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Myocardial infarction: diagnosis
Medical expert of the article
Last reviewed: 06.07.2025
Myocardial infarction should be suspected in men over 30 years of age and women over 40 years of age (at a younger age in patients with diabetes mellitus) if the leading symptom is chest pain or discomfort. The pain should be differentiated from pain due to pneumonia, pulmonary embolism, pericarditis, rib fracture, esophageal spasm, acute aortic dissection, renal colic, splenic infarction, or various abdominal diseases. In patients with a previously diagnosed hernia, peptic ulcer, or gallbladder pathology, the clinician should not attempt to explain new symptoms solely by these diseases.
For any ACS, the approaches to patient management are the same: perform an initial and serial ECG, study the activity of cardiac-specific enzymes in dynamics, which allows us to differentiate unstable angina, HSTHM and STHM. Each emergency department should have a diagnostic system for the immediate identification of patients with chest pain for their urgent examination and ECG. Pulse oximetry and chest X-ray are also performed (primarily to detect mediastinal widening, indicating aortic dissection).
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Electrocardiography
ECG is the most important investigation and should be performed within 10 minutes of admission. ECG is a key moment in determining the tactics, since the administration of fibrinolytic drugs brings benefit to patients with STHM, but may increase the risk in patients with HSTHM.
In patients with STHM, the initial ECG is usually diagnostic because it shows segment elevation > 1 mm in two or more contiguous leads that represent the location of the lesion. An abnormal wave is not necessary for diagnosis. The ECG must be read carefully because the segment elevation may be small, especially in the inferior leads (II, III, aVF). Sometimes the physician's attention is mistakenly focused on leads that show segment depression. In the presence of characteristic symptoms, segment elevation has a specificity of 90% and a sensitivity of 45% for the diagnosis of myocardial infarction. Serial analysis of the ECG series (performed every 8 hours on the first day, then daily) allows one to identify the dynamics of changes with their gradual reverse development or the appearance of abnormal waves, which allows one to confirm the diagnosis within a few days.
Because nontransmural myocardial infarction usually occurs in the subendocardial or intramural layer, it does not produce diagnostic waves or significant segment elevations. Typically, such myocardial infarctions are characterized by various ST-T changes that are less significant, variable, or uncertain and sometimes difficult to interpret (HSTHM). If such changes improve (or worsen) somewhat with repeat ECGs, ischemia is likely. However, when repeat ECGs remain unchanged, the diagnosis of acute myocardial infarction is unlikely, and if clinical findings suggestive of myocardial infarction persist, other criteria for making the diagnosis must be used. A normal ECG in a patient without pain does not exclude unstable angina; A normal electrocardiogram recorded against the background of pain syndrome, although it does not exclude angina, indicates the likelihood of another cause of pain.
If right ventricular myocardial infarction is suspected, a 15-lead ECG is usually performed; additional leads are recorded in V 4 R and (to detect posterior myocardial infarction) in V 8 and V 9.
ECG diagnosis of MI is more difficult if left bundle branch block is present because the ECG findings resemble those of STHM. Segment elevation concordant with the QRS complex is suggestive of MI, as is segment elevation of more than 5 mm in at least two precordial leads. In general, any patient with clinical features suggestive of MI and the development of left bundle branch block (or if it was not known to be present before the event) is treated as a patient with STHM.
ECG in myocardial infarction with Q wave
Large-focal changes. The ECG is used to diagnose myocardial infarction with a Q wave, determine the stage of myocardial infarction and localize large-focal changes.
Pathological Q wave in most cases begins to form after 2 hours and is fully formed within 12-24 hours. In some patients, pathological Q wave forms within one hour after the onset of myocardial infarction symptoms. A Q wave with a width of 0.04 s or more (or 0.03 s if its depth is more than 1/3 of the R wave) or a QS complex is considered pathological. In addition, any, even a "tiny" Q wave (q) is considered pathological if it is recorded in the chest leads V1-V3 or in the inferior leads (II, III, aVF) - qrS complexes. The American College of Cardiologists proposed to consider Q waves with a width of 0.03 s or more and a depth of 1 mm or more, as well as any Q in leads V1-V3, as a sign of infarction. The occurrence of left bundle branch block is classified as “unspecified type of MI” (ACC, 2001).
Localization of large focal changes
It is customary to distinguish 4 main localizations of infarction: anterior, lateral, inferior, and posterior. Myocardial infarction of inferior localization is sometimes called posterior or posterior diaphragmatic, and posterior infarction is also called postero-basal or "true posterior".
If large-focal ECG changes are recorded in leads V1-4, an anterior-septal infarction is diagnosed; if in leads I, aVL, V5-6, a lateral infarction is diagnosed (if large-focal changes are recorded only in lead aVL, they speak of a “high lateral infarction”); with changes in the lower leads II, III, aVF, an inferior infarction is diagnosed. Posterior (or posterobasal) myocardial infarction is recognized by reciprocal changes in leads V1-2 - everything is "inverted" ("inverted MI"): instead of Q - an increase and widening of the R wave, instead of an elevation of the ST segment - depression of the ST segment, instead of a negative T wave - a positive T wave. Of additional importance in identifying direct ECG signs of posterior myocardial infarction (Q waves) is the registration of posterior leads V8-V9 (on the left along the scapular and paravertebral lines). In most cases, patients with posterior infarction simultaneously develop an inferior or lateral infarction, often involving the right ventricle. Isolated posterior infarction is a rather rare phenomenon.
Among the listed localizations of myocardial infarction, the most difficult to detect are changes in the 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 infarction in these localizations (changes in leads V1-2 or aVL).
Patients with large-focal inferior infarction often (up to 50%) also have right ventricular infarction, with 15% of them having hemodynamically significant right ventricular MI (signs of right ventricular failure, hypotension, shock, and grade II-III AV block developing much more often). A sign of right ventricular involvement is ST segment elevation in lead VI in a patient with inferior infarction. To confirm the presence of right ventricular infarction, it is necessary to record an ECG in the right chest leads VR4-VR6 - an ST segment elevation of 1 mm or more is a sign of right ventricular involvement. It should be noted that the ST segment elevation in the right chest leads does not last long - about 10 hours.
As already noted, it is impossible to accurately determine the localization of the lesion in non-Q-wave MI using ECG, since ST segment depression or negative T waves do not reflect the localization of ischemia or focal myocardial necrosis. However, it is customary to note the localization of ECG changes (anteroseptal, inferior, or lateral) or simply indicate the ECG leads in which these changes are recorded. In 10-20% of patients with non-Q-wave MI, ST segment elevation is observed in the early phase - in these cases, it is possible to more or less accurately determine the localization of myocardial infarction (after which ST segment depression and/or T wave inversion are usually observed).
The duration of ECG changes in MI without a Q wave can be anything from several minutes or hours to several weeks or months.
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Cardiac specific markers
Cardiac markers are myocardial enzymes (eg, CK-MB) and cellular components (eg, troponin I, troponin T, myoglobin) that are released into the circulation after myocardial cell necrosis. Markers appear at different times after injury and decline to different degrees. Several different markers are typically measured at intervals, usually every 6 to 8 hours for 1 day. Newer point-of-care tests are more convenient and sensitive when done at shorter intervals (eg, at presentation 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 myocardial necrosis markers begin to be determined only 4-6 hours after the onset of myocardial infarction and therefore they are usually determined after the patient is hospitalized. Moreover, at the prehospital stage there is no need to identify signs of myocardial necrosis, since this does not affect the choice of treatment measures.
The main marker of myocardial necrosis is an increase in the level of cardiac troponins T ("ti") and I ("ai"). An increase in the level of troponins (and subsequent dynamics) is the most sensitive and specific marker of MI (myocardial necrosis) in clinical manifestations corresponding to the presence of acute coronary syndrome (an increase in the level of troponins can also be observed in myocardial damage of "non-ischemic" etiology: myocarditis, pulmonary embolism, heart failure, chronic renal failure).
Troponin determination can detect myocardial damage in approximately one third of patients with myocardial infarction who do not have elevated MB CPK. Troponin elevation begins 6 hours after the onset of myocardial infarction and remains elevated for 7-14 days.
The "classic" marker of myocardial infarction is an increase in the activity or mass of the MB CPK isoenzyme ("cardiac-specific" isoenzyme of creatine phosphokinase). Normally, the activity of MB CPK is no more than 3% of the total CPK activity. In myocardial infarction, an increase in MB CPK of more than 5% of the total CPK (up to 15% or more) is observed. Reliable lifetime diagnostics of small-focal myocardial infarction became possible only after the introduction of methods for determining the activity of MB CPK into clinical practice.
Less specific is the change in the activity of LDH isoenzymes: an increase in the activity of predominantly LDH1, an increase in the LDH1/LDH2 ratio (more than 1.0). Earlier diagnosis can be made by determining the isoforms of CPK. The maximum increase in activity or an increase in the mass of CPK ("peak CPK") is observed on the first day of myocardial infarction, after which a decrease and return to the initial level is observed.
Determination of the activity of LDH and its isoenzymes is indicated in late admission of patients (after 24 hours or more). The peak of LDH is noted on the 3rd-4th day of MI. In addition to an increase in the activity or mass of enzymes, an increase in the content of myoglobin is noted in myocardial infarction. Myoglobin is the earliest (in the first 1-4 hours), but non-specific marker of myocardial necrosis.
Troponin levels are the most reliable markers for diagnosing myocardial infarction, but may be elevated in myocardial ischemia without infarction; high values (actual values depend on the method of determination) are considered diagnostic. Borderline troponin levels in patients with progressive angina indicate a high risk of future adverse events and, thus, the need for further evaluation and treatment. False-positive results are sometimes obtained in cardiac and renal failure. CK-MB activity is a less specific marker. False-positive results occur in renal failure, hypothyroidism, and skeletal muscle damage. Myoglobin levels are not specific for myocardial infarction, but since their levels increase earlier than other markers, they may be an early diagnostic clue that aids in diagnosis in the presence of unusual changes in ECG data.
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Echocardiography
Echocardiography is widely used to detect areas of regional contractility disorders. In addition to detecting areas of hypokinesia, akinesia or dyskinesia, an echocardiographic sign of ischemia or infarction is the absence of systolic thickening of the left ventricular wall (or even its thinning during systole). Echocardiography helps to detect signs of posterior wall myocardial infarction, right ventricular myocardial infarction, and to determine the localization of myocardial infarction in patients with left bundle branch block. Echocardiography is very important in diagnosing many complications of myocardial infarction (rupture of the papillary muscle, rupture of the interventricular septum, aneurysm and "pseudoaneurysm" of the left ventricle, pericardial effusion, detection of thrombi in the heart cavities and assessment of the risk of thromboembolism).
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Other studies
Routine laboratory tests are not diagnostic, but can demonstrate some abnormalities that may occur with tissue necrosis (eg, increased ESR, moderate increase in leukocyte count with a left shift in the leukocyte count).
Imaging studies are not necessary for diagnosis if cardiac markers or ECG findings support the diagnosis. However, in patients with myocardial infarction, bedside echocardiography is invaluable in identifying abnormalities in myocardial contractility. Patients with signs of ACS but normal ECG findings and normal cardiac markers undergo stress testing with imaging (radioisotope or echocardiographic study performed during exercise or pharmacologic stress) before or shortly after hospital discharge. Changes detected in such patients indicate a high risk of complications in the next 3 to 6 months.
Right heart catheterization using a balloon-type pulmonary catheter can be used to measure right heart pressure, pulmonary artery pressure, pulmonary artery occlusion pressure, and cardiac output. This test is usually performed only if the patient has severe complications (e.g., severe heart failure, hypoxia, hypotension).
Coronary angiography 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 (based on ECG and clinical findings), hemodynamic instability, ongoing ventricular tachyarrhythmias, and other conditions indicating recurrence of ischemic episodes.
Formulation of the diagnosis of myocardial infarction
"Anteroseptal Q-wave myocardial infarction (date of onset of symptoms of myocardial infarction); "Non-Q-wave myocardial infarction (date of onset of symptoms)." In the first few days of myocardial infarction, many cardiologists include the definition of "acute" in the diagnosis (formally, the acute period of myocardial infarction is considered to be 1 month). Specific criteria for the acute and subacute periods are defined only for ECG signs of uncomplicated Q-wave myocardial infarction. After the diagnosis of myocardial infarction, complications and concomitant diseases are indicated.