In garbage

ISBN 978-5-9704-3974-6
Publisher : "GEOTAR-Media"

The year of publishing : 2017

TO number of pages: 960

Edition: per. from English
Format: in per.

Price: 5800 rub.

The European Guidelines for Acute Cardiology is an official guideline prepared by the Acute Cardiovascular Care Association (ACCA). The manual provides comprehensive information on all matters of intensive and urgent cardiac care.

The book discusses the various acute cardiovascular conditions that require specialized acute care, as well as organizational issues, collaboration between different specialists, and an interdisciplinary approach.

The guide is addressed to all specialists in the field of intensive and urgent cardiac care: cardiologists, cardiovascular and endovascular surgeons, resuscitators, emergency doctors and other medical professionals.

Chapter 1. Intensive and emergency care in cardiology: an introduction
Suzanne Price, Marco Tubaro, Pascal Vranks, Christian Vrinz
Chapter 2. Training and Certification in Emergency Cardiac Care
Magda Geas, Alessandro Zionis, Suzanne Price
Chapter 3. Patient Safety and Clinical Practice Guidance
Elizabeth Huxby, Suzanne Walker
Chapter 4. Databases, registers and quality of care
Nicholas Dunchin, Fiona Ecarnot, Francois Schiele
Part 1 Prehospital and emergency departments
Chapter 5. Sudden cardiac death: epidemiology and prevention
Hans-Richard Arntz
Chapter 6. Cardiopulmonary resuscitation and postresuscitation disease
Jerry P. Nolan
Chapter 7. Emergency medical assistance system
Mark Sabbe, Cohen Bronzeler,
Olivier Hugmartens
Chapter 8. Acute chest pain and branches of "chest pain"
Eric Durand, Aures Chaib, Nicholas Danchin
Chapter 9. Acute dyspnea in the emergency room
Christian Müller
Part 2 Cardiology intensive care unit
Chapter 10. Recommendations for the structure, organization and work of the department
emergency cardiology
Menachem Nahir, Doron Zachger, Yonatan Hasin
Chapter 11. Team of the Department of Emergency Cardiology (cardioreanimation)
Tom Queen, Eva Swan
Chapter 12. Cardiology team in the emergency cardiology system
help
Ari Peter Cuppetine, Stefan Windecker
Chapter 13. Ethical Issues in Cardiac Arrest and Emergency Cardiac Care: A European Perspective
Jean-Louis Vincent
Part 3 Monitoring and Diagnostic Activities in the Cardiac Intensive Care Unit
Chapter 14. Pathophysiology and clinical evaluation of the cardiovascular system (including pulmonary artery catheterization)
Romain Barthélemy, Etienne Guyat, Alexander Mebaza
Chapter 15. Respiratory system
Antoine Vieillard-Baron
Chapter 16. Neurological examination of patients with acute cardiac
pathology
Katie De Daney, Joe Dance
Chapter 17. Monitoring the functions of the kidneys, liver and other vital organs
Karl Verdant, Brides Patel, Mathias Girndt, Genning Ebelt, Johan Schroeder, Sebastian Nuding
Chapter 18. Analysis of blood gas composition: acid-base balance and water-electrolyte balance
Richard Paul, Pavlos Miriantefs, George Baltopolos, Sean McMaster
Chapter 19. Clinical evaluation and monitoring of chest x-ray
Alexander Parkhomenko, Olga S. Guryeva, Tatiana Yalinska
Chapter 20. Echocardiography and chest ultrasound
Frank A. Flaxskampf, Pavlos Miriantefs, Raxandra Beyer
Chapter 21. Ultrasound-Guided Vascular Access in Intensive Care / Emergency Cardiology
Richard Paul
Chapter 22. Computed tomographic angiography and other methods of computed tomography
Michelle A. de Graaf, Arthur J. Hitch A. Scholt, Lucia Croft, Jeroen J. Bucks
Chapter 23. Magnetic resonance imaging of the heart in cardiac resuscitation
Jürg Schwitter, Jens Bremerich
Part 4 Procedures in the Cardiac Intensive Care Unit
Chapter 24. Artificial ventilation of the lungs
Gian Abuella, Andrew Rhodes
Chapter 25. Non-invasive ventilation of the lungs
Joseph Masip, Kenneth Planas, Arantksa Mas
Chapter 26. Temporary electrocardio-stimulation
Bulent Gorenek
Chapter 27. Pericardiocentesis
Gerard Marty Agwasca, Bruno Garcia del Blanco, Jaume Sagrista Sauleda
Chapter 28. Drainage tubes
Arthur Atchabayan, Christian Laplace, Karim Tazarurte
Chapter 29. Maintaining kidney function
Claudio Ronco, Zacaria Ricci
Chapter 30. Portable mechanical devices for temporary support
circulation
Suzanne Price, Pascal Vrancks
Chapter 31. Implantable circulatory support devices
Andrew Morley-Smith, Andre R. Simon,
John R. Pepper
Chapter 32. Nutritional support in emergency cardiac care
Michael P. Cesar, Grit Van den Berge
Chapter 33. Physical therapy for critically ill patients
Rick Gosselink, Jean Roseler
Chapter 34. Organizing organ donation
Arne P. Neirink, Patrick Ferdinand, Dirk Van Raemdonk, Mark Van de Velde
Part 5 Laboratory diagnostics in cardiology and other intensive care units
Chapter 35. Use of biomarkers in acute cardiovascular diseases
Allan S. Jaff
Chapter 36. Biomarkers in acute coronary syndrome
Evangelos Giannitsis, Hugo A. Catus
Chapter 37. Biomarkers in acute heart failure
Rajiv Chaudhary, Kevin Shah, Alan Meisel
Chapter 38. Biomarkers of the clotting process and thrombosis
Anna-Matt Hwas, Eric L. Grove, Steen Dalby Christensen
Chapter 39. Biomarkers of renal and hepatic failure
Mario Plebani, Monica Maria Mien,
Martina Zaninotto
Part 6 Acute coronary syndrome
Chapter 40. Atherosclerosis and Atherothrombosis
Lina Badimon, Gemma Vilagur
Chapter 41. Universal definition of myocardial infarction
Christian Thigesen, Joseph S. Alpert,
Allan S. Jaff, Harvey D. White
Chapter 42. Regional systems of care for patients with acute coronary syndrome with ST-segment elevation (regional networks)
Kurt Huber, Tom Queen
Chapter 43. ST-segment elevation myocardial infarction
Adrian Cheong, Gabrielle Steg, Stefan K. James
Chapter 44. Fibrinolytic, antithrombotic and antiplatelet agents in the treatment of acute coronary syndrome
Peter Sinnawy, Frans Van de Werf
Chapter 45. Mechanical complications of myocardial infarction
Jose Lopez Sendon, Esteban Lopez de Sa
Chapter 46. Acute coronary syndrome without ST-segment elevation
Hector Bueno, Jose A. Barrabes
Chapter 47. Percutaneous coronary interventions in acute coronary syndrome
Victor Kochka, Steen Dalby Christensen,
William Wines, Petr Teishek, Petr Widimski
Chapter 48. Operations of coronary artery bypass grafting
Piroz M. Davierwala, Friedrich W. Mohr
Chapter 49. Cardiogenic shock in acute coronary syndrome
Holger Thiele, Uwe Seimer
Chapter 50. Gender characteristics of the course of acute coronary syndrome
Eva Swan, Joachim Alfredsson, Sofia Sedergolm Lawsson
Part 7 Acute heart failure
Chapter 51. Acute heart failure: epidemiology, classification and pathophysiology
Dimitros Farmakis, John Parisis, Gerasimos Filippatos
Chapter 52. Acute heart failure: intensive pharmacotherapy
Jonathan R. Dalzell, Colette E. Jackson, John J. W. McMurray, Roy Gardner
Chapter 53. Non-pharmacological therapy of acute heart failure: when drugs are not enough
Pascal Vranks, Wilfred Mullens, Johan Weigen
Chapter 54. Acute heart failure: surgery and transplantation
Aykaterini N. Vizuli, Antonis A. Pitsis
Part 8 Arrhythmias
Chapter 55. Conduction disorders and pacemaker
Carlo Lavalle, Renato Pietro Ricci, Massimo Santini
Chapter 56. Atrial fibrillation and supraventricular arrhythmias
Demosthenes Katritsis, A. John Gamm
Chapter 57. Ventricular tachyarrhythmias and implantable cardioverter defibrillator
Joachim R. Ehrlich, Stefan H. Hohnloser
Part 9 Other acute cardiovascular pathology
Chapter 58. Myocarditis and pericarditis
Michelle Nutsias, Bernard Maisch
Chapter 59. Acute valvular pathology and endocarditis
Gregory Ducroc, Frank Thani, Bernard Jung, Alec Vakhanyan
Chapter 60. Congenital heart defects in adults
Suzanne Price, Brian F. Keough, Lorna Swan
Chapter 61. Emergencies in diseases of the aorta
Parla Astarchi, Laurent de Kerkov, Gebrin el-Khuri
Chapter 62. Cardiac complications after trauma
Demetrios Demetriades, Leslie Kobayashi, Lydia Lam
Chapter 63. Emergency cardiac conditions during pregnancy
Patrizia Presbyero, Dennis Zavalloni, Benedetta Agnoli
Part 10 Associated acute conditions
Chapter 64. Acute respiratory failure and acute respiratory distress syndrome
Luciano Gattinoni, Eleanor Carlesso
Chapter 65. Pulmonary hypertension
Nazzareno Gallier, Alexandra Meines, Massimiliano Palazzini
Chapter 66. Pulmonary embolism
Adam Torbitski, Martin Kurzhina, Stavros Konstantinides
Chapter 67. Stroke
Didier Leys, Charlotte Cordonier, Valeria Caso
Chapter 68. Acute kidney injury
Sophie A. Gevert, Eric Host, John A. Kellum
Chapter 69. Hyperglycemia, diabetes and other emergency conditions in endocrinology
Yves Debavier, Diete Mesotten, Grit Van den Berge
Chapter 70. Bleeding and hemostasis disorders
Pierre Manuccio Manucci
Chapter 71. Anemia and transfusion
Jean-Pierre Bassand, Francois Schiele, Nicholas Menevue
Chapter 72. Infections, sepsis and multi-organ dysfunction syndrome
Julian Arias Ortiz, Rafael Favori, Jean-Louis Vincent
Chapter 73. Acute pain in the practice of intensive cardiac care unit
Sian Jaggar, Helen Laycock
Chapter 74. Acute Cognitive Disorders: Recognizing and Treating Delirium in the Cardiovascular Intensive Care Unit
Jennifer Guzeffi, John McPerson, Chad Wagner, E. Wesley Eli
Chapter 75. Management of immunosuppressed patients
Anna Sophia More, Raphael Favori, Alain Durocher
Chapter 76. Perioperative management of high-risk noncardiac patients
Martin Balik
Chapter 77. Perioperative management of high-risk surgical patients: cardiac surgery
Marco Ranucci, Serenella Castelvechio, Andrea Ballotta
Chapter 78. Palliative care in the intensive care unit
Jane Wood, Maureen Carruthers
Subject index

Indications for research methods are indicated in accordance with the classes: class I - research is useful and effective; IIA - data on the usefulness are contradictory, but more data in favor of the effectiveness of the study; IIB - data on the usefulness are conflicting, but the benefits of the study are less obvious; III - research is useless.

The level of evidence has three levels: level A - there are several randomized clinical trials or meta-analyzes; Level B - data obtained from a single randomized study or from non-randomized studies; Level C - Recommendations based on expert agreement.

  • with stable angina pectoris or other symptoms associated with coronary artery disease, such as shortness of breath;
  • with established coronary artery disease, currently asymptomatic due to treatment;
  • patients in whom symptoms are noted for the first time, but it has been established that the patient has a chronic stable disease (for example, from the anamnesis it has been revealed that such symptoms have been present for several months).

Thus, stable coronary artery disease includes different phases of the disease, with the exception of a situation when the clinical manifestations are determined by coronary artery thrombosis (acute coronary syndrome).

In stable coronary artery disease, symptoms during exercise or stress are associated with stenosis of the left trunk of the coronary artery> 50% or stenosis of one or more large arteries> 70%. This edition of the Guidelines discusses diagnostic and prognostic algorithms not only for such stenoses, but also for microvascular dysfunction and coronary artery spasm.

Definitions and pathophysiology

Stable coronary artery disease is characterized by a mismatch between the demand for oxygen and its delivery, leading to myocardial ischemia, which is usually triggered by physical or emotional stress, but sometimes occurs spontaneously.

Episodes of myocardial ischemia are associated with chest discomfort (angina pectoris). Stable coronary artery disease also includes the asymptomatic phase of the course of the disease, which can be interrupted by the development of acute coronary syndrome.

Various clinical manifestations of stable coronary artery disease are associated with different mechanisms, including:

  • obstruction of the epicardial arteries,
  • local or diffuse arterial spasm without stable stenosis or in the presence of atherosclerotic plaque,
  • microvascular dysfunction,
  • dysfunction of the left ventricle associated with a previous myocardial infarction or with ischemic cardiomyopathy (myocardial hibernation).

These mechanisms can be combined in one patient.

Natural course and prognosis

In a population of patients with stable coronary artery disease, individual prognosis may vary depending on clinical, functional and anatomical characteristics.

It is necessary to identify patients with more severe forms of the disease, whose prognosis may be better with aggressive intervention, including revascularization. On the other hand, it is important to identify patients with mild forms of the disease and a good prognosis, in whom unnecessary invasive interventions and revascularization should be avoided.

Diagnosis

Diagnostics includes clinical assessment, instrumental studies, and imaging of the coronary arteries. Studies can be used to confirm the diagnosis in patients with suspected coronary artery disease, identify or exclude concomitant conditions, stratify risk, and evaluate the effectiveness of therapy.

Symptoms

In assessing chest pain, the Diamond A.G. classification is used. (1983), according to which a typical, atypical angina pectoris and non-cardiac pain are distinguished. Objective examination of a patient with suspected angina pectoris reveals anemia, arterial hypertension, valvular lesions, hypertrophic obstructive cardiomyopathy, rhythm disturbances.

It is necessary to assess body mass index, identify vascular pathology (pulse in the peripheral arteries, noise in the carotid and femoral arteries), determine comorbid conditions such as thyroid disease, kidney disease, diabetes mellitus.

Non-invasive research methods

The optimal use of non-invasive studies is based on an assessment of the pretest probability of coronary artery disease. Once diagnosed, patient management depends on the severity of symptoms, risk, and patient preference. It is necessary to choose between drug therapy and revascularization, the choice of the method of revascularization.

The main studies in patients with suspected coronary artery disease include standard biochemical tests, ECG, 24-hour ECG monitoring (if symptoms are suspected to be associated with paroxysmal arrhythmia), echocardiography and, in some patients, chest X-ray. These studies can be done on an outpatient basis.

Echocardiography provides information about the structure and function of the heart. In the presence of angina pectoris, it is necessary to exclude aortic and subaortic stenosis. Global contractility is a prognostic factor in patients with coronary artery disease. EchoCG is especially important in patients with heart murmurs, myocardial infarction, symptoms of heart failure.

Thus, transthoracic echocardiography is indicated for all patients for:

  • exclusion of an alternative cause of angina pectoris;
  • detecting violations of local contractility;
  • ejection fraction (EF) measurements;
  • assessment of left ventricular diastolic function (Class I, level of evidence B).

There are no indications for repeated studies in patients with uncomplicated coronary artery disease in the absence of changes in the clinical state.

Ultrasound examination of the carotid arteries necessary to determine the thickness of the intima-media complex and / or atherosclerotic plaque in patients with suspected coronary artery disease (Class IIA, level of evidence C). The identification of changes is an indication for preventive therapy and increases the pretest probability of coronary artery disease.

24-hour ECG monitoring rarely provides additional information in comparison with stress ECG tests. The study is useful in patients with stable angina pectoris and suspected arrhythmias (Class I, level of evidence C) and if vasospastic angina is suspected (class IIA, level of evidence C).

X-ray examination indicated for patients with atypical symptoms and suspected pulmonary disease (Class I, level of evidence C) and with suspected heart failure (class IIA, level of evidence C).

Step-by-step approach to the diagnosis of coronary artery disease

Step 2 - the use of non-invasive methods for the diagnosis of coronary artery disease or non-obstructive atherosclerosis in patients with an average probability of ischemic heart disease. Once diagnosed, optimal drug therapy and risk stratification of cardiovascular events are required.

Step 3 - non-invasive tests to select patients in whom invasive intervention and revascularization are more beneficial. Depending on the severity of symptoms, early coronary angiography (CAG) can be performed without going through steps 2 and 3.

The pretest probability is estimated taking into account age, gender and symptoms (table).

Principles of using non-invasive tests

The sensitivity and specificity of non-invasive imaging tests is 85%, hence 15% of results are false positive or false negative. In this regard, testing of patients with a low (less than 15%) and high (more than 85%) pretest probability of coronary artery disease is not recommended.

Exercise ECG tests have low sensitivity (50%) and high specificity (85-90%); therefore, tests are not recommended for diagnosis in the group with a high probability of coronary artery disease. In this group of patients, the purpose of carrying out stress ECG tests is to assess the prognosis (risk stratification).

Patients with low ejection fraction (less than 50%) and typical angina pectoris are shown CAG without non-invasive tests, since they have a very high risk of cardiovascular events.

Patients with a very low likelihood of coronary artery disease (less than 15%) need to exclude other causes of pain. With an average probability (15-85%), non-invasive testing is indicated. In patients with a high probability (more than 85%), testing is necessary for risk stratification, but in severe angina pectoris, it is advisable to perform CAG without non-invasive tests.

The very high negative predictive value of computed tomography (CT) makes the method important for patients with lower mean risk values ​​(15-50%).

Stress ECG

VEM or treadmill are shown with a pretest probability of 15-65%. Diagnostic testing is performed when anti-ischemic drugs are discontinued. The sensitivity of the test is 45-50%, the specificity is 85-90%.

The study is not indicated for left bundle branch block, WPW syndrome, the presence of a pacemaker due to the inability to interpret changes in the ST segment.

False positive results are observed with ECG changes associated with left ventricular hypertrophy, electrolyte disturbances, intraventricular conduction disturbances, atrial fibrillation, and digitalis intake. In women, the sensitivity and specificity of the samples is lower.

In some patients, testing is not informative due to the failure to reach the submaximal heart rate in the absence of symptoms of ischemia, with restrictions associated with orthopedic and other problems. Pharmacological loading imaging techniques are an alternative for these patients.

  • for the diagnosis of coronary artery disease in patients with angina pectoris and an average probability of ischemic heart disease (15-65%) who are not receiving anti-ischemic drugs, who can perform physical activity and do not have ECG changes that do not allow the interpretation of ischemic changes (Class I, level of evidence B);
  • to assess the effectiveness of treatment in patients receiving anti-ischemic therapy (Class IIA, level C).

Stress echocardiography and myocardial perfusion scintigraphy

Stress echocardiography is performed using physical activity (VEM or treadmill) or pharmacological agents. Exercise is more physiological, but pharmacologic exercise is preferable when contractility is impaired at rest (dobutamine to assess viable myocardium) or in patients unable to exercise.

Indications for stress echocardiography:

  • for the diagnosis of coronary artery disease in patients with a pretest probability of 66-85% or with ejection fraction<50% у больных без стенокардии (Класс I, уровень доказанности В);
  • for the diagnosis of ischemia in patients with resting ECG changes that do not allow interpretation of the ECG during exercise tests (Class I, level of evidence B);
  • exercise stress testing echocardiography is preferred over pharmacological (Class I, level of evidence C);
  • in symptomatic patients who have undergone percutaneous intervention (PCI) or coronary artery bypass grafting (CABG) (Class IIA, level of evidence B);
  • to assess the functional significance of moderate stenoses identified in CAG (Class IIA, level of evidence B).

Perfusion scintigraphy (BREST) ​​with technetium (99mTc) reveals myocardial hypoperfusion during exercise compared with resting perfusion. Possible provocation of ischemia by physical activity or medication with the use of dobutamine, adenosine.

Research with thallium (201T1) is associated with a higher radiation load and is currently used less frequently. The indications for perfusion scintigraphy are similar to those for stress echocardiography.

Positron emission tomography (PET) has advantages over BREST in terms of image quality, but is less readily available.

Non-invasive methods for assessing coronary anatomy

CT can be performed without the introduction of contrast (calcium deposition in the coronary arteries is determined) or after intravenous administration of an iodine-containing contrast drug.

Calcium deposition is a consequence of coronary atherosclerosis, except in patients with renal failure. In determining coronary calcium, the Agatston index is used. The amount of calcium correlates with the severity of atherosclerosis, but the correlation with the degree of stenosis is poor.

Coronary CT angiography with the introduction of a contrast agent allows you to assess the lumen of the vessels. The conditions are the patient's ability to hold his breath, the absence of obesity, sinus rhythm, heart rate less than 65 per minute, the absence of pronounced calcification (Agatston index< 400).

Specificity decreases with increasing coronary calcium. CT angiography is inappropriate when the Agatston index is> 400. The diagnostic value of the method is available in patients with the lower limit of the average probability of coronary artery disease.

Coronary angiography

CAG is rarely needed for diagnosis in stable patients. The study is indicated if the patient cannot undergo stress-imaging research methods, with an EF of less than 50% and typical angina pectoris, or in persons of special professions.

CAG is indicated after non-invasive risk stratification in the high-risk group to determine the indications for revascularization. In patients with a high pretest probability and severe angina pectoris, early CAG is indicated without prior non-invasive tests.

CAG should not be performed in patients with angina pectoris who refuse PCI or CABG or in whom revascularization will not improve functional status and quality of life.

Microvascular angina

Primary microvascular angina should be suspected in patients with typical angina pectoris, positive results of stress ECG tests in the absence of stenotic lesions of the epicardial coronary arteries.

Research required to diagnose microvascular angina pectoris:

  • stress echocardiography with exercise or dobutamine to detect abnormalities of local contractility during an attack of angina pectoris and ST segment changes (Class IIA, level of evidence C);
  • Transthoracic Doppler EchoCG of the anterior descending artery with measurement of diastolic coronary blood flow after intravenous administration of adenosine and at rest for non-invasive assessment of coronary reserve (Class IIB, Level of Evidence C);
  • CAG with intracoronary acetylcholine and adenosine in normal coronary arteries to assess coronary reserve and determine microvascular and epicardial vasospasm (Class IIB, level of evidence C).

Vasospastic angina

For diagnosis, it is necessary to register an ECG during an attack of angina pectoris. CAH is indicated for the assessment of coronary arteries (Class I, Level of Evidence C). 24-hour ECG monitoring to detect ST-segment elevation in the absence of an increase in heart rate (Class IIA, level of evidence C) and CAG with intracoronary administration of acetylcholine or ergonovine to identify coronary spasm (Class IIA, level of evidence C).

On June 3-4, 2005, in Bucha, a scientific and practical conference of the working group on urgent cardiology of the Association of Cardiologists of Ukraine was held, entered in the register of scientific and practical activities of the Ministry of Health of Ukraine for 2005. The conference reviewed the main pathophysiological mechanisms of acute coronary syndromes (ACS), acute heart failure (HF), life-threatening ventricular arrhythmias and sudden cardiac death, as well as analyzed the latest research in this area concerning the diagnosis, treatment and prevention of cardiovascular diseases (CVD). ).

Prepared by Irina Starenkaya

The main tasks of the working group are the development and implementation into practice of national recommendations for the treatment of ACS and acute heart failure, the definition of rational modern approaches to stratification and treatment of other CVDs, an overview of the possibilities of emergency care in cardiology. The conference participants were guided, first of all, by international norms and standards of treatment and diagnostics, therefore, in the reports and discussions, the main attention was paid to the analysis and discussion of the recommendations of European and American experts and, accordingly, the possibility of their application in Ukraine.

The educational grant for the conference was provided by Sanofi-Aventis, Boehringer-Ingelheim and Orion. We offer a brief overview of the most interesting speeches to the attention of our readers.

Member of the Board of the European Society of Cardiology, Head of the Working Group on Emergency Cardiology of the Ukrainian Association of Cardiologists, Head of the Department of Reanimation and Intensive Care at the Institute of Cardiology named after I. N. D. Strazhesko AMS of Ukraine, Doctor of Medical Sciences, Professor Alexander Nikolaevich Parkhomenko.

- The draft national guidelines for treatment and diagnostics, based on the recommendations of the European Society of Cardiology (ESC), are currently being actively discussed by the members of the working group and are being prepared for publication. In order to approach such an important document with full responsibility, it is necessary to carefully study the recommendations of the ESC, highlight the most relevant aspects for Ukraine, and determine the tasks that are actually feasible in our conditions.

The European guidelines for the treatment and diagnosis of acute heart failure were approved as recently as April this year. According to this document, acute HF is considered as a condition associated with the rapid development of symptoms and manifestations of HF and is caused by dysfunction of the heart both without previous pathology and against the background of cardiac pathology (heart dysfunction associated with both systolic and diastolic disorders, cardiac arrhythmias , changes in pre- and afterload, and other reasons). This life-threatening condition requires urgent treatment. However, the given definition is not the best one. An attempt to combine all possible aspects of acute heart failure has led to some ambiguity and vagueness of terminology. The ESC guidelines highlight these forms of acute heart failure.

  1. Acute decompensated HF (first or developing in chronic forms of HF) is a slowly progressive, relatively mild course, without signs of cardiogenic shock, pulmonary edema or hypertensive crisis.
  2. Hypertensive acute HF - manifested by symptoms of cardiac dysfunction against a background of high blood pressure, but, as a rule, with preserved systolic heart function and without pulmonary edema.
  3. An important form of acute heart failure is pulmonary edema, for the diagnosis of which verification by radiography is required. Pulmonary edema is associated with severe distress syndrome, wheezing in the lungs, orthopnea, oxygen saturation less than 90% before treatment.
  4. The most severe form of acute heart failure is cardiogenic shock, which is manifested by a sharp decrease in cardiac output and, as a result, tissue hypoperfusion. Signs of cardiogenic shock are well known: a decrease in blood pressure below 90 mm Hg. Art., heart rate - below 60 beats / min, urine output - below 0.5 ml / kg / hour.
  5. High cardiac output syndrome is usually associated with significant tachycardia (with arrhythmias, thyrotoxicosis, anemias, Paget's syndrome, iatrogenic interventions). A feature of this form of acute heart failure is “warm” peripheral tissues, high heart rate, and sometimes low blood pressure.
  6. The syndrome of right ventricular failure is manifested by low cardiac output, high pressure in the jugular vein, enlarged liver, and arterial hypotension.

In Europe, 40% of patients hospitalized for acute heart failure are admitted to the hospital with shortness of breath - the main complaint of patients. Among the manifestations of acute HF, the second place is taken by the progression of chronic HF (aggravation of shortness of breath, edema, weakness, etc.). It should be noted that many patients are hospitalized with stable heart failure, with an ejection fraction of more than 40%. Therefore, in the diagnosis of acute heart failure, one cannot focus only on standard studies; it is necessary to actively look for the cause of the patient's condition disorder, even in the absence of obvious signs of cardiac dysfunction.

The diagnosis of acute heart failure is based on symptoms and clinical examination of the patient, an important role is played by ECG, X-ray examination, blood test for biological markers, Doppler echocardiography. Laboratory research methods are becoming increasingly important in the diagnosis of heart diseases. So, in all patients hospitalized with acute heart failure, it is imperative to do a complete blood count, determine the number of platelets, blood glucose levels, urea, creatinine and electrolytes, CRP, D-dimer, troponins. The issue of widespread introduction of plasma natriuretic peptide analysis in acute heart failure, which is manifested mainly by shortness of breath, is considered. With severe cardiac dysfunction, as well as with concomitant diabetes mellitus, it is important to pay attention to the indicators of arterial blood gases, in severe condition and while taking anticoagulants - to INR (international normalized thromboplastin time ratio).

The basic principles for the treatment of acute heart failure are as follows.

  1. Providing ventilation and oxygenation.
  2. Drug treatment:
    • morphine and its analogs with pronounced stagnation in the pulmonary circulation;
    • antithrombotic therapy for ACS and atrial fibrillation;
    • vasodilators to combat peripheral tissue hypoperfusion (nitrates, sodium nitroprusside, nesiretide - recombinant human natriuretic peptide, calcium antagonists);
    • ACE inhibitors;
    • loop diuretics;
    • β-blockers;
    • inotropic drugs (dopamine, dobutamine, phosphodiesterase inhibitors, levosimendan, epinephrine, norepinephrine, cardiac glycosides).
  3. Surgical treatment is rarely indicated (for example, with postinfarction rupture of the interventricular septum, acute mitral regurgitation).
  4. Use of mechanical assistive devices (intra-aortic balloon contrapulsation) or heart transplantation.

Patients with acute HF may respond well to treatment, depending on the underlying cause of the HF. But even in these cases, they need long-term treatment and supervision of specialists.

The meeting devoted to ACS was opened by the head of the Department of Myocardial Infarction and Rehabilitation Treatment of the Institute of Cardiology. N. D. Strazhesko AMS of Ukraine, Doctor of Medical Sciences, Professor Valentin Aleksandrovich Shumakov, who spoke about the current problems and prospects for the diagnosis and treatment of ACS without ST segment elevation.

- In 2 million patients in the United States with an ACS clinic, ECG signs of acute myocardial damage are detected: in 600 thousand - with ST segment elevation; the rest - without it. The risk of developing ACS increases with age: as shown by S. Kulkarni et al. (ACC, 2003, CRUSADE Presentation), the risk of death, development of myocardial infarction (MI), HF sharply increases in people over 75 years old. Of great importance is the presence of diabetes mellitus, against the background of which the risk of ACS also increases, as was shown in the same study.

The term "acute coronary syndrome" includes:

  • unstable angina and non-Q-MI;
  • Q-IM;
  • sudden cardiac death;
  • acute ischemic complications of angioplasty, stenting, and other interventions on the coronary arteries.

In recent years, the understanding of the pathogenesis of ACS has undergone a number of changes, in particular, much attention has been paid to the factors of systemic and local inflammation, which contributes to the destabilization of atheromatous plaques. Its formation, rupture and erosion, subsequent thrombosis, vasoconstriction lead to ischemia, damage, necrosis of cardiocytes and, as a consequence, to myocardial dysfunction. Possible causes of systemic inflammation, contributing to the destabilization of an atheromatous plaque, can be oxidative stress (radiation, psycho-emotional and physical overload, diet errors), hemodynamic stress, exposure to infectious factors, including exacerbation of chronic inflammatory diseases, systemic immune and allergic reactions. The activation of inflammation of the vascular wall with oxidized LDL occurs with the participation of activated resident (fat) and migrated inflammatory blood cells, with the release of proteolytic enzymes (metalloproteases), free radicals, apoptosis and necrosis of plaque cellular elements. In the future, a hematoma forms inside the plaque, its size grows rapidly, and the degree of stenosis of the vessel increases accordingly. Eventually, the connective tissue matrix and the lining of the plaque are destroyed with the development of local thrombosis.

In accordance with new views on the pathophysiology of ACS, the factors of systemic inflammation have begun to receive more attention in the diagnosis and treatment of this pathology. So, in the diagnosis of ACS, C-reactive protein and fibrinogen are currently important diagnostic markers in IHD, since the value of these parameters is associated with mortality in unstable IHD (Lindahl et al., 2000).

In 2002, the ESC adopted an algorithm for managing patients with suspected ACS, according to which, after clinical suspicion of ACS, it is necessary to conduct a routine physical examination, ECG monitoring, and blood tests. If a patient has persistent ST elevation, thrombolysis or intravascular interventions are indicated. In the absence of persistent ST elevation, patients are prescribed heparin (low molecular weight or unfractionated), aspirin, clopidogrel, β-blockers, nitrates, and the question of the degree of risk in this patient is decided. If the patient is in a high-risk group, he should be prescribed glycoprotein receptor blockers and coronary ventriculography. In the future, based on clinical and angiographic prerequisites, intravascular intervention, coronary artery bypass grafting (CABG) is performed, or drug treatment is continued. Patients with a low risk are re-determined the level of troponin in the blood and only with a twice negative result of this test, the question of further treatment tactics is decided, otherwise, the patient is treated in the same way as patients in the high-risk group.

Thus, one of the most important steps determining the tactics of treating a patient is to determine the degree of risk. The simplest way to assess risk is ECG analysis (patients with depression or ST elevation, as well as those with a higher ST elevation, are at the highest risk); the degree of risk also increases depending on the frequency of ischemic episodes. Troponin is an effective marker of increased risk in ACS. The high-risk group also includes patients with early postinfarction unstable angina pectoris, with unstable hemodynamics during the observation period, with severe rhythm disturbances (repeated episodes of ventricular tachycardia, ventricular fibrillation), diabetes mellitus, as well as with an ECG graph that makes it impossible to assess changes segment ST. The group of low-risk patients includes patients without recurrent episodes of chest pain during follow-up, without depression or ST elevation, but with negative T waves, flat T waves, or with a normal ECG picture, without elevation of troponin or other biochemical markers.

The management of high-risk patients is as follows. During preparation for angiography, it is necessary to administer low-molecular-weight heparin (enoxaparin), as well as a GP IIb / IIIa receptor blocker, which lasts 12 (absiximab) or 24 (tirofiban, eptifibatid) hours in case of angioplasty. If the patient is shown PCI, it is advisable to prescribe clopidogrel, but if CABG is planned, clopidogrel should be discontinued 5 days before the proposed operation.

The benefits of low molecular weight heparins (LMWH) have long been appreciated by doctors of all specialties. They differ significantly better than conventional heparin in the predictability of the antithrombotic effect due to the lack of binding to plasma proteins and endotheliocyte membranes. Accordingly, LMWH therapy does not require such careful individual laboratory control. LMWH have high bioavailability (up to 90% after deep subcutaneous injection), which allows them to be prescribed subcutaneously not only for prophylactic, but also for therapeutic purposes, as well as longer antithrombotic activity (half-life is more than 4.5 hours after intravenous administration versus 50 -60 minutes for ordinary heparin) with the appointment 1-2 times a day.

In the ESSENCE study (M. Cohen et al., 1997; SG Goodman et al., 2000), when studying the effect of LMWH of enoxaparin on the triple endpoint (death, acute myocardial infarction, refractory angina pectoris), the risk of one of the events in the enoxaparin group was significantly lower by the 14th day, and the differences between the patients of the enoxaparin and placebo groups persisted by the 30th day. According to some reports, the high efficiency of enoxaparin persists even after a year (Fox KAA. Heart, 1998).

Thus, enoxaparin, according to multicenter randomized placebo-controlled trials, is the only LMWH with proven greater efficacy than unfractionated heparin.

The ARMADA study - a randomized comparison of the effect of enoxaparin, dalteparin, and unfractionated heparin on markers of cellular activation in patients with ACS without ST-segment elevation - showed that only enoxaparin had a positive effect on the dynamics of all three markers. Although the study design did not involve comparison of clinical efficacy parameters, the incidence of death, reinfarction, and recurrent ischemia was lower in the enoxaparin group (13%) than in the dalteparin (18.8%) and heparin (27.7%) groups.

Coronary angiography should be planned as early as possible in the absence of undue urgency. Only in a relatively small group of patients, coronary angiography should be performed within the first hour: with severe prolonged ischemia, severe arrhythmias, hemodynamic instability. In other cases, this technique is performed within 48 hours or during hospitalization. In the presence of lesions, the anatomy of which allows for myocardial revascularization, after a thorough assessment of the extent and other characteristics of the lesion, the question of further treatment tactics is decided.

The management of patients at low risk consists in drug treatment with oral forms of drugs: aspirin, clopidogrel (loading dose of clopidogrel 300 mg, then 75 mg per day), β-blockers, possibly nitrates and calcium antagonists. In this group of patients, it is recommended to start secondary prevention activities, and stop LMWH treatment if there are no ECG changes at the end of the observation period, and no increase in troponin activity was detected in the second consecutive analysis.

Long-term management of patients with ACS should include a number of measures:

  • aggressive modification of risk factors;
  • aspirin at a dose of 75-150 mg; in addition to it, taking into account the results of the CURE study, the appointment of clopidogrel (Plavix) at a dose of 75 mg is indicated for at least 9, preferably 12 months (in this case, the dose of aspirin should be reduced to 75-100 mg);
  • β-blockers improve the prognosis in patients with myocardial infarction;
  • lipid-lowering therapy (HMG-CoA reductase inhibitors significantly reduce mortality and the likelihood of coronary events, while not only regression of the atherosclerotic process occurs, but first of all, the deactivation of the inflamed plaque, the reverse development of endothelial dysfunction, a decrease in the activity of prothrombotic factors);
  • ACE inhibitors can play an independent role in the secondary prevention of coronary syndromes (SOLVD, 1991; SAVE, 1992; HOPE, 2000), the action of which may also be associated with the stabilization of atherosclerotic plaque.

The search for effective methods of treatment and prevention of coronary events continues. In particular, interesting results were obtained in a study on the impact of influenza vaccination in MI (FLUVACS). The study shows a positive effect - a change in the immune response to the invasion of the influenza virus in relation to the destabilization of coronary artery disease. The incidence of CVD was also studied in persons registered with three insurance companies in Minneapolis - 140,055 in the 1998-1999 season. and 146,328 in the 1999-2000 season. at the same time, about half of the surveyed persons were vaccinated. The comparison results showed a significant significant decrease in morbidity (in terms of hospitalization rates) in vaccinated individuals (K.L. Nichol, J. Nordin, J. Mullooly et al., 2003). There is evidence that the addition of red wine to the traditional treatment of ACS patients increases the antioxidant blood capacity and significantly improves endothelial function (E. Guarda, I. Godoy, R. Foncea, D. Perez, C. Romero, R. Venegas, F. Leighton, Catholic University of Chile, Santiago, Chile).

The problem of ACS with ST elevation was highlighted in her report by Corresponding Member of the Academy of Medical Sciences of Ukraine, Chief Cardiologist of the Ministry of Health of Ukraine, Head of the Department of Hospital Therapy No. 1 of the N.M. A.A. Bogomolets, Doctor of Medical Sciences, Professor Ekaterina Nikolaevna Amosova.

- Every doctor in Ukraine wants to treat his patients according to the most modern European recommendations. At the same time, familiarity with these recommendations causes some dissatisfaction among domestic doctors, since in our practice it is difficult to follow European treatment standards due to many financial and organizational problems. Therefore, today, when it is impossible to achieve the standards adopted in the developed countries of the world, Ukrainian doctors must determine for themselves the golden mean - a reasonable compromise between the requirements of international experts and the realities of our country.

First of all, we must be aware of the limitations of thrombolytic therapy in patients with ACS. Reperfusion at the tissue level is highly time dependent. Serious problems of thrombolytic therapy remain retrombosis, reocclusion, residual thrombosis and stenosis of the coronary artery, microembolization of the distal bed, the phenomenon of no-reflow in the "open" coronary artery, complications in the form of intracranial bleeding.

Currently, the effectiveness of thrombolytic therapy is clinically determined by a significant decrease or disappearance of pain in a patient, with an objective improvement in the patient's condition, and positive trends on the ECG. Almost no one is engaged in the exact determination of how fully reperfusion has passed, although this is an extremely important issue in assessing the patient's risk degree, on which the patient's discharge time from the hospital depends, his referral to coronary angiography and other aspects of care. I would like to emphasize that a simple indicator - the dynamics of the ST segment 60-180 minutes after the opening of the coronary artery - is a fairly accurate criterion for the effectiveness of reperfusion. Assessment of ST dynamics is very simple, allowing the physician to understand how effective his or her reperfusion therapy has been.

A new thrombolytic agent, tenecteplase, has recently appeared in Ukraine. Its advantages are obvious: the drug has a high fibrin-specificity and an increased half-life in blood plasma, which makes it possible to administer tenecteplase as a bolus, starting thrombolysis at the prehospital stage. In addition, tenecteplase is resistant to type 1 plasminogen activator inhibitors. Compared with streptokinase, the introduction of tenecteplase allows in 80% of cases to achieve patency of the coronary artery more often, which provides a higher clinical efficacy. But how do these benefits actually manifest themselves in terms of clinical efficacy? As shown by numerous clinical studies (GUSTO-I, 1993; INJECT, 1995; GUSTO-III, 1997; ASSENT-2, 1999; In TIME-2, 2000), thrombolytic drugs of the tissue plasminogen activator group have a very limited increase in clinical efficacy, and all their advantages lie mainly in the ease of administration and some reduction in the frequency of severe complications of therapy (intracranial bleeding).

Thus, to date, improving the effectiveness of reperfusion therapy consists in improving adjuvant antithrombin therapy, which is aimed at preventing early and late rethrombosis, reducing the frequency of microembolization of the distal vessels, and increasing the completeness of tissue perfusion. Drugs with adjuvant action include LMWH (enoxaparin), indirect anticoagulants, antiplatelet drugs.

Until recently, adjuvant therapy focused on two areas: the replacement of unfractionated heparin with LMWH and the use of powerful glycoprotein receptor blockers for safe combination with a half-dose of thrombolytics. These new directions have provided a number of benefits for the endpoints (recurrent heart attacks, mortality), but, unfortunately, the use of absiximab was fraught with a significant increase in the number of serious bleeding. Therefore, inhibitors of glycoprotein receptors were not included in the European and American recommendations for thrombolytic therapy.

A decrease in the frequency of relapses can be achieved with the help of new regimens of accompaniment therapy - one of the most promising is the regimen with the inclusion of enoxaparin. However, even with this scheme, an unfavorable effect was noted - an increase in the frequency of dangerous bleeding in the group of patients over 75 years old. Based on this, the American recommendations (2004) for the use of enoxaparin are more restrained than in European ones. American experts do not recommend prescribing the drug to patients of this age group. Taking this into account, an amendment was introduced to the protocol of the large study ExTRACT-TIMI-25, in which Ukraine is also involved - for patients over 75 years old, the enoxaparin bolus was excluded, and the dose of the drug was reduced to 0.75 mg / kg 2 times a day (in other cases - 1 mg / kg). This study should provide a definitive answer to the question of the comparative efficacy of enoxaparin and unfractionated heparin in thrombolysis. The results of the study are expected to be fundamental in the revised guidelines for the use of LMWH as an adjuvant treatment in reperfusion therapy.

Both European and American experts pay great attention to antiplatelet therapy. The CLARITY-TIMI-28 study, completed this year, confirmed the use of clopidogrel in addition to aspirin for ST-elevation ACS, which was previously widely used empirically without evidence. The study confirmed that the addition of clopidogrel to the treatment regimen can improve coronary patency during reperfusion and reduce the frequency of MI recurrence, although it was not possible to obtain a difference in mortality due to the small number of patients. Moreover, this effect was the same and did not depend on gender, age, localization of the infarction, thrombolytics and heparins used. Advantages were noted not only in relation to revascularization, but also in relation to reperfusion at the tissue level, which is much more important for patient survival. With such a powerful antithrombin therapy, safety indicators are very important: as it turned out, the use of clopidogrel did not increase the incidence of severe intracranial bleeding, although the incidence of non-severe bleeding increased slightly.

An interesting study was conducted in China (COMMIT / CSS-2, 2005), which included about 46 thousand patients with acute myocardial infarction lasting up to 24 hours, regardless of whether they received thrombolytic therapy or not (the average time to randomization was 10 hours) ... As a result, this study revealed significant differences in mortality: when clopidogrel was used in the therapy regimen, mortality significantly decreased. In this case, severe bleeding, as in the previous study, did not increase its frequency.

Thus, intensification of antiplatelet therapy by using clopidogrel opens up some additional opportunities for urgent cardiology in increasing the clinical effectiveness of reperfusion therapy. Therefore, domestic cardiologists intend to raise the issue of including clopidogrel in the national recommendations for the treatment of MI. Currently, the Ministry of Health of Ukraine is developing a national CVD program, which, in particular, plans to include many modern drugs and treatment regimens. Thus, Ukrainian patients can hope for more significant than before, state funding for emergency cardiology, including the possible provision of highly effective drugs such as clopidogrel. Undoubtedly, the improvement of the organization system is of great importance in improving medical care in emergency cardiology, which will speed up the start of treatment.

Interesting reports were made at the meeting devoted to cardiac arrhythmias in the practice of urgent cardiology. So, the head of the department of cardiac arrhythmias at the Institute of Cardiology. N. D. Strazhesko AMS of Ukraine, Doctor of Medical Sciences, Professor Oleg Sergeevich Sychev in his report touched upon the problem of syncope (SS).

- Due to the variety of possible causes of SS, it is often difficult to identify the underlying disease. ESC experts offer a special examination program for such patients. Differential diagnosis is largely based on the differences between the course of fainting: the characteristics of pre- and post-fainting states, the duration of loss of consciousness. Neurogenic syncope often occurs after a sudden unpleasant sight, sound or smell, within one hour after eating, accompanied by nausea, vomiting. Vasovagal syncope is caused by stress, acute pain, prolonged standing in an upright position (at attention or in stuffy rooms). Carotid sinus syndrome is a common cause of fainting in men over 60 years of age, the diagnostic test in this case is carotid sinus massage. Orthostatic syncope can be registered in the presence of documented orthostatic hypotension (a decrease in systolic blood pressure by 20 mm Hg or when blood pressure is below 90 mm Hg) in combination with a syncope or presyncopal state. Fainting of arrhythmogenic genesis can be different in origin - due to tachycardia, bradycardia, blockade. Therefore, for the differential diagnosis of syncope, an ECG is necessary: ​​arrhythmogenic syncope is diagnosed in the presence of signs of bradycardia (below 40 beats / min), repeated sinoatrial blockades with pauses of more than 3 seconds, atrioventricular block II (Mobits II) or III degree, alterations of blockades of the left and right legs bundle of His, paroxysmal supraventricular tachycardia, ventricular tachycardia, disturbances in the work of the artificial pacemaker with the presence of pauses. Fainting due to organic pathology of the heart and blood vessels is determined due to the identification of the underlying disease, which can manifest itself clinically and electrophysiologically - on the ECG, a wide QRS complex (> 0.12 seconds), a violation of AV conduction, sinus bradycardia (< 50) или синоатриальные паузы, удлиненный интервал QT.

Treatment of CVS of neurogenic genesis involves avoiding trigger mechanisms for the development of syncope; modification or withdrawal of medications (antihypertensive drugs), if they are a provoking factor; in case of cardiodepressor or mixed carotid sinus syndrome, implantation of a pacemaker is recommended (in case of more than 5 episodes of obfuscation during the year, in case of injuries or accidents caused by fainting in patients over 40 years old). For patients with vasovagal genesis of CC, training with a change in body position is indicated.

Fainting resulting from orthostatic hypotension usually requires modification of medication (usually antihypertensive drugs).

With arrhythmogenic SS, treatment with antiarrhythmic drugs is necessary. In many cases, implantation of a cardioverter is recommended. Indications for pacing: frequent recurrent fainting of the cardio-inhibitory type, refractory to drug therapy and significantly reducing the quality of life of patients.

Atrial fibrillation is considered one of the most common supraventricular arrhythmias. This rhythm disturbance more than doubles the risk of general and cardiac death. Among the adverse consequences of atrial fibrillation, one of the most dangerous is the high probability of thromboembolic complications. According to the recommendations of European and American experts, the strategic goals in patients with paroxysmal atrial fibrillation are the restoration of sinus rhythm and its retention with the help of antiarrhythmic drugs. With a stable form, it is possible both to restore the sinus rhythm using cardioversion or medication, and to decrease the heart rate with simultaneous anticoagulant therapy. The permanent form of atrial fibrillation presupposes the preservation of atrial fibrillation, control of the ventricular response with the use of adequate anticoagulant therapy, therefore, antiplatelet therapy is so important in atrial fibrillation, the standards of which are aspirin and Plavix, as well as anticoagulant therapy - the drug of choice is most often LMW Clexan. The choice of the optimal treatment for atrial fibrillation depends on the structural damage to the heart, the state of hemodynamics, heart rate, the risk of thromboembolism and other factors.

Fainting associated with low cardiac output is due to obstructive heart disease and vascular disease, so treatment for these CVDs is determined by the underlying disease.

Thus, SS can be signs of a large number of different diseases, including very dangerous ones. Their timely diagnosis, correctly prescribed treatment will not only significantly improve the patient's quality of life, but also improve the further prognosis.

An employee of the Department of Resuscitation and Intensive Care of the Institute of Cardiology named after V.I. N. D. Strazhesko AMS of Ukraine, Doctor of Medical Sciences Oleg Igorevich Irkin.

  • Electrical instability of the myocardium reflects its vulnerability to the development of life-threatening arrhythmias (ventricular fibrillation and persistent ventricular tachycardia) when applying threshold force extrastimuli (B. Lown, 1984). The components of electrical instability were determined in 1987 by P. Coumel:
    • arrhythmogenic substrate (persistent, unstable);
    • provoking factors (electrolyte imbalance, catecholaminemia, drugs);
    • triggers (ventricular premature beats, myocardial ischemia).

Electrophysiological studies show that electrical instability of the myocardium is observed in patients with CV after myocardial infarction; therefore, practitioners face an important problem - to reduce the risk of death of patients due to electrical instability of the myocardium.

In 1993, K. Teo (JAMA) showed the prophylactic effect of various antiarrhythmic drugs in myocardial infarction. Virtually all classes of antiarrhythmic drugs that are widely used in clinical practice increase the risk of death in patients. An exception to these are b-blockers, as well as amiodarone. In the same year, Held and Yusuf published the results of a study examining the effect of long-term use of β-blockers after acute myocardial infarction on the possible risk of death in patients. It turned out that b-blockers, compared with placebo, significantly reduce the risk of all deaths by 23%, sudden death by 32%, and other deaths by 5%.

Studies examining the effect of other antiarrhythmic drugs on the risk of death and coronary events in patients have not led to encouraging results. Encainide / flecainide (class I) in the CAST-1 study (Echt et al., 1991) showed a decrease in the number of patients without coronary events compared with placebo. Similar results were obtained in the study of d-sotalol (class III) in 1996 (SWORD, Waldo et al.), When in the placebo group the overall mortality, cardiac and arrhythmic mortality were significantly lower. In the DIAMOND-MI study (Kober et al., 2000), dofetilide showed a slight decrease in total, cardiac and arrhythmic mortality, at the same time slightly increased the incidence of HF compared with placebo.

Interesting SSSD (Spanish Study on Sudden Death) study with a follow-up of 2.8 years, which compared two different antiarrhythmic drugs. A total of 368 patients with myocardial infarction, low LV ejection fraction and complex ventricular extrasystoles were examined. Therapy was carried out with amiodarone in one group and metoprolol in the other. The results showed that arrhythmic mortality was significantly lower in the amiodarone group than in the metoprolol group (3.5% versus 15.4%, respectively). In subsequent studies (EMIAT, CAMIAT), amiodarone also showed better patient survival and a lower risk of arrhythmic death.

In 1997, a meta-analysis of studies with amiodarone in acute myocardial infarction (5101 patients) and heart failure (1452 patients) once again confirmed that the use of amiodarone significantly reduced total, arrhythmic and sudden mortality compared with placebo.

It was also found that the effectiveness of the use of amiodarone depends on the heart rate. In the EMIAT study (Fance et al., 1998), when taking amiodarone with a baseline level of more than 84 beats / min, the risk of arrhythmic events was 54%, and with a baseline heart rate of less than 63 bpm, only 17%. The ECMA study (Boutitue et al., 1999) showed that when the heart rate slows down to a heart rate of more than 80 beats per minute, the risk of arrhythmic events while taking amiodarone is 59%, while when slowing down below 65 beats per minute - 12%.

In 1999, the results of the ARREST study (“Amiodarone in community-acquired resuscitation for Refractory Persistent Ventricular Tachycardia,” Kudenchuk et al.) Were published, which evaluated the effectiveness of amiodarone in a standard resuscitation regimen. The algorithm of actions for ventricular fibrillation (VF) or ventricular tachycardia (VT) included cardiopulmonary resuscitation (CPR) before connecting the ECG monitor, in the presence of VF / VT on the monitor: three consecutive defibrillator shocks with increasing energy, in case of persistence or recurrence of VF / VT continued CPR, tracheal intubation was performed, vein punctured, adrenaline was injected (1 mg every 3-5 minutes). Repeated defibrillator shocks and intravenous antiarrhythmics (lidocaine, bretylium, procainamide) were supplemented with amiodarone (300 mg) or placebo. The duration of resuscitation measures was almost the same in both groups, but the number of defibrillator shocks in the placebo group was large (6 ± 5 versus 4 ± 3 in the amiodarone group), and the number of patients who survived by the time of hospitalization in group A.