Treatment of acute coronary syndrome without st. Approach to the treatment of acute coronary syndrome without ST-segment elevation
Spicy coronary syndrome Non-ST segment elevation (ACS) is a type of myocardial infarction with less severe damage to the heart muscle compared to ST-segment elevation myocardial infarction, which is more common.
Differences between ACS without ST segment elevation and ACS with ST segment elevation
Each contraction of the heart muscle is displayed on the electrocardiogram (ECG) in the form of a curve. Despite the fact that clinically ACS without ST elevation and ACS with ST elevation look the same, on the cardiogram the curves for these types of ACS are very different.
Signs of ACS without ST elevation on ECG:
Decreased ST or T wave inversion
No Q wave changes
Incomplete closure of the coronary artery
Signs of ACS with ST elevation:
ST segment elevation
Q wave changes
Complete occlusion of the coronary artery
Risk factors for ACS without ST segment elevation:
Smoking
Inactive lifestyle
Increased blood pressure or high cholesterol
Diabetes mellitus
Overweight or obesity
Family history of heart disease or stroke
Symptoms:
Feeling of tightness or discomfort in the chest
Pain or discomfort in the jaw, neck, back, or stomach
Dizziness
Sharp weakness
Nausea
Sweating
The occurrence of such symptoms should be taken very seriously and promptly called emergency assistance. When it comes to chest pain, it is better not to take risks and play it safe, since in the event of a heart attack, every minute counts.
Diagnosis of ACS without ST elevation
Diagnosis is carried out using a blood test and ECG.
Blood tests reveal increased levels of cardiac creatine kinase, troponins I and T. These markers indicate possible damage to cardiac muscle cells and, in comparison with ACS without ST elevation, their levels increase moderately. A blood test alone cannot diagnose a myocardial infarction. On the ECG you can see how the ST segment “behaves” and, based on this, judge both the presence of a heart attack and its type.
Treatment
Tactics depend on the degree of blockage of blood flow and the severity of the disease. The GRACE score determines low, moderate, or high risk of death due to ACS. The following parameters are used for risk stratification:
Age
Heart rate
Systolic blood pressure
Class by Killip
Serum creatinine level
Cardiac arrest upon patient admission
Changes in the ST segment on the ECG
Increased levels of cardiac markers
In patients with ACS without ST elevation at low risk, drug therapy is used. These may be anticoagulants, antiplatelet agents, beta blockers, nitrates, statins, ACE inhibitors or blockers.
In patients at average or high risk, percutaneous coronary artery grafting or coronary artery bypass surgery is performed.
Prevention
Prevention measures involve reducing risk factors. The most important change in lifestyle is:
Healthy balanced diet (fruits, vegetables, whole grains, healthy fats)
Limit your intake of saturated and trans fats
Minimum 30 minutes physical activity 5 days a week
Stress management practices: yoga, deep breathing, walking
Quitting smoking
Fighting excess weight
In addition, measures should be taken to reduce blood pressure or cholesterol levels, properly control diabetes.
If you have previously had a heart attack or are at risk, plan what you will do in the event of a heart attack. emergency. Always keep with you the doctor's phone number, a list of your medications, and a list of drugs to which you are allergic.
Acute coronary syndrome is a pathological process in which the natural blood supply to the myocardium through the coronary arteries is disrupted or completely stopped. In this case, oxygen does not reach the heart muscle in a certain area, which can lead not only to a heart attack, but also to death.
The term "ACS" is used by clinicians to refer to certain heart diseases, including unstable heart disease. This is due to the fact that the etiology of these diseases lies. In this condition, the patient requires emergency medical care. In this case, we are talking not only about the development of complications, but also a high risk of death.
Etiology
The main cause of acute coronary syndrome is damage to the coronary arteries by atherosclerosis.
In addition, the following possible factors in the development of this process are identified:
- strong, nervous overstrain;
- narrowing of the lumen of the vessel;
- mechanical damage to the organ;
- complications after surgery;
- coronary arteries;
- inflammation of the coronary artery;
- congenital pathologies of the cardiovascular system.
Separately, it is necessary to highlight factors that predispose to the development of this syndrome:
- overweight;
- smoking, drug use;
- practically complete absence physical activity;
- imbalance of fats in the blood;
- alcoholism;
- genetic predisposition to cardiovascular pathologies;
- increased blood clotting;
- frequent stress, constant nervous tension;
- taking certain medications which lead to a decrease in pressure in the coronary arteries (coronary steal syndrome).
ACS is one of the most life-threatening conditions for humans. In this case, not only emergency medical care is required, but also urgent resuscitation measures. The slightest delay or incorrect first aid actions can lead to death.
Pathogenesis
Due to thrombosis of the coronary vessels, which is provoked by a certain etiological factor, platelets begin to be released biologically active substances- thromboxane, histamine, thromboglobulin. These compounds have a vasoconstrictor effect, which leads to a deterioration or complete cessation of blood supply to the myocardium. This pathological process can be aggravated by adrenaline and calcium electrolytes. At the same time, the anticoagulant system is blocked, which leads to the production of enzymes that destroy cells in the necrosis zone. If at this stage of development pathological process not stopped, the affected tissue will transform into a scar, which will not take part in the contraction of the heart.
The mechanisms of development of acute coronary syndrome will depend on the degree of thrombus or plaque occlusion of the coronary artery. The following stages are distinguished:
- with a partial decrease in blood supply, attacks of angina may occur periodically;
- with complete overlap, areas of dystrophy appear, which later transform into necrosis, which will lead to;
- sudden pathological changes lead to ventricular fibrillation and, as a consequence, clinical death.
It is also necessary to understand that a high risk of death is present at any stage of the development of ACS.
Classification
Based on modern classification, highlight such clinical forms OKS:
- acute coronary syndrome with ST segment elevation - the patient has typical ischemic pain in the chest, reperfusion therapy is mandatory;
- acute coronary syndrome without ST segment elevation – typical for coronary disease changes, angina attacks. Thrombolysis is not required;
- myocardial infarction diagnosed by changes in enzymes;
- unstable angina.
Forms of acute coronary syndrome are used only for diagnostic purposes.
Symptoms
First and most characteristic feature The disease is acute pain in the chest. The pain syndrome can be paroxysmal in nature and radiate to the shoulder or arm. With angina pectoris, the pain will be squeezing or burning in nature and short-lived. In case of myocardial infarction, the intensity of this symptom can lead to painful shock, so immediate hospitalization is required.
In addition, the following symptoms may be present in the clinical picture:
- cold sweating;
- unstable blood pressure;
- excited state;
- confusion;
- panic fear of death;
- fainting;
- pale skin;
- the patient feels a lack of oxygen.
In some cases, symptoms may be accompanied by nausea and vomiting.
With such a clinical picture, the patient needs to urgently provide first aid and call an emergency room. medical care. Under no circumstances should the patient be left alone, especially if there is nausea with vomiting and loss of consciousness.
Diagnostics
The main method for diagnosing acute coronary syndrome is electrocardiography, which must be done as soon as possible after the onset of a painful attack.
A full diagnostic program is carried out only after the patient’s condition has been stabilized. Be sure to notify the doctor about what medications were given to the patient as first aid.
The standard program of laboratory and instrumental examinations includes the following:
- general blood and urine analysis;
- biochemical blood test - the level of cholesterol, sugar and triglycerides is determined;
- coagulogram - to determine the level of blood clotting;
- ECG is a mandatory method of instrumental diagnostics for ACS;
- echocardiography;
- coronary angiography - to determine the location and degree of narrowing of the coronary artery.
Treatment
The therapy program for patients with acute coronary syndrome is selected individually, depending on the severity of the pathological process; hospitalization and strict bed rest are required.
The patient's condition may require emergency measures. first aid, which are as follows:
- provide the patient with complete rest and access to fresh air;
- put a nitroglycerin tablet under your tongue;
- Call emergency medical services and report your symptoms.
Treatment of acute coronary syndrome in a hospital may include the following therapeutic measures:
- oxygen inhalation;
- administration of medications.
As part of drug therapy, the doctor may prescribe the following drugs:
- narcotic or non-narcotic painkillers;
- anti-ischemic;
- beta blockers;
- calcium antagonists;
- nitrates;
- disaggregants;
- statins;
- fibrinolytics.
In some cases conservative treatment it turns out to be insufficient or not at all appropriate. In such cases, the following surgical intervention is performed:
- stenting of the coronary arteries - a special catheter is passed to the site of narrowing, after which the lumen is expanded using a special balloon, and a stent is installed at the site of narrowing;
- coronary artery bypass grafting - the affected areas of the coronary arteries are replaced with shunts.
Such medical measures make it possible to prevent the development of myocardial infarction from ACS.
In addition, the patient must follow general recommendations:
- strict bed rest until stable improvement;
- complete elimination of stress, strong emotional experiences, nervous tension;
- exclusion of physical activity;
- as the condition improves, daily walks in the fresh air;
- exclusion from the diet of fatty, spicy, too salty and other heavy foods;
- complete exclusion of alcoholic beverages and smoking.
You need to understand that acute coronary syndrome, if the doctor’s recommendations are not followed, can lead to serious complications at any time, and the risk of death in case of relapse always remains.
Separately, diet therapy for ACS should be highlighted, which implies the following:
- limiting the consumption of animal products;
- the amount of salt should be limited to 6 grams per day;
- exclusion of overly spicy, seasoned dishes.
It should be noted that compliance with this diet is necessary constantly, both during the treatment period and as a preventive measure.
Possible complications
Acute coronary insufficiency syndrome can lead to the following:
- violation heart rate in any form;
- acute development, which can lead to death;
- inflammation of the pericardium;
It should also be understood that even with timely medical measures, there remains a high risk of developing the above complications. Therefore, such a patient should be systematically examined by a cardiologist and strictly follow all his recommendations.
Prevention
Prevent development cardiovascular diseases It is possible if you follow the following doctor’s recommendations in practice:
- complete cessation of smoking, moderate consumption of alcoholic beverages;
- proper nutrition;
- moderate physical activity;
- daily walks in the fresh air;
- elimination of psycho-emotional stress;
- control of blood pressure indicators;
- control blood cholesterol levels.
In addition, we should not forget about the importance of a preventive examination by specialized medical specialists and compliance with all doctor’s recommendations regarding the prevention of ailments that can lead to acute coronary insufficiency syndrome.
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Treatment of acute coronary syndrome without persistent ST segment elevation on ECG
Developed by a committee of experts of the All-Russian Scientific Society of Cardiologists
Moscow 2006
All-Russian Scientific Society of Cardiologists
Moscow, 2006
© All-Russian Scientific Society of Cardiologists Reproduction in any form and reprinting of these materials is possible only with permission from VNOK
Dear colleagues!
These guidelines have been updated to reflect new evidence that has become available since the first version was published in 2001. They can be considered a single standard of treatment for patients with non-ST segment elevation acute coronary syndrome, based on the most modern ideas about the pathogenesis, diagnosis and treatment of this group of diseases and, of course, taking into account the specific conditions of Russian healthcare.
The proposed treatment methods, based on a clear stratification of risk factors, are confirmed by the results of recent international, multicenter studies and have proven their effectiveness in thousands of treated patients.
The All-Russian Scientific Society of Cardiologists hopes that Russian Recommendations on the treatment of acute coronary syndrome without ST segment elevation will become a guide to action for every cardiologist.
President of the All-Russian Scientific and Cultural Organization, academician R.G. Oganov
1. Introduction................................................... ........................................................ .................... |
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1.1. Some definitions..................................................................................................... |
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1.1.1. Correlation between the concepts of NS and STEMI ST. NS with elevated CStr levels...... |
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2. Diagnosis................................................... ........................................................ .................... |
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2.1. Clinical symptoms............................................................. ........................................................ |
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2.2. Physical examination................................................................... ........................................................ |
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2.3. ECG................................................. ........................................................ ............................ |
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2.4. Biochemical markers of myocardial damage.................................................................. ............... |
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2.5. Risk assessment................................................ ........................................................ ............. |
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2.5.1. FR................................................... ........................................................ ........................ |
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2.5.1.1.Clinical data............................................................ ........................................................ ...... |
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2.5.1.2. ECG................................................. ........................................................ ........................ |
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2.5.1.3. Markers of myocardial damage – CStr.................................................... ........................ |
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2.5.1.4. EchoCG......................................................... ........................................................ ...................... |
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2.5.1.5. Stress tests before discharge.................................................................... ........................... |
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2.5.1.6. KAG................................................... ........................................................ ........................ |
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3. Treatment methods.................................................. ........................................................ ......... |
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3.1. Anti-ischemic drugs................................................... ........................................... |
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3.1.1.BAB................................................... ........................................................ ........................... |
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3.1.2.Nitrates................................................... ........................................................ ............... |
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3.1.3. AK................................................ ........................................................ ........................ |
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3.2. Antithrombotic drugs. Antithrombins........................................................ ............. |
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3.2.1.Heparins (UFH and LMWH)............................................ ........................................................ ... |
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3.2.1.1. Long-term administration of LMWH in patients with signs of increased risk of complications11 |
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3.2.2.Direct thrombin inhibitors............................................................ ....................................... |
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3.2.3. Treatment of hemorrhagic complications associated with antithrombin therapy........... |
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3.3. Antithrombotic drugs. Antiplatelet drugs................................................... |
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3.3.1. Aspirin (acetyl salicylic acid) ..................................................................... |
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3.3.1.1. Aspirin dose................................................... ........................................................ ........ |
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3.3.1.2. Resistance to aspirin.................................................................... .................................... |
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3.3.2. ADP receptor antagonists: thienopyridines.................................................... ......... |
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3.3.3. Blockers of GP IIb/IIIa platelet receptors.................................................... .......... |
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3.3.3.1. Antagonists of GP IIb/IIIa platelets and LMWH.................................................... ............ |
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3.4. Indirect anticoagulants for ACS.................................................... ................................... |
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3.5. Fibrinolytic (thrombolytic) treatment.................................................. ............... |
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3.6. Coronary revascularization................................................................. ........................................ |
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3.6.1. KAG................................................... ........................................................ ....................... |
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3.6.2. PCI. Stents........................................................ ........................................................ ....... |
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3.6.2.1. ATT after PCI................................................... ........................................................ ........ |
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3.6.2.2. PCI and LMWH................................................... ........................................................ ............. |
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3.6.3. KS......................................................... ........................................................ ...................... |
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3.6.4. Indications for PCI and surgical interventions.................................................. ..... |
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3.6.5. Comparison of the effectiveness of invasive and drug treatment methods........... |
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4. Treatment strategy for patients with ACS.................................................... ........................................ |
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4.1. Initial assessment of the patient................................................................... ........................................... |
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4.2. Patients with signs of acute occlusion of a large coronary artery............................................................ ............ |
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4.3. Patients with suspected ST-ACS.................................................... ................................ |
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4.3.1. Use of heparin................................................... ................................................... |
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4.3.1.1. NFG........................................................ ........................................................ ....................... |
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4.3.1.2. NMG......................................................... ........................................................ ...................... |
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4.3.2. Patients with a high immediate risk of death or development of myocardial infarction |
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results of initial observation (8-12 hours) .................................................... .................... |
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4.3.3. Patients with a low risk of death or development of myocardial infarction in the near future.................................... |
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4.4. Management of patients after stabilization................................................................. ................ |
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5. Approximate sequence of actions in the management of patients with ST-ACS .................. |
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5.1. First contact with a doctor (local doctor, clinic cardiologist)................................................. |
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5.2. Emergency doctor......................................................... ........................................................ ..... |
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5.3. Hospital waiting room......................................................... ........................................................ |
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5.3.1. Hospitals without cardiac ICU or with emergency facilities |
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treatment of patients in the emergency room................................................................... ......................................... |
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5.3.2. Hospitals with cardiac intensive care units.................................................................... ........................... |
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5.4. BIT (in its absence, the department in which treatment is carried out) .............................. |
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5.4.1. Facilities with surgical services or PCI capabilities...... |
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5.5. Cardiology department after transfer from the hospital.................................................... .......... |
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Application................................................. ........................................................ ............... |
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Literature................................................. ........................................................ ................ |
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Composition of the GFCI Expert Committee for the preparation of recommendations.................................................... |
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List of abbreviations and symbols used in the recommendations |
ACC/AAC – American College of Cardiology/American
what is the association of the heart |
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coronary artery bypass grafting. |
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antithrombotic therapy |
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adenosine triphosphate |
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activated partial thromboplastin |
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β-blockers |
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balloon angioplasty |
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block intensive care |
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LBBB – left bundle branch block |
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upper limit of normal for the method used |
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intravenously |
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LVH – |
LV hypertrophy |
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HMG-CoA – hydroxy methylglutaryl coenzyme A |
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GP IIb/IIIa receptors – |
glycoprotein IIb/IIIa receptor |
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platelet tori. |
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GP IIb/IIIa of platelets – glycoproteins IIb/IIIa of platelets
HTG – hypertriglyceridemia DBP – diastolic blood pressure
ACE inhibitors – angiotensin-converting enzyme inhibitors
left ventricle |
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MB (Muscle Brain) CPK fraction |
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international normalized ratio |
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MI without Q wave |
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low molecular weight heparin(s) |
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unstable angina |
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unfractionated heparin |
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s/c – |
subcutaneously |
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acute MI |
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acute coronary syndrome(s) |
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OKSBP ST – |
acute coronary syndrome without elevations |
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ST segment on ECG |
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ST OKSP – OKS with ST segment elevation on ECG |
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total cholesterol |
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systolic blood pressure |
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heart failure |
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stable angina |
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cardiac troponins |
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thrombotic therapy |
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troponins |
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ejection fraction |
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functional class |
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risk factors |
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low-density lipoprotein cholesterol |
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high density lipoprotein cholesterol |
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percutaneous coronary intervention (PCA) |
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and/or wall installation, atherectomy, others |
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methods for eliminating coronary stenosis, devices for |
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which, as a rule, are introduced through |
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peripheral vessel) |
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heart rate |
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electrocardiogram |
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echocardiography |
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SaO2 – |
arterial blood oxygen saturation |
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TXA2 – |
thromboxane A2 |
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1. Introduction
For KBS as chronic disease, characterized by periods of stable course and exacerbations. The period of exacerbation of CAD is designated as ACS. This term combines such clinical conditions, as MI, including non-Q-MI, small-focal, micro-, etc.) and NS. NS and MI are different clinical manifestations of a single pathophysiological process - thrombosis of varying severity over rupture of an atherosclerotic plaque or erosion of the coronary artery endothelium, and subsequent distal thromboembolism.
The term ACS was introduced into clinical practice when it became clear that the issue of using certain active treatment methods, in particular TLT, should be resolved before the final diagnosis of the presence or absence of large-focal MI.
At the first contact of a doctor with a patient if the presence of ACS is suspected based on clinical and ECG signs it can be classified into one of its two main forms.
OKSP ST. These are patients with pain or other unpleasant sensations (discomfort) in the chest and persistent elevations of the ST segment or “new”, newly occurring, or presumably newly occurring LBBB on the ECG. Persistent ST segment elevations reflect the presence of acute complete coronary artery occlusion. The goal of treatment in this situation is rapid and lasting restoration of the lumen of the vessel. For this purpose, in the absence of contraindications, thrombolytic agents or direct angioplasty - PCI - are used.
OKSBP ST. Patients with chest pain and ECG changes indicating acute myocardial ischemia, but PD ST. These patients may exhibit persistent or transient ST depression, inversion, flattening or pseudo-normalization of the T wave; The ECG on admission may be normal. The management strategy for such patients is to eliminate ischemia and symptoms, monitor with repeated (serial) ECG recordings and determine markers of myocardial necrosis: CP and CF CK. Thrombolytic agents are not effective and are not used in the treatment of such patients. Therapeutic tactics depend on the degree of risk (severity of the condition) of the patient.
1.1. Some definitions ACS is any group of clinically recognized
symptoms or symptoms suggestive of acute AMI or UA include AMI, ST UTI, ST NSTEMI, MI diagnosed by enzyme changes, biomarkers, late ECG findings, and UA. The term appeared in connection with the need to choose treatment tactics before the final diagnosis of the listed conditions. Used to designate patients upon first contact and implies the need for treatment as patients with MI or NS.
STEMI ST is an acute process of myocardial ischemia of sufficient severity and duration to cause myocardial necrosis. There are no ST elevations on the initial ECG. In most patients whose disease begins as STEMI, Q waves do not appear and are eventually diagnosed as non-Q-MI. STEMI ST differs from NS by the presence (increased levels) of markers of myocardial necrosis, which are absent in NS.
NS is an acute process of myocardial ischemia, the severity and duration of which is insufficient for the development of myocardial necrosis. There are usually no ST elevations on the ECG. There is no release of biomarkers of myocardial necrosis into the bloodstream in quantities sufficient to diagnose MI.
1.1.1. Correlation between the concepts of NS and STEMI ST. NS with elevated CTr levels
The concept of STEMI ST appeared in connection with the widespread introduction of the definition of ST into clinical practice. Patients with ST-ACSBP with increased level STRs have a worse prognosis (higher risk) and require more aggressive treatment and monitoring. The term STEMI ST is used to “mark” the patient for a short time until it is finally determined whether he has developed a large-focal MI or whether the process is limited to the occurrence of non-Q-MI. Isolating STEMI ST without determining CTr on the basis of less sensitive markers of necrosis, in particular CF CK, is possible, but leads to the identification of only a part of patients with foci of necrosis in the myocardium and, therefore, at high risk.
Thus, to quickly differentiate within ST-ACS, ST-NSEMI, and UA, determination of CTr levels is required.
NS and STEMI ST are very similar conditions, having a common pathogenesis and a similar clinical picture, they may differ only in the severity (severity) of symptoms. In Russia, medical institutions use different, both quantitative and qualitative methods for determining Str. Accordingly, depending on the sensitivity of the method for determining necrosis markers, the same condition can be assessed differently: NS or STEMI ST. Until now, the attitude towards the diagnosis of MI based on the fact of an increase in the content of CTr of any severity has not been officially formulated. On the other hand, a positive test for TP (increased levels with quantification) significantly influences the choice of method and place of treatment and must somehow be reflected in the diagnosis. Therefore, it is acceptable to use the wording “NS with an increased level of STr” (T or I) as equivalent to the term STEMI ST. This formulation is provided for by the classification of NS Hamm CW and Braunwald E - NS class IIIB, TP positive (Table 1).
2. Diagnosis
2.1. Clinical symptoms
Patients suspected of developing ST-CSD, the treatment of which is discussed in these guidelines, when seeking
medical care can be classified into the following clinical groups:
patients after prolonged >15 min. attack of anginal pain at rest. This condition usually serves as a basis for calling an ambulance or an emergency visit to a medical facility in some other way. It corresponds to class III NS according to the classification of Hamm CW and Braunwald E (Table 1). Patients belonging to this group constitute the main object of these recommendations;
patients with new onset in previous 28-30 days of severe angina;
patients who have experienced destabilization of a pre-existing CV with the appearance of characteristics inherent in at least class III angina according to the Canadian Heart Association classification (Appendix), and/or attacks of pain at rest (progressive angina, crescendo angina).
ACS may present atypically, especially in young (25–40 years) and elderly (>75 years) patients, patients with diabetes, and women. Atypical manifestations of NS include pain that occurs predominantly at rest, epigastric pain, acute onset of digestive disorders, stabbing pain in the chest, pain with signs characteristic of pleural damage, or increasing shortness of breath. In these
Table 1
Classification of NS Hamm CW, Braunwald E.
I – First appearance of severe angina, progressive angina; without angina at rest
II – Angina at rest in the previous month, but not in the next 48 hours; (angina at rest, subacute)
III – Angina at rest in the previous 48 hours; (angina at rest, acute)
Note: * Circulation 2000; 102:118.
In cases, correct diagnosis is facilitated by indications of a more or less long-term existence of CHD.
2.2. Physical examination
The objectives of the examination are: to exclude non-cardiac causes of pain, heart diseases of non-ischemic origin (pericarditis, valve damage), as well as non-cardiac causes that potentially contribute to increased ischemia (anemia); identification of cardiac causes that increase (or cause) myocardial ischemia (HF, hypertension).
Resting ECG is the main method for assessing patients with ACS. An ECG should be recorded when symptoms are present and compared with an ECG taken after symptoms have resolved. It is advisable to compare the recorded ECG with the “old” ones obtained before the current exacerbation, especially in the presence of LVH or previous MI. Q waves, indicating post-MI scarring, are highly specific for advanced coronary atherosclerosis but do not indicate current instability.
ECG signs of unstable CAD are ST segment displacement and T wave changes. The likelihood of the presence of NS is especially high when the corresponding clinical picture is combined with ST segment depression > 1 mm in two or more adjacent leads, as well as T wave inversion > 1 mm in leads with a predominant wave R; the latter sign is less specific. Deep symmetrical T wave inversions in the anterior chest leads often indicate severe proximal stenosis of the anterior descending branch of the LMCA; nonspecific displacements of the ST segment and changes in the T wave, amplitude ≤1 mm, are less informative.
Fully normal ECG in patients with symptoms suggestive of ACS does not exclude its presence. However, if during severe pain a normal ECG is recorded, you should look harder for others possible reasons patient complaints.
ST segment elevation indicates transmural myocardial ischemia due to coronary artery occlusion. Persistent ST segment elevation is characteristic of developing MI. Preho-
A prolonged rise in the ST segment may occur with Prinzmetal's angina (vasospastic angina).
2.4. Biochemical markers of myocardial damage
In case of acute coronary artery disease ST, CTr T and I as markers of myocardial necrosis, due to their greater specificity and reliability, are preferable to the traditionally determined CPK and its MB fraction. Elevated levels of CTr T or I reflect necrosis of myocardial cells. In the presence of other signs of myocardial ischemia - chest pain, changes in the ST segment, such an increase should be called MI.
Determination of CTr makes it possible to detect myocardial damage in approximately a third of patients without an increase in CPK MV. To confirm or rule out myocardial injury, repeat blood draws and measurements are required within 6 to 12 hours of admission and after any episode of severe chest pain.
Changes in the content of various markers of myocardial necrosis over time in relation to a painful attack are presented in Figure 1. Myoglobin is a relatively early marker, while an increase in CK and CP appears later. CTP may remain elevated for 1–2 weeks, making it difficult to diagnose recurrent necrosis in patients with recent MI (Appendix Table 6).
2.5. Risk assessment
U In patients diagnosed with ST-ACSBP, in each specific case the choice of treatment strategy depends on the risk of developing MI or death.
The risk of death and MI increases with age. An increased risk of coronary complications is associated with male gender and previous manifestations of CAD, such as severe and long-term angina or previous MI. Signs of increased risk include impaired LV function, congestive heart failure, as well as hypertension and diabetes. Most of the well-known risk factors for CAD are also signs of poor prognosis in ACS.
* Vertical axis– marker content in the blood relative to the level sufficient for the diagnosis of AMI (diagnostic level for MI), taken as one.
Rice. 1 Biochemical markers of myocardial necrosis and changes in their content in the blood after a painful attack.
2.5.1.1. Clinical data
Prognostically important are the time elapsed since the last episode of ischemia, the presence of angina at rest and the response to drug treatment. These characteristics, along with the CTr concentration, are taken into account in the classification of Hamm CW and Braunwald E. (Table 1).
ECG data are crucial for diagnosing ACS and assessing prognosis. Patients with ST segment depression have a higher risk of subsequent complications than patients whose only change is T wave inversion. In turn, the latter have a greater risk of complications compared to patients with a normal ECG.
Painless (“silent”) episodes of myocardial ischemia cannot be detected using a conventional ECG. Therefore, Holter ECG monitoring is advisable, although its capabilities are limited to recording only
two or three leads and obtaining results no less than a few hours after recording*.
2.5.1.3. Markers of myocardial damage – CTr
Patients with elevated CTr levels have less favorable short- and long-term prognoses compared to patients without such an increase. The risk of new coronary events correlates with the degree of increase in Tr. The increased risk associated with high levels of CTr is independent of other risk factors, including ECG changes at rest or during long-term monitoring. Identification of patients with elevated CTr levels is important for choosing a treatment method.
2.5.1.4. EchoCG
EchoCG allows one to assess the state of LV systolic function, which has important prognostic significance. During myocardial ischemia, local
* A promising technique is continuous 12-lead ECG monitoring with constant analysis of the results using a computer. Continuous ST segment monitoring is also useful for assessing the effect of treatment on ischemia
hypokinesia or akinesia of the LV wall, and after the disappearance of ischemia - restoration of normal contractility. To assess the prognosis and select management tactics for patients, it is important to diagnose conditions such as aortic stenosis or hypertrophic cardiomyopathy.
2.5.1.5. Stress tests before discharge
A stress test performed after stabilization of the patient's condition and before discharge is useful to confirm the diagnosis of CAD and to assess the risk of its complications. A significant proportion of patients are unable to complete stress tests, and this in itself is associated with a poor prognosis. The addition of imaging modalities to detect myocardial ischemia, such as echocardiography, further improves the sensitivity and specificity of prognosis. However, large, long-term, prognostic studies using stress echocardiography in patients after an episode of ST-ACS are lacking.
This research method provides information about the presence of stenotic changes in the coronary artery and their severity. Patients with multivessel disease and patients with LMCA stenosis have a higher risk of serious complications. CAG assessment of the degree and location of the stenosis that caused the deterioration and other stenoses is necessary if PCI is planned. The greatest risk is associated with the presence of filling defects indicating intracoronary thrombus.
3. Treatment methods
3.1. Anti-ischemic drugs
These drugs reduce myocardial oxygen consumption by reducing heart rate, blood pressure, suppressing LV contractility, or causing vasodilation.
evidence that a particular BAB is more effective. Therapy can be started with metoprolol, propranolol or atenolol. In cases where, in the opinion of the doctor, a very rapid cessation of the action of beta blockers is necessary, it is advisable to use esmolol.
With the shortest active drugs Treatment should be started in the presence of concomitant diseases, such as pulmonary pathology or LV dysfunction. Parenteral administration of beta blockers requires careful monitoring of blood pressure, preferably continuous ECG monitoring. The goal of subsequent administration of beta blockers per os should be to achieve a heart rate of 50-60 beats/min. You should not use beta blockers in patients with severe AV conduction disorders (1st degree AV block with PQ>0.24 sec, II or III degrees) without a working artificial pacemaker, bronchial asthma history of severe acute LV dysfunction with signs of HF*.
Particular caution should be observed in patients with chronic obstructive pulmonary diseases, starting treatment with a relatively short-acting, cardioselective beta blocker, for example, metoprolol in reduced doses.
3.1.2. Nitrates
It should be borne in mind that the use of nitrates in NS is based on pathophysiological premises and clinical experience. There are no controlled studies available to demonstrate optimal dosage and duration of use.
In patients with persistent episodes of myocardial ischemia (and/or coronary pain), it is advisable to prescribe IV nitrates. The dose should be gradually increased (“titrate”) until symptoms disappear or side effects appear: headache, hypotension. It should be remembered that long-term use nitrates can be addictive.
As symptoms are controlled, IV nitrates should be replaced with non-parenteral forms, while maintaining a certain nitrate-free interval.
* For the use of beta blockers after the elimination of acute myocardial ischemia in patients with chronic HF, see the relevant GFCI recommendations.
10 Supplement to the journal “Cardiovascular Therapy and Prevention”
TO 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 the 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 bed. In this regard, unstable angina and developing myocardial infarction are currently united by the term acute coronary syndrome (ACS) .
Acute coronary syndrome is a preliminary diagnosis that allows the doctor to determine urgent therapeutic and organizational measures. Accordingly, the development of clinical criteria, 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 prescribing invasive interventions. During the creation of such criteria, all acute coronary syndromes were divided into those accompanied and those not accompanied by persistent ST segment elevation. Currently, optimal treatment interventions, the effectiveness of which is based on the results of well-planned randomized clinical trials, have already been largely developed. Thus, in acute coronary syndrome with persistent ST segment elevation (or new-onset complete block of the left bundle branch), reflecting acute total occlusion of one or more coronary arteries, the goal of treatment is rapid, complete and persistent restoration of the lumen of the coronary artery using thrombolysis (if it is not contraindicated) or primary coronary angioplasty (if technically feasible). The effectiveness of these therapeutic measures has been proven in a number of studies.
For acute coronary syndrome without ST segment elevation we're talking about about patients with chest pain and ECG changes indicating acute myocardial ischemia (but not necessarily necrosis). Such patients often exhibit persistent or transient ST segment depression, as well as inversion, flattening, or “pseudonormalization” of T waves. In addition, ECG changes in acute coronary syndrome without ST segment elevation may be nonspecific or completely absent. Finally, some patients with the above changes on the electrocardiogram, but without subjective symptoms (i.e., cases of painless “silent” ischemia and even myocardial infarction) may also be included in this category of patients.
In contrast to situations with persistent ST-segment elevation, previous treatment proposals for acute coronary syndrome without ST-segment elevation were less clear. It was not until 2000 that the recommendations of the European Society of Cardiology Working Group on the treatment of non-ST segment elevation acute coronary syndrome were published. Soon, corresponding recommendations will be developed for Russian doctors.
This article discusses only the management of patients with suspected acute coronary syndrome who do not have persistent ST segment elevation. In this case, the main attention is paid directly to diagnosis and the choice of therapeutic tactics.
But first we consider it necessary to make two remarks:
- First, the recommendations below are based on the results of a number of clinical studies. However, these trials were performed on specially selected groups of patients and, accordingly, do not reflect all conditions encountered in clinical practice.
- Secondly, it should be borne in mind that cardiology is developing rapidly. Accordingly, these recommendations should be reviewed regularly as new clinical trial results accumulate.
Level A: Conclusions are based on data that were obtained in several randomized trials clinical studies or meta-analyses.
Level B: Conclusions are based on data that have been obtained from single randomized trials or non-randomized studies.
Level C. Conclusions are based on consensus expert opinion.
In the further presentation, after each point the level of its validity will be indicated.
Tactics for managing patients with acute coronary syndrome Initial assessment of the patient's condition The initial assessment of a patient complaining of chest pain or other symptoms suggestive of ACS includes:
1. Careful history taking . Classic characteristics of anginal pain, as well as typical exacerbations of coronary artery disease (prolonged [> 20 minutes] anginal pain at rest, new-onset severe [at least class III according to the Canadian Cardiovascular Society (CCS) classification] angina pectoris, recent worsening of stable angina pectoris of at least to III FC according to CCS) are well known. However, it should be noted that ACS can also manifest itself with atypical symptoms, including chest pain at rest, epigastric pain, sudden dyspepsia, stabbing chest pain, “pleural” pain, and increased shortness of breath. Moreover, the frequency of these manifestations of ACS is quite high. Thus, according to the Multicenter Chest Pain Study (Lee T. et al., 1985), acute myocardial ischemia was diagnosed in 22% of patients with acute and stabbing pain in the chest, as well as in 13% of patients with pain characteristic of pleural lesions , and in 7% of patients in whom painful sensations were completely reproduced by palpation. Atypical manifestations of ACS are especially often observed in young (25-40 years old) and old (over 75 years old) patients, as well as in women and patients with diabetes mellitus.
2. Physical examination . The results of examination and palpation of the chest, cardiac auscultation data, as well as heart rate and blood pressure are usually within normal limits. The purpose of the physical examination is primarily to exclude noncardiac causes of chest pain (pleurisy, pneumothorax, myositis, inflammatory diseases musculoskeletal system, chest trauma, etc.). In addition, physical examination should identify heart diseases not associated with coronary artery disease (pericarditis, heart defects), as well as assess hemodynamic stability and the severity of circulatory failure.
3. ECG . Recording an ECG at rest is a key method for diagnosing ACS. Ideally, you should record an ECG during a painful attack and compare it with an electrocardiogram recorded after the pain has disappeared. For recurring pain, multichannel ECG monitoring can be used for this. It is also very useful to compare the ECG with “old” films (if available), especially if there are signs of left ventricular hypertrophy or previous myocardial infarction.
The most reliable electrocardiographic signs of ACS are the dynamics of the ST segment and changes in the T wave. The likelihood of ACS is greatest if the corresponding clinical picture is combined with depression of the ST segment with a depth of more than 1 mm in two or more adjacent leads. A somewhat less specific sign of ACS is T wave inversion, the amplitude of which exceeds 1 mm, in leads with a predominant R wave. Deep negative symmetrical T waves in the anterior precordial leads often indicate severe proximal stenosis of the anterior descending branch of the left coronary artery. Finally, shallow (less than 1 mm) ST segment depression and slight T wave inversion are the least informative.
It should be remembered that a completely normal ECG in patients with characteristic symptoms does not exclude the diagnosis of ACS.
Thus, in patients with suspected ACS, a resting ECG should be recorded and long-term multichannel ST segment monitoring should be initiated. If monitoring is not feasible for any reason, then frequent ECG registration(level of evidence: C).
Hospitalization
Patients with suspected non-ST segment elevation ACS should be immediately hospitalized in specialized emergency cardiology departments/intensive care units and cardiac intensive care units (level of evidence: C).
Study of biochemical markers of myocardial damage
“Traditional” cardiac enzymes, namely creatine phosphokinase (CPK) and its isoenzyme MB CPK are less specific (in particular, possible false positive results in case of injury skeletal muscles). In addition, there is a significant overlap between normal and pathological serum concentrations of these enzymes. The most specific and reliable markers of myocardial necrosis are cardiac troponins T and I . The concentration of troponins T and I should be determined 6-12 hours after admission to the hospital, as well as after each episode of intense chest pain.
If a patient with suspected non-ST segment elevation ACS has elevated levels of troponin T and/or troponin I, then this condition should be regarded as myocardial infarction and appropriate medical and/or invasive treatment should be provided.
It should also be taken into account that after cardiac muscle necrosis, the increase in the concentration of various markers in the blood serum does not occur simultaneously. Thus, the earliest marker of myocardial necrosis is myoglobin, and the concentrations of CPK and troponin increase somewhat later. In addition, troponins remain elevated for one to two weeks, making it difficult to diagnose recurrent myocardial necrosis in patients who have recently suffered a myocardial infarction.
Accordingly, if ACS is suspected, troponins T and I should be determined at the time of admission to the hospital and re-measured after 6-12 hours of observation, as well as after each painful attack. Myoglobin and/or MB CPK should be determined at recent (less than six hours) onset of symptoms and in patients with a recent (less than two weeks ago) myocardial infarction (Level of Evidence: C).
Initial treatment of patients with suspected non-ST segment elevation ACS
For non-ST segment elevation ACS, the initial therapy should be:
1. Acetylsalicylic acid (level of evidence: A);
2. Sodium heparin and low molecular weight heparins (level of evidence: A and B);
3. b-blockers (level of evidence: B);
4. For persistent or recurrent chest pain - nitrates orally or intravenously (level of evidence: C);
5. If there are contraindications or intolerance to b-blockers, calcium antagonists (level of evidence: B and C).
Dynamic observation
During the first 8-12 hours, it is necessary to carefully monitor the patient's condition. The subject of special attention should be:
- Recurrent chest pain. During each painful attack, it is necessary to record an ECG, and after it, re-examine the level of troponins in the blood serum. Continuous multichannel ECG monitoring is highly advisable to identify signs of myocardial ischemia, as well as cardiac arrhythmias.
- Signs of hemodynamic instability (arterial hypotension, congestive wheezing in the lungs, etc.)
Patients with acute coronary syndrome represent a very heterogeneous group of patients who differ in the extent and/or severity of atherosclerotic lesions of the coronary arteries, as well as in the degree of “thrombotic” risk (i.e., the risk of developing myocardial infarction in the coming hours/days). The main risk factors are presented in Table 1.
Patients with acute coronary syndrome represent a very heterogeneous group of patients who differ in the extent and/or severity of atherosclerotic lesions of the coronary arteries, as well as in the degree of “thrombotic” risk (i.e., the risk of developing myocardial infarction in the coming hours/days). The main risk factors are presented in Table 1.
Based on follow-up data, ECG and biochemical studies, each patient should be classified into one of the two categories below.
1. Patients at high risk of myocardial infarction or death
- repeated episodes of myocardial ischemia (either recurrent chest pain or ST segment dynamics, especially depression or transient ST segment elevations);
- increased concentration of troponin T and/or troponin I in the blood;
- episodes of hemodynamic instability during the observation period;
- life-threatening heart rhythm disturbances (repeated paroxysms of ventricular tachycardia, ventricular fibrillation);
- the occurrence of ACS without ST segment elevation in the early post-infarction period.
2. Patients at low risk of myocardial infarction or death
- chest pain did not recur;
- there was no increase in the level of troponins or other biochemical markers of myocardial necrosis;
- There were no ST segment depressions or elevations in the presence of inverted T waves, flattened T waves, or a normal ECG.
Differentiated therapy depending on the risk of myocardial infarction or death
For patients at high risk of these events, the following treatment tactics may be recommended:
1. Administration of IIb/IIIa receptor blockers: abciximab, tirofiban or eptifibatide (level of evidence: A).
2. If it is impossible to use IIb/IIIa receptor blockers, intravenous administration of sodium heparin according to the scheme (Table 2) or low molecular weight heparins (level of evidence: B).
The following are widely used in modern practice: low molecular weight heparins : adreparin, dalteparin, nadroparin, tinzaparin and enoxaparin. As an example, let’s take a closer look at nadroparin. Nadroparin is a low molecular weight heparin obtained from standard heparin by depolymerization. The drug is characterized by pronounced activity against factor Xa and weak activity against factor IIa. The anti-Xa activity of nadroparin is more pronounced than its effect on aPTT, which distinguishes it from sodium heparin. For the treatment of ACS, nadroparin is administered subcutaneously 2 times a day in combination with acetylsalicylic acid (up to 325 mg/day). The initial dose is determined at 86 units/kg and should be administered as an IV bolus. Then the same dose is administered subcutaneously. Duration further treatment- 6 days, in doses determined depending on body weight (Table 3).
3. In patients with life-threatening cardiac arrhythmias, hemodynamic instability, development of ACS soon after myocardial infarction, and/or a history of CABG, coronary angiography (CAG) should be performed as quickly as possible. In preparation for coronary angiography, heparin administration should be continued. If there is an atherosclerotic lesion that allows revascularization, the type of intervention is chosen taking into account the characteristics of the damage and its extent. The principles for choosing a revascularization procedure for ACS are similar to the general recommendations for this type of treatment. If percutaneous transluminal coronary angioplasty (PTCA) with or without stent placement is chosen, it can be performed immediately after angiography. In this case, the administration of IIb/IIIa receptor blockers should be continued for 12 hours (for abciximab) or 24 hours (for tirofiban and eptifibatide). Level of validity: A.
In patients at low risk of myocardial infarction or death, the following strategies may be recommended:
1. Ingestion acetylsalicylic acid, b-blockers, possibly nitrates and/or calcium antagonists (level of evidence: B and C).
2. Discontinuation of low-molecular-weight heparins if during follow-up there were no changes in the ECG and the troponin level did not increase (level of evidence: C).
3. Stress test to confirm or establish a diagnosis of coronary artery disease and assess the risk of adverse events. Patients with severe ischemia during a standard exercise test (bicycle ergometry or treadmill) should undergo coronary angiography followed by revascularization. If standard tests are not informative, stress echocardiography or stress myocardial perfusion scintigraphy may be useful.
Management of patients with ACS without ST segment elevation after discharge from hospital
1. Administration of low molecular weight heparins if there are repeated episodes of myocardial ischemia and revascularization cannot be performed (level of evidence: C).
2. Taking b-blockers (level of evidence: A).
3. Broad impact on risk factors. First of all, stopping smoking and normalizing the lipid profile (level of evidence: A).
4. Reception ACE inhibitors(level of evidence: A).
Conclusion Currently, many medical institutions in Russia do not have the capabilities to carry out the above-mentioned diagnostic and therapeutic measures (determination of the level of troponins T and I, myoglobin; emergency coronary angiography, use of IIb/IIIa receptor blockers, etc.). We can expect, however, their increasingly wider inclusion in medical practice in our country in the near future.
The use of nitrates for unstable angina is based on pathophysiological reasons and clinical experience. There are no data from controlled studies indicating optimal dosages and duration of use.
Acute coronary syndrome without segment elevation ST (unstable angina and small focal myocardial infarction).
- with incomplete obstruction of the coronary artery.
It is characterized by anginal attacks and the absence of ST segment elevation on the ECG. ACS without ST segment elevation includes unstable angina and small focal MI.
A typical clinical manifestation is a feeling of pressure or heaviness in the chest (angina pectoris) radiating to the chest. left hand, neck or jaw, which may be temporary or permanent.
Traditionally, the following clinical manifestations are distinguished:
* Prolonged (more than 20 minutes) anginal pain at rest;
* New-onset angina of functional class II or III;
* Recent worsening of previously stable angina, at least to functional class III - progressive angina;
* Post-infarction angina.
Diagnostics.
ECG— a first-line method for examining patients with suspected ACS without ST-segment elevation. It should be done immediately after the first contact with the patient. Depression of the ST segment below the isoline and changes in the T wave are characteristic, but not obligatory.
Primary ECG data are also risk predictors. The number of leads with ST depression and the magnitude of depression indicate the degree and severity of ischemia and correlate with prognosis. Deep symmetrical T wave inversion in the anterior precordial leads is often associated with significant stenosis of the proximal left anterior descending coronary artery or the main trunk of the left coronary artery.
A normal ECG does not exclude the presence of non-ST segment elevation ACS.
Biochemical markers. With myocardial necrosis, the contents of the dead cell enter the general bloodstream and can be determined in blood samples. Cardiac troponins play a major role in diagnosis and risk stratification, and also help distinguish between non-ST segment elevation ACS and unstable angina. The test is capable of excluding and confirming ACS with a high probability. In order to differentiate a chronic increase in troponin from an acute one, the dynamics of changes in troponin levels compared to the initial value is of great importance.
It is necessary to remember about possible non-coronary causes of increased troponin levels. These include: pulmonary embolism, myocarditis, stroke, aortic aneurysm dissection, cardioversion, sepsis, and extensive burns.
Any increase in troponin in ACS is associated with a poor prognosis.
There is no fundamental difference between troponin T and troponin I. Cardiac troponins increase after 2.5-3 hours and reach a maximum after 8-10 hours. Their levels return to normal after 10-14 days.
- CPK MB increases after 3 hours, reaching a maximum after 12 hours.
- Myoglobin increases after 0.5 hours, reaching a maximum after 6-12 hours.
Markers of inflammation. Currently, much attention is paid to inflammation as one of the main causes of destabilization of atherosclerotic plaque.
In this regard, so-called inflammatory markers, in particular C-reactive protein, are widely studied. Patients with the absence of biochemical markers of myocardial necrosis, but with elevated levels of CRP are also considered to be at high risk of developing coronary complications.
Echocardiography necessary for all patients with ACS to assess local and global LV function and conduct differential diagnosis. To determine treatment tactics for patients with non-ST segment elevation ACS, stratification models for determining the risk of developing MI or death are currently widely used in practice: the Grace and TIMI scales.
TIMI risk:
7 independent predictors
- Age 65 years (1 point)
- Three factors risk of ischemic heart disease(cholesterol, family history of coronary artery disease, hypertension, diabetes, smoking) (1 point)
- Previously known CAD (1 point) (stenoses > 50% on coronary angiography)
- Aspirin in the next 7 days (!)
- Two episodes of pain (24 hours) - 1
- ST displacements (1 point)
- Presence of cardiac markers (CK-MB or troponin) (1 point)
Risk of MI or death according to TIMI:
– low – (0-2 points) – up to 8.3%
– average – (3-4 points) – up to 19.9%
– high – (5-7 points) – up to 40.9%
Risk assessment according to the GRACE scale
- Age
- Systolic blood pressure
- Creatinine content
- SN class according to Killip
- ST segment deviation
- Heart failure
- Increased markers of myocardial necrosis
Treatment
Etiotropic therapy
— the use of statins has been proven to be highly effective in stabilizing the cap of an unstable fibrous plaque. The statin dose should be higher than typical and titrated further to achieve a target LDL cholesterol level of 2.5 mmol/L. Initial doses of statins are rosuvastatin 40 mg per day, atorvastatin 40 mg per day, simvastatin 60 mg per day.
The effects of statins that determine their use in ACS:
- impact on endothelial dysfunction
- decreased platelet aggregation
- anti-inflammatory properties
- decreased blood viscosity
- plaque stabilization
- suppression of the formation of oxidized LDL.
AAC/ACC (2010): Statins should be prescribed within the first 24 hours of hospitalization
regardless of cholesterol level.
EKO (2009): Lipid-lowering therapy should be prescribed without delay.
Pathogenetic therapy has two goals:
1) The effect is aimed at preventing and inhibiting the development of increasing parietal thrombosis of the coronary arteries - anticoagulant and disaggregant therapy.
2) Traditional coronary therapy - beta-blockers and nitrates.__
Antiplatelet agents
Platelet activation and aggregation play a dominant role in the formation of arterial thrombosis. Platelets can be inhibited by three classes of drugs: aspirin, P2Y12 inhibitors and glycoprotein Ilb/IIIa inhibitors.
1) Acetylsalicylic acid. The mechanism of action is due to the inhibition of COX in tissues and platelets, which causes a blockade of the formation of thromboxane A2, one of the main inducers of platelet aggregation. Blockade of platelet cyclooxygenase is irreversible and persists throughout life.
Aspirin in patients with ACS without ST elevation is considered as a first-line drug, since the direct substrate of the disease is the activation of the vascular-platelet and plasma coagulation cascades. That is why the effect of aspirin in this category of patients is even more pronounced than in patients with stable angina.
2) P2Y12 inhibitors: Clopidogrel, Prasugrel, Ticagrelor, Thienopyridine, Thienopyridine, Triazolopyrimidine.
Inhibitor P2Y12 should be added to aspirin as soon as possible and continued for 12 months, provided there is no risk of increased bleeding.
Clopidogrel(Plavike, Zilt, Plagryl) - a representative of the thienopyridine group, is a powerful antiplatelet agent, the mechanism of action of which is associated with the inhibition of ADP-induced platelet activation due to the blockade of purine receptors P2Y12. Pleiotropic effects of the drug were revealed - anti-inflammatory due to inhibition of the production of platelet cytokines and cell adhesion molecules (CD40L, P-selectin), which is manifested by a decrease in the level of
SRB. The advantages of clopidogrel over aspirin have been proven for long-term use in patients with high and very high risk coronary artery disease - with myocardial infarction, a history of stroke, and diabetes.
Recommended doses. The first dose of the drug (as early as possible!) is 300 mg (4 tablets) orally once (loading dose), then the daily maintenance dose is 75 mg (1 tablet) once a day, regardless of food intake, for 1 to 9 months . The antiplatelet effect develops 2 hours after taking a loading dose of the drug (reduction of aggregation by 40%). The maximum effect (60% suppression of aggregation) is observed on days 4-7 of continuous administration of a maintenance dose of the drug and persists for 7-10 days (platelet life period). Contraindications: individual intolerance; active bleeding; erosive and ulcerative processes in the gastrointestinal tract; severe liver failure; age less than 18 years.
3) Abciximab- antagonist of glycoprotein Ilb/IIIa platelet receptors.
As a result of platelet activation, the configuration of these receptors changes, which increases their ability to fix fibrinogen and other adhesive proteins. The binding of fibrinogen molecules to the Ilb/IIIa receptors of various platelets leads to the connection of the plates with each other - aggregation. This process does not depend on the type of activator and is the final and only mechanism of platelet aggregation
For ACS: intravenous bolus (10-60 minutes before PCI) at a dose of 0.25 mg/kg, then 0.125 mcg/kg/min. (maximum 10 mcg/min.) for 12-24 hours.
When administered intravenously, the steady-state concentration of abciximab is maintained only by continuous infusion; after its cessation, it decreases within
6 hours quickly, and then slowly (over 10-14 days) due to the platelet-bound fraction of the drug.
Anticoagulants
They are able to inhibit the thrombin system and/or its activity, thereby reducing the likelihood of complications associated with thrombosis. There is evidence that anticoagulants are effective in addition to inhibiting platelet aggregation and that the combination is more effective than treatment with one drug alone (Class I, Level A).
The drug with the most favorable profile efficiency - safety is fondaparinux (2.5 mg SC daily) (Class I, Level A).
If fondaparinux or enoxaparin are not available, unfractionated heparin with a target APTT of 50–70 sec or other low molecular weight heparins at specific recommended doses is indicated (Class I, Level C).
Unfractionated heparin (UFH).
When using heparin, it is necessary to measure the activated partial thromboplastin time (aPTT) and maintain it in the therapeutic range - prolongation of the aPTT by 1.5-2.5 times higher than the control. The reference (normal) aPTT value depends on the sensitivity of the reagent used in a given laboratory (usually 40 seconds). Determination of aPTT should be carried out every 6 hours after each change in the dose of heparin and once every 24 hours when the desired aPTT is maintained in two consecutive analyzes. Currently, it is still recommended to administer heparin intravenously using a dispenser - around the clock, along with aspirin under careful monitoring of the platelet count in the blood serum. Discontinuation of treatment—stabilization of angina (no angina attacks).
Basic side effect- bleeding. Possible allergic reactions, with long-term use - thrombocytopenia.
They reduce myocardial oxygen demand (by reducing heart rate, blood pressure, preload and myocardial contractility) and increase myocardial oxygen supply through stimulation of coronary vasodilation.
Anti-ischemic drugs include nitrates, beta blockers and calcium antagonists.