Ministry of health of republic of uzbekistan tashkent medical academy

Acute coronary syndromes without persistent ST elevation RS-T. To the category of acute coronary syndromes without persistent ST elevation RS-T, related patients with chest pain and / or suddenly appearing electrocardiographic changes, indicating acute myocardial ischemia. In ECG ofthese patients, recorded at rest, there may be persistent or transient segment depression of RS-T and / or T-wave inversion, but no persistent elevation of RS-T. In some cases, the ECG can be less changed, while in other cases, by contrast, the diagnosis of this category of acute coronary syndrome can be made in the presence of painless ischemic changes.
On the base of acute myocardial ischemia, patients have formation of wall, mainly platelet ("white"), a blood clot, and as a rule, in the region of the complicated atherosclerotic plaque.Later, in most patients with acute coronary syndromes without persistent ST elevation RS-T may occur either unstable angina or acute myocardial infarction without tooth Q. These two forms of ischemic heart disease (HC and IM without tooth Q) differ in the absence or presence of markers of necrosis (elevated levels of troponin, creatine kinase and creatine kinase MB).
It is found that patients with acute coronary syndromes without persistent ST elevation RS-T, use of thrombolytic therapy is ineffective. Treatment of such patients should be directed at addressing the severity of myocardial ischemia and prevent further blood clots.
The main goal of treatment of patients with acute coronary syndromes without persistent ST elevation RS-T, which is then transformed into the NS, is to reduce the risk of myocardial infarction and sudden death, and reduce the impact of common acute ischemic myocardium (rhythm and conduction disturbances, heart failure progression, etc.). According to the recommendations of the European Society of Cardiology (2000) and the Russian expert committee recommendations of GFCF (2001), for this goal, may be used the following medication and non-medication effects.
1. Anti-ischemic (antianginal) PM:
• β-blockers;
• nitrates;
• Calcium channel blockers slow.
2. Antithrombin agents:
• heparins (unfractionated and low molecular weight);]
• direct thrombin inhibitors.
3. Antiplatelet agents:
• aspirin;
• adenosine receptor antagonists (thienopyridines);
• blockers, glycoprotein IIb / IIIa receptor inhibitors.
4. Coronary revascularization:
• transluminal coronary angioplasty;
• coronary artery bypass surgery.
Treatment of patients with the following methods should be started immediately, as soon as the clinical data and results of ECG - study alone gives impression of presence of acute coronary syndromes without persistent ST elevation RS-T (the most typical of the NS) and a clinical assessment of the risk of myocardial infarction and sudden death. In the resumption of attacksof pain, shownusage of nitroglycerin, including intravenously, if necessary - the use of intravenous β-blockers and narcotic analgesics.

It should be emphasized that in acute coronary syndrome without persistent ST elevation RS-T, precisely, the vast majority of patients with HC, it is not recommended to use thrombolytic therapy as increasing the risk of bleeding complications, this treatment does not reduce mortality and MI, and according to some data, even increase them. An entirely different approach can be traced on patients with acute coronary syndrome with persistent elevation RS-T or the "new" blockade bundle branch block in which this method of treatment is the method of choice (see section 6.4).

β-blockers. In absence of contradictions, β-blockers are recommended to use in all patients of the NS. The positive effect of using these drugs is primarily based on negative inotropic and chronotropic effects. The decrease of demand in myocardial oxygen and slowing heart rate caused by β-blockers, usually accompanied by a pronounced anti-ischemic effect and id reduces the risk of subsequent myocardial infarctionabout 13%.
Since there is no evidence of greater effectiveness of a β-blocker in the treatment of the NS, the choice of drug should be primarily based on account of the individual clinical situation: the presence of comorbid conditions (hypertension or hypotension, diabetes, lung disease, etc.) available to the patient's symptoms of left ventricular dysfunction, the presence of sinus tachycardia or bradycardia, etc. We note that, on the treatment of UA patients, should be avoided assigning β-blockers in severe acute heart failure associated with bronchial asthma, severe hypotension, sinus bradycardia (<50-55 bpm. Per minute) and AV block II, III and I degree (by at least at P-Q (R)> 0,24 s). Drugs carefully are used for chronic lung disease, and in these cases it is advisable to use short-cardioselective β 1-adrenoceptor antagonists in small doses.
Patients with high risk of myocardial infarction and sudden death (see above), it is shown the intravenous infusion of β-blockers with their subsequent transfer to oral. It should be remembered that in patients with a tendency to spasm SC β-blockers, should be used with great caution and in vasospastic angina Prinzmetal is contraindicated. Β-blockers, which have additional vasodilating properties (carvedilol) are exluded.
Nitrates
Nitrates are used in patients with HC, firstly, in order to hemodynamic unloading of the left ventricle and reduce or relieve symptoms (eg, persistent pain in the heart, shortness of breath and other symptoms of left ventricular failure). In the latter case, nitrates administered parenterally, gradually increasing the dose until the relief of the symptoms of the disease or the side effects (headache, hypotension).
Initial speed of intravenous infusion of nitroglycerin is 10 mcg / min. It then increases to 10 mcg / min every 3-5 minutes until the reaction or changes in blood pressure symptoms. If the pain in the heart and other signs of ischemia decrease or disappear, the rate of increase does not increase the dose. If there is a corresponding reaction in blood pressure, and symptoms of acute myocardial ischemia is saved, then speed of drug increases with big long intervals and under the constant control of blood pressure. Extra care must be in the situation when the systolic blood pressure is below 110 mm Hg. Art. or in patients with high blood pressure - 25% below the baseline. If within 12 hours the pain and other symptoms of myocardial ischemia does not occur, you should try to reduce the dose and begin the use of other medicines of nitrate (ingestion, buccally, transkutanealno), considering the possibility of side effects and contraindications of using nitrates.
Blockers of slow calcium canals.Blockers of slow calcium channels (calcium antagonists) are appointed by the NS of patients with symptomatic objective, because, having vasodilating action (especially the preparations of nifedipine and diltiazem) and reducing myocardial contractility and oxygen demand (verapamil and diltiazem), they do not prevent the development of acute myocardial infarction and reduce mortality of patients with HC. Particularly,there are indicated calcium antagonists in patients with variant angina, vasospasticPrinzmetal, as well as the presence of contraindications to β-blockers (eg, associated with bronchial asthma).
Verapamil and diltiazem are shown in the presence of patients with hyperactivity of CAC, sinus tachycardia and the need to reduce myocardial oxygen demand. Preparations of nifedipine, which have the most pronounced vasodilating action, are indicated for concomitant hypertension and vasospastic angina Prinzmetal. While using calcium antagonists of nifedipine, should be used drugs with prolonged effect, because there is evidence that the systematic use of short-acting drugs nifedipine may be accompanied by an increase in mortality in patients with coronary artery disease.
The main goal of curing patients withNS is to prevent further progression of coronary thrombosis and the development of acute myocardial infarction. Today, for that purpose, there are used several groups of drugs that affect the focal point of the process of thrombosis:
1. Antiplatelet drugs:
• aspirin;
• adenosine receptor antagonists (thienopyridines);
• blockers, glycoprotein IIb / IIIa receptor inhibitors.
2. Antithrombin agents:
• indirect thrombin inhibitors (unfractionated and low-molecular gepariny);
• direct thrombin inhibitors (hirudin, etc.).
Antiplatelet agents
Aspirin.To all the patients of the NS, it is recommended aspirin (acetylsalicylic acid), which is the "gold standard" for antiplatelet therapy. As with stable CHD, it is reasonable to assign low-dose aspirin (75-325 mg daily); because aspirin in this dose inhibits platelet cyclooxygenase, preventing the formation of thromboxane A2, almost not effecting on the metabolism of arachidonic acid in the vascular endothelium and reduces the production of prostacyclin. Patients with acute coronary syndrome should start taking aspirinas early as possible. For example, for the first meeting between emergency doctor and patient or on coming to hospital, along with measures to relief the pain, patients are encouraged to chew one tablet of aspirin, not coated (250-500 mg). Later moving to take aspirin orally 1 time a day (75-325 mg).
Thienopyridines.In intolerance to aspirin, UA patients may be assigned ticlopidine (tiklid) or clopidogrel, in order to effectively suppress the adhesion and aggregation of platelets. They exhibit antagonist of ADP-receptor inhibitors and according to some inhibits IIb / IIIa receptors. Asticlopidine features a large number of side effects, including the occurrence of neutropenia and thrombocytopenia, it is preferably to use clopidogrel, the reception of which is accompanied by a much smaller number of adverse events. It should be remembered that the therapeutic effects of ticlopidine and clopidogrel does not occur at once, recommended early treatment so-called loading doses of these drugs, such as clopidogrel - 300 mg once a day and then taking 75 mg a day.
Since the mechanisms of action of aspirin and clopidogrel are different, it is possible to combine the two drugs, which in patients with HC is differ with high effect in preventing myocardial infarction and sudden death compared with taking aspirin alone. In absence of contradictions, from the first day, for the patients with HC is recommended to use this combination of aspirin and clopidogrel.
Chimes (dipyridamole), having a pronounced effect of antiplatelet, is recommend to use in patients with stable angina I-II FC. Patients with UA and MI chimes are not appointed, although there are reports of the successful use of the drug in some patients with NA.
Blockers of glycoprotein IIb / IIIa receptor inhibitors - is a relatively new group of anti-platelet drugs that prevent the formation of platelet thrombus formation at the final stage of the process. Note that activated IIb / IIIa receptorsof inhibitors interact with the fibrinogen molecule, contributing to the formation of dense platelet clot permeated strands of fibrin. Currently, extensive clinical trials were passed three drugs related to this class of antiplatelet drugs:
• abciximab (monoclonal antibodies to glycoprotein IIb / IIIa receptor inhibitors;
• eptifibatide (a synthetic cyclic peptide);
• tirofibatid (non-peptide selective blocker IIb / IIIa receptor inhibitors).
All three drugs are administered intravenously. Also, there are set up blockers IIb / IIIa receptor of inhibitors for oral use (orbofiban, sibrofiban etc.). Clinical trials of infusion blockers IIb / IIIa receptor of inhibitors have shown that the addition of these drugs to heparin in patients with NA, reduces the risk of myocardial infarction and death from cardiovascular causes. Especially, it is shown their use during coronary angioplasty and coronary artery bypass grafting.
Antithrombin funds
Almost all patients with acute coronary syndrome, including patients with UA, there is the need for antithrombin drugs. They are:
• indirect thrombin inhibitors (unfractionated and low-molecular weight heparin);
• direct thrombin inhibitors (hirudin, etc.).
Unfractionated heparin for many years has been used successfully to treat patients with acute myocardial infarction. It was found that its use was shown in patients with UA. Heparin - a natural anticoagulant factor in the body, produced by the mast cells. Heparin has anticoagulant effect mainly by binding to antithrombin III, which is a natural inhibitor of thrombin. In connecting with heparin, activity of antithrombin increases 700 times, and it inhibits some key activated coagulation factors: IIa, VIIa, Xa, HIa, HIIa. Heparin also increases the activity of lipoprotein lipase, reduces the concentration of cholesterol and LDL, anti-inflammatory, immunosuppressive, and hypoglycemic diuretic effect (VG Kukes). Heparin can reduce CSO by increasing resistance vessels, removes spasm spacecraft. Using large doses can cause thrombocytopenia and leukopenia, increases lymphocytes, monocytes and eosinophils.
In case of NA, heparin is used to prevent further thrombosis of spacecraft. According to the recommendations of the European Society of Cardiology (2000) and GFCF Russian Federation (2001), for the patients with acute coronary syndrome, unfractionated heparin is injected intravenously - first jet, as a bolus dose of 60-80 IU / kg (maximum 5000 U ) followed by long-term (48-72 h) intravenous infusion at a dose of 12-18 IU / kg / h (but no more than 1250 IU / kg / h). APTTshould be usedas a means of control. Heparin dose is adjusted so that at 6 h after the start of APTT, 1.5-2.5 times increased the control (normal) rate of the laboratory and in the future firmly held on these «therapeutic» levels. If this level is determined by the APTT in 2 consecutive measurements, the following measurements can be carried out after 24 hours.
Myocardial infarction (MI) - is ischemic necrosis of the heart muscle that is developed as a result of acute failure of the coronary circulation.
MI is one of the most common causes of death and disability in the population, both in this country and abroad. In the Russian Federation annually infarction occurs in 0.2-0.6% of men aged 40 to 59 years (NA Mazur). In men, the older age group (60-64 g), its incidence is even higher, reaching 1.7% in the year. Women develop MI in 2.5-5 times less often than men, especially in young and middle age, which is usually associated with the later (about 10 years), their development of atherosclerosis. After menopause (age 55-60 years), the difference in incidence between men and women is significantly reduced.
In recent years, incidence of MI, especially among the young and middle age is increased. Despite the widespread reduction in hospital mortality from myocardial infarction, mortality from this disease remains high, reaching 30-50% of the total number of cases. With most of the deaths occur in the prehospital setting.
Modern classification of IM provides its divisions:
• the size and depth of damage to the heart muscle;
• the nature of the disease;
• localization of MI;
• the stage of the disease;
• the presence of complications of MI.
1. According to the magnitude and depth, damage of heart muscle is distinguished by intransmuralandtransmural infarction.
In transmural MI (myocardial infarction tooth Q), necrosis captures the entire thickness of the heart muscle from subendocardial to subepicardial layers miokardaa), or most of it, which is reflected on the surface ECG as a form of pathological Q waves or QS complex in several electrocardiographic leads. Here, the synonym of transmural infarction - "myocardial infarction with tooth Q". Typically, such heart muscle damage is extensive enough and necrosis extended to two or more segments of the left ventricle (macrofocal MI).
When netransmuralnom MI (myocardial infarction without wave Q) necrosis only captures subendocardial or intramural departments of LV and is not accompanied by pathological changes of the complex QRS ("myocardial infarction without wave Q"). For a long time, in our literature, myocardial infarction without wave Q is used with the term "small focal myocardial infarction." Indeed, in most cases without Q-wave myocardial infarction is much smaller in extent than transmural infarction, but often there are cases of extensive subendocardial infarction that span multiple LV segments, but only affects the subendocardial layers of the myocardium.
2. According to the nature of the disease, thereare primary, secondary and recurrent MI.
Primary MI diagnosed in the absence of anamnestic and instrumental signs of myocardial infarction in the past.
Repeated MI is diagnosed when a patient who has documented information on previous MI, there are appeared reliable signs of new foci of necrosis, often formed in the basin of the other satellites in a period exceeding 28 days from the date of previous myocardial infarction.
In repeated MI clinical laboratory and instrumental signs of formation of new foci of necrosis occur in a period of 72 hours (3 days) and 28 days after myocardial infarction, precisely, before the end of the main processes to scarring.
3. According to the localization of MI:
• anteseptal (anteseptulum);
• anterosuperior;
• anterolateral;
• antebasal(high front);
• the prevalence of anterior (septal, apical and lateral);
• posterodiaphragmatic (lower);
• posterolateral;
• posterobasal;
• the prevalence of back;
• right ventricular infarction.
MI often localized in the left ventricle, hitting him front, back, side and / or the interventricular septum (IVS), which depends on the location of the critical stenosis or occlusion of a spacecraft. Poor circulation to LAD may lead to the development of myocardial infarction anteseptulum, tops and much rarer - posterodiaphragmatic(lower) wall of the left ventricle. Cessation of blood flow in the LCA agents is accompanied by the emergence of antebasal, lateral or posterobasalinfarction (occlusion of the distal left main OS). With poor circulation, in the pool of RCA, there may be developedposterodiaphragmatic(with the defeat of the proximal segment) or posterobasalinfarction (occlusion of the distal segment). Isolatedinfarction of right ventricular is relatively rare. Often there is a combination of its various locations.
4. On the stage of the disease are distinguished:
• acute period - up to 2 hours after onset of myocardial infarction;
• acute period - up to 10 days from the onset of MI;
• subacute period - from 10 days to the end of 4-8 weeks;
• postinfarction period - usually after 4-8 weeks.
5. The most common complications of MI are:
• acute left ventricular failure (pulmonary edema);
• cardiogenic shock;
• ventricular and supraventricular arrhythmias;
• conduction abnormalities (CA-blockade, AV block, bundle-branch block, block);
• acute left ventricular aneurysm;
• external and internal ruptures infarction, cardiac tamponade;
• aseptic pericarditis (epistenokarditichesky);
• thromboembolism.
• Physical Examination
• The purpose of the physical examinations of patients with MI is not to establish a diagnosis of MI, which is confirmed in the main data of laboratory and ECG - studies as evaluation of the functional state of the cardiovascular system and the timely diagnosis of serious complications of a heart attack.
Inspection. With the general examination in the first minutes or 1-1.5 hours elapsed from the start of the disease, attention is drawn to marked agitation and restlessness of patients experiencing at this time of great pain. They are trying to change positions or even walk across the room, sit in a chair, lie on the bed in search of provisions, to relieve the suffering. This feature is characteristics of patients with MI, distinguishes them from patients with angina who, during a pain attack as if frozen in place. After the relief of pain stimulation in patients with developing myocardial infarction, usually goes. The exception is the situations with progressive left ventricular failure accompanied suddenly appeared and rapidly increasing shortness of breath and asthma.
On examination, often marked pallor, cold extremities, and severe sweating, indicating the possible development of acute circulatory failure (shock, short-term reflex pain) or the initial clinical manifestation of true cardiogenic shock (see below). In most cases, it is determined by cyanosis of the lips.
Severe cyanosis, orthopnea position in combination with wet finely wheezing in the lower lung and increased respiratory rate indicate the presence of severe left ventricular failure.
Palpation and percussion of the heart. On palpation of the heart, there may be local tenderness in the left precordium. For percussion noticeable expansion of the LV cavity in the acute period of the disease can not be identified. The exception of patients with previous myocardial diseases, accompanied ventricular dilatation (AG, atherosclerotic and myocardial infarction, etc.).
Auscultation of the heart. In the acute period of myocardial infarction in patients can be identified several auscultatory phenomena:
1. Weakening and I muted tones on top associated with a decrease in contractility of the ischemic myocardium.
2. Weakening II tone caused deceleration of early diastolic LV relaxation or reducing the pressure in the aorta. When the pressure in the pulmonary artery, caused by venous congestion in the pulmonary circulation,there is determined accent II tone on the pulmonary artery. Finally, some patients with myocardial infarction and severe atherosclerotic aortic seal can listen accent II tone of the aorta.
3. Sinus tachycardia, which in the first 2-3 hours after the start of MI, shows not the presence of heart failure, but a significant activation of CAC, taking place in the background of painful stress.
4. Sinus bradycardia, sometimes detectable in patients with myocardial infarction is associated, on the contrary, with a predominance of parasympathetic nervous system activity and the inhibition of CA-node automaticity, most often observed in the field of MI posterodiaphragmaticof LV. Additionally, in rarer cases, bradycardia may be caused by CA-lock or AV block II and even III degree.
Arterial pulse and blood pressure. Blood pressure in the first minutes and hours of MI can increase, which is often associated with elevated CAC, high concentrations of catecholamines in the blood that appeared as a result of the pain and emotional stress. The development of acute vascular insufficiency of blood pressure decreases, mainly due to systolic BP. At the same time a decrease in the content, voltage and size of arterial pulse, and its acceleration.
Laboratory confirmation of acute myocardial infarction based on the identification of: 1) non-specific indicator of tissue necrosis and myocardial inflammatory response, 2) hyperenzymemia and 3) increase in the blood levels of myoglobin and troponin.
Non-specific reaction to the occurrence of acute myocardial infarction is associated primarily with the collapse of the muscle fibers, absorption through the breakdown of proteins in the blood and local aseptic inflammation of the heart muscle, mainly in developing peri-infraction zone. The main clinical and laboratory findings that reflect these processes are:
1. Increase in body temperature (from subfebrile figures to 38,5-39 ° C).
2. Leukocytosis, usually not more than 12-15 x 109 / l.
3. Aneozinofiliya.
4. Small stab shift of the blood left.
5. Increased ESR.
All patients with suspected MI with emerging tooth Q, precisely patients with acute coronary syndrome and persistent elevation RS-T, should immediately be taken to the intensive care of specialized cardiology units. Basic therapy, which is implemented in all patients with MI tooth Q, regardless of the presence or absence of certain complications, includes the following:
• relief of pain (analgesia);
• thrombolytic therapy (of course, to the individual indications and contraindications);
• antithrombotic and antiplatelet therapy;
• oxygen therapy;
• use of anti-ischemic drugs;
• ACE inhibitors and angiotensin receptor antagonists II.
Thus, the basic principles of the basic treatment of MI with a tooth Q (treatment of uncomplicated MI) are similar to those in patients with HC.
List of the literature
1. Jeffrey Bender, Kerry Russell, Lynda Rosenfeld, Sabeen Chaudry-Oxford American Handbook of Cardiology, 2011
2. A.Zaza An introduction to cardiac electrophysiology
3.ABC of Interventional Cardiology - Ever D. Grech, 2004
4. Cardiovascular Disease in the Elderly - Wilbert S.Aronow, Jerome L.Fleg,
5.www.vidal.ru /кардиология
6.medlistok.com./infarct.asp
7.health. mail.ru /disease/infarct/