Clinical guidelines for aux with the rise of st. Acute coronary syndrome without ST segment elevation. Clinic. Diagnostics. Treatment: etiotropic, pathogenetic. Treatment with folk remedies
For citation: Kashtalap V.V., Barbarash O.L. Controversial issues in the management of patients with non-ST elevation acute coronary syndrome (review of recommendations of the European Society of Cardiology 2015) // BC. 2015. No. 26. S. 1524-1527
The article deals with controversial issues in the management of patients with non-ST elevation acute coronary syndrome 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 non-ST elevation acute coronary syndrome (review of recommendations of the European Society of Cardiology 2015) // BC. 2015. No. 26. S. 1524–1527.
Currently, the problem of choosing the optimal method for 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 rather diverse cohort of patients. It may include patients with clinical manifestations of acute coronary syndrome (ACS) without changes in the ECG and the reaction of cardiospecific 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 with patients with acute coronary syndrome with ST segment elevation (ACS-ST). However, this is not the case: hospital mortality in NSTE-ACS can be 2–3 times higher than in patients with NSTE-ACS, however, in the long-term (annual) 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. patients with ST-ACS.
It should be said that practitioners have no doubts about the optimal treatment tactics for patients with ST-ACS and has fully justified itself - this is the most complete and early myocardial reperfusion by any available method (surgical or medical) in the next few hours from the onset of the disease.
The tactics regarding revascularization in patients with NSTE-ACS is individual and depends on the objectification of risk factors for the development of an unfavorable course of ACS in a particular patient. The main problem in the management of patients with NSTE-ACS is the correct assessment by the practitioner of individual risk and, based on this assessment, the timing of the application of an invasive strategy (urgent on 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 ST-ACS.
Due to the existing objective difficulties of practitioners regarding the choice of optimal tactics for the treatment of patients with NSTE-ACS, the updated recommendations of the European Cardiology Society for the management of patients with NSTE-ACS were adopted in August 2015 in London at the regular European Congress of Cardiology.
Clinical manifestations of NSTE-ACS may include prolonged (>20 min) anginal pain at rest; first-time angina pectoris II or III functional class (FC) according to the Canadian classification; progression of manifestations of previously stable angina pectoris to III–IV FC; post-infarction angina.
In elderly patients, women, patients with diabetes mellitus (DM), renal failure and dementia, atypical clinical forms of NSTE-ACS are often found: abdominal, asthmatic, peripheral, which requires increased attention to these categories of patients.
In case of any suspicion that a patient has ACS, the first-line diagnostic study is a 12-lead ECG recording at rest within 10 minutes from the start of the patient's first contact with the doctor. In 1/3 of patients with NSTE-ACS, ischemic changes on the ECG may be absent, which does not reject the diagnosis of an acute coronary event. In other patients, the ECG may show changes in the ST segment: depression, transient (up to 20 minutes) elevation, changes in the T wave in the form of its inversion. If an unchanged ECG is detected in a patient against the background of persistent ischemic discomfort, then it is useful in this case to record additional leads: V7–V9 and right thoracic (V3R–V4R). In any case, only the absence of persistent ST segment elevation on the ECG classifies the patient as a patient with NSTE-ACS. If the clinical manifestations of myocardial ischemia persist during treatment, a serial ECG recording is required in the course of monitoring the patient and comparison with previous results.
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 studies can determine further patient management. And the diagnosis of MI itself, according to the latest universal definition of this disease, must necessarily be confirmed by positive results of determining the biomarkers of myocardial necrosis in a quantitative way. Such biomarkers of myocardial damage as MB-fraction of creatine kinase, total fraction of creatine kinase, myoglobin have proven themselves well. However, at present, troponin (types T or I) is the leader in cardiospecificity, it is this that is preferable and the authors of the recommendations propose to determine it in patients with NSTE-ACS. Its significant drawback for practical use is a 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 in MI, but also in myocarditis, sepsis, shock of any etiology, life-threatening arrhythmias, aortic dissection, and pulmonary embolism. Positive positive troponin results should be interpreted with caution in patients with coronary artery disease and severely impaired renal function, 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 guidelines suggest the use of creatine kinase MB-fraction and copeptin. Copeptin is the C-terminal portion of the prohormone vasopressin, which can quantify the severity of endogenous stress in a variety of medical conditions, including MI.
The European guidelines of 2015 describe diagnostic algorithms that allow, based on an assessment of clinical, electrocardiographic and laboratory data (serial determination of hfT) 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 management of the patient with NSTE-ACS or start looking 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 a serial assessment of hfT (T or I) upon admission of the patient to the intensive care unit and after 1 hour of intensive treatment. Determination of initial concentrations of hsT 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 probably non-cardiac causes of chest pain. Such an algorithm makes it possible to quickly stratify patients in relation to the risk of complications of the acute period of ACS and apply earlier invasive tactics for managing these patients. The only drawback of this algorithm is a clear binding 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 borderline values of HF are described, which serve to stratify patients depending on the likelihood of an ischemic nature of chest pain.
The 0h/3h algorithm is more accessible for practical use. It also involves evaluating HCT in a patient with chest pain and no ECG criteria for ACS-ST on admission to the hospital. If the values of HCT 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 the hfT is not carried out. The patient should be given analgesia, assess the likelihood of adverse events on the GRACE scale, prescribe exercise tests before discharge, and conduct 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 observation ward, it is necessary to re-determine the values of HF. If a difference of 2 values of the TsT above the upper limit of normal is detected, the patient is considered as a candidate for invasive treatment. If there is no difference between the 2 hT values, the patient is stratified into the observation group with a risk assessment according to the GRACE scale and exercise testing before discharge. If in a patient with signs of NSTE-ACS, upon admission to the hospital, hsT values are determined above the upper limit of normal, then it is necessary to act as follows: 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 the values of hsT slightly exceed the level of the upper limit of the norm, it is permissible to re-examine after 3 hours with the determination of the difference between 2 values. If it 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 shown additional examination in the general ward and early discharge after stress tests. The above algorithms for accelerated 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 quite familiar to practitioners in our country. The main purpose of their implementation, according to European cardiologists, is the possibility of rapid stratification of patients with suspected ACS, depending on the identified risk of an unfavorable outcome, to determine indications for invasive patient management, or for early transfer to the outpatient stage of additional examination after carrying out stress tests. The 2015 European Heart Society Guidelines 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, resting echocardiography and stress testing, magnetic resonance imaging of the heart with perfusion, multispiral computed tomography of the coronary arteries can be performed. Echocardiography is recommended for assessing regional and global left ventricular contractility in a patient with NSTE-ACS and for the differential diagnosis of chest pain. Multispiral computed coronary angiography may be discussed 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 at admission, the authors of the European guidelines do not deny the need for an individual assessment of the risk of developing an adverse cardiovascular event in the short-term follow-up period. To do this, it is proposed to use the GRACE scale known to practitioners 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 fairly objective risk stratification of the patient both on admission and discharge. The use of the improved GRACE 2.0 risk calculator makes it possible to predict in-hospital mortality and mortality in patients after NSTE-ACS after 6, 12, and 36 months. . The GRACE 2.0 scale uses patient age, systolic blood pressure, heart rate, serum creatinine concentration, Killip class of acute heart failure (HF) on admission, data on cardiac arrest on admission, the fact of an increase in cardiospecific markers on admission, and deviations ST segment. If data on HF class and serum creatinine values are not available, the modified GRACE 2.0 scale allows risk assessment based on additional history of chronic kidney disease and diuretic use.
Episodes of major bleeding, even when adequately corrected by 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 coagulation (combinations of antiplatelet agents 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 CRUSADE scale for assessing the risk of bleeding in patients with NSTE-ACS seems to be preferable for practical use.
All patients with NSTE-ACS require continuous ECG monitoring for 24 hours or until percutaneous coronary intervention (PCI) prior to primary risk stratification. A patient with a preliminary diagnosis of NSTE-ACS in the ward without the possibility of ECG monitoring is unacceptable. ECG monitoring in patients with NSTE-ACS for more than 24 hours may be used at high risk of arrhythmic complications.
The drug treatment of patients with NSTE-ACS has not changed significantly in the new guidelines. Beta-blockers are prescribed as early as possible for symptoms of ischemia in patients without contraindications (acute HF III–IV classes according to Killip). In patients with vasospastic angina, beta-blockers should be excluded from treatment, replacing them with calcium antagonists and nitrovasodilators. IV nitrovasodilators are recommended if ischemic discomfort, uncontrolled hypertension, and pulmonary congestion persist.
A number of well-known drugs are used as antiplatelet agents in the treatment of patients with NSTE-ACS: acetylsalicylic acid (ASA), clopidogrel, ticagrelor, prasugrel. The recommendations also include a new drug with antiplatelet action by intravenous injection - cangrelor.
ASA during the initial examination of a patient with suspected ACS is prescribed by a doctor at a loading dose of 150–300 mg in an “uncoated” form, then the patient receives ASA indefinitely at a dosage of 75–100 mg 1 r./day in a “protected” form.
The appointment of platelet P2Y12 receptor inhibitors in addition to ASA is recommended for 12 months if the patient has no contraindications, such as a high risk of bleeding.
Ticagrelor at a loading dose of 180 mg and a maintenance dose of 90 mg b.i.d. initial management, including patients previously treated with clopidogrel at a loading dose. Treatment with clopidogrel should be discontinued if ticagrelor is available. Greater efficacy of ticagrelor in preventing recurrent cardiovascular events in patients for 12 months. after NSTE-ACS compared with clopidogrel was shown in the PLATO study.
Prasugrel (not available in Russia) at a loading dose of 60 mg and a maintenance dose of 10 mg daily is prescribed 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 who need additional prescription of 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 with a 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 a thorough assessment of the risk of ischemic events and bleeding.
The place for a new drug - cangrelor in the recommendations - is defined rather modestly in the recommendations - 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 when the diagnosis of ACS is established. As anticoagulants in the acute phase of NSTE-ACS, the use of drugs such as:
- unfractionated heparin (should be administered only in / in);
- low molecular weight heparin (enoxaparin, i.v. bolus and s.c. injection);
– fondaparinux (s/c introduction);
- bivalirudin (should be administered only in / in).
It is noted that fondaparinux (2.5 mg/day sc) is recommended as a drug that has an optimal efficacy/safety profile in patients with NSTE-ACS, regardless of the chosen treatment tactics. If fondaparinux cannot be administered, enoxaparin or unfractionated heparin is an alternative for 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 an invasive management strategy.
Stop anticoagulant therapy in patients with NSTE-ACS after PCI, if there are no additional indications for this (prevention of venous thromboembolism, atrial fibrillation). Additionally, it is stipulated that in patients with NSTE-ACS without a history of stroke and transient ischemic attacks, with a high risk of recurrent ischemic events and a low risk of bleeding after discontinuation of anticoagulant therapy, additional rivaroxaban at a dosage of 2.5 mg 2 r./day 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 NSTE-ACS patients in the hospital for 1 day of illness 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 given to patients with NSTE-ACS with documented LVEF<35%, клиникой СН или выявленным СД. Однако у пациента не должно быть тяжелых проявлений почечной недостаточности и гиперкалиемии.
Separately, the 2015 guidelines describe an approach to the choice of invasive management of patients with NSTE-ACS based on individual risk stratification. Emergency invasive management (performing coronary angiography up to 2 hours from the patient's admission to the hospital) is used when signs of very high risk are detected in patients with NSTE-ACS (hemodynamic instability or cardiogenic shock; persistent ischemic chest pain refractory to medical treatment; cardiac arrest or life-threatening rhythm disturbances; mechanical complications of MI (myocardial ruptures); acute HF; recurrent dynamic changes in the ST segment on the ECG, especially transient elevations). If such patients are hospitalized without the possibility of emergency coronary angiography and PCI, they must be transferred to the appropriate specialized intervention center immediately.
Early invasive management of a patient with NSTE-ACS involves coronary angiography up to 24 hours after the patient's admission to the hospital and is performed 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 number of points on the GRACE scale >140. If such patients are in the hospital without the possibility of emergency coronary angiography and PCI, they must be transferred to the appropriate specialized intervention center within 1 day after hospitalization.
Invasive patient management involves 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 (decrease in 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.
Low-risk patients are shown to perform stress tests and coronary angiography according to 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 total myocardial revascularization for multivessel coronary atherosclerosis. Currently, the decision on the preferred method of myocardial revascularization in 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 on the issue of the benefits of PCI or CABG in patients with NSTE-ACS. Emergency CABG is used in NSTE-ACS with hemodynamic instability, recurrent myocardial ischemia, and in patients with very high-risk coronary disease, regardless 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, and prasugrel 7 days before. In patients with NSTE-ACS, it is acceptable to evaluate platelet function after discontinuation of the platelet receptor P2Y12 inhibitor to reduce the waiting time for CABG. The resumption of dual antiplatelet therapy after CABG is possible at a time that doctors consider safe for this. At the same time, it is recommended to continue therapy with low doses of ASA until the time of 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 guidelines is a chapter on efforts to change the lifestyle of a patient who has experienced 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 the implementation of medical prescriptions.
It should be summarized that not all the positions indicated in the new recommendations of our European colleagues on the management of patients with NSTE-ACS can be fully implemented in the real clinical practice of hospitals in the Russian Federation. It should be taken into account that a clear understanding of the principles of managing this heterogeneous cohort of patients will contribute to greater activity of practitioners in relation to risk stratification, stress testing and referral of patients for invasive coronary studies.
Literature
1. Wallentin L., Becker R.C., Budaj A., Cannon C.P., Emanuelsson H., Held C., Horrow J., Husted S., James S., Katus H., Mahaffey K.W., Scirica B.M., Skene A., Steg P.G., Storey R.F., Harrington R.A., Freij A., Thorsen M. Ticagrelor versus clopidogrel in patients with acute coronary syndromes // N Engl J Med. 2009 Vol. 361. R. 1045-1057.
2. Rubini Gimenez M., Reiter M., Twerenbold R., Reichlin T., Wildi K., Haaf P., Wicki K., Zellweger C., Hoeller R., Moehring B., Sou S. M., Mueller M., Denhaerynck K., Meller B., Stallone F., Henseler S., Bassetti S., Geigy N., Osswald S., Mueller C. Sex-specific chest pain characteristics in the early diagnosis of acute myocardial infarction // JAMA Intern Med . 2014. Vol. 174. R. 241-249.
3. Thygesen K., Alpert J.S., Jaffe A.S., Simoons M.L., Chaitman B.R., White H.D., Katus H.A., Apple F.S., Lindahl B., Morrow D.A., Chaitman B.A., Clemmensen P.M., Johanson P., Hod H., Underwood R ., Bax J.J., Bonow R.O., Pinto F., Gibbons R.J., Fox K.A., Atar D., Newby L.K., Galvani M., Hamm C.W., Uretsky B.F., Steg P.G., Wijns W., Bassand J.P., Menasche P., Ravkilde J., Ohman E.M., Antman E.M., Wallentin L.C., Armstrong P.W., Januzzi J.L., Nieminen M.S., Gheorghiade M., Filippatos G., Luepker R.V., Fortmann S.P., Rosamond W.D., Levy D., Wood D., Smith S.C., Hu D., Lopez-Sendon J.L., Robertson R.M., Weaver D., Tendera M., Bove A.A., Parkhomenko A.N., Vasilieva E.J., Mendis S. Third universal definition of myocardial infarction // Eur Heart J. 2012. Vol. 33. R. 2551-2567.
4. Irfan A., Twerenbold R., Reiter M. , Reichlin T., Stelzig C., Freese M., Haaf P., Hochholzer W., Steuer S., Bassetti S., Zellweger C., Freidank H., Peter F., Campodarve I., Meune C., Mueller C. Determinants of high-sensitivity troponin T among patients with a noncardiac cause of chest pain // Am J Med. 2012. Vol. 125. R. 491-498, e491.
5. URL address: http://www.gracescore.org/WebSite/default.aspx?Return Url=%2f.
6. URL address: http://www.timi.org/index.php?page=calculators.
7. Fox K.A., Fitzgerald G., Puymirat E., Huang W., Carruthers K., Simon T., Coste P., Monsegu J., Gabriel Steg P., Danchin N., Anderson F. Should patients with acute coronary disease be stratified formanagement according to their risk? Derivation, external validation and outcomes using the updated GRACE risk score // BMJ Open. 2014. Vol. four.; e004425.
8. Subherwal S., Bach R.G., Chen A.Y., Gage B.F., Rao S.V., Newby L.K., Wang T.Y., Gibler W.B., Ohman E.M., Roe M.T., Pollack C.V. Jr, Peterson E.D., Alexander K.P. Baseline risk of major bleeding in non-ST-segment-elevationmyocardial infarction: the CRUSADE (Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the ACC/AHA guidelines) bleeding score // Circulation. 2009 Vol. 119. R. 1873-1882.
9. URL address http://www.crusadebleedingscore.org.
10. Parikh S.V., de Lemos J.A., Jessen M.E., Brilakis E.S., Ohman E.M., Chen A.Y., Wang T.Y., Peterson E.D., Roe M.T., Holper E.M. Timing of in-hospital coronary artery bypass graft surgery for non-ST-segment elevation myocardial infarction patients results from the National Cardiovascular Data Registry ACTION Registry-GWTG (Acute Coronary Treatment and Intervention Outcomes Network Registry-GetWith The Guidelines) // JACC Cardiovasc Interv . 2010 Vol. 3. R. 419-427.
As previously stated, non-elevated acute coronary syndrome ST(ACSbnST) includes two nosological forms of coronary artery disease:
Unstable angina;
MI without segment elevation ST.
Unstable angina
Unstable angina is one of the clinical forms of coronary artery disease, characterized by the development of acute myocardial ischemia, the severity and duration of which is insufficient for the occurrence of myocardial necrosis. Unstable angina is manifested by typical chest pains, during which the ECG shows signs of myocardial ischemia in the form of persistent or transient ST segment depression, inversion, smoothing or pseudo-normalization of the wave T, however, there is no increase in the level of biochemical markers of myocardial necrosis (cardiac troponins I or T or MB-CPK) in the blood plasma. It must be emphasized that outside of an attack of pain, the ECG may be normal.
Epidemiology
According to the US National Registry, in 1999, the number of patients who underwent NSTE-ACS was 1,932,000 people, while 953,000 people were discharged from hospitals with a diagnosis of unstable angina, and 530,000 people with a diagnosis of myocardial infarction without a tooth Q. National MI registries in the USA (NRMI I, II and III) showed that over the period 1990-1999. there was a relative increase in the frequency of ACS without segment elevation ST from 45 to 63%.
Clinical picture
The main complaint of patients with unstable angina is typical anginal pain in the chest, most often localized in the region of the heart. However, already on first stage of diagnostic search it is possible to determine a number of features that make one suspect "instability" of angina pectoris, therefore, in accordance with the clinical picture of unstable angina, the following clinical variants are distinguished:
First time angina pectoris. This term refers to exertional angina pectoris that has occurred within the last 2 months and has a severity of at least FC III according to the classification of the Canadian Cardiovascular Society.
progressive angina pectoris, those. progression of pre-existing stable angina pectoris by at least class 1 (according to the classification of the Canadian Cardiovascular Society) with the achievement of at least FC III. Anginal pains become more frequent, longer, occur with lower physical exertion.
rest angina, arising within the last 7 days, with a duration of attacks up to 20-30 minutes, including angina at rest, transformed from angina pectoris.
All these variants of the clinical course of unstable angina pectoris can occur both in a patient who has not previously endured MI, and in a patient who had a history of MI. All of them require an early ECG registration and a decision on the issue of hospitalization. From a formal point of view, all patients with one or another of the above clinical presentations should be hospitalized, since they have ACS without segment elevation. ST(unstable angina). However, the risk of death and myocardial infarction is undoubtedly higher in individuals who have had prolonged rest angina attacks in the last 48 hours, compared with those who had moderate exertional angina pectoris 3-4 weeks ago.
Early postinfarction angina pectoris. Strenuous or rest angina pectoris that occurred in the coming days after myocardial infarction, especially after successful thrombolytic therapy in patients with ST-segment elevation myocardial infarction. This variant of angina pectoris is fraught with the development of recurrent MI and requires an early coronary angiography to resolve the issue of myocardial revascularization. Currently, the generally accepted clinical classification of unstable angina, proposed by E. Braunwald in 1989 (Table 2-10).
Table 2-10. Clinical classification of unstable angina
The clinical manifestations of coronary heart disease are stable angina, silent myocardial ischemia, unstable angina, myocardial infarction, heart failure, and sudden death. For many years, unstable angina was considered as an independent syndrome, occupying an intermediate position between chronic stable angina and acute myocardial infarction. However, in recent years, it has been shown that unstable angina and myocardial infarction, despite differences in their clinical manifestations, are consequences of the same pathophysiological process, namely, rupture or erosion of an atherosclerotic plaque in combination with associated thrombosis and embolization of more distally located areas of the vascular channels. In this regard, unstable angina and developing myocardial infarction are currently combined by the term acute coronary syndrome (ACS) .
Acute coronary syndrome is a preliminary diagnosis that allows the doctor to determine urgent therapeutic and organizational measures. Accordingly, the development of clinical criteria is of great importance, allowing the doctor to make timely decisions and choose the optimal treatment, which is based on an assessment of the risk of complications and a targeted approach to the appointment of invasive interventions. In the course of creating such criteria, all acute coronary syndromes were divided into those accompanied and not accompanied by persistent ST segment elevation. Currently, the optimal therapeutic interventions, the effectiveness of which is based on the results of well-designed randomized clinical trials, have already been largely developed. So, in acute coronary syndrome with persistent ST segment elevation (or first-time complete blockade of the left bundle branch block), reflecting acute total occlusion of one or more coronary arteries, the goal of treatment is the rapid, complete and persistent restoration of the lumen of the coronary artery using thrombolysis (if it is not contraindicated) or primary coronary angioplasty (if it is technically feasible). The effectiveness of these therapeutic measures has been proven in a number of studies.
Non-ST elevation acute coronary syndrome refers to patients with chest pain and ECG changes suggestive of acute ischemia (but not necessarily necrosis) of the myocardium.
These patients often present with persistent or transient ST-segment depression, as well as T-wave inversion, flattening, or ｫpseudo-normalizationｻ. In addition, non-ST-elevation ACS ECG changes may be nonspecific or absent. Finally, some patients with the above changes on the electrocardiogram, but without subjective symptoms (i.e. cases of painless "silent" ischemia and even myocardial infarction) can be included in this category of patients.
In contrast to situations with persistent ST-segment elevation, previous proposals for the treatment of non-ST-segment elevation acute coronary syndrome were less clear-cut. It was only in 2000 that the recommendations of the European Society of Cardiology Working Group for the treatment of non-ST elevation acute coronary syndrome were published. Relevant recommendations will soon be developed for Russian doctors as well.
This article only considers the management of patients with suspected acute coronary syndrome who do not have persistent ST elevation. At the same time, the main attention is paid directly to the diagnosis and the choice of therapeutic tactics.
But beforehand we consider it necessary to make two remarks:
First, the recommendations below are based on the results of a number of clinical studies. However, these tests were performed on specially selected groups of patients and, accordingly, do not reflect all the conditions encountered in clinical practice.
Secondly, it should be taken into account that cardiology is developing rapidly. Accordingly, these guidelines should be reviewed regularly as new clinical trial results accumulate.
The degree of persuasiveness of conclusions about the effectiveness of various methods of diagnosis and treatment depends on the data on the basis of which they were made. In accordance with generally accepted recommendations, the following are distinguished: three levels of validity (“proof”) of conclusions:
Level A: Conclusions are based on data from several randomized clinical trials or meta-analyses.
Level B: Conclusions are based on data from single randomized trials or non-randomized trials.
Level C. The conclusions are based on the consensus opinion of the experts.
In the following discussion, after each item, the level of its validity will be indicated.
Tactics of managing patients with acute coronary syndrome
Initial assessment of the patient's condition
The initial assessment of a patient presenting with chest pain or other symptoms suggestive of ACS includes:
1. Careful history taking . Classical characteristics of anginal pain, as well as typical CAD exacerbations (protracted [> 20 minutes] anginal pain at rest, first-onset severe [not lower than Canadian Cardiovascular Society (CCS) Class III] angina pectoris, recent worsening of stable angina pectoris of at least up to III FC according to CCS) are well known. However, it should be noted that ACS can also present with atypical symptoms, including chest pain at rest, epigastric pain, sudden onset dyspepsia, stabbing chest pain, ｫpleuralｻ pain, and increased dyspnoea. Moreover, the frequency of these manifestations of ACS is quite high. Thus, according to the Multicenter Chest Pain Study (Lee T. et al., 1985), acute myocardial ischemia was diagnosed in 22% of patients with acute and stabbing pain in the chest, as well as in 13% of patients with pain characteristic of pleural lesions. , and in 7% of patients in whom pain was fully reproduced on palpation. Especially often, atypical manifestations of ACS are observed in young (25-40 years old) and senile (over 75 years old) patients, as well as in women and patients with diabetes mellitus.
2. Physical examination . Chest examination and palpation, cardiac auscultation, and heart rate and blood pressure are usually within normal limits. The purpose of a physical examination is primarily to exclude non-cardiac causes of chest pain (pleurisy, pneumothorax, myositis, inflammatory diseases of the musculoskeletal system, chest trauma, etc.). In addition, physical examination should detect heart disease not associated with coronary artery disease (pericarditis, heart defects), as well as assess the stability of hemodynamics and the severity of circulatory failure.
3. ECG . Resting ECG recording is a key diagnostic tool for ACS. Ideally, an ECG should be recorded during a pain attack and compared with an electrocardiogram recorded after the pain disappeared.
With recurring pain, multi-channel ECG monitoring can be used for this. It is also very useful to compare the ECG with ｫoldｻ films (if available), especially if there are signs of left ventricular hypertrophy or a previous myocardial infarction.
The most reliable electrocardiographic signs of ACS are ST segment dynamics and T wave changes. The likelihood of ACS is greatest if the corresponding clinical picture is combined with ST segment depression more than 1 mm deep in two or more adjacent leads. A slightly less specific sign of ACS is T-wave inversion greater than 1 mm in R-wave-dominant leads. Deep negative, symmetrical T waves in the anterior chest leads often indicate severe proximal stenosis of the anterior descending branch of the left coronary artery. Finally, shallow (less than 1 mm) ST segment depression and slight T-wave inversion are the least informative.
It should be remembered that a completely normal ECG in patients with characteristic symptoms does not exclude the diagnosis of ACS.
Thus, in patients with suspected ACS, an ECG at rest should be recorded and long-term multichannel monitoring of the ST segment should be started. If monitoring is not feasible for any reason, then frequent ECG recording is necessary (level of evidence: C).
Hospitalization
Patients with suspected non-ST-segment elevation ACS should be immediately admitted to a specialized cardiology emergency/intensive care unit (LE) (Level of Evidence: C).
Study of biochemical markers of myocardial damage
ｫTraditionalｻ cardiac enzymes, namely creatine phosphokinase (CPK) and its CPK MB isoenzyme, are less specific (in particular, false positive results are possible in skeletal muscle injury). In addition, there is significant overlap between normal and abnormal serum concentrations of these enzymes. The most specific and reliable markers of myocardial necrosis are cardiac troponins T and I. . Troponin T and I concentrations should be determined 612 hours after admission to the hospital, and also after each episode of intense chest pain.
If a patient with suspected non-ST elevation ACS has elevated levels of troponin T and/or troponin I, then this condition should be regarded as a myocardial infarction and appropriate medical and/or invasive treatment should be carried out.
It should also be taken into account that after cardiac muscle necrosis, the increase in the concentration of various markers in the blood serum does not occur simultaneously. Thus, the earliest marker of myocardial necrosis is myoglobin, while the concentrations of CPK MB and troponin increase somewhat later. In addition, troponins remain elevated for one to two weeks, making it difficult to diagnose recurrent myocardial necrosis in patients with a recent myocardial infarction.
Accordingly, if ACS is suspected, troponins T and I should be determined at the time of admission to the hospital and re-measured after 612 hours of observation, as well as after each pain attack. Myoglobin and/or CPK MV should be measured in recent (less than six hours) onset of symptoms and in patients who have recently (less than two weeks ago) myocardial infarction (level of evidence: C).
Initial Therapy in Patients with Suspected Non-ST Elevation ACS
For non-ST-segment elevation ACS, the initial therapy should be:
1. Acetylsalicylic acid (level of validity: A);
2. Sodium heparin and low molecular weight heparins (level of evidence: A and B);
3. bblockers (level of evidence: B);
4. For persistent or recurrent chest pain, oral or intravenous nitrates (level of evidence: C);
5. In the presence of contraindications or intolerance to b-blockers, calcium antagonists (level of evidence: B and C).
Dynamic Surveillance
During the first 8-12 hours, it is necessary to carefully monitor the patient's condition. Special attention should be:
Recurrent chest pain. During each pain attack, it is necessary to record an ECG, and after it, re-examine the level of troponins in the blood serum. It is highly advisable continuous multichannel ECG monitoring to detect signs of myocardial ischemia, as well as cardiac arrhythmias.
Signs of hemodynamic instability (arterial hypotension, congestive rales in the lungs, etc.)
Assessing the risk of myocardial infarction or death
Patients with acute coronary syndromes represent a highly heterogeneous group of patients that differ in the prevalence and/or severity of atherosclerotic coronary artery disease, as well as in the degree of ｫthromboticｻ risk (i.e.
risk of myocardial infarction in the coming hours/days). The main risk factors are presented in Table 1.
Based on follow-up data, ECG and biochemical studies, each patient should be assigned to one of the two categories below.
1. Patients at high risk of myocardial infarction or death
repeated episodes of myocardial ischemia (either recurring chest pain or ST segment dynamics, especially depression or transient ST segment elevations);
an increase in the concentration of troponin T and / or troponin I in the blood;
episodes of hemodynamic instability during the observation period;
life-threatening cardiac arrhythmias (repeated paroxysms of ventricular tachycardia, ventricular fibrillation);
the occurrence of ACS without ST segment elevation in the early postinfarction period.
2. Patients at low risk of myocardial infarction or death
no recurrence of chest pain;
there was no increase in the level of troponins or other biochemical markers of myocardial necrosis;
there were no ST depressions or elevations associated with inverted T waves, flattened T waves, or normal ECG.
Differentiated therapy depending on the risk of myocardial infarction or death
For patients at high risk of these events, the following treatment tactics may be recommended:
1. Administration of IIb/IIIa receptor blockers: abciximab, tirofiban, or eptifibatide (level of evidence: A).
2. If it is impossible to use IIb/IIIa receptor blockers, intravenous administration of sodium heparin according to the scheme (Table 2) or low molecular weight heparins (level of evidence: B).
In modern practice, the following are widely used low molecular weight heparins : adreparin, dalteparin, nadroparin, tinzaparin and enoxaparin. Let us take a closer look at nadroparine as an example. Nadroparin is a low molecular weight heparin obtained from standard heparin by depolymerization.
The drug is characterized by a pronounced activity against factor Xa and weak activity against factor IIa. The anti-Xa activity of nadroparin is more pronounced than its effect on APTT, which distinguishes it from sodium heparin. For the treatment of ACS, nadroparin is administered s / c 2 times a day in combination with acetylsalicylic acid (up to 325 mg / day). The initial dose is determined at the rate of 86 units / kg, and it should be administered as an intravenous bolus. Then the same dose is administered subcutaneously. The duration of further treatment is 6 days, in doses determined depending on body weight (Table 3).
3. In patients with life-threatening cardiac arrhythmias, hemodynamic instability, development of ACS soon after myocardial infarction and/or a history of CABG, coronary angiography (CAG) should be performed as soon as possible. In preparation for CAG, the administration of heparin should be continued. In the presence of atherosclerotic damage, allowing for revascularization, the type of intervention is chosen taking into account the characteristics of the damage and its extent. The principles for choosing a revascularization procedure for ACS are similar to the general recommendations for this type of treatment. If percutaneous transluminal coronary angioplasty (PTCA) with or without a stent is chosen, it can be performed immediately after angiography. In this case, administration of IIb/IIIa receptor blockers should be continued for 12 hours (for abciximab) or 24 hours (for tirofiban and eptifibatide). Level of justification: A.
In patients at low risk of myocardial infarction or death, the following tactics may be recommended:
1. Ingestion of acetylsalicylic acid, b-blockers, possibly nitrates and / or calcium antagonists (level of evidence: B and C).
2. Cancellation of low molecular weight heparins in the event that during the dynamic observation there were no changes in the ECG and the level of troponin did not increase (level of evidence: C).
3. Stress test to confirm or establish the diagnosis of coronary artery disease and assess the risk of adverse events. Patients with severe ischemia during a standard exercise test (bicycle ergometry or treadmill) should undergo CAG followed by revascularization. If standard tests are not informative, stress echocardiography or exercise myocardial perfusion scintigraphy may be useful.
Management of patients with non-ST elevation ACS after discharge from the hospital
1. The introduction of low molecular weight heparins in the event that repeated episodes of myocardial ischemia occur and it is impossible to perform revascularization (level of evidence: C).
2. Taking b-blockers (level of evidence: A).
3. Widespread impact on risk factors. First of all, smoking cessation and normalization of the lipid profile (level of evidence: A).
4. Taking ACE inhibitors (level of evidence: A).
Conclusion
Currently, many medical institutions in Russia do not have the capacity to carry out the above-mentioned diagnostic and therapeutic measures (determination of the level of troponins T and I, myoglobin; emergency coronary angiography, the use of IIb / IIIa receptor blockers, etc.). We can expect, however, their ever wider inclusion in medical practice in our country in the near future.
The use of nitrates in unstable angina is based on pathophysiological considerations and clinical experience. Data from controlled studies indicating the optimal dosage and duration of their use are not available.
Acute coronary syndrome with ST segment elevation (myocardial infarction).
Myocardial infarction is an acute disease caused by the occurrence of foci of ischemic necrosis in the heart muscle due to absolute insufficiency of coronary blood flow, caused by thrombosis of the coronary artery.
Cause: The rupture of a “soft” atherosclerotic plaque triggers a cascade of blood coagulation reactions, which leads to acute thrombotic occlusion of the coronary artery. If the restoration of blood perfusion through the artery does not occur, then myocardial necrosis develops (starting from the subendocardial regions). Depending on the duration of ischemia, the state of the coronary vessels and related circumstances (the so-called premorbid background), both reversible damage to cardiomyocytes and their irreversible necrosis can occur.
Classification.
In the most acute stage of MI, which is based on the processes of ischemic damage, it is recommended to use the term acute coronary syndrome with ST elevation (as an intermediate diagnosis). With the formation of infarct changes on the ECG (the appearance of a pathological Q or QS wave), it is necessary to diagnose acute myocardial infarction of one or another localization.
Myocardial infarction without a pathological Q wave (in our country, it is often referred to as a small-focal myocardial infarction). It is also based on thrombosis of the coronary artery, but unlike large-focal MI, it does not completely obstruct the lumen of the vessel. Accordingly, it is not accompanied by changes in the QRS complex and the rise of the ST segment on the ECG. Currently, together with unstable angina, it is included in the category of ACS without ST elevation.
Clinic.
1. Pain syndrome - intense retrosternal pain lasting more than 15 minutes, which does not go away after taking nitroglycerin, usually accompanied by
shortness of breath. In the vast majority of patients, at the same time, there are signs of activation of the autonomic nervous system (pallor, cold sweat), which is very typical for anginal pain.
2. Syndrome of acute left ventricular failure - suffocation (a feeling of lack of air at rest). Develops in 100% with acute myocardial infarction, in parallel
with pain syndrome. With repeated and recurrent myocardial infarctions, it is often the leading one in the clinic (with mild or even no pain syndrome) - an asthmatic variant of MI.
3. Electrocardiographic syndrome. Even in the early stages of myocardial infarction, ECG parameters rarely remain normal.
- Small-focal myocardial infarction (myocardial infarction without a Q wave) - is characterized by the appearance on the ECG of a coronary T wave (negative, peaked
and isosceles).
- Large-focal myocardial infarction - characterized by the appearance of a pathological Q wave in at least two leads:
- Transmural myocardial infarction is determined by the appearance of an abnormal QS wave (no R wave):
4. Resorption-necrotic syndrome is caused by resorption of necrotic masses and the development of aseptic inflammation of the myocardium. The most important signs:
An increase in body temperature lasting up to 10 days, at a body temperature of not more than 38 degrees
Leukocytosis up to 10-12 OOO from the first days
Acceleration of ESR by 5-6 days
The appearance of biochemical signs of inflammation - an increase in the level of fibrinogen, seromucoid, haptoglobin, sialic acids, a2-globulin, Y-globulin, C-reactive protein.
The appearance of biochemical markers of myocardial death - aspartate aminotransferase, lactate dehydrogenase, creatine phosphokinase, glycogen phosphorylase, myoglobin, myosin, cardiotroponins T, I.
5. Arrhythmic syndrome - with myocardial infarction in 100% of cases, cardiac arrhythmias are recorded (in the vast majority of cases, ventricular),
which in the most acute and acute stage of myocardial infarction often determine the prognosis of patients due to the high risk of developing against their background arrhythmic death as a result of ventricular fibrillation.
6. Cardiogenic shock syndrome occurs in 3 variants - pain (reflex shock as a result of intense retrosternal pain), arrhythmic - significant
increase (more than 180 beats/min) or decrease (less than 40 beats/min) in the number of heartbeats with the regular development of hemodynamic disturbances as a result of a fall in cardiac output. The third option is the most unfavorable - true cardiogenic shock (it is based on the death of a significant part of the myocardium of the left ventricle).
Clinical options:
1. Anginal - a classic variant, the main clinical manifestation is severe retrosternal pain, accompanied by a feeling of lack of air and severe sweating.
2. Asthmatic variant - the syndrome of acute left ventricular failure dominates. It occurs frequently, especially in repeated and recurrent myocardial infarctions, in elderly and senile patients, especially against the background of previous CHF. Anginal pain may be mild or absent, and an attack of cardiac asthma or pulmonary edema is the first and only clinical symptom of MI.
3. Gastralgic - very often causes diagnostic errors. It is more common in diaphragmatic MI. It is characterized by pain in the upper abdomen, dyspeptic symptoms - nausea, vomiting, flatulence, and in some cases paresis of the gastrointestinal tract. On palpation of the abdomen, there may be tension in the abdominal wall. In the abdominal form of MI, the clinical picture resembles an acute disease of the digestive tract. Wrong diagnosis is the cause of erroneous treatment tactics. There are cases when such patients undergo gastric lavage and even surgery. Therefore, in every patient with suspected "acute abdomen" it is necessary to register an ECG.
4. Arrhythmic variant - debuts with paroxysmal cardiac arrhythmias, syncope. In the arrhythmic form of MI, the pain syndrome may be absent or may be slightly expressed. If severe rhythm disturbances occur against the background of a typical anginal attack or simultaneously with it, they speak not of an atypical form of MI, but of its complicated course, although the conventionality of such a division is obvious.
5. The cerebral variant is characterized by intense headaches, loss of consciousness, nausea, vomiting, may be accompanied by transient focal symptoms, which greatly complicates the diagnosis. Diagnosis of MI is possible only with timely and dynamic ECG recording. This variant of MI is most common in patients with initially stenotic extracranial and intracranial arteries, often with cerebrovascular accidents in the past.
6. "Asymptomatic" variant - very often diagnosed already by the presence of cicatricial changes on the ECG.
Diagnostics
EchoCG. The main symptom of MI is the zone of impaired myocardial contractility.
Using this research method, it is possible to determine the localization of MI, which is especially important if there are no diagnostic signs of the disease on the ECG. Echocardiography is the main method for diagnosing a number of complications of MI: rupture of the interventricular septum, rupture of the free wall or the formation of an aneurysm of the left ventricle, intrapo-
abdominal thrombosis.
Coronary angiography. The detection of acute coronary artery occlusion, along with clinical symptoms, allows for an accurate diagnosis.
Treatment
When fibrinolytic therapy is carried out in the first hours of the disease, it is possible to save an additional 50-60 lives per 1000 patients, and in many more to avoid the development of heart failure, other complications of myocardial infarction or reduce their severity. The essence of the treatment is the enzymatic destruction of fibrin filaments, which form the basis of an occlusive coronary thrombus, with the restoration of adequate coronary circulation.
Indications for fibrinolytic therapy - clinic + ST segment elevation or acute blockade of the left bundle branch block. The exception is patients with true cardiogenic shock, in which the time from the onset of the disease is not taken into account.
The goals of treating acute MI with thrombolytics are:
— Rapid recanalization of an occluded coronary artery
- Relief of chest pain
– Limiting the size of acute MI and preventing its spread
— Preservation of LV function due to the maximum preservation of its muscle mass in the affected area.
Contraindications for thrombolytic therapy:
1) stroke;
2) lack of consciousness;
3) major trauma, surgery, suffered during the last 3 weeks;
4) gastrointestinal bleeding during the last month;
4) hemorrhagic diathesis;
5) dissecting aortic aneurysm;
6) arterial hypertension over 160 mm Hg. Art.
In our country, for the treatment of MI, the use of tissue plasminogen activator, alteplase (actilyse), is currently optimal. After intravenous administration, alteplase, binding to fibrin, is activated and causes the conversion of plasminogen to plasmin, which leads to the dissolution of thrombus fibrin. As a result of clinical studies, actilyse has proven to be much more effective in recanalization of the coronary arteries - in comparison with other thrombolytics, in particular streptokinase. The continued use of streptokinase to date is determined only by the relative "cheapness" of the drug in comparison with actilyse.
Indicators of successful thrombolysis:
1. Resolution of anginal pain;
2. ECG dynamics: | ST by 70% of the initial value in case of posterior inferior infarction and by 50% in case of anterior MI;
3. t the level of isoenzymes (MF-CPK, Tnl, TpT) after 60-90 minutes from the onset of thrombolysis;
4. Reperfusion arrhythmias (ventricular extrasystole, accelerated idioventricular rhythm)
2) Direct anticoagulants.
Simultaneously with the introduction of actilyse, heparin should be started for a period of 24 hours or more (when using streptokinase, heparin is contraindicated). Heparin is administered intravenously at a rate of 1000 units per hour. The dose of heparin should be adjusted depending on the results of repeated determination of activated partial thromboplastin time (APTT) - the values of this indicator should exceed the initial level by 1.5-2.0 times, but not more (threat of bleeding). An alternative to this method of treatment is the use of low molecular weight heparins - enoxaparin (Clexane) 1 mg per kg of the patient's body weight, subcutaneously 2 times a day. With proven equal clinical efficacy, this type of anticoagulant therapy is determined by ease of use and the absence of the need for thorough laboratory
control.
3. The effectiveness of thrombolytic and anticoagulant therapy increases significantly if it is combined with aspirin at a therapeutic dose of 325 mg.
4. Clopidogrel (Plavike, Zilt, Plagril) is indicated for all patients with ST-segment elevation ACS. The loading dose is 300 mg orally, the maintenance dose is 75 mg per day. The use of this drug is indicated throughout the entire period of hospitalization.
5. Statins. Indicated from the first day of treatment for acute MI.
6. Nitrates (nitroglycerin, isoket, perlinganite) - administered intravenously, improve myocardial perfusion, reduce pre- and afterload on the left ventricle, determining
decrease in myocardial oxygen demand.
Clinical indications for which the appointment of nitrates is necessary:
- anginal attack
- signs of heart failure
- uncontrolled hypertension.
Contraindications for nitrates:
GARDEN< 90 мм рт. ст. или его снижение более чем на 30 мм рт. ст. от исходного
heart rate<50 уд/мин
Heart rate >100 bpm
right ventricular MI
7. Beta-blockers - by reducing myocardial oxygen demand, improve perfusion in the ischemic zone, providing antiarrhythmic, antifibrillatory effects, reduce mortality not only in the long-term, but also in the early stages from the onset of myocardial infarction. It is recommended to use highly selective
drugs that do not have their own sympathomimetic effect. Preference is given to metoprolol, bisoprolol and betaxolol.
8. Calcium antagonists are not recommended in the early stages of myocardial infarction.
9. ACE inhibitors.
Term acute coronary syndrome (ACS) used to denote an exacerbation of coronary artery disease. This term combines such clinical conditions as myocardial infarction (MI) and unstable angina. The experts of the All-Russian Scientific Society of Cardiology adopted the following definition of ACS and unstable angina (2007):
Acute Coronary Syndrome is a term for any group of clinical signs or symptoms suggestive of AMI or unstable angina. Includes AMI, STEMI, STEMI ECG, MI diagnosed by enzyme changes, by other biomarkers, by late ECG signs, and unstable angina.
The term “ACS” was introduced into clinical practice when it became clear that the use of certain active therapies, in particular thrombolytic therapy, must be resolved quickly, often before the final diagnosis of MI. It has been established that the nature and urgency of intervention to restore coronary perfusion is largely determined by the position of the ST segment relative to the isoelectric line on the ECG: when the ST segment is shifted upward (ST elevation), coronary angioplasty is the method of choice for restoring coronary blood flow, but if it is impossible to perform it at the appropriate time, it is effective and, accordingly, thrombolytic therapy is indicated. Restoration of coronary blood flow in ACS-ST should be carried out without delay. In NSTE-ACS, thrombolytic therapy is not effective, and the timing of coronary angioplasty (in rare cases, coronary bypass surgery) depends on the degree of risk of the disease. If in a patient with a clear exacerbation of coronary artery disease, the choice of the main method of treatment depends on the presence or absence of ST elevation, then from a practical point of view, it has become expedient at the first contact of a doctor with a patient who has a suspicion of the development of ACS, the use of the following diagnostic terms (identification of the following forms of ACS ): “OKSpST” and “OKSbpST”.
ACS with ST-segment elevation and ACS without ST-segment elevation
ST-ACS is diagnosed in patients with an anginal attack or other unpleasant sensations (discomfort) in the chest and persistent (lasting for at least 20 minutes) ST-segment elevation or "new" (first-time) LBBB on the ECG. Typically, patients who begin as ACS-ST will later develop evidence of myocardial necrosis—elevated biomarker levels and ECG changes, including Q wave formation.
The appearance of signs of necrosis means that the patient has developed MI. The term “MI” reflects the death (necrosis) of heart muscle cells (cardiomyocytes) as a result of ischemia (Appendix 1).
OKSbpST. These are patients with an anginal attack and, usually, with ECG changes indicating acute myocardial ischemia, but without ST segment elevation. They may have persistent or transient ST depression, T-wave inversion, flattening, or pseudo-normalization. The ECG may be normal on admission. In many cases, non-occlusive (parietal) coronary thrombosis is found. In the future, some patients show signs of myocardial necrosis, caused (except for the initial cause of the development of ACS) by embolism of small myocardial vessels, fragments of a thrombus and material from a ruptured AB. However, the Q wave on the ECG rarely appears, and the developed condition is referred to as “MI without ST segment elevation”.
About correlation of diagnostic terms "ACS" and "MI"
The term "ACS" is used when diagnostic information is still insufficient for a final judgment on the presence or absence of necrosis foci in the myocardium. Accordingly, ACS is a working diagnosis in the first hours, while the concepts of “MI” and “unstable angina” (ACS that did not result in signs of myocardial necrosis) are retained for use in formulating the final diagnosis.
If signs of myocardial necrosis are found in a patient with ACS who has persistent ST elevations on the initial ECG, this condition is referred to as STEMI. Further, depending on the ECG picture, the maximum level of cardiac troponin or enzyme activity and imaging data, the diagnosis is specified: MI can be large-focal, small-focal, with Q waves, without Q waves, etc.
