocardial infarction. It is also very rare.

In fact, all of these pathologies can also be included in the definition of ACS. This diagnosis will be relevant until all the details of heart damage are clarified. Only then can the diagnosis be clarified from the collective term ACS to a specific clinical form, indicating the stage and localization of the process.

Causes of coronary syndrome

Coronary syndrome is a disease that can have a variety of underlying causes. In general, as mentioned above, myocardial damage is caused by impaired arterial blood flow. Most often, blood flow disturbances are caused by a limited set of standard changes. This is the so-called pathophysiology of coronary syndrome.

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

It should be noted that most patients experience a combination of several of the above mechanisms. For example, against the background of atherosclerotic damage to the arteries, ischemic heart disease occurs. If, against this background, the myocardial oxygen demand increases, IHD turns into ACS and there is a direct threat to the patient’s life.

The classic cause of the development of coronary artery disease and subsequent ACS is considered to be atherosclerotic damage to the coronary arteries. 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 greatly influence the risk of developing acute coronary syndrome.

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

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, damage to the coronary arteries develops rather as a complication of other diseases. That is, acute coronary syndrome is not preceded by coronary heart disease, as happens in the classical version. Most often, non-atherosclerotic causes of ACS lead to the development of acute myocardial infarction. Because of this, they are considered more dangerous. Neither the patient nor the doctor can often predict heart damage in advance. Other pathologies are considered here as causes.

Non-atherosclerotic causes of ACS can be:

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

Arteritis

As mentioned above, the inflammatory process leads to temporary thickening of the walls of the arteries and narrowing of their lumen. There are a number of diseases in which such inflammation develops without cholesterol deposition. Endothelial cells in the walls are affected due to infectious or immunological reasons.

Diseases that can cause myocardial infarction due to arteritis are:

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

Deformation of the coronary arteries

In contrast to inflammation of the coronary arteries, deformation is usually understood as a permanent change in their structure. If in the first case, taking anti-inflammatory drugs restores blood flow, then in the second, the process is irreversible. Deformation may be a consequence ( residual phenomenon) after an inflammatory process or develop independently. Most often it is caused by excessive accumulation of substances in the walls of the arteries. The final stage is fibrosis ( connective tissue proliferation).

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

mucopolysaccharidosis;
Fabry disease;
fibrosis after radiation therapy;
idiopathic ( reason is unclear) calcium deposits in the arterial wall ( more common in children).

Congenital anomalies

In some cases, coronary circulatory disorders are a consequence of congenital anomalies. In other words, during the intrauterine development of the child, the heart vessels formed incorrectly. This is often a consequence of congenital diseases ( within the framework of any syndromes) or exposure to toxic substances on the mother's body during pregnancy. Due to the abnormal structure of the arteries in humans, already in adulthood, certain parts of the myocardium are less well supplied with blood. Accordingly, under certain conditions, favorable conditions are created for the development of a heart attack. This cause of ACS is extremely rare.

Injuries

Local circulatory disorders can also be caused by injury, especially if the blow was in the chest area. If the heart is directly affected, they speak of myocardial contusion. Due to local concussion, partial release of fluid from the vessels occurs, circulatory disturbances and, as a result, necrosis of cardiomyocytes. Injuries in other anatomical areas not directly related to cardiac injury pose some risk of blood clot formation. In addition, pain stress can cause the heart to work faster and increase the myocardial oxygen demand.

Heart irradiation

A fairly rare cause of myocardial infarction is irradiation of the heart area. It may occur as part of radiotherapy for malignant neoplasms. Intense ionizing radiation, in addition to tumor cells, also affects endothelial cells in the coronary arteries and the cardiomyocytes themselves. The consequence may be direct death of a section of the myocardium, deformation or inflammation of the arteries, and the creation of favorable conditions for the formation of blood clots and atherosclerotic plaques.

Coronary artery embolism

Coronary artery embolism is very similar to thrombosis. The only difference is that the thrombus forms directly in the coronary artery, usually through the growth of an atherosclerotic plaque. An embolism is the same blockage of a vessel as with thrombosis, but the embolus itself has formed somewhere else. Then it accidentally entered the coronary artery through the bloodstream and disrupted the blood flow.

Coronary artery embolism can occur with the following diseases:

bacterial endocarditis;
thromboendocarditis ( a blood clot formed in the heart cavity without the participation of microbes);
heart valve malformations ( Normal blood flow is disrupted, turbulence and blood clots form);
blood clots formed in inserted catheters ( during medical procedures);
blood clots after heart surgery.

Thyrotoxicosis

Thyrotoxicosis is an increased level of thyroid hormones in the blood. This condition can develop with various pathologies of this organ. Thyrotoxicosis itself very rarely causes a heart attack. Most often, it provokes ACS in people with existing coronary artery disease. The mechanism of heart damage is very simple. Thyroxine and triiodothyronine ( thyroid hormones) stimulate a faster and stronger heartbeat. Because of this, the myocardial need for oxygen increases. With limited capacity of the coronary vessels, acute ischemia and infarction occur.

Increased blood clotting

In some diseases, blood clotting is impaired, which is why even without the influence of external factors or atherosclerosis, a blood clot can form in the coronary artery. Among these causes, disseminated intravascular coagulation is usually called ( ICE), thrombocytosis ( elevated platelet count), some malignant blood diseases.

Thus, acute coronary syndrome can have many different causes. Most often this is associated with atherosclerosis and coronary heart disease, but secondary damage to the coronary arteries also occurs. The mechanism of development of angina and heart attack may also be different. All these pathologies are united by common clinical manifestations and similar diagnostic and treatment tactics. That is why, from a practical point of view, it was convenient to combine such diverse forms into the collective concept of OKS.

Symptoms of coronary syndrome

Compared to many other diseases, ACS has rather sparse symptoms ( few different manifestations of the disease). However, the combination of the patient’s complaints and his general condition are so characteristic of this particular pathology that experienced doctors can accurately make a preliminary diagnosis at the first glance at the patient.

Typical symptoms of ACS are:

pain;
sweating;
pale skin;
fear of death;

Pain

Pain syndrome in ACS is the most important symptom. Sometimes it is the only manifestation of the disease. Pain can vary in location and intensity, but most often have a number of characteristic features that suggest their true nature. In ACS, the pain is also called anginal. This term is used specifically for those pains that are caused by oxygen starvation of cardiomyocytes.

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

Thus, pain syndrome is the main complaint and manifestation of ACS. Unlike stable angina, its manifestation here is more intense. The pain is acute, most often unbearable. Without taking medications ( nitroglycerin under the tongue) she doesn't back down. Distinguish pain during a heart attack from pain of another nature ( for pancreatitis, renal colic, etc.) can be very difficult at times.

Sweating

Most often it occurs suddenly. The patient turns pale at the first attack, and large drops of cold, sticky sweat appear on the forehead. This is explained by the acute reaction of the autonomic nervous system to painful stimulation.

Dyspnea

In angina pectoris and myocardial infarction, shortness of breath can be caused by two main mechanisms. Most often it occurs due to irritation of pain receptors. With a sharp attack of pain, the patient seems to lose his breath. When inhaling, the pain may intensify, so he is afraid to take a deep breath. Shortness of breath occurs - a violation of the breathing rhythm. Somewhat later, if there has been necrosis of the heart muscle or arrhythmia has occurred, circulatory disorders appear. The heart pumps blood intermittently, which is why it can stagnate in the small circle ( in the vessels of the lungs), disrupting breathing.

Pale skin

Pale skin in patients with ACS is explained not so much by circulatory disorders, but, as with sweating, by irritation of the autonomic parts of the nervous system. This reaction is triggered by intense pain. Only after some time, if there is necrosis, blockade of conduction bundles or arrhythmia, circulatory disorders occur. Then pallor and cyanosis ( blue skin) are explained by insufficient oxygen supply to the tissues. In the acute period, this symptom is of a vegetative nature.

Fear of death

Fear of death is often considered as a separate symptom, since so many patients describe their condition this way. Usually this subjective sensation appears due to a temporary stop of the heartbeat, interruptions in breathing, and severe pain.

Fainting

Fainting ( syncope) condition in the classic course of myocardial infarction occurs infrequently. It does not occur with angina pectoris. Loss of consciousness is caused by a short-term attack of arrhythmia or circulatory disorders. Because of this, at some point the brain stops receiving enough oxygen, and it loses control over the body. Syncope occurs only immediately after a heart attack. Repeated episodes indicate an atypical course of the disease ( cerebral form).

Cough

Cough is a fairly rare symptom. It appears for a short period and is unproductive ( without sputum separation). Most often, the occurrence of this symptom is caused by stagnation of blood in the pulmonary circulation. Almost always, a cough appears simultaneously with shortness of breath.

A different picture can be observed with the following atypical forms of myocardial infarction:

Abdominal form

In the abdominal form, the area of necrosis is usually located on the posteroinferior surface of the heart, which is adjacent to the diaphragm. This is a flat muscle that separates the abdominal cavity from the chest cavity. This form of heart attack occurs in approximately 3% of patients. Due to irritation of the nerves in this area, a number of gastrointestinal symptoms appear. This creates serious difficulties in making a diagnosis.

Typical symptoms of abdominal myocardial infarction are:

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

It is especially difficult to diagnose a heart attack if the patient has chronic gastrointestinal diseases ( gastritis, stomach ulcer, colitis). All these pathologies can cause the above symptoms during an exacerbation.

Asthmatic form

This form occurs in almost 20% of patients and is therefore very common. With it, circulatory disorders come first. If the heart attack is localized in the wall of the left ventricle, then the latter stops pumping blood normally. Left ventricular failure develops rapidly. Due to stagnation of blood in the pulmonary circulation, symptoms resembling an attack of bronchial asthma begin to appear in the lungs. This is a subjective feeling of suffocation, a forced position ( orthopnea), severe shortness of breath, increasing cyanosis. When listening to the lungs, you can hear characteristic wheezing, and the patient himself may complain of a wet cough. In the asthmatic form, pain in the heart area may be mild or absent altogether.

Painless form

This form is one of the rarest and most dangerous. The fact is that with it, most of the symptoms typical of myocardial infarction are very mild. Instead of pain, a short-term feeling of discomfort appears behind the sternum, cold sweat appears, but quickly passes. The patient may feel a disturbance in heart rhythm or breathing, but within seconds the rhythm is restored. Due to the absence of serious symptoms, such patients often do not seek medical help. They are diagnosed only by ECG data, when a small healed area is detected. Death with this form is quite rare. The fact is that a painless form is possible only with a small-focal heart attack, which rarely seriously disrupts the functioning of the organ as a whole.

Cerebral form

This form is more typical for older people, in whom blood circulation in the vessels of the brain is already difficult ( usually due to atherosclerosis). Against the background of a myocardial infarction, a temporary disruption of blood circulation occurs, and a sufficient amount of oxygen ceases to flow to the brain. Then it is the symptoms of damage to the central nervous system that come to the fore. This form occurs in 4–8% of cases of all atypical forms, and is more often observed in men.

Typical symptoms of the cerebral form of myocardial infarction are:

severe sudden dizziness;
severe headaches;
attack of nausea;
repeated fainting;
darkening of the eyes and temporary visual disturbances.

If a heart attack causes arrhythmia and normal blood circulation is not restored for a long time, then motor and sensory disturbances may also appear. This indicates serious damage to brain tissue.

Collaptoid form

This form is characterized by a serious disturbance of the systemic circulation. The appearance of symptoms is caused by a sharp drop in blood pressure. Because of this, the patient may be disoriented ( but he rarely loses consciousness). Characterized by profuse sweating and darkening of the eyes. The patient has difficulty standing on his feet and often falls, losing control of his muscles. At the same time, kidney function may be impaired ( urine is not filtered). This form indicates the threat of a serious complication of myocardial infarction - cardiogenic shock. As a rule, it occurs with extensive necrosis affecting all layers of the heart wall. Pain in the heart area may be mild. The pulse in such patients is rapid, but weak and difficult to palpate.

Edema form

This form is usually a sign of an extensive heart attack with a serious disturbance of the systemic circulation and the establishment of heart failure. The main symptoms in patients in the first hours after a heart attack are heartbeat disturbances, periodic attacks of shortness of breath, general muscle weakness and dizziness. During the same period, cardiac edema gradually begins to form. They involve the area of the feet, ankles and legs, and in severe cases, fluid even begins to accumulate in the abdominal cavity ( ascites).

Arrhythmic form

In principle, heart rhythm disturbances are one of the most common ( almost constant) symptoms of myocardial infarction. A separate arrhythmic form is diagnosed only when rhythm interruptions are the leading symptom. That is, the patient does not complain of pain or shortness of breath, but constantly notes an increased and uneven heartbeat. This form occurs in only 1–2% of patients. As a rule, the ECG shows a blockage of the conduction pathways, which causes arrhythmia. The prognosis in this case is poor, since rhythm disturbances can at any time turn into ventricular fibrillation and quickly lead to the death of the patient. In this regard, such patients must be hospitalized. The problem is that the symptoms of this form of heart attack can be very similar to an ordinary attack of arrhythmia. Then an ECG and detection of signs of resorption-necrotic syndrome ( lab tests).

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 and knows that he has 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

Diagnosis of ACS in the first stages is aimed at detecting oxygen starvation of the heart muscle. As a rule, to make a preliminary diagnosis, it is enough to analyze the patient’s complaints. A similar nature of pain practically does not occur in other heart pathologies. In the hospital ( cardiology department) more complex procedures are carried out in order to clarify the diagnosis and prescribe complex treatment.

The following methods are used in the diagnosis of acute coronary syndrome:

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

General inspection and analysis of complaints

In addition to the characteristic complaints and symptoms of ACS, which were listed in the corresponding section, the doctor may take a number of standard measurements during the initial examination. For example, in patients who have suffered a myocardial infarction, the temperature may rise as part of the resorption-necrotizing syndrome. It begins to grow on days 1–2 and reaches a peak on days 2–3. In case of extensive myocardial infarction with the appearance of a Q wave, the temperature can last a week. Its values usually do not exceed 38 degrees. Heart rate ( pulse) decreases slightly immediately after a heart attack ( bradycardia up to 50 – 60 beats per minute). If the frequency remains high ( tachycardia more than 80 beats per minute), this may indicate an unfavorable prognosis. The pulse is often arrhythmic ( intervals between beats of different lengths).

In addition to taking your temperature, your doctor may use the following standard physical examination techniques:

Palpation. During palpation, the doctor probes the area of the heart. In the case of ACS, a slight displacement of the apical impulse may be observed.
Percussion. Percussion is tapping the area of the heart with your fingers to determine the boundaries of the organ. In ACS, the boundaries are usually not greatly changed. Characterized by moderate expansion of the left border of the heart, as well as expansion of vascular dullness in the second intercostal space on the left.
Auscultation. Auscultation is listening to heart sounds using a stethoscope. Here you can hear pathological noises and heart sounds that arise due to disturbances in blood flow inside the cavities. Characteristic features include the appearance of a systolic murmur at the apex of the heart, the appearance of a pathological third sound, and sometimes a 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 likelihood of a heart attack. Immediately after a heart attack, blood pressure may be low.

Another important diagnostic criterion is the reaction to nitroglycerin. As a rule, with its sublingual ( under the tongue) application of pain weakens or disappears. This can be used as a diagnostic criterion. For pain in the heart area that is not caused by ACS, its intensity will not decrease after taking nitroglycerin.

General blood analysis

In patients with ACS, there may be no specific changes in the general blood test. However, with necrosis of the heart muscle, certain abnormalities are recorded in some patients. The most common is an increase in erythrocyte sedimentation rate ( ESR) . It is explained by the presence of resorption-necrotic syndrome. ESR increases on days 2–3 and reaches a maximum after about a week. In general, this indicator may remain elevated for another month after a heart attack. Normally, the maximum permissible ESR value for men is 10 mm/h, and for women – 15 mm/h.

Another important indicator of resorption-necrotic syndrome is leukocytosis ( increased white blood cell count). These cells are engaged in “cleansing” the blood and tissues of foreign elements. In the case of necrosis, these elements are dead myocardial tissue. Leukocytosis is registered within 3–4 hours after a heart attack and reaches a maximum on days 2–3. The white blood cell count 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. The number of band neutrophils increases proportionally ( shift of the leukocyte formula to the left).

Blood chemistry

In case of ACS, there may be no visible changes in the biochemical blood test for a long time. As a rule, the first deviations from the norm are biochemical markers of resorption-necrotic syndrome. These are substances that accompany the inflammatory process at the site of ischemic damage to the heart muscle.

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

Seromucoid. It can be determined on the very first day after a myocardial infarction. Its concentration remains elevated for another 1–2 weeks. Normally, it is contained 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 for 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 normal level 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 may increase on days 2–3 after a heart attack, reaching a maximum in the period from days 3 to 5. The analysis is informative for 2 weeks. The normal level of fibrinogen in the blood is 2 – 4 g/l.
C-reactive protein. This indicator is of great importance in 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 a rapid positive reaction to troponin ( biomarker of necrosis) almost 10% of patients die within 2 weeks. If the C-reactive protein level is lower and the reaction to troponin is negative, the survival rate is as much as 99.5%. These indicators are relevant for unstable angina and myocardial infarction without the formation of a Q wave.

As a rule, other parameters of the biochemical blood test remain normal. Changes can only occur in chronic diseases not directly related to ACS, or after some time ( weeks) due to complications.

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 the patient. To do this, measure the level of cholesterol in the blood, triglycerides and lipoproteins ( low and high density). If these indicators are elevated, there is a high probability that coronary artery disease has developed precisely against the background of atherosclerosis of the coronary arteries.

Coagulogram

Coagulation is a blood clotting process in which a very large number of different substances and cells take part. A coagulogram is a set of tests that are designed to check how a patient’s blood clots. This test is usually ordered to determine your risk of developing blood clots. In addition, coagulogram data are necessary to accurately calculate the dose of anticoagulants - a group of substances that is included in the treatment of almost all patients with ACS.

To obtain accurate results of a coagulogram, you should donate blood on an empty stomach. Eating should be stopped at least 8 hours before the test.

The coagulogram measures the following indicators:

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

If necessary, other, more detailed studies of the blood coagulation system are carried out.

Determination of biomarkers of necrosis

During acute myocardial infarction, death occurs ( necrosis) muscle cells. Since cardiomyocytes are unique cells, they contain certain enzymes and substances inside them that are not typical ( or less characteristic) for other body tissues. Normally, these substances are practically not detected in the blood during analysis. However, in the midst of cell death and immediately after a heart attack, these substances enter the blood and circulate for some time before being eliminated from the body. Specific tests make it possible to determine their concentration, assess the severity of damage to the heart muscle, and also establish the fact of necrosis ( reliably confirm a heart attack and distinguish it from angina or other pain in the heart area).

Markers of myocardial necrosis are:

These markers are the most specific signs of the resorption-necrotizing syndrome discussed above. When taking blood for analysis, you need to take into account that not all of them will be elevated. As follows from the above data, each marker circulates in the blood only for a certain period of time. However, the identification of even a few of them in combination with other signs of a heart attack is sufficient confirmation of the diagnosis. An isolated increase in one of the markers should still make the doctor wonder whether the death of the heart muscle is taking place. The severity of the infarction usually corresponds to the level of marker elevation.

Electrocardiography

ECG is the most common way to diagnose ACS. It is based on recording a bioelectrical impulse that passes through the heart in various directions. Under the influence of this impulse, the heart muscle normally contracts. On modern electrocardiographs, the sensitivity is high enough to sense the slightest deviation from the norm. The doctor, examining the electrocardiogram, sees which parts of the myocardium conduct the electrical impulse worse, and which do not conduct it at all. In addition, this method allows you to evaluate the frequency and rhythm of heart contractions.

When performing an ECG, the patient lies supine or semi-recumbent ( for severe patients) position. Before the procedure, the patient should not perform heavy physical activity, smoke, drink alcohol or take 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 to 10 minutes after the patient has taken a comfortable position. The fact is that in a number of patients, heart function may be disrupted even with a rapid change in body position. Another important condition is to remove all metal objects and turn 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 moistened with a special solution or just water. This improves metal-to-skin contact and helps obtain more accurate data.

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 shin;
black – on the lower part of the right shin;
chest electrodes ( 6 items) - on the anterior left part of the chest.

Color coding is needed so as not to confuse the so-called leads. The leads are formed as follows. The device registers the conduction of impulses in a certain plane. Depending on which electrodes are taken into account when forming the plane, different leads are obtained. By recording impulses in different directions, doctors have the opportunity to find out in which part of the myocardium there is not enough oxygen.

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 hand – negative, left leg – positive;
aVR – enhanced abduction from the right arm ( relative to the average potential of the remaining electrodes);
aVL – enhanced abduction from the left arm;
aVF – increased abduction from the left leg;
V 1 – V 6 – leads from the chest electrodes ( from right to left).

Thus, there are 3 standard, 3 enhanced and 6 chest leads. The electrode on the right leg performs the grounding function. If the electrodes are correctly positioned and all the above requirements are met, when turned on, the electrocardiograph itself records in all leads.

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

Isoline. Indicates a lack of momentum. Also, no deviations may be observed if the pulse propagates strictly perpendicular to the measurement axis. Then the vector projection onto the axis will be equal to zero and there will be no changes on the ECG.
Wave P. Reflects the spread of the impulse through the atrial myocardium and the contraction of the atria.
PQ segment. Registers the delay of the excitation wave at the level of the atrioventricular node. This ensures that blood is completely pumped from the atria to the ventricles and the valves close.
QRS complex. Displays the propagation of the impulse through the ventricular myocardium and their contraction.
ST segment. Usually located on an 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 state of rest. After the T wave, a new cardiac cycle begins.

In acute coronary syndrome, there are a number of possible abnormalities on the cardiogram. Depending on which leads these deviations are recorded, a conclusion is made about the localization of the infarction. Also, it is during an ECG that it is possible to determine the severity of ACS. The procedure shows the degree of damage to myocardial tissue - from the mildest ( without cell death) to necrosis of muscle tissue ( with ST segment elevation).

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 blood clot.
ST segment elevation in leads V 1 – V 6, I, aVL, plus signs of bundle branch block. Speaks of an extensive infarction of the anterior wall ( left ventricle). The mortality rate reaches 25.5%.
ST segment elevation in leads V 1 – V 6, I, aVL without bundle branch block. This indicates a large area of infarction in the anterior wall. The mortality rate is about 12.5%.
ST segment elevation in leads V 1 – V 4 or I, aVL and V 5 – V 6. Speaks of anteropical or anterolateral myocardial infarction. The mortality rate is approximately 10.5%.
A sign of a large inferior myocardial infarction is ST segment elevation in leads II, III, aVF. If the wall of the right ventricle is damaged, a rise occurs in leads V 1, V 3 r, V 4 r. For inferolateral infarction - in leads V 5 - V 6. In case of infarction of the posterior wall, the R wave is larger than the S wave in leads V 1 – V 2. The mortality rate in these cases is approximately 8.5%.
Isolated ST segment elevation in leads II, III, aVF indicates a small lower myocardial infarction, in which mortality does not exceed 7%.

There are other signs of myocardial infarction on the ECG. As noted above, the appearance of a pathological Q wave, which indicates a transmural infarction, is of great importance. It is also important to determine how the conduction system of the heart works. Sometimes a heart attack is accompanied by a blockade of the bundle branches or their branches ( the impulse does not propagate to any area of the myocardium). This indicates more severe heart damage and a less favorable prognosis.

Echocardiography

EchoCG is performed in many ways similar to a conventional ultrasound examination ( Ultrasound) area of the heart. The doctor obtains images of various anatomical structures of the heart using a special sensor. For unstable angina or myocardial infarction, this study is of great importance. The fact is that the doctor receives the image in real time. The heart continues to beat ( in contrast to the static image on an x-ray, where the heart is “photographed” at a specific moment). By analyzing the movements of the walls of the heart, the doctor notes whether muscle contractions occur evenly. Typically, areas suffering from a lack of oxygen ( for unstable angina), or area of necrosis ( during a heart attack) are far behind neighboring, healthy areas. This lag is an important diagnostic criterion for confirming ACS and determining a specific clinical form.

Echocardiographic signs of ACS are:

Changes in the functioning of heart valves (tricuspid - for right ventricular infarction and mitral - for left ventricular infarction). They are explained by hemodynamic disturbances. The damaged heart muscle cannot cope with the incoming blood volume, the chamber is stretched, and with it the fibrous ring of the valve is stretched.
Expansion of the heart chamber. In this case, the chamber in the wall of which the infarction occurred usually expands.
Turbulence in the blood flow. Occur due to uneven contraction of muscle walls.
Bulging of the wall. It is formed during a 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 healthy myocardium. Due to constant movement ( with heart contractions) this fabric does not have time to gain sufficient strength. The damaged area swells under the influence of internal pressure ( especially in the left ventricle).
Dilatation of the inferior vena cava. Observed during myocardial infarction of the right ventricle. Since the right side of the heart can no longer cope with the flow of blood, this blood stagnates in the large veins leading to the heart. The inferior vena cava expands earlier and stronger than the superior one, since under the influence of gravity a larger volume of blood accumulates in it.

It should be noted that small areas of infarction may not be visible on echocardiography. At the same time, the patient may have typical ECG signs and complaints. Therefore, this study is widely used to clarify the diagnosis, but is not the main one in terms of making a diagnosis.

Myocardial scintigraphy

Scintigraphy ( radionuclide research) is a relatively new and expensive method for diagnosing ACS. Most often it is used when there are difficulties in determining the location of the infarction. The essence of the method is that healthy cardiomyocytes and dead cells have different biochemical activities. When special chemically active substances are introduced into the patient’s body, they will accumulate selectively in healthy or necrotic areas ( depending on the chosen substance). After this, visualizing the damaged areas will no longer be difficult.

The procedure proceeds as follows. Special reagents are injected into the patient's vein. The most commonly used isotope is technetium with a molecular weight of 99 ( 99 mTc-pyrophosphate). It has the special property of accumulating only in the area of myocardial necrosis. This is due to the accumulation of excess calcium in 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 results are obtained between 24 and 48 hours. Weaker accumulation is observed for another 1 – 2 weeks.

Another option with a similar technology is the thallium isotope – 201 Tl. On the contrary, it is retained only by viable cardiomyocytes. Thus, places where the isotope does not accumulate will be areas of necrosis. True, accumulation defects can also be detected in some forms of angina, 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 within which reliable results can be obtained. Also, the study does not provide a clear answer as to what is the cause of necrosis. Storage defects can also be detected in cardiosclerosis of other origins ( not after a heart attack).

Coronary angiography

Coronary angiography is a rather complex, but very informative study in terms of diagnosing coronary artery disease and ACS. It is an invasive method that requires special medication and psychological preparation of the patient. The essence of the method is the introduction of a special contrast agent into the cavity of the coronary arteries. It is evenly distributed in the blood, and the subsequent x-ray image reliably shows the boundaries of the vessels.

To conduct this study, an incision is made in the femoral artery, and a special catheter is placed through it to the heart. A contrast agent is injected through it near the aortic valve. Most of it ends up in the coronary arteries. If the cause of coronary artery disease is atherosclerosis, then coronary angiography will reveal areas of vascular narrowing and the presence of plaques that pose a threat in the future. If the contrast does not spread along any of the branches 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 preventative measure to understand the nature of angina. In case of heart attack and other acute conditions, its use is dangerous. In addition, there is a certain risk of complications ( provocation of arrhythmia or infection). Coronary angiography is clearly indicated before surgery, bypass surgery or angioplasty. In these cases, surgeons need to know exactly at what level the thrombus or narrowing is located.

Magnetic resonance imaging

Magnetic resonance imaging ( MRI) is currently one of the most accurate diagnostic methods. It allows you to visualize even very small formations in the human body, based on the movement of hydrogen ions, which are present in varying quantities in all human tissues.

MRI is used relatively rarely to diagnose ACS due to its high cost. It is prescribed before surgical treatment to clarify the location of the thrombus. With the help of this study, it is possible to determine the condition of the so-called fibrous cap ( assess the chance of atherosclerotic plaque rupture), detect calcium deposits in the thickness of the plaque. All this supplements information about the patient’s condition and allows for a more accurate diagnosis.

Pulse oximetry

Pulse oximetry is an important diagnostic method in the acute period, when the patient’s life is threatened. During myocardial infarction, the pumping function of the heart can be severely affected. This will lead to circulatory problems and interruptions in the supply of oxygen to the organs. Pulse oximetry uses a special sensor on the patient’s finger to record the concentration of oxyhemoglobin in the blood ( compound in red blood cells that attaches oxygen atoms). If this indicator falls below 95%, this may affect the general condition of the patient. Low oxygen levels are an indication for oxygen administration. Without this, the heart muscle will not receive enough saturated arterial blood, and patients with ACS are at increased risk of recurrent infarction.

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

Separately, the diagnosis of unstable angina should be highlighted. This pathological condition is sometimes very difficult to recognize. Its diagnosis is based on the principles of so-called evidence-based medicine. According to them, a diagnosis can be made only according to certain criteria. If, after 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, attention is paid to changes in the nature of pain. During the last month before seeing a doctor, the duration of the attacks increased ( more than 15 minutes). Along with them, attacks of suffocation, arrhythmia, and sudden inexplicable weakness began to appear.
Sudden attacks of pain or shortness of breath after activities that were previously tolerated normally.
Attacks of angina at rest ( without visible provoking factors) during the last 2 days before seeing a doctor.
Reduced effect of using nitroglycerin under the tongue ( the need to increase the dose, slow relief of pain).
An attack of angina within the first 2 weeks after a myocardial infarction ( is regarded as unstable angina, threatening recurrent infarction).
First angina attack in my life.
A shift of the ST interval on the ECG by more than 1 mm upward from the isoline in 2 or more leads simultaneously, or the presence of arrhythmia attacks on the ECG. In this case, 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 ( changes remain during a heart attack).
There were no signs of resorption-necrotic syndrome in the patient's tests, which would indicate the death of cardiomyocytes.

Treatment of coronary syndrome

As noted above, ACS is accompanied by oxygen starvation of the heart muscle, in which there is a high risk of developing myocardial infarction. If a significant part of the heart muscle dies, the risk of death is quite high. Without qualified medical care, it reaches 50% or more. Even with intensive treatment and timely hospitalization, the mortality rate for heart attacks remains high. In this regard, it is necessary to hospitalize all patients with confirmed ACS, as well as ( preferably) all patients suspected of having this pathology.

The International Health Organization recommends that patients be distributed as follows:

A preliminary diagnosis is made on site and basic assistance measures are carried out. At this stage, treatment is carried out by emergency doctors.
Patients with confirmed myocardial infarction and signs of circulatory impairment are hospitalized immediately in the intensive care unit.
Patients with suspected heart attacks and signs of circulatory disorders are also hospitalized directly in the intensive care unit.
Hemodynamically stable patients ( no signs of circulatory problems) with a confirmed heart attack can be placed both in the intensive care unit and in a regular cardiology hospital.
Hemodynamically stable patients with suspected myocardial infarction or unstable angina should also be hospitalized. In the emergency room, they must 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.

In this case, signs of hemodynamic instability mean a drop in blood pressure below 90 mmHg. Art., incessant anginal pain, any heart rhythm disturbances. After hospitalization, treatment is carried out in several stages. First aid is provided by people nearby. Next, a preliminary diagnosis is made by emergency doctors. Full treatment is carried out in the intensive care section or a highly specialized cardiology department.

Treatment of ACS is carried out in the following areas:

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

Drug treatment

Drug treatment is the main way to combat ACS. It is aimed, first of all, at eliminating the main symptoms and restoring the oxygen supply to the heart. Nowadays, there are many drugs and treatment regimens that are prescribed for patients with ACS. The choice of a specific regimen is made by the attending physician based on a comprehensive examination of the patient. The main drugs used in the treatment of ACS are given below in the form of tables.

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 to do everything at the first symptoms to restore normal blood flow to the heart muscle.

Drugs used as part of first aid for ACS

Drug name	Mechanism of action	Recommended dose	special instructions
*Nitroglycerine*	Reduces the need for myocardial cells for oxygen. Improves blood supply to the myocardium. Slows down the death of muscle cells in the heart.	0.4 mg sublingually at intervals of 5–10 minutes 2–3 times. Next they switch to intravenous administration ( concentrate for infusion). Drop by drop, infusion rate – 5 mcg/min with a gradual increase ( every 5 – 10 minutes at 15 – 20 mcg/min).	It is not given under the tongue if blood pressure drops below 100 mmHg. Art. or an increase in heart rate of more than 100 beats per minute.
*Isosorbide dinitrate*	Similar to nitroglycerin. Dilates coronary vessels ( increases blood flow to the myocardium), reduces the tension of the ventricular walls.	Intravenous drip at an initial rate of 2 mg per hour. The maximum dose is 8 – 10 mg/hour.	Side effects from taking are intensified by drinking alcohol.
*Oxygen*	Helps fill the blood with oxygen, improves myocardial nutrition, and slows down the death of muscle cells.	Inhalation at a rate of 4 – 8 l/min.	Prescribed if pulse oximetry indicates oxygenation below 90%.
*Aspirin*	Prevents the formation of blood clots, thins the blood. As a result, blood passes more easily through the narrowed coronary vessels, and oxygen supply to the myocardium improves.	150 – 300 mg in tablet form – immediately, chew. The subsequent dose is 75 – 100 mg/day.	When administered simultaneously with anticoagulants, the risk of bleeding increases.
*Clopidogrel*	Changes platelet receptors and affects their enzyme system, preventing the formation of blood clots.	Initial dose 300 mg once ( maximum – 600 mg for faster action). Then 75 mg/day in tablet form ( orally).	May lower blood platelet levels and lead to spontaneous bleeding ( most often – bleeding gums, increased menstruation in women).
*Ticlopidine*	Prevents platelet aggregation, reduces blood viscosity, inhibits the growth of wall thrombi and endothelial cells ( inner lining of blood vessels).	The initial dose is 0.5 g orally, then 250 mg twice a day with meals.	In case of renal failure, the dose is reduced.

Another important group in the treatment of ACS are beta-blockers. They are especially often prescribed to patients who simultaneously have tachycardia and increased blood pressure. The range of drugs in this group is quite wide, which allows you to select a drug that is best tolerated by the patient.

Beta blockers used in the treatment of ACS

Drug name	Mechanism of action	Recommended dose	special instructions
*Propranolol*	Blocks beta-adrenergic receptors in the heart. The strength of heart contractions and the myocardium's need for oxygen decreases. Heart rate decreases ( Heart rate), the passage of the impulse through the conduction system of the heart slows down.	Intravenous 1 mg every 5 minutes until the heart rate is established within 55 - 60 beats per minute. After 1 - 2 hours, start taking 40 mg tablets 1 - 2 times a day.	Use with caution in case of concomitant disorders of the liver and kidneys.
*Atenolol*		Intravenously once 5 – 10 mg. After 1–2 hours, 50–100 mg/day orally.	Can be used for angina pectoris to prevent heart attack.
*Metoprolol*		5 mg intravenously every 5 minutes for a total dose of 15 mg ( three injections). After 30 - 60 minutes, take 50 mg orally every 6 - 12 hours.	For moderate renal impairment, the dose may not be changed. In case of liver dysfunction, the dose is reduced based on the patient's condition.
*Esmolol*		Intravenous 0.5 mg/kg patient weight.	Not used for bradycardia less than 45 beats per minute and atrioventricular block II - III degree.

Some patients with ACS are not prescribed beta blockers. The main contraindications in this case are the duration of the P – Q interval on the ECG of more than 0.24 seconds, low heart rate ( less than 50 beats/min), low blood pressure ( systolic below 90 mm Hg. Art.). Also, drugs in this group are not prescribed for chronic obstructive pulmonary disease, since such patients may develop serious breathing problems.

As noted above, one of the main manifestations of ACS is pain in the heart area, 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 undesirable symptoms as anxiety and fear of death.

Drugs for pain relief in ACS

Drug name	Mechanism of action	Recommended dose	special instructions
*Morphine*	A powerful opioid drug. Has a strong analgesic effect.	10 mg in 10 – 20 ml NaCl 0.9%. It is administered intravenously, slowly. After 5 - 10 minutes, you can repeat 4 - 8 mg until the pain disappears.	May cause a sharp decrease in blood pressure and bradycardia. For breathing problems ( overdose or side effect) Naloxone is used; for severe nausea, metoclopramide is used.
*Fentanyl*	Similar to morphine.	0.05 – 0.1 mg intravenously slowly.	They are often used together for so-called neuroleptanalgesia for severe pain.
*Droperidol*	Blocks dopamine receptors in the brain. Has a powerful sedative effect.	2.5 – 10 mg intravenously. The dose is selected depending on the initial blood pressure, individually.
*Promedol*	Powerful analgesic effect, relaxes muscle spasms ( which may appear against a background of severe pain). Gives a hypnotic effect.	10 – 20 mg once intravenously, subcutaneously or intramuscularly.	The drug may cause addiction.
*Diazepam*	A drug from the group of benzodiazepines. Gives a good calming and hypnotic effect. Eliminates fear, anxiety and tension in patients.	2.0 ml of 0.5% solution per 10 ml of 0.9% NaCl solution. It is administered intravenously or intramuscularly.	May cause dependence with prolonged use. In a number of countries it is classified as a potent psychotropic substance.

A number of drugs to dissolve the clot can also be considered as drug therapy. Such drugs are combined into the group of thrombolytic agents. The selection of the drug and dose in this case is done individually based on the preliminary or final diagnosis. What these drugs have in common is an increased risk of side effects, which include spontaneous bleeding. If possible, thrombolysis ( clot dissolution) is carried out locally by administering the medicine through a special catheter. Then the risk of side effects is reduced.

The following drugs can be used as a thrombolytic agent:

streptokinase;
urokinase;
alteplase;
tenecteplase.

In the absence of ST segment elevation on the ECG, treatment with thrombolytics is not indicated. Then it is possible to prescribe anticoagulants. This is a group of drugs that are similar in action to thrombolytics. They prevent blood clotting and platelet aggregation. The only difference is that anticoagulants do not dissolve an already formed blood clot, but only prevent the formation of new ones. This category of drugs is used to treat all patients with acute coronary syndrome. The most common drugs are heparin ( direct anticoagulant) and warfarin ( indirect anticoagulant). Doses are selected individually depending on the patient’s condition, final diagnosis, and prognosis of the disease.

Prevention of exacerbations

Preventive measures are a very important component in the complex treatment of ACS. If the disease develops against the background of atherosclerosis and ischemic heart disease, then it is chronic. In patients who have had a myocardial infarction, the risk of recurrent episodes cannot be excluded, since the coronary arteries remain narrowed, despite the fact that the acute period is over. Therefore, all patients with angina, as well as those who have already had a heart attack, are recommended to follow simple preventive rules. This will reduce the likelihood of recurrent ACS.

The main preventive measures are:

Elimination of risk factors for atherosclerosis. The most important thing in this case is to stop drinking alcohol and smoking. Patients with diabetes should check their blood sugar levels regularly to prevent prolonged highs. 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 likelihood 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 stay fit. For people who have had a heart attack or suffer from angina, exercise may be contraindicated. This point should be clarified with your doctor. If necessary, a special test is done with an ECG taken during exercise ( treadmill test, bicycle ergometry). It allows you to understand what load is critical for the patient.
Diet. In case of atherosclerosis, the proportion of animal fats in the diet should be reduced. Also limit your salt intake to reduce the risk of hypertension. The energy value is practically unlimited if the patient does not have problems with excess weight or severe hemodynamic disturbances. In the future, the subtleties of the diet should be discussed with your attending cardiologist or nutritionist.
Regular monitoring. All patients who have had a myocardial infarction or have angina are at risk of developing ACS. In this regard, it is necessary to regularly ( at least once every six months) visiting the attending physician and performing the necessary diagnostic procedures. In certain cases, more frequent monitoring may be required.

Without compliance with preventive measures, any medical or surgical treatment will be only temporary. The risk of ACS will still increase over time and the patient will most likely die from another heart attack. Following the doctor's instructions in this case actually prolongs life for many years.

Treatment with folk remedies

Folk remedies for acute coronary syndrome are used to a limited extent. During the period of a heart attack and immediately after it, it is recommended to abstain from their use or coordinate a treatment regimen with a cardiologist. In general, among the recipes of traditional medicine there are quite a lot of remedies for combating coronary artery disease. They help supply the heart muscle with oxygen. These recipes are advisable to use in chronic ischemic heart disease to prevent ACS or after completion of the main course of treatment to prevent recurrent heart attacks.

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

Infusion of oat grains. The grains are poured in a ratio of 1 to 10 ( for 1 cup oat grains 10 cups boiling water). Infusion lasts at least a day ( preferably 24 – 36 hours). Drink half a glass of infusion 2-3 times a day before meals. It should be taken for several days until periodic heart pain disappears.
Nettle decoction. Nettles are collected before flowering and dried. For 5 tablespoons of chopped herbs you need 500 ml of boiling water. After this, the resulting mixture is boiled for another 5 minutes over low heat. When the decoction has cooled, take it 50-100 ml 3-4 times a day. You can add a little sugar or honey for taste.
Centaury infusion. For 1 tablespoon of dry herb 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.
Eryngium decoction. The grass is collected during flowering and thoroughly dried in the sun for several days. For 1 tablespoon of chopped herb you need 1 cup of boiling water. The product is boiled over low heat for 5 - 7 minutes. Take it 4 – 5 times a day, 1 tablespoon.

Surgeries to treat coronary syndrome

Surgical treatment of acute coronary syndrome is aimed primarily at restoring blood flow in the coronary arteries and stable supply of arterial blood to the myocardium. This can be achieved using two main methods - bypass surgery and stenting. They have significant differences in the technique of execution and various indications and contraindications. An important feature is that not every patient with ACS can resort to surgical treatment. Most often, it is indicated for patients suffering from atherosclerosis, congenital defects in the development of arteries, and fibrosis of the coronary arteries. In the case of inflammatory processes, these methods will not help, since the cause of the disease is not eliminated.

Coronary artery bypass surgery

The essence of this method is to create a new path for arterial blood, bypassing the narrowed or blocked area. To do this, doctors cut out a small superficial vein from the patient ( usually in the lower leg area) and use it as a shunt. This vein is sutured to the ascending aorta on one side, and the other to the coronary artery below the site of blockage. Thus, along a new path, arterial blood begins to flow freely into areas of the myocardium that previously suffered from a lack of oxygen. In most patients, angina disappears and the risk of heart attack decreases.

This operation has the following advantages:

ensures reliable supply of arterial blood to the myocardium;
risk of infection or autoimmune reactions ( rejection) is extremely small, since the patient’s own tissue is used as a shunt;
there is almost no risk of complications associated with blood stagnation 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 remote area);
The walls of the vein have a different cellular structure than the arteries, so the risk of damage to the shunt by atherosclerosis is very small.

Among the main disadvantages of the method, the main one is that the operation usually has to be performed using a heart-lung machine. Because of this, the execution technique becomes more complicated and more time is required ( on average 3 – 4 hours). Sometimes it is possible to perform bypass surgery on a beating heart. Then the duration and complexity of the operation are reduced.

Most patients tolerate coronary artery bypass grafting well. The postoperative period lasts several weeks, during which it is necessary to regularly clean the incision sites on the lower leg and chest to avoid infection. It takes several months for the sternum, which is cut during surgery, to heal ( up to six months). The patient will have to be regularly monitored by a cardiologist and undergo preventive examinations ( ECG, EchoCG, etc.). This will allow you to evaluate the effectiveness of blood supply through the shunt.

Many points concerning the course of the operation are determined individually. This is explained by 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 influenced by the patient’s age, severity of the disease, and the presence of allergies to certain medications.

Stenting of coronary arteries

The operation for stenting the coronary arteries differs significantly in the technique of execution. Its essence is to install a special metal frame into the lumen of the vessel. When introduced into the coronary artery, it is compressed, but expands inside and keeps the lumen in an expanded state. Stent insertion ( the frame itself) is performed using a special catheter. This catheter is inserted into the femoral artery and, under fluoroscopic guidance, the narrowing in the coronary artery is reached. This method is most effective for atherosclerotic vascular lesions. A properly placed stent prevents plaque from growing or breaking off, causing acute thrombosis.

The main advantages of stenting are:

the use of a heart-lung machine is not required, which reduces the risk of complications and shortens the operation time ( On average, stent installation 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 high and long-term survival of patients after this operation;
low risk of serious complications, since the chest cavity is not opened.

The main disadvantage is that in 5–15% of patients the vessel narrows again over time. Most often this is caused by a local reaction of the vessel to a foreign body. The growth of connective and muscle tissue on the sides of the stent gradually impedes blood flow, and the symptoms of CAD return. Postoperative complications may include only minor bleeding or hematoma formation in the area where the catheter was inserted. Patients, as well as after bypass surgery, are advised to undergo regular examination by a cardiologist for the rest of their lives.

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

- with incomplete obstruction of the coronary artery.

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

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

Traditionally, the following clinical manifestations are distinguished:

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

* New-onset angina of functional class II or III;

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

* Post-infarction angina.

Diagnostics.

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

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

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

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

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

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

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

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

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

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

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

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

TIMI risk:

7 independent predictors

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

Risk of MI or death according to TIMI:

– low – (0-2 points) – up to 8.3%

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

– high – (5-7 points) – up to 40.9%

Risk assessment according to the GRACE scale

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

Treatment

Etiotropic therapy

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

The effects of statins that determine their use in ACS:

- impact on endothelial dysfunction

- decreased platelet aggregation

- anti-inflammatory properties

- decreased blood viscosity

- plaque stabilization

- suppression of the formation of oxidized LDL.

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

regardless of cholesterol level.

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

Pathogenetic therapy has two goals:

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

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

Antiplatelet agents

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

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

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

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

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

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

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

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

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

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

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

When administered intravenously, the steady-state concentration of abciximab is maintained only by continuous infusion; after its cessation, it decreases within

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

Anticoagulants

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

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

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

Unfractionated heparin (UFH).

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

The main side effect is bleeding. Allergic reactions are possible, and with long-term use - thrombocytopenia.

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

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

Treatment of acute coronary syndrome without persistent ST segment elevation on ECG

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

Moscow 2006

All-Russian Scientific Society of Cardiologists

Moscow, 2006

Dear colleagues!

These guidelines have been updated to reflect new evidence that has become available since the first version was published in 2001. They can be considered a unified standard of treatment for patients with acute coronary syndrome without ST segment elevation, based on the most modern ideas about the pathogenesis, diagnosis and treatment of this group of diseases and, necessarily, taking into account the specific conditions of Russian healthcare.

The proposed treatment methods, 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 Cardiologists hopes that the Russian Recommendations for the treatment of acute coronary syndrome without ST segment elevation will become a guide to action for every cardiologist.

President of the All-Russian Scientific and Cultural Organization, academician R.G. Oganov


1. Introduction............................................... ........................................................ ....................
1.1. Some definitions.....................................................................................................
1.1.1. Correlation between the concepts of NS and STEMI ST. NS with elevated CStr levels......
2. Diagnosis................................................... ........................................................ ....................
2.1. Clinical symptoms............................................................. ...........................................
2.2. Physical examination................................................................... ...........................................
2.3. ECG................................................. ........................................................ ............................
2.4. Biochemical markers of myocardial damage.................................................................. ...............
2.5. Risk assessment................................................ ........................................................ .............
2.5.1. FR................................................... ........................................................ .........................
2.5.1.1.Clinical data............................................................ ........................................................ ......
2.5.1.2. ECG................................................. ........................................................ .........................
2.5.1.3. Markers of myocardial damage – CStr.................................................... ........................
2.5.1.4. EchoCG......................................................... ........................................................ ......................
2.5.1.5. Stress tests before discharge.................................................................... ...........................
2.5.1.6. KAG................................................... ........................................................ ........................
3. Treatment methods.................................................. ........................................................ .........
3.1. Anti-ischemic drugs................................................... ...........................................
3.1.1.BAB................................................... ........................................................ ...........................
3.1.2.Nitrates.................................................... ........................................................ ...............
3.1.3. AK................................................ ........................................................ ........................
3.2. Antithrombotic drugs. Antithrombins........................................................ .............
3.2.1.Heparins (UFH and LMWH)............................................ ........................................................ ...
3.2.1.1. Long-term administration of LMWH in patients with signs of increased risk of complications11
3.2.2.Direct thrombin inhibitors.................................................... .......................................
3.2.3. Treatment of hemorrhagic complications associated with antithrombin therapy...........
3.3. Antithrombotic drugs. Antiplatelet drugs...................................................
3.3.1. Aspirin (acetyl salicylic acid) .................................................... .........................
3.3.1.1. Aspirin dose................................................... ........................................................ ........
3.3.1.2. Resistance to aspirin.................................................................... ....................................
3.3.2. ADP receptor antagonists: thienopyridines.................................................... .........
3.3.3. GP IIb/IIIa platelet receptor blockers.................................................... ..........
3.3.3.1. Antagonists of GP IIb/IIIa platelets and LMWH.................................................... ............
3.4. Indirect anticoagulants for ACS.................................................... ...................................
3.5. Fibrinolytic (thrombolytic) treatment.................................................. ...............
3.6. Coronary revascularization................................................................. ........................................
3.6.1. KAG................................................... ........................................................ .......................
3.6.2. PCI. Stents........................................................ ........................................................ .......
3.6.2.1. ATT after PCI................................................... ........................................................ ........
3.6.2.2. PCI and LMWH................................................... ........................................................ .............
3.6.3. KS......................................................... ........................................................ ......................
3.6.4. Indications for PCI and surgical interventions.................................................. .....
3.6.5. Comparison of the effectiveness of invasive and drug treatment methods...........
4. Treatment strategy for patients with ACS.................................................... ........................................
4.1. Initial assessment of the patient................................................................... ...........................................
4.2. Patients with signs of acute occlusion of a large coronary artery............................................................ ............
4.3. Patients with suspected ST-ACS.................................................... ................................
4.3.1. Use of heparin................................................... ...................................................
4.3.1.1. NFG........................................................ ........................................................ .......................
4.3.1.2. NMG................................................... ........................................................ ......................

4.3.2. Patients with a high immediate risk of death or development of myocardial infarction
results of initial observation (8-12 hours) .................................................... ....................
4.3.3. Patients with a low risk of death or development of myocardial infarction in the near future....................................
4.4. Management of patients after stabilization................................................................. ................
5. Approximate sequence of actions in the management of patients with ST-ACS ..................
5.1. First contact with a doctor (local doctor, clinic cardiologist).................................................
5.2. Emergency doctor......................................................... ........................................................ .....
5.3. Hospital waiting room......................................................... ...........................................
5.3.1. Hospitals without cardiac ICU or with emergency facilities
treatment of patients in the emergency room................................................................... .........................................
5.3.2. Hospitals with cardiac intensive care units................................................................. ...........................
5.4. BIT (in its absence, the department in which treatment is carried out) ..............................
5.4.1. Facilities with surgical services or PCI capabilities......
5.5. Cardiology department after transfer from the hospital.................................................... ..........
Application................................................. ........................................................ ...............
Literature................................................. ........................................................ ................
Composition of the VNOK Expert Committee for the preparation of recommendations..................................................
List of abbreviations and symbols used in the recommendations

ACC/AAC – American College of Cardiology/American

	what is the association of the heart
	coronary artery bypass grafting.
	antithrombotic therapy
	adenosine triphosphate
	activated partial thromboplastin

	β-blockers
	balloon angioplasty
	intensive care unit
LBBB – left bundle branch block
	upper limit of normal for the method used
	intravenously
LVH –	LV hypertrophy
HMG-CoA – hydroxy methylglutaryl coenzyme A
GP IIb/IIIa receptors –		glycoprotein IIb/IIIa receptor
	platelet tori.

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

HTG – hypertriglyceridemia DBP – diastolic blood pressure

ACE inhibitors – angiotensin-converting enzyme inhibitors


	left ventricle

	MB (Muscle Brain) CPK fraction
	international normalized ratio
	MI without Q wave
	low molecular weight heparin(s)
	unstable angina
	unfractionated heparin
s/c –	subcutaneously
	acute MI
	acute coronary syndrome(s)
OKSBP ST –		acute coronary syndrome without elevations
	ST segment on ECG
ST OKSP – OKS with ST segment elevation on ECG
	total cholesterol
	systolic blood pressure
	diabetes
	heart failure
	stable angina
	cardiac troponins
	thrombotic therapy
	troponins
	ejection fraction
	functional class
	risk factors
	low-density lipoprotein cholesterol
	high density lipoprotein cholesterol
	percutaneous coronary intervention (PCA)
	and/or wall installation, atherectomy, others
	methods for eliminating coronary stenosis, devices for
	which, as a rule, are introduced through
	peripheral vessel)
	heart rate
	electrocardiogram
	echocardiography
SaO2 –	arterial blood oxygen saturation
TXA2 –	thromboxane A2

1. Introduction

CHD as a chronic disease is characterized by periods of stable progression and exacerbations. The period of exacerbation of CAD is designated as ACS. This term combines 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 rupture of an atherosclerotic plaque or erosion of the coronary artery endothelium, and subsequent distal thromboembolism.

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

At the first contact of a doctor with a patient when the presence of ACS is suspected, based on clinical and ECG signs, it can be classified as one of its two main forms.

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

OKSBP ST. Patients with chest pain and ECG changes indicating acute myocardial ischemia, but PD ST. These patients may exhibit persistent or transient ST depression, inversion, flattening or pseudo-normalization of the T wave; The ECG on admission may be normal. The management strategy for such patients is to eliminate ischemia and symptoms, monitor with repeated (serial) ECG recordings and determine markers of myocardial necrosis: CP and CF CK. Thrombolytic agents are not effective and are not used in the treatment of such patients. Therapeutic tactics depend on the degree of risk (severity of the condition) of the patient.

1.1. Some definitions ACS is any group of clinically recognized

symptoms or symptoms suggestive of acute AMI or UA include AMI, ST UTI, ST NSTEMI, MI diagnosed by enzyme changes, biomarkers, late ECG findings, and UA. The term appeared in connection with the need to choose treatment tactics before the final diagnosis of the listed conditions. Used to designate patients upon first contact and implies the need for treatment as patients with MI or NS.

STEMI ST is an acute process of myocardial ischemia of sufficient severity and duration to cause myocardial necrosis. There are no ST elevations on the initial ECG. In most patients whose disease begins as STEMI, Q waves do not appear and are eventually diagnosed as non-Q-MI. STEMI ST differs from NS by 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 is insufficient for the development of myocardial necrosis. There are usually no ST elevations on the ECG. There is no release of biomarkers of myocardial necrosis into the bloodstream in quantities sufficient to diagnose MI.

1.1.1. Correlation between the concepts of NS and STEMI ST. NS with elevated CTr levels

The concept of STEMI ST appeared in connection with the widespread introduction of the definition of ST into clinical practice. ST-ACSLD patients with elevated CTr levels have a worse prognosis (higher risk) and require more aggressive treatment and monitoring. The term STEMI ST is used to “mark” the patient for a short time until it is finally determined whether he has developed a large-focal MI or whether the process is limited to the occurrence of non-Q-MI. Isolating STEMI ST without determining CTr on the basis of less sensitive markers of necrosis, in particular CF CK, is possible, but leads to the identification of only a part of patients with foci of necrosis in the myocardium and, therefore, at high risk.

Thus, to quickly differentiate within ST-ACS, ST-NSEMI, and UA, determination of CTr levels is required.

NS and STEMI ST are very similar conditions, having a common pathogenesis and a similar clinical picture, they may 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 STEMI ST. Until now, the attitude towards the diagnosis of MI based on the fact of an increase in the content of CTr of any severity has not been officially formulated. On the other hand, a positive TP test (elevated levels when quantified) significantly influences the choice of method and site 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 STEMI ST. This formulation is provided for by the classification of NS Hamm CW and Braunwald E - NS class IIIB, TP positive (Table 1).

2. Diagnosis

2.1. Clinical symptoms

Patients suspected of developing ST-ACSPD, the treatment of which is discussed in these guidelines, when seeking

medical care can be classified into the following clinical groups:

patients after prolonged >15 min. attack of anginal pain at rest. This condition usually serves as a basis for calling an ambulance or an emergency visit to a medical facility in some other way. It corresponds to class III NS according to the classification of Hamm CW and Braunwald E (Table 1). Patients belonging to this group constitute the main object of these recommendations;

patients with new onset in previous 28-30 days of severe angina;

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

ACS may present atypically, especially in young (25–40 years) and elderly (>75 years) patients, patients with diabetes, and women. Atypical manifestations of NS include pain that occurs predominantly at rest, epigastric pain, acute onset of digestive disorders, stabbing pain in the chest, pain with signs characteristic of pleural damage, or increasing shortness of breath. In these

Table 1

Classification of NS Hamm CW, Braunwald E.

I – First appearance of severe angina, progressive angina; without angina at rest

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

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

Note: * Circulation 2000; 102:118.

In cases, correct diagnosis is facilitated by indications of a more or less long-term existence of CHD.

2.2. Physical examination

The objectives of the examination are: to exclude non-cardiac causes of pain, heart diseases of non-ischemic origin (pericarditis, valve damage), as well as non-cardiac causes that potentially contribute to increased ischemia (anemia); identification of cardiac causes that increase (or cause) myocardial ischemia (HF, hypertension).

Resting ECG is the main method for assessing patients with ACS. An ECG should be recorded when symptoms are present and compared with an ECG taken after symptoms have resolved. It is advisable 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 post-MI scarring, are highly specific for advanced coronary atherosclerosis but do not indicate current instability.

ECG signs of unstable CAD are ST segment displacement and T wave changes. The likelihood of the presence 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 latter sign is less specific. Deep symmetrical T wave inversions in the anterior precordial leads often indicate severe proximal stenosis of the anterior descending branch of the LMCA; nonspecific displacements of the ST segment and changes in the T wave, amplitude ≤1 mm, are less informative.

A completely normal ECG in patients with symptoms suggestive of ACS does not exclude its presence. However, if during severe pain a normal ECG is recorded, you should look more persistently 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-

A prolonged rise in the ST segment may occur with Prinzmetal's angina (vasospastic angina).

2.4. Biochemical markers of myocardial damage

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

Determination of CTr allows detecting myocardial damage in approximately a third of patients without an increase in CPK MV. To confirm or rule out myocardial injury, repeat blood draws and measurements are necessary within 6 to 12 hours of admission and after any episode of severe chest pain.

Changes in the content of various markers of myocardial necrosis over time in relation to a painful attack are presented in Figure 1. Myoglobin is a relatively early marker, while an increase in CK and CP appears later. CTP may remain elevated for 1–2 weeks, making it difficult to diagnose recurrent necrosis in patients with recent MI (Appendix Table 6).

2.5. Risk assessment

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

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

* Vertical axis – marker content in the blood relative to the level sufficient for the diagnosis of AMI (diagnostic level for MI), taken as one.

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

2.5.1.1. Clinical data

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

ECG data are crucial for diagnosing ACS and assessing 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 detected using a conventional ECG. Therefore, Holter ECG monitoring is advisable, although its capabilities are limited to recording only

two or three leads and obtaining results no less than a few hours after recording*.

2.5.1.3. Markers of myocardial damage – CTr

Patients with elevated CTr levels have less favorable short- and long-term prognoses compared to 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 levels of CTr is independent of other risk factors, including ECG changes at rest or during long-term monitoring. Identifying patients with elevated CTr levels is important for choosing a treatment method.

2.5.1.4. EchoCG

EchoCG allows one to assess the state of LV systolic function, which has important prognostic significance. During myocardial ischemia, local

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

hypokinesia or akinesia of the LV wall, and after the disappearance of ischemia - restoration of normal contractility. To assess the prognosis and select management tactics for 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 to confirm the diagnosis of CAD and to assess the risk of its complications. A significant proportion of patients are unable to complete stress tests, and this in itself is associated with a poor prognosis. The addition of imaging modalities to detect myocardial ischemia, such as echocardiography, further improves the sensitivity and specificity of prognosis. However, large, long-term, prognostic studies using stress echocardiography in patients after an episode of ST-ACS are lacking.

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

3. Treatment methods

3.1. Anti-ischemic drugs

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

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

Treatment should be started with the shortest-acting drugs in the presence of concomitant diseases, such as pulmonary pathology or LV dysfunction. Parenteral administration of beta blockers requires careful monitoring of blood pressure, preferably continuous ECG monitoring. The goal of subsequent administration of beta blockers per os should be to achieve a heart rate of 50-60 beats/min. Blockers 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 HF*.

Particular caution should be observed in patients with chronic obstructive pulmonary diseases, starting treatment with a relatively short-acting, cardioselective beta blocker, for example, 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 premises and clinical experience. There are no data from controlled studies to demonstrate optimal dosage and duration of use.

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

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

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

10 Supplement to the journal “Cardiovascular Therapy and Prevention”