Myocardial Infarction

Myocardial Infarction

Myocardial Infarction-Myocardial infarction. Myocardial infarction (MI) usually results from the occlusion of one or more coronary arteries by atheroma and subsequent thrombus.

It presents with severe central chest pain, having the same site and character as the pain of angina pectoris but usually lasting for more than 30 minutes.

in other word

Myocardial infarction is death of cardiac myocytes (necrosis) caused by prolonged ischemia. Ischemia is the result of a mismatch of myocardial perfusion to his needs.


ECG is still considered to be one of the most important diagnostic tools in acute coronary pathology. With its help, acute myocardial infarction can be supplied in 70% of cases.

In other 30%, difficulties of diagnosis may be associated with delayed withdrawal ECG, presence of comorbidities, atypical localization of necrosis associated with impaired conduction and excitability.

Myocardial infarction is death of cardiac myocytes (necrosis) caused by prolonged ischemia. Ischemia is the result of a mismatch of myocardial perfusion to his needs.

The main cause of myocardial infarction is the cessation of blood flow to the area of the heart muscle on coronary arteries abruptly changed as a result of atherosclerosis.

In addition, ischemic necrosis may develop as a result of total obstruction of a coronary artery by a thrombus, embolus. Sometimes the disease has a hereditary nature. More precisely,

inherited anomalies of development of the network of coronary vessels which fail to provide adequate blood supply to the heart while strengthening it. In addition to the immediate causes of this disease,

there are risk factors. These include advanced age, arterial hypertension, disruption of carbohydrate, obesity, Smoking, lack of physical activity, nervous stress, overwork.

With the development of myocardial infarction simultaneously or sequentially three main pathophysiological process occur they are myocardial ischemia, myocardial damage (injury) and necrosis.

Traditionally, for ischemia the T wave is responsible on the ECG, for injury – ST segment, the zone of necrosis – pathological Q (wide and deep) or QS. Depending on the polarity of the T wave and the ST position on the isoline,

it is possible to judge the “start” of the process (subendo or subepicardial) that indirectly indicates the severity and prognosis of the disease.

The modern course of myocardial infarction taking into account the depth of the lesion occurs in several stages. Below is a modern phasic ECG changes in uncomplicated myocardial infarction with Q (subepicardial, transmural infarction).

1. The most acute phase. On ECG at this time high isosceles and peaked T wave (coronary) appears, as a manifestation ischemia. The duration of this stage is 15-30 minutes, so these changes can rarely be fixed not ECG.

2. Acute stage or phase cardiomyocytes damage is characterized by elevation ST segment above the isoline and merge ( its association) with coronary T wave, thus forming the phenomenon Pardee or “back of the cat”. The duration of this phase can vary from several hours to 2-3 days.

In the center of the damaged zone the focus of necrosis is formed, it is characterized by the appearance of pathological Q wave, decrease of the R wave (QRS complex) or complete absence of the R wave (QS) in transmural infarction.

In this stage the last part of the repolarization changes (T wave). On the 4-5 day first inversion of the T wave (negative T wave) occurs, associated with subendocardial ischemia, which is 6-8 day can take place due to the development of collaterals.

The second inversion of the T wave develops by the 10th day due to the autoimmune inflammation in a necrosis zone, and it is deeper than the first one.

The characteristic feature of the acute phase is reciprocal (mirrored) ST-segment depression in leads opposite to those in which there is ST-segment elevation.

The duration of this depression can be 1-2 days. With 10 days, as a rule, ST segment begins slowly approaching to the isoline, it indicates the end of the acute phase.

4. Subacute phase

In this stage only with the ST segment and the T wave changes occur. The ST segment continues to approach the isoelectric line and the T wave continues to deepen. Eventually it becomes negative and deep pointed equilateral, i.e. “coronary”.

Subacute stage is complete when the ST segment returns to the isoline and there is no dynamics of the T wave (it is stable). The duration of the subacute stage, on average, 4-6 weeks.

5. The phase of scarring

Usually preserved pathological Q wave, transferred as a marker of necrosis, ST segment on the isoline, and T wave changes. Over time it becomes less deep (5 mm) or two-phase (+/- ; -/+), iso electrical, rarely positive. The process of scarring a long, one year and more.

In the development of subendocardial infarction (according to the old terminology of small focus) there is no staging on ECG. For a long period of time persistent changes in phase of repolarization (ST segment and T) without pathological Q observed.

The diagnosis of myocardial infarction (of any form) is a combination in various combinations of three signs: the clinic, the typical signs ECG and cardiac enzymes reaction.

There is no uniform classification of myocardial infarction still, in parallel both Russian and the World Health Organization`s classifications exist. According to the WHO classification, we can distinguish Q-positive (with Q) and Q is negative (no Q wave) myocardial infarction.

Criteria Q-positive myocardial infarction:

1)- the presence of pain (typical or atypical)

2) the presence of pathological Q wave (QS)

3) ST-segment elevation (elevation) with subsequent phasic dynamics

4) the response of cardiac enzymes (lactate dehydrogenase, creatine kinase, troponins)

Criteria Q-negative myocardial infarction:

1) the presence of pain (typical or atypical)

2) no pathological Q wave (QS)

3) persistent ST-segment depression and change of T wave

4) the reaction of the cardiac enzymes.

Russian ECG classification extends the concept of multiple heart attacks with Q and without Q.

In the Q-positive myocardial infarction they allocate 2 forms:

1) transmural (there is a QS complex);

2) large-focal (there is a QR complex).

In Q-negative myocardial infarction they allocate 2 forms:

1) subendocardial (ST-segment depression more than 48 hours and negative or positive T wave in a significant group of leads);

2) intramural process (there is only pathological negative T wave). The diagnosis can only be made during dynamic observation (monitoring) ECG: within 3 weeks there is no improvement on the ECG, but rather the depth of T is increased.

Modern topical classification (A. P. Meshkov (1998) myocardial infarction reflects, primarily, the process in the left ventricle and is closely associated with coronary artery disease.

Isolated anterior localization, which in turn is divided into: – septal (direct signs of infarction in leads V1-2),
-apical (V3-4,),
-anterolateral (I, aVL, V5),
-is common anterior (I, avl, V1-4),
-extensive anterior (I, avl, V1-6),
-high lateral (isolated changes in avl).

At all locations of the anterior process expressed stenotic changes are in trunk and branches of the left coronary artery. The second localization is a lower infarction. Lower infarctions are associated with pathology of the right coronary artery and its branches.

It comes in two variants: true lower (changes in II, III and avF), – posterior-basal (no direct indication in 12 standard leads and requires removing the left additional leads V7-9, which are fixed infarct changes (pathological Q, ST and T).

Isolated circular-apical infarction, in which there is a slight discrepancy between clinical manifestations and marked changes on the ECG (I, II, III, avL, avF, V3-6).

This is due to the fact that affects the final anastomosis branch of the left and right coronary arteries. The prognosis of this type of infarction is favorable.

Pathology of the right ventricle, including myocardial infarction is not visible on a standard ECG at rest and requires of making additional right chest leads V3R-V4R. Experienced doctors functionalists can supply the right ventricle myocardial infarction by circumstantial evidence (described in the literature).

Focal abnormalities in the anterior-septal-apical wall with a zone of injury and ischemia with diffusion on the lateral wall
Focal abnormalities in the anterior-septal-apical wall with a zone of injury and ischemia with diffusion on the lateral wall


Acute large-focal myocardial infarction inferior wall of the left ventricle
Acute large-focal myocardial infarction inferior wall of the left ventricle


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