Myocardial infarction: diagnosis

Myocardial infarction should be assumed in men over the age of 30 and women over 40 years of age (in patients with diabetes mellitus - at a younger age) if the leading symptom is chest pain or discomfort. Pain must be differentiated from pain in pneumonia, pulmonary embolism, pericarditis, rib fracture, esophageal spasm, acute aortic dissection, renal colic, spleen infarction, or various abdominal diseases. In patients with a pre-diagnosed hernia, peptic ulcer, or gall bladder pathology, the clinician should not attempt to explain the new symptoms solely to these diseases.

At any ACS, the approaches to conducting the patient are the same: they perform the initial and series of ECG, study the activity of cardiospecific enzymes in dynamics, which makes it possible to distinguish unstable angina, HSTHM and STHM. Each reception unit should have a diagnostic system for the immediate identification of patients with chest pain for the purpose of their urgent examination and ECG. They also perform pulse oximetry and chest X-ray examination (primarily to identify the expansion of the mediastinum, which is evidence in favor of aortic dissection).

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Electrocardiography

ECG is the most important study that must be performed within 10 minutes after receiving the patient. ECG is a key point in determining tactics, since the introduction of fibrinolytic drugs benefits patients with STHM, but may increase the risk in patients with HSTHM.

In patients with STHM, the initial ECG is usually diagnostic, as it demonstrates a segment elevation> 1 mm in two or more adjacent leads reflecting the localization of the affected area. The pathological prong is not necessary for the diagnosis. The electrocardiogram should be read carefully, since the segment elevation may be small, especially in the lower leads (II, III, aVF). Sometimes the doctor's attention is mistakenly focused on leads where there is a decrease in the segment. In the presence of characteristic symptoms, the segment elevation has a specificity of 90% and a sensitivity of 45% for the diagnosis of myocardial infarction. A sequential analysis of a series of ECG data (performed on the first day every 8 hours, daily) can reveal the dynamics of changes with a gradual reverse development or the appearance of pathological teeth, which allows confirming the diagnosis within a few days.

Since non-transfural myocardial infarction usually occurs in the subendocardial or intramural layer, it is not accompanied by the appearance of diagnostic teeth or significant segment elevations. Typically, such myocardial infarctions are characterized by various changes in the ST-T segment , which are less significant, variable or uncertain and sometimes interpreted with difficulty (HSTHM). If such changes improve somewhat (or worsen) with repeated ECG, ischemia is likely. However, when repeated ECG data remain unchanged, the diagnosis of acute myocardial infarction is unlikely, and if clinical data are maintained in favor of myocardial infarction, other criteria for diagnosis should be used. A normal electrocardiogram obtained from a patient without pain does not exclude unstable angina; a normal electrocardiogram recorded against a background of pain syndrome, although it does not exclude angina, indicates the likelihood of another cause of pain.

If the right ventricle is suspected of myocardial infarction, an ECG in 15 leads is usually performed; additional exhaust recorded in V ₄ R u (for the detection of myocardial infarction adjustable) to V ₈ and V ₉.

ECG diagnostics of myocardial infarction is more difficult if there is a left bundle branch block, as the ECG data resemble the changes characteristic of STHM. Segment elevation , a concordant QRS complex, supports myocardial infarction, as does the rise of a more than 5 mm segment in at least two thoracic leads. In general, any patient with clinical signs of myocardial infarction and the appearance of a blockade of the left leg of the bundle of His (or if it was not known about her presence before this episode) receives treatment as a patient with STHM.

ECG with myocardial infarction with a Q

Large-scale changes. The electrocardiogram is diagnosed with myocardial infarction with Q-wave, determines the stage of myocardial infarction and localization of large-scale changes.

The pathological tooth Q in most cases begins to form after 2 hours and is fully formed within 12-24 hours. In some patients, the pathological Q tooth is formed within one hour after the onset of symptoms of myocardial infarction. Pathological Q is considered to be a 0.04-cm wide or more (or 0.03 s if its depth is more than 1/3 of the R-wave) or QS complex. In addition, any, even a "tiny" tooth Q (q) is considered pathological if it is registered in the thoracic leads V1-V3 or in the lower leads (II, III, aVF) - complexes of the qrS type. The American College of Cardiologists suggested that the Q-wave denticles with a width of 0.03 s and more and a depth of 1 mm or more, as well as any Q in leads V1-V3, should be considered a sign of a heart attack. The appearance of the left bundle branch block is classified as an "indeterminate type of MI" (ACC, 2001).

Localization of large-scale changes

It is accepted to distinguish 4 main localizations of the infarct: anterior, lateral, inferior and posterior. Myocardial infarction of the lower localization is sometimes called posterior or posterior diaphragmatic, and the posterior infarct is also called the posterior basal or "true posterior".

If large-scale ECG changes are recorded in leads V1-4 - diagnose an anteroposterior infarction, if in leads I, aVL, V5-6 - lateral (if large-scale changes are recorded only in the lead aVL - talk about "high lateral infarction"), with changes in the lower leads II, III, aVF - lower infarction. The posterior (or posterior-basal) myocardial infarction is recognized by the reciprocal changes in the leads V1-2 - all "inverted" ("inverted MI"): instead of Q - the increase and broadening of the R wave, instead of the ST segment elevation, the ST segment depression, instead of the negative T wave - a positive T wave. Additional value in the detection of direct ECG signs of posterior myocardial infarction (Q teeth) is recorded in the rear leads V8-V9 (on the left along the scapula and paravertebral line). In most cases, patients with a posterior localization infarction simultaneously develop a lower or lateral infarction, often with the involvement of the right ventricle. Isolated posterior infarction is a rare phenomenon.

Among the listed localizations of myocardial infarction, it is most difficult to detect changes in posterior and high lateral localization. Therefore, in the absence of obvious ECG changes in a patient with suspected myocardial infarction, it is necessary first of all to exclude the presence of signs of a heart attack of precisely these localizations (changes in leads V1-2 or aVL).

In patients with large-focal infarction of the lower localization, right heart ventricular infarction is quite often (up to 50%), and in 15% of them the hemodynamically significant right ventricular myocardial infarction (signs of right ventricular failure, hypotension, shock, degree). Sign of involvement of the right ventricle is the rise of the ST segment in lead VI in a patient with a lower infarction. To confirm the presence of a right ventricular infarction, it is necessary to register the ECG in the right thoracic leads VR4-VR6 - lifting the ST segment by 1 mm or more is a sign of right ventricular involvement. It should be noted that the rise of the ST segment in the right thoracic leads is not long - about 10 hours.

As already noted, an accurate definition of lesion localization in infarction without a Q-wave on the ECG is impossible, because Depression of the ST segment or negative T wave does not reflect localization of ischemia or small-focal myocardial necrosis. Nevertheless, it is customary to note the localization of ECG changes (anteroposterior, lower or lateral) or simply indicate the ECG leads in which these changes are recorded. In 10-20% of patients with non-Q-wave infarction, the ST segment is elevated in the early phase. In these cases, the localization of myocardial infarction can be more or less accurately determined (ST depression and / or T wave inversion are usually observed after this).

The duration of ECG changes in MI without a Q wave can be any - from several minutes or hours to several weeks or months.

[2], [3], [4], [5], [6], [7],

Cardiospecific markers

Cardiospecific markers are myocardial enzymes (for example, CK-MB) and cell components (eg, troponin I, troponin T, myoglobin) that go to the blood after necrosis of the myocardial cell. Markers appear at different times after damage, and their number decreases in varying degrees. Usually several different markers are examined at regular intervals, often every 6-8 hours for 1 day. Newer tests performed directly at the patient's bed are more convenient; they are also sensitive when performed at shorter intervals (for example, at the time of admission, and then at 1.3 and 6 hours).

The criterion for establishing the diagnosis of myocardial infarction is the detection of an increase in the level of biochemical markers of myocardial necrosis. However, elevated levels of markers of myocardial necrosis begin to be detected only 4-6 hours after the onset of myocardial infarction and therefore usually their determination is carried out after hospitalization of the patient. Moreover, at the pre-hospital stage there is no need to identify signs of myocardial necrosis, because this does not affect the choice of therapeutic measures.

The main marker for the onset of myocardial necrosis is an increase in the level of cardiac troponins T ("ti") and I ("ay"). An increase in the level of troponins (and subsequent dynamics) is the most sensitive and specific marker of myocardial infarction (myocardial necrosis) in clinical manifestations corresponding to the presence of acute coronary syndrome (an increase in the level of troponins can also occur with damage to the myocardium of non-ischemic etiology: myocarditis, PE, heart failure, CRF).

The determination of troponins allows the detection of myocardial damage in about one third of patients with myocardial infarction who do not have an increase in MB CK. Elevation of troponins begins 6 hours after the development of myocardial infarction and remains elevated for 7-14 days.

"Classic" marker of myocardial infarction is an increase in activity or an increase in the mass of the isoenzyme MB CKK ("cardiospecific" isoenzyme of creatine phosphokinase). Normally, the activity of MB CK is not more than 3% of the total activity of CKK. With myocardial infarction there is an increase of MB CK by more than 5% of the total CK (up to 15% or more). A reliable intravital diagnosis of small-focal myocardial infarction became possible only after the introduction into clinical practice of methods for determining the activity of MB CK.

Less specific is the change in the activity of LDH isoenzymes: an increase in the activity of predominantly LDH1, an increase in LDH1 / LDH2 ratio (more than 1.0). An earlier diagnosis allows the determination of CK isoforms. The maximum increase in activity or increase in the mass of CK ("peak CK") is observed on the first day of myocardial infarction, after which there is a decrease and return to the baseline level.

Determination of the activity of LDH and its isoenzymes is indicated with late admission of patients (24 hours or more). The LDH peak is observed on day 3-4 of the IM. In addition to increasing the activity or mass of enzymes in myocardial infarction, there is an increase in myoglobin content. Myoglobin is the earliest (in the first 1-4 hours), but a nonspecific marker of myocardial necrosis.

The content of troponins is most reliable for diagnosis of myocardial infarction, but it is possible to increase it with myocardial ischemia without infarction; high figures (actual values depend on the method of determination) are considered diagnostic. Troponin borderline indicators in patients with progressive angina indicate a high risk of adverse events in the future and, thus, the need for further examination and treatment. False positive results are sometimes obtained with cardiac and renal insufficiency. The activity of CK-MB is a less specific indicator. False-positive results occur with renal failure, hypothyroidism and skeletal muscle damage. The amount of myoglobin is an indicator that is not specific for myocardial infarction, however, since its content is increased earlier than other markers, it can be an early diagnostic feature that facilitates diagnosis in uncharacteristic changes in ECG data.

[8], [9], [10], [11], [12], [13], [14], [15],

Echocardiography

Echocardiography is widely used to identify areas of regional contractility. In addition to identifying areas of hypokinesia, akinesia or dyskinesia, the echocardiographic sign of ischemia or infarction is the absence of systolic thickening of the left ventricular wall (or even its sinking during systole). Carrying out of echocardiography allows to reveal signs of a myocardial infarction of a back wall, a myocardium infarction of a right ventricle, to define localization of a myocardial infarction at patients with blockade of the left leg. Very important is the conduct of echocardiography in the diagnosis of many complications of myocardial infarction (rupture of the papillary muscle, rupture of the interventricular septum, aneurysm and left ventricular pseudoaneurism, effusion in the pericardial cavity, detection of thrombi in the cavities of the heart and evaluation of the risk of thromboembolism).

[16], [17], [18], [19], [20], [21], [22], [23],

Other studies

Conventional laboratory tests are not diagnostic, but are able to demonstrate some abnormalities that may occur with tissue necrosis (for example, an increase in ESR, a moderate increase in the number of leukocytes with a shift of the leukocyte formula to the left).

Visualization methods of investigation are not needed for diagnosis, if cardiac-specific markers or ECG data confirm the diagnosis. However, in patients with myocardial infarction, bedside echocardiography is invaluable as a method to detect abnormalities in myocardial contractility. Before discharge from the hospital or shortly thereafter, patients with signs of ACS, but no changes in ECG data and normal cardiospecific markers, perform a stress test with visualization (radioisotope or echocardiographic examination performed against the background of a physical or pharmacological load). The revealed changes in such patients indicate a high risk of complications in the next 3-6 months.

A catheterization of the right heart chambers using a balloon-type pulmonary catheter can be used to measure pressure in the right heart, pulmonary arteries, pulmonary artery wedge pressure and cardiac output. This study is usually performed only if the patient develops serious complications (for example, severe heart failure, hypoxia, arterial hypotension).

Coronarography is most often used for simultaneous diagnosis and treatment (eg, angioplasty, stenting). However, it can be used for diagnostic purposes in patients with signs of ongoing ischemia (by ECG and clinical picture), hemodynamically unstable, with ongoing ventricular tachyarrhythmias and other conditions indicative of recurrence of ischemic episodes.

The formulation of the diagnosis of myocardial infarction

"Myocardial infarction with a Q wave of anterior-septal localization (date of onset of symptoms of myocardial infarction); "Myocardial infarction without a Q wave (date of onset of symptoms)". In the first few days of myocardial infarction, many cardiologists include in the diagnosis the definition of "acute" (a formally acute period of myocardial infarction is 1 month). Specific criteria for acute and subacute periods are defined only for ECG signs of uncomplicated myocardial infarction with a Q wave. After diagnosis of myocardial infarction, complications and concomitant diseases are indicated.