Acute Coronary Syndrome

In recent years, the term "acute coronary syndrome (ACS)." The acute coronary syndrome includes acute variants of IHD: unstable angina (NS) and myocardial infarction (MI). Since unstable angina and myocardial infarction are not distinguishable at the clinic, at the first examination of the patient, after ECG recording, one of two diagnoses is established.

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

The final diagnosis of a specific variant of acute coronary syndrome is always retrospective. In the first case, myocardial infarction with Q wave is very likely, in the second case, unstable angina or development of myocardial infarction without Q wave is more likely. The division of acute coronary syndrome into two options is primarily necessary for an early onset of targeted therapeutic measures: in acute coronary syndrome with elevation the ST segment shows the appointment of thrombolytics, and in acute coronary syndrome without ST elevation, thrombolytics are not shown. It should be noted that in the process of examining patients, a “non-ischemic” diagnosis can be identified, for example, pulmonary embolism, myocarditis, aortic dissection, neurocirculatory dystonia, or even extracardiac pathology, for example, acute diseases of the abdominal cavity.

[1], [2], [3],

What causes acute coronary syndrome?

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

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

The development of one or another variant of the acute form of coronary heart disease is determined mainly by the degree, duration and the associated structure of the thrombotic narrowing of the coronary artery. So, at the stage of unstable angina, the thrombus is predominantly platelet - “white”. At the stage of myocardial infarction, it is more fibrin - “red”.

Such conditions as arterial hypertension, tachyarrhythmia, hyperthermia, hyperthyroidism, intoxication, anemia, etc. Lead to an increase in heart demand for oxygen and a decrease in oxygen supply, which can provoke or aggravate the existing myocardial ischemia.

The main causes of acute reduction of coronary perfusion are spasm of the coronary vessels, a thrombotic process against the background of stenotic sclerosis of the coronary arteries and damage to atherosclerotic plaque, intima detachment and hemorrhage into the plaque. Cardiomyocytes switch from aerobic to anaerobic metabolic pathway. There is an accumulation of anaerobic metabolism products, which activates the peripheral pain receptors of the C7-Th4 segments in the spinal cord. Pain develops, initiating the release of catecholamines. There is tachycardia, shortening the time of diastolic filling of the left ventricle, and even more increasing myocardial need for oxygen. As a result, myocardial ischemia worsens.

Further deterioration of the coronary circulation is associated with a local violation of the contractile function of the myocardium and dilatation of the left ventricle.

Approximately in 4-6 hours from the moment of development of myocardial ischemia, a zone of necrosis of the heart muscle is formed, corresponding to the blood supply zone of the affected vessel. Until this point occurs, the viability of cardiomyocytes may be restored, provided coronary blood flow is restored.

How does acute coronary syndrome develop?

Acute coronary syndrome begins with inflammation and rupture of a “vulnerable” plaque. At inflammation, activation of macrophages, monocytes and T-lymphocytes, production of inflammatory cytokines and secretion of proteolytic enzymes are observed. The reflection of this process is an increase in acute coronary inflammation (acute phase reactants), for example, C-reactive protein, amyloid A, and interleukin-6, in acute coronary syndrome. As a result, the plaque capsule is damaged, followed by rupture. The idea of the pathogenesis of acute coronary syndrome can be represented as 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. A "white" thrombus can be a source of microemboli in smaller myocardial vessels with the formation of small foci of necrosis ("microinfarction"). 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.

[4], [5], [6], [7], [8]

How does acute coronary syndrome manifest?

[9], [10], [11], [12],

Acute coronary syndrome without ST elevation

Unstable angina and myocardial infarction without ST elevation are very similar in nature. The main difference is that the degree and duration of ischemia in myocardial infarction without ST-segment elevation are sufficient for the development of cardiac muscle necrosis.

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

Patients with acute coronary syndrome without ST elevations with elevated levels of cardiac troponins (that is, patients with myocardial infarction without ST elevations) have a worse prognosis (higher risk of complications) and need more active methods of treatment and observation.

The electrocardiographic pattern is characterized by signs of acute myocardial ischemia without ST segment elevations. As a rule, it is a transient or persistent depression of the ST segment, inversion, smoothness or pseudonormalization of the teeth of T. The T tooth on the electrocardiogram is extremely rare. In some cases, the electrocardiogram may remain normal.

The main symptom that allows to differentiate myocardial infarction without elevating the ST segment from unstable angina pectoris is an increase in the levels of myocardial necrosis markers in the blood.

[13], [14], [15], [16], [17], [18],

Acute coronary syndrome with ST elevation

The diagnosis of myocardial infarction with ST-segment elevation "set" patients with:

• an anginal attack or its equivalents;
• persistent rise of the ST segment;
• or a blockade of the left leg of the His bundle on the electrocardiogram that first arose or presumably first appeared (within 6 hours after the onset of an attack);
• increased levels of biomarkers of myocardial necrosis (positive troponin test).

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

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

[19], [20], [21], [22],

Diagnosis of acute coronary syndrome

The diagnosis of acute coronary syndrome is made when there is still insufficient 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 of the onset of the disease.

The diagnoses of “myocardial infarction” and “unstable angina pectoris” are made when there is enough information to put it on. Sometimes this possibility is already at the initial examination, when the data of electrocardiography and laboratory tests allow to determine the presence of necrosis foci. More often, the possibility of differentiation of these states appears later, then the concepts of “myocardial infarction” and various variants of “unstable angina pectoris” are used in formulating the final diagnosis.

The defining criteria for the diagnosis of acute coronary syndrome at the initial stage are the clinical symptoms of an anginal seizure and electrocardiography data, which must be performed within the first 10 minutes after the first treatment. Further, 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 the further tactics of therapy.

It should be remembered that a normal electrocardiogram in patients with symptoms that give rise to suspect acute coronary syndrome does not exclude it. It should also be borne in mind that in young (25–40 years) and elderly (> 75 years) patients, as well as diabetic patients, manifestations of acute coronary syndrome can occur without typical anginal status.

The final diagnosis is often made retrospectively. It is almost impossible to predict the initial stages of the development of the disease and how the exacerbation of coronary heart disease will end - stabilization of angina pectoris, myocardial infarction, sudden death.

The only method for diagnosing any variant of ACS is ECG recording. When ST elevation is detected, myocardial infarction with a Q wave subsequently develops in 80-90% of cases. In patients without a persistent ST segment elevation, ST segment depression, negative T teeth, pseudonormalization of inverted T teeth or ECG changes are observed (besides, approximately 10% of patients with ACS without sustained ST elevation occur episodes of transient ST elevation. The probability of myocardial infarction with Q wave or death for 30 days in patients with ST segment depression averages about 12%, with registration of negative T teeth - about 5%, in the absence of ECG changes - from 1 to 5%.

[23], [24], [25], [26], [27],

Q wave myocardial infarction

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

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

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

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

The level of troponin T: 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 signs of high risk is an indication for an invasive treatment strategy.

[28], [29], [30], [31], [32]

Myocardial infarction without Q wave

The criterion for the diagnosis of myocardial infarction without Q wave is the presence of increased levels of markers of myocardial necrosis: troponins and / or isoenzyme KFK MB.

[33], [34], [35], [36], [37],

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 enters the unit with a diagnosis of "acute coronary syndrome with ST segment elevation" or "acute coronary syndrome without ST segment elevation"), and in the process of treatment, after additional examination, determine the option of acute coronary syndrome: unstable angina or myocardial infarction. Patients with acute coronary syndrome with ST-segment elevation are shown to have thrombolytic therapy. The main thing in the treatment of acute coronary syndrome is to reduce the likelihood of myocardial infarction and death.

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

Acceptance of aspirin in doses of 75-325 mg is the primary means for 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 chew and drink water. The effect of aspirin begins within 20 minutes. Next, take aspirin 75-100 mg per day.

Heparin is prescribed in a dose of 5000 IU in / in the jet, then drip under the control of blood clotting indicators. Instead of conventional heparin, subcutaneous administration of low molecular weight heparins can be used.

Aspirin is the primary treatment for patients with unstable angina. With its use, there is a decrease in the incidence of myocardial infarction by 50%! If there are contraindications for the appointment of aspirin, you can use bedcloth. However, a disadvantage of clopidogrel is that its action occurs slowly (within 2-3 days), therefore, unlike aspirin, it is not suitable for the treatment of acute unstable angina. To some extent, this disadvantage can be compensated by using a loading dose of clopidogrel of 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, in the treatment of unstable angina pectoris, platelet receptor antagonists (blockers of glycoprotein IIb / IIIa platelet receptors) are used: abciximab, tirofiban, eptifibatid. 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 results of the troponin test (“troponin-positive”), i.e. In patients with myocardial infarction without Q wave.

Antianginal treatment

In the presence of pain and in the absence of severe hypotension, sublingual nitroglycerin is used. With a lack of effect of nitroglycerin shown in / in the introduction of morphine or other narcotic analgesics.

The main drugs for the treatment of pain in ACS without ST-segment elevation are / 2-blockers without internal symptomatic activity — an urgent decrease in heart rate to 50-60 min. (/ 9-blockers are the "cornerstone" of ACS treatment). Treatment begins with the appointment, for example, propranolol 5-10 mg IV, then ingestion 160-320 mg / day, metoprolol - 100-200 mg / day, atenolol - 100 mg / day. In the presence of contraindications for the appointment of beta-blockers use verapamil, diltiazem, cordarone (intravenously and inside). In case of persistent pain syndrome, intravenous drip of nitroglycerin is used (“protective umbrella” on the first day of unstable angina). The average injection rate is 200 µg / min. Systolic blood pressure should not fall below 100 mm Hg. Art., and the heart rate should not rise more than 100 per minute. Instead of nitroglycerin infusion, you can use isosorbid dinitrate or isosorbide-5-mononitrate, for example, nitrosorbid under the tongue, 10-20 mg every 1-2 hours, while improving, go to oral administration (up to 40-80 mg after 3-4 h) or use prolonged forms of nitrates. It should be emphasized that nitrates should be prescribed only according to indications, i.e. While maintaining angina or painless ischemia, despite the use of beta-blockers, or if there are contraindications for beta-blockers.

Calcium antagonists are used with insufficient effect of the combination of nitrates and beta-blockers, if there are contraindications for taking beta-blockers or for vasospastic angina. Use verapamil, diltiazem or prolonged forms of dihydropyridine calcium antagonists, such as amlodipine.

Short-acting dihydropyridine calcium antagonists are not recommended.

The appointment of tranquilizers is useful for all patients, for example, diazepam (Relanium) in 1 tab. 3-4 times a day.

An ambulance doctor during the process of transporting a patient with ACS should stop pain, give aspirin, enter heparin (normal unfractionated IV intravenous heparin or low-molecular-weight heparin subcutaneously) and beta-blockers.

In the majority of patients (approximately 80%), it is possible to achieve the cessation of recurrence of angina pectoris within a few hours. Patients who fail to achieve stabilization within 2 days, a coronary angiography is shown 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, coronary angiography is shown in order to determine the prognosis and refine the tactics of further management.

Thus, acute coronary syndrome without ST-segment elevation is treated with drugs such as: aspirin (+ clopidogrel) + heparin + beta-blockers. In 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 for patients with an increased risk, it is desirable to use an “invasive strategy” of treatment, i.e. Early coronary angiography followed by revascularization: coronary angioplasty or coronary artery bypass surgery. Patients who are planned revascularization, in addition to conventional therapy, are assigned platelet receptor blockers.

After stabilization of the state within 24 hours, they switch to ingestion of drugs (“non-intensive phase” of management of patients with acute coronary syndrome).

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

Of interest are reports on the possible role of infectious agents, in particular, chlamydia pneumonie in the occurrence of acute coronary syndromes. In two studies, a decrease in mortality and the incidence of myocardial infarction was observed during antibiotic treatment with macrolides (azithromycin and roximycin).

Risk assessment is a continuous process. Two days after stabilization, patients with acute coronary syndrome without ST-segment elevation and low or intermediate risk level are recommended to conduct an exercise test. Signs of high risk are inability to achieve a load level of more than 6.5 MET (approximately 100 W) in combination with signs of myocardial ischemia on an ECG.

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

[38], [39], [40], [41], [42], [43], [44], [45], [46], [47], [48], [49]