Acute coronary syndrome

In recent years, the term "acute coronary syndrome (ACS)" has become widespread. Acute coronary syndrome includes acute variants of coronary heart disease: unstable angina (UA) and myocardial infarction (MI). Since unstable angina and myocardial infarction are not distinguishable clinically, one of two diagnoses is established during the first examination of the patient, after recording an ECG.

Acute coronary syndrome serves as a preliminary diagnosis, allowing the physician to determine the order and urgency of diagnostic and therapeutic measures. The main purpose of introducing this concept is the need to use active treatment methods (thrombolytic therapy) until the final diagnosis is restored (the presence or absence of a large-focal myocardial infarction).

The final diagnosis of a specific variant of acute coronary syndrome is always retrospective. In the first case, the development of myocardial infarction with a Q wave is very likely, in the second case, unstable angina or the development of myocardial infarction without a Q wave are more likely. Subdivision of acute coronary syndrome into two variants is primarily necessary for the early initiation of targeted treatment measures: in acute coronary syndrome with ST segment elevation, thrombolytics are indicated, and in acute coronary syndrome without ST elevation, thrombolytics are not indicated. It should be noted that during the examination of patients, a "non-ischemic" diagnosis may be revealed, for example, pulmonary embolism, myocarditis, aortic dissection, neurocirculatory dystonia, or even extracardiac pathology, for example, acute abdominal diseases.

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What causes acute coronary syndrome?

The immediate cause of acute coronary syndrome is acute myocardial ischemia, which occurs due to a discrepancy between the supply of oxygen to the myocardium and its need for it. The morphological basis of this discrepancy is most often an atherosclerotic lesion of the coronary arteries with a rupture or splitting of the atherosclerotic plaque, thrombus formation and increased platelet aggregation in the coronary artery.

It is the thrombotic processes at the site of the defect in the surface of the atherosclerotic plaque of the coronary artery that serve as the morphological basis for all types of acute coronary syndrome.

The development of one or another variant of acute ischemic heart disease is determined mainly by the degree, duration and associated structure of thrombotic stenosis of the coronary artery. Thus, at the stage of unstable angina, the thrombus is predominantly platelet - "white". At the stage of myocardial infarction, it is mostly fibrinous - "red".

Conditions such as arterial hypertension, tachyarrhythmia, hyperthermia, hyperthyroidism, intoxication, anemia, etc. lead to an increase in the heart's need for oxygen and a decrease in oxygen supply, which can provoke or aggravate existing myocardial ischemia.

The main causes of acute decrease in coronary perfusion are coronary vessel spasm, thrombotic process against the background of stenosing sclerosis of the coronary arteries and damage to the atherosclerotic plaque, intimal detachment and hemorrhage into the plaque. Cardiomyocytes switch from aerobic to anaerobic metabolism. There is an accumulation of anaerobic metabolism products, which activates peripheral pain receptors of the C7-Th4 segments in the spinal cord. Pain syndrome develops, initiating the release of catecholamines. Tachycardia occurs, shortening the time of diastolic filling of the left ventricle, and further increasing the myocardial oxygen demand. As a result, myocardial ischemia worsens.

Further deterioration of coronary circulation is associated with local impairment of myocardial contractile function and dilation of the left ventricle.

Approximately 4-6 hours after the development of myocardial ischemia, a zone of cardiac muscle necrosis is formed, corresponding to the blood supply zone of the affected vessel. Before this moment, provided that coronary blood flow is restored, it is possible to restore the viability of cardiomyocytes.

How does acute coronary syndrome develop?

Acute coronary syndrome begins with inflammation and rupture of a "vulnerable" plaque. During inflammation, activation of macrophages, monocytes and T-lymphocytes, production of inflammatory cytokines and secretion of proteolytic enzymes are observed. This process is reflected in an increase in the level of acute phase inflammation markers (acute phase reactants) in acute coronary syndrome, for example, C-reactive protein, amyloid A, interleukin-6. As a result, damage to the plaque capsule occurs with subsequent rupture. The concept of the pathogenesis of acute coronary syndrome can be presented in the form of the following sequence of changes:

• inflammation of the "vulnerable" plaque
• plaque rupture
• platelet activation
• vasoconstriction
• thrombosis

The interaction of these factors, progressively increasing, can lead to the development of myocardial infarction or death.

In acute coronary syndrome without ST-segment elevation, a non-occlusive "white" thrombus is formed, consisting mainly of platelets. The "white" thrombus can be a source of microembolism into smaller myocardial vessels with the formation of small foci of necrosis ("microinfarctions"). In acute coronary syndrome with ST-segment elevation, an occlusive "red" thrombus is formed from the "white" thrombus, which consists mainly of fibrin. As a result of thrombotic occlusion of the coronary artery, transmural myocardial infarction develops.

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How does acute coronary syndrome manifest itself?

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Acute coronary syndrome without ST segment elevation

Unstable angina and non-ST-segment elevation myocardial infarction are very similar in nature. The main difference is that the degree and duration of ischemia in non-ST-segment elevation myocardial infarction are sufficient to cause myocardial necrosis.

As a rule, in myocardial infarction without ST segment elevation, there is non-occlusive thrombosis of the coronary artery with the development of necrosis caused by embolism of small myocardial vessels by particles of the coronary thrombus and material from the ruptured atherosclerotic plaque.

Patients with non-ST-elevation acute coronary syndrome with elevated cardiac troponin levels (i.e., patients with non-ST-elevation myocardial infarction) have a worse prognosis (higher risk of complications) and require more aggressive treatment and monitoring.

The electrocardiographic picture is characterized by signs of acute myocardial ischemia without ST segment elevations. As a rule, this is a transient or persistent depression of the ST segment, inversion, smoothing or pseudo-normalization of the T waves. The T wave on the electrocardiogram appears extremely rarely. In some cases, the electrocardiogram may remain normal.

The main sign that allows differentiating myocardial infarction without ST segment elevation from unstable angina is an increase in the levels of myocardial necrosis markers in the blood.

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Acute coronary syndrome with ST segment elevation

The diagnosis of myocardial infarction with ST segment elevation is made in patients with:

• angina attack or its equivalents;
• persistent ST segment elevation;
• or a newly developed or presumably newly developed left bundle branch block on the electrocardiogram (within 6 hours after the onset of the attack);
• increased levels of myocardial necrosis biomarkers (positive troponin test).

The most significant signs when making a diagnosis are: persistent ST segment elevation (at least 20 minutes) and increased levels of myocardial necrosis biomarkers. Such a clinical picture, electrocardiographic and laboratory data indicate that the patient has acute complete thrombotic occlusion of the coronary artery. Most often, when the disease begins as a myocardial infarction with ST segment elevation, a Q wave is subsequently formed.

Depending on the electrocardiographic picture and the results of instrumental examination methods, myocardial infarction can be large-focal, small-focal, Q-wave myocardial infarction and non-Q-wave myocardial infarction.

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Diagnosis of acute coronary syndrome

The diagnosis of acute coronary syndrome is made when there is not yet enough information for a final judgment on the presence or absence of foci of necrosis in the myocardium. This is a working and legitimate diagnosis in the first hours and days from the onset of the disease.

The diagnoses of "myocardial infarction" and "unstable angina" are made when there is enough information to make them. Sometimes this is possible already during the initial examination, when electrocardiography and laboratory test data allow us to determine the presence of necrosis foci. More often, the possibility of differentiating these conditions appears later, then the concepts of "myocardial infarction" and various variants of "unstable angina" are used to formulate the final diagnosis.

The determining criteria for the diagnosis of acute coronary syndrome at the initial stage are the clinical symptoms of an angina attack and the electrocardiography data, which should be performed within the first 10 minutes after the first visit. Subsequently, based on the electrocardiographic picture, all patients are divided into two groups:

• patients with acute coronary syndrome with ST segment elevation;
• patients with acute coronary syndrome without ST segment elevation. This division determines further treatment tactics.

It should be remembered that a normal electrocardiogram in patients with symptoms that give reason to suspect acute coronary syndrome does not exclude it. It should also be taken into account that in young (25-40 years) and elderly (> 75 years) patients, as well as in patients with diabetes mellitus, manifestations of acute coronary syndrome may occur without a typical anginal status.

The final diagnosis is most often made retrospectively. It is practically impossible to predict at the initial stages of the disease's development how the exacerbation of ischemic heart disease will end - stabilization of angina, myocardial infarction, sudden death.

The only method for diagnosing a particular variant of ACS is ECG recording. If ST segment elevation is detected, Q-wave myocardial infarction subsequently develops in 80-90% of cases. Patients without persistent ST segment elevation have ST segment depression, negative T waves, pseudo-normalization of inverted T waves, or no ECG changes (in addition, approximately 10% of patients with ACS without persistent ST segment elevation have episodes of transient ST segment elevation). The probability of Q-wave myocardial infarction or death within 30 days in patients with ST segment depression averages about 12%, with negative T waves - about 5%, and without ECG changes - from 1 to 5%.

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Q-wave myocardial infarction

Myocardial infarction with Q wave is diagnosed by ECG (appearance of Q wave). To detect MI without Q wave, it is necessary to determine markers of myocardial necrosis in the blood. The method of choice is determination of the level of cardiac troponins T or I. In second place is determination of the mass or activity of the MB fraction of creatine phosphokinase (MB CK). A sign of MI is a troponin T level of more than 0.1 μg/l (troponin I - more than 0.4 μg/l) or an increase in MB CK by 2 times or more. In approximately 30% of patients with an increase in the level of troponins in the blood ("troponin-positive" patients), MB CK is within the normal range. Therefore, when using the determination of troponins, a diagnosis of MI will be made in a greater number of patients than when using MB CK. It should be noted that an increase in troponins can also be observed in non-ischemic myocardial damage, for example, in pulmonary embolism, myocarditis, heart failure, and chronic renal failure.

For rational implementation of treatment measures, it is advisable to assess the individual risk of complications (MI or death) in each patient with ACS. The risk level is assessed based on clinical, electrocardiographic, biochemical parameters and response to treatment.

The main clinical signs of high risk are recurrent myocardial ischemia, hypotension, heart failure, and severe ventricular arrhythmias.

ECG: low risk - if the ECG is normal, unchanged or with minimal changes (T wave depression, T wave inversion less than 1 mm deep); intermediate risk - if there is ST segment depression less than 1 mm or negative T waves more than 1 mm (up to 5 mm); high risk - if there is transient ST segment elevation, ST depression more than 1 mm or deep negative T waves.

Troponin T level: less than 0.01 μg/L - low risk; 0.01-0.1 μg/L - intermediate risk; more than 0.1 μg/L - high risk.

The presence of high-risk features is an indication for an invasive treatment strategy.

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Non-Q wave myocardial infarction

The criterion for the diagnosis of non-Q-wave myocardial infarction is the presence of an increase in the level of myocardial necrosis markers: troponins and/or the CPK MB isoenzyme.

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Treatment of acute coronary syndrome without ST segment elevation

The presence of signs of acute coronary syndrome is an indication for hospitalization in the intensive care unit. The patient is admitted to the unit with a diagnosis of "acute coronary syndrome with ST segment elevation" or "acute coronary syndrome without ST segment elevation"), and during treatment, after additional examination, the variant of acute coronary syndrome is determined: unstable angina or myocardial infarction. Patients with acute coronary syndrome with ST segment elevation are indicated for thrombolytic therapy. The main thing in the treatment of acute coronary syndrome is to reduce the likelihood of myocardial infarction and death.

To prevent myocardial infarction, acetylsalicylic acid (aspirin) and heparin are prescribed.

Taking aspirin in doses of 75-325 mg is the main means of preventing myocardial infarction. At the first suspicion of ACS, it is necessary to take aspirin (regular aspirin without enteric coating). The first (loading) dose of aspirin is 325 mg or 500 mg. Aspirin is chewed and washed down with water. The effect of aspirin begins in 20 minutes. Then aspirin is taken at 75-100 mg per day.

Heparin is administered in a dose of 5000 U intravenously by jet stream, then by drip under the control of blood coagulation parameters. Subcutaneous administration of low-molecular heparins can be used instead of regular heparin.

Aspirin is the main treatment for patients with unstable angina. Its use has been shown to reduce the incidence of myocardial infarction by 50%! If there are contraindications to prescribing aspirin, clopidogrel can be used. However, the disadvantage of clopidogrel is that its action occurs slowly (within 2-3 days), so unlike aspirin, it is not suitable for the treatment of acute unstable angina. To some extent, this disadvantage can be compensated for by using a loading dose of clopidogrel at 300 mg, then 75 mg per day. Even more effective is the use of a combination of aspirin and clopidogrel.

In addition to aspirin, clopidogrel and heparin, platelet receptor antagonists (blockers of glycoprotein IIb/IIIa platelet receptors) are used in the treatment of unstable angina: abciximab, tirofiban, eptifibatide. Indications for the use of platelet receptor antagonists are refractory ischemia and/or coronary angioplasty. It has been established that the use of these drugs is most effective in patients with positive troponin test results ("troponin positive"), i.e. in patients with myocardial infarction without a Q wave.

Antianginal treatment

In the presence of pain syndrome and the absence of pronounced hypotension, sublingual administration of nitroglycerin is used. If the effect of nitroglycerin is insufficient, intravenous administration of morphine or other narcotic analgesics is indicated.

The main drugs for the treatment of pain in ACS without ST segment elevation are /2-blockers without intrinsic sympathomimetic activity - it is necessary to urgently reduce the heart rate to 50-60 beats per minute (/9-blockers are the "cornerstone" of ACS treatment). Treatment begins with the prescription of, for example, propranolol 5-10 mg intravenously, then oral administration of 160-320 mg / day, metoprolol - 100-200 mg / day, atenolol - 100 mg / day. If there are contraindications for the prescription of beta-blockers, verapamil, diltiazem, cordarone (intravenously and orally) are used. In case of persistent pain syndrome, intravenous drip administration of nitroglycerin is used (a "protective umbrella" on the first day of unstable angina). The average rate of administration is 200 mcg / min. Systolic blood pressure should not decrease below 100 mm Hg. st., and the heart rate should not increase more than 100 per minute. Instead of nitroglycerin infusion, it is possible to use isosorbide dinitrate or isosorbide-5-mononitrate preparations, for example, nitrosorbide sublingually at 10-20 mg every 1-2 hours, with an improvement in the condition - a transition to oral administration (up to 40-80 mg every 3-4 hours) or use prolonged forms of nitrates. It should be emphasized that nitrates should be prescribed only according to indications, i.e. if angina or painless ischemia persists, despite the use of beta-blockers, or if there are contraindications for beta-blockers.

Calcium antagonists are used when the combination of nitrates and beta-blockers is insufficient, when there are contraindications for taking beta-blockers, or in vasospastic angina. Verapamil, diltiazem, or prolonged forms of dihydropyridine calcium antagonists, such as amlodipine, are used.

Short-acting dihydropyridine calcium antagonists are not recommended.

All patients benefit from tranquilizers, such as diazepam (Relanium), 1 tablet 3-4 times a day.

During the transportation of a patient with ACS, the emergency physician must relieve pain, administer aspirin, heparin (regular unfractionated heparin intravenously or low molecular weight heparin subcutaneously) and beta-blockers.

In most patients (approximately 80%), it is possible to achieve cessation of recurrent angina within a few hours. Patients who fail to achieve stabilization within 2 days are recommended to undergo coronary angiography to assess the possibility of surgical treatment. Many researchers believe that patients with unstable angina, even with a good effect of drug treatment, after stabilization of the condition are recommended to undergo coronary angiography to determine the prognosis and clarify the tactics of further management.

Thus, acute coronary syndrome without ST segment elevation is treated with such drugs as: aspirin (+ clopidogrel) + heparin + beta-blockers. In case of refractory or recurrent myocardial ischemia, nitroglycerin and platelet receptor blockers are used. This is the so-called "conservative strategy" of treatment. If invasive interventions are possible, it is advisable for patients with an increased risk to use an "invasive strategy" of treatment, i.e. early coronary angiography followed by revascularization: coronary angioplasty or coronary bypass surgery. In addition to conventional therapy, patients who are planned to undergo revascularization are prescribed platelet receptor blockers.

After the condition has stabilized for 24 hours, they switch to taking medications orally (“non-intensive phase” of managing patients with acute coronary syndrome).

In addition to prescribing antiplatelet, antithrombotic and antianginal drugs to all patients with acute coronary syndrome, in the absence of contraindications, it is recommended to prescribe statins and ACE inhibitors.

Of interest are reports on the possible role of infectious agents, in particular Chlamydia pneumoniae, in the development of acute coronary syndromes. Two studies have noted a decrease in mortality and the incidence of myocardial infarction with treatment with macrolide antibiotics (azithromycin and roximycin).

Risk assessment is an ongoing process. Two days after stabilization, patients with non-ST-segment elevation acute coronary syndrome and low or intermediate risk are recommended to undergo exercise testing. High-risk indicators include inability to achieve a stress level greater than 6.5 METs (approximately 100 W) in combination with ECG evidence of myocardial ischemia.

Acute coronary syndrome with ST-segment elevation is treated to achieve the fastest possible restoration of vessel lumen and myocardial perfusion in the affected area by thrombolytic therapy, percutaneous angioplasty, or coronary artery bypass grafting.

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