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Kuzhel, G.V. Matyushin, T.D. Fedorova E.A., Savchenko, T.M. Zadoenko KGUZ "Krasnoyarsk Regional Hospital No. 2" GOUVPO "Krasnoyarsk State Medical Academy"
An electrocardiogram in 12 standard leads is the method of choice in the diagnosis of acute myocardial infarction (AMI). Quick and accurate diagnosis of AMI is vital, as it makes it possible to immediately begin reperfusion therapy, which reduces the area of necrosis and improves the patient's prognosis. One of the generally accepted criteria for myocardial infarction is ST segment elevation in two or more anatomically adjacent leads [10]. The importance of timely identification of ST segment elevation associated with AMI is emphasized by the fact that neither ST segment depression nor increased biochemical markers of cardiac necrosis (MCN) in the blood serum are indications for thrombolytic therapy [4, 9].
In the early stages of AMI, diagnosis can be significantly difficult, since the ECG is often normal or has minimal abnormalities. Moreover, only half of patients with AMI have obvious diagnostic changes on the first ECG. At the same time, approximately 10% of patients with proven AMI (based on clinical data and positive MCI) will not develop typical changes on the ECG, such as ST segment elevation or depression [4]. However, in most cases, serial ECGs in individuals with AMI show a characteristic evolution that usually corresponds to the typical changes observed in myocardial infarction. In the domestic school of cardiology, it is customary to distinguish four stages of the course of AMI [1].
I.
The most acute stage
. In this stage, which lasts from several hours to several days, changes in the ECG affect only the ST segment and the T wave. The earliest signs of acute myocardial infarction are difficult to distinguish and usually include an increase in the amplitude of the T wave in the affected area, which becomes symmetrical and directional ( hyperacute). Typically, hyperacute T waves are most evident in the anterior precordial leads and are most noticeable when an older ECG is available for comparison. Changes in T wave amplitude can be observed within a few minutes of the onset of infarction and are accompanied by corresponding changes in the ST segment. The optimal time for delivery of a patient to a medical facility is considered to be an interval of up to four hours from the onset of AMI. Unfortunately, ECG changes in the acute stage of myocardial infarction are often not properly assessed, which significantly increases the time it takes for the patient to be delivered to a specialized facility and prolongs the start of reperfusion therapy.
II. Acute stage.
In the acute stage, which usually lasts up to one week, ST segment elevation is recorded and Q waves begin to form. In practice, ST segment elevation is often the earliest sign of AMI and usually becomes noticeable within a few hours from the onset of symptoms. At the initial stages, the angle between the T wave and the ST segment, characteristic of a normal ECG, is lost. The T wave becomes wide and the ST segment rises, losing its normal concavity. During further ascent, the ST segment becomes convex upward. The degree of ST segment elevation varies between small changes of less than 1 mm to pronounced elevation of more than 10 mm. Sometimes the QRS complex, ST segment and T wave merge, forming the so-called monophasic curve.
III. Subacute stage.
The subacute stage of myocardial infarction lasts up to several weeks. During this stage, the ST segment begins to approach the isoline, and negative T waves are formed. In the case of transmural myocardial infarction, the necrosis process is accompanied by changes in the QRS complex, which include a decrease in the amplitude of the R waves and the development of pathological Q waves. Such changes develop as a result of the loss of viable myocardium under recording electrode, therefore Q waves are the only ECG criterion that verifies myocardial necrosis. Q waves can develop within 1 to 2 hours of the onset of AMI symptoms, although this often takes 12 to 24 hours. The presence of pathological Q waves, however, does not necessarily indicate a completed infarction. If ST segment elevation and Q waves are detected on the ECG and the chest pain is of recent onset, the patient may still benefit from thrombolysis or interventional therapy.
IV. Scar stage.
Consolidation of scar tissue ends on average 8 weeks after myocardial infarction. At this stage, the ST segment reverts to the isoline and the amplitude of negative T waves decreases. In the case of extensive myocardial infarction, pathological Q waves are a stable marker of cardiac necrosis. In small infarcts, scar tissue may include viable myocardium, which may reduce the size of the electrically inert region and even cause the eventual disappearance of Q waves.
One of the curious features of the ECG in AMI is the so-called pseudonormalization phenomenon. Wilson's theory of the formation of Q waves implies the formation of a so-called electrical window in case of necrosis, through which the recording electrode records the electrical potentials of the opposite wall. However, despite necrosis, some of the myocardial fibers in the infarction zone remain viable, which explains the characteristic flattening of Q waves during myocardial infarction. However, the potentials of these fibers remain hidden behind the powerful electric vector of the opposite wall. With a repeated infarction, which involves the opposite wall, this vector is significantly reduced, which, in turn, makes it possible to record the potentials of myocardial fibers in the area of the old scar. As a result, in the area of the old scar with pathological Q waves (for example, in the anterior wall), in the event of a re-infarction of the opposite wall (for example, the posterior wall), R waves begin to be recorded. Thus, the registration of R waves in the area where pathological Q waves were previously observed, strongly suggests the formation of an infarction in the opposite wall.
Dynamics of changes in the ST segment and T wave in AMI
The ECG picture during myocardial infarction has its own characteristic development. Firstly, ST segment elevation, as a rule, leads to the formation of Q waves. Secondly, the formation of negative T waves occurs against the background of a characteristic arcuate ST segment elevation.
ST segment elevation associated with myocardial infarction in the anterior wall can persist for a long time if dyskinesia or left ventricular (LV) aneurysm develops. Negative T waves can also persist for a long period and sometimes remain a permanent sign of myocardial infarction. It should be noted that the absence of formation or “restoration” of pre-inverted T waves in the acute stage of myocardial infarction strongly suggests the development of post-infarction pericarditis [11].
Myocardial infarction: symptoms and signs
The development of symptoms depends on the form of the heart attack, its extent and type of manifestations.
The most important thing for the patient is the ability to recognize the symptoms of a pre-infarction condition. This will help you react in a timely manner and take life-saving measures.
The first signs of a heart attack:
- severe angina pectoris;
- dyspnea;
- labored breathing;
- pain in the abdomen;
- headache;
- discomfort in the chest area - a feeling of compression, pressure;
- discomfort in the upper body;
- feeling of anxiety and severe restlessness, insomnia.
The pre-infarction stage is observed in 50% of cases. It can last from 2-3 days to several weeks.
Following this, the actual acute myocardial infarction begins, which consists of several stages.
The most acute stage is manifested by severe sharp chest pain, which radiates to the neck, arms, and under the shoulder blades. The nature of the pain can be burning, bursting. The general pre-infarction symptoms include increased sweating (sticky, cold sweat), panic attacks, nausea, vomiting, pallor of the integument and mucous membranes, sudden surges in pressure, dizziness with loss of consciousness.
The acute stage is the most dangerous and decisive period in the development of a heart attack, lasting several days. During this period, the following may occur:
- rupture of the heart muscle;
- blockage of a coronary vessel by a thrombus;
- cerebral circulatory disorders.
Body temperature rises, the level of leukocytes increases sharply.
Subacute stage – the beginning of the pathological process subside, can take up to 1 month. At this time, it is necessary to reduce the temperature and level of leukocytes to normal values, restore blood circulation, start tissue regeneration processes and prevent the development of post-infarction syndrome.
The post-infarction stage is the final stage of pathology development with a period of active formation of scar tissue at the site of injury. It is at this stage that possible complications should be expected. If everything goes well, the patient’s condition quickly returns to normal.
Attention!
Without proper care and reparative therapy, 35% of patients may experience a recurrent heart attack within 3 years.
Reciprocal ST segment depression
ST segment depression in leads opposite the affected area, otherwise known as reciprocal depression, is a highly sensitive indicator of AMI. The pathogenesis of reciprocal changes remains unknown. Reciprocal changes have high sensitivity and a positive predictive value of up to 90% and are observed in approximately 70% of lower and up to 30% of infarcts involving the anterior wall of the LV, although, of course, their absence does not exclude the diagnosis of AMI [4, 5]. As a rule, ST segment depression is horizontal or oblique. The presence of reciprocal changes is especially important when there is doubt about the clinical significance of the recorded ST segment elevation. We especially note that reciprocal changes may be the only sign of AMI against the background of still unobvious ST segment elevation. Similar situations often occur in cases of myocardial infarction with damage to the lower wall. The presence of severe ST segment depression in the precordial leads against a background of normal heart rate or bradycardia in a patient with an ischemic painful attack strongly requires the exclusion of AMI.
Stages of the disease and main signs of myocardial infarction
Myocardial infarction goes through several stages in its development. The duration and severity of each depends on the size of the lesion, the condition of the blood vessels, concomitant diseases and complications, as well as the correctness of the chosen treatment tactics. There are acute, subacute periods, periods of scarring and post-infarction periods. Many patients noted that the acute period was preceded by some signs of unstable heart function - angina pectoris, arrhythmia.
Acute period
can last up to 10 days. This is the most difficult time for the patient, when all sorts of complications arise and the likelihood of death is quite high. A characteristic clinical picture of the acute period of myocardial infarction is severe pain in the chest area radiating to the left shoulder, collarbone, neck, ear, and shoulder blades. The sensations of spasm can be different - cutting, stabbing, pressing, burning. This condition during myocardial infarction lasts from thirty minutes to several hours. An attack during myocardial infarction occurs in waves. The pain may increase or decrease. It is impossible to stop them with nitroglycerin. At the same time, during myocardial infarction, the patient experiences severe weakness, a feeling of lack of air, and anxiety. Pallor of the skin, cyanosis (acrocyanosis) of the nasolabial triangle, arrhythmia, and profuse sticky sweat are also noted. Possible increase in blood pressure.
Subacute period of myocardial infarction
characterized by the disappearance of pain. Their preservation indicates the addition of pericarditis (inflammation of the outer lining of the heart). Necrotic processes in the area of inflammation can cause fever with a rise in body temperature. The patient is concerned about persistent low blood pressure.
Scarring period
in case of myocardial infarction, it is characterized by gradual healing of the affected area through the formation of scars. The duration of the process ranges from several weeks to several months. The patient's condition improves significantly. Painful symptoms disappear.
Post-infarction period
– time for recovery and return to normal life. It is recommended to avoid moving heavy objects on your own, give up alcohol and smoking, follow a diet, monitor your body weight, monitor your pulse and blood pressure, and avoid prolonged exposure to the sun.
It is important to know that there are atypical forms of myocardial infarction, in which the signs of a life-threatening condition are not always obvious. They make diagnosis and timely provision of medical care difficult. Among the most common:
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Myocardial infarction of the anterior wall
Anteroseptal ST-segment elevation infarction in leads V1-V3 is a highly accurate indicator of left anterior descending coronary artery (LADCA) involvement. ST segment elevation in these three leads and in lead aVL, combined with ST segment depression of more than one mm in lead aVF, indicates occlusion of the proximal segment of the LCA. ST-segment elevation in leads V1, V2, and V3 without significant ST-segment depression in the inferior leads suggests occlusion of the LCA after origin of the first diagonal branch.
In some cases, the LPNCA wraps around the apex of the LV and supplies blood to the apical parts of the inferior wall in the distal part of the posterior interventricular groove. Rarely, the LCA extends along the entire length of the posterior sulcus, replacing the posterior descending artery. In the case of ST segment elevation in leads V1, V2 and V3 with ST elevation in the inferior leads, occlusion of the LCA of the distal origin of the first diagonal branch, in the area that irrigates the inferoapical parts of the LV, can be assumed [7].
Main causes of myocardial infarction
There is a risk group - a population whose likelihood of developing myocardial infarction is higher than the rest of the population. It includes:
- men over 50 years old.
- hypertensive patients.
- smokers and alcohol abusers.
- overweight.
- persons leading a sedentary lifestyle.
- persons who have previously had a heart attack.
The main cause of myocardial infarction
It is considered to be a narrowing of the lumen of the coronary arteries caused by atherosclerotic changes. Increased blood clotting leads to the formation of blood clots that disrupt blood circulation in the heart muscle. The tissues of a vital organ suffer from a lack of nutrients. Myocardial infarction can be triggered by severe emotional and physical stress, the presence of coronary heart disease or angina, as well as diabetes, obesity, addiction to alcoholic beverages and smoking.
Lower IM
AMI with isolated ST-segment elevation in leads II, III, and aVF is usually associated with damage to the right coronary artery (RCA) or the distal circumflex artery (CA). A rather unpleasant feature of AMI with damage to the inferior wall is that the ST segment elevation associated with the infarction can develop over a long period, up to two weeks, to become evident on the ECG [4]. The inferior wall can be supplied with blood from the right coronary artery (in 80% of cases) or from the OA, which is a branch of the left coronary artery.
ST segment elevation in lead III is greater than in lead II, and ST segment depression of more than one mm in leads I and aVL suggests damage to the RCA, which supplies the inferior wall. In the case of blood supply to the lower wall from the OA, the rise of the ST segment in lead III does not exceed the rise in lead II. In this case, either an elevation of the ST segment in aVL is observed, or it is located on the isoline [6, 7].
Right ventricular myocardial infarction
Right ventricular MI is usually associated with occlusion at the level of the proximal RCA. The most sensitive ECG sign of right ventricular MI is ST segment elevation of more than one mm in lead V4R with a positive T wave in this lead [5]. This sign is rarely observed more than 12 hours after AMI, so right leads should be recorded as soon as possible in all patients with inferior wall infarction. On a standard 12-lead ECG, signs of AMI involving the right ventricle are ST segment elevation in lead V1 combined with ST segment elevation in leads II, III, and aVF (STIII greater than STII).
Right ventricular infarction is often missed because the standard 12-lead ECG does not have high sensitivity for right ventricular infarction. At the same time, the diagnosis of right ventricular infarction is important, as it may be associated with a state of hypotension caused by treatment with nitrates or diuretics. At the same time, in contrast to cardiogenic shock, which requires differential diagnosis, the patient responds well to fluid administration.
In approximately 40% of cases, inferior wall AMI is complicated by right ventricular infarction [2, 6]. Less commonly, right ventricular infarction is associated with occlusion of the circumflex artery and, if this branch is dominant, may be associated with inferolateral infarction. Right ventricular infarction can complicate anterior wall AMI and can rarely occur as an isolated phenomenon [15].
Complications of myocardial infarction
In the first hours of myocardial infarction, various complications may arise that aggravate the patient's condition. This is the appearance of an aortic aneurysm, myocardial rupture, cardiogenic shock, cessation of cardiac activity (asystole), pulmonary edema. The consequences of a heart attack can accompany the patient for life. These are heart rhythm disturbances, cardiosclerosis and other problems associated with disruption of the cardiovascular system. Experts do not guarantee absolute recovery after a heart attack and recommend following all the instructions of a cardiologist in order to avoid a relapse. The next attack threatens the appearance of a new area of necrosis. It is almost impossible to compensate for such consequences for the heart.
Myocardial infarction of the posterior wall
The posterior descending coronary artery (PDCA), which supplies blood to the posterobasal sections, can be a branch of the RCA (in 85-90% of cases) or a branch of the OA (12), which determines the right or left type of coronary circulation. The diagnosis of AMI with posterior-basal lesions is often difficult when using a standard 12-lead ECG, while early detection of coronary thrombosis is very important from the point of view of prescribing thrombolytic therapy.
Changes in the ECG during AMI of the posterior basal sections are indirectly manifested in the anterior precordial leads. Leads V1-V3 record the potentials of not only the anterior, but also the opposite (posterior) wall, and changes in blood supply in this area are reflected in these leads. Typically, there is an increase in R waves that become wider and more dominant, as well as ST segment depression and high amplitude T waves pointing toward the posterior wall [3]. The use of leads V7-V9, recording posterobasal potentials, will show ST segment elevation in patients with AMI.
These additional leads provide valuable information and help in identifying patients who may benefit from urgent invasive therapy. In any case, registration of ST segment depression in leads V1-V2 should serve as a reason to exclude AMI of the posterobasal parts of the LV. In the cicatricial stage, a previous myocardial infarction in the posterior-basal sections will be indicated by the ratios R/S > 1 in lead V2 and RV2 > RV6, recorded against the background of the horizontal position of the electrical axis of the heart [2].
Lateral wall infarction.
Lesions in the proximal circumflex artery are often associated with lateral infarction and changes in leads I, aVL, V5-V6. Often, AMI can manifest itself as changes that occur isolated in lead aVL. In such cases, it is customary to diagnose AMI with damage to the high lateral parts of the LV [3].
ECG predictors of reperfusion
Pathogenetic therapy for AMI has the goal of restoring blood flow in the affected artery. Lack of restoration of blood flow (reperfusion) is the most powerful predictor of the development of LV systolic dysfunction and the risk of death after AMI. In the absence of reperfusion, 30-day mortality can reach 15% [14]. In turn, the resolution of ST segment elevation is an indicator of improved short-term (30-day) and long-term (one-year) prognosis [5]. Assessing ST segment resolution is also useful for deciding on further management of the patient.
Failure to resolve the ST segment within the first 90-120 minutes after thrombolytic administration should be a reason to consider angioplasty. A specific marker of reperfusion that has occurred is considered to be a reduction in ST segment elevation by more than 50-70% in the lead with maximum elevation, which is associated with the most favorable further prognosis. At the same time, a number of authors propose a criterion of 50% reduction in ST segment elevation after 60 minutes of reperfusion therapy as a predictor of a good prognosis in individuals with AMI [13]. Considering that the maximum effect from subsequent angioplasty after thrombolysis is achieved no later than 6-8 hours from the onset of AMI [14], reducing the time for assessing reperfusion has good reason.
Other ECG markers of reperfusion include T wave inversion within four hours of AMI onset. T wave inversion, which occurs within the first hours of reperfusion therapy, is a highly specific sign of restoration of blood flow. T wave inversion, which develops after more than four hours, is associated with natural ECG dynamics during AMI and does not indicate restoration of blood flow. Accelerated idioventricular rhythm 60-120 beats/min, late, paired, ventricular extrasystoles are also a highly specific marker of reperfusion. These rhythms are considered not dangerous and, as a rule, do not require antiarrhythmic therapy. Polymorphic ventricular tachycardia and ventricular fibrillation can also be associated with reperfusion, but are rare and more often a consequence of persistent coronary occlusion.
