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Myocardial Infarction

*Infarctus myocardii*

For medical students2 min readUpdated 2026-10-10

Myocardial infarction (MI) is a life-threatening condition characterized by a severe imbalance between the myocardial oxygen demand and its actual supply. If the patient survives the acute phase, the necrotic area of the heart muscle is inevitably replaced by fibrous connective tissue, leading to cardiosclerosis.

Core PathologyCritical mismatch between myocardial oxygen demand and supply

ComplicationsCardiogenic shock, pulmonary edema, cardiac wall rupture, and severe arrhythmias

Arterial ThrombosisTriggered by polycythemia, atherosclerosis, hypercoagulability, and turbulent blood flow

DiagnosisSignificant focal coronary artery stenoses are identified on coronary angiography

Key Pathophysiological Mechanisms

In pathophysiology, there are precisely three groups of factors that lead to a critical mismatch between myocardial oxygen demand and supply:

Factors that decrease blood flow to the heart muscle via the coronary arteries.
Factors that increase myocardial consumption of oxygen and metabolic substrates.
Factors that reduce the content of oxygen and/or metabolic substrates in the blood and myocardial cells.

Classification of Causes

All causes leading to this pathology are classified into two main categories:

Coronary causes. These include any factors that decrease and/or completely stop blood flow through the coronary arteries.
Non-coronary causes. This group includes factors that increase myocardial consumption of oxygen and/or metabolic substrates, as well as factors that directly reduce oxygen and/or substrate levels in the blood and myocardium.

Coronary Artery Involvement

Organic vascular narrowing plays a key role. Coronary angiograms in patients reveal significant focal stenoses of the lumen of at least one coronary artery. Such lesions are found in angina pectoris (including in young patients), systemic vasculitis, diabetes mellitus (DM), and the systemic form of juvenile idiopathic arthritis.

Thrombi, predominantly erythrocyte- and platelet-rich, frequently form in the coronary arteries. This process is facilitated by the following factors:

Atherosclerotic changes. Especially dangerous in the presence of diabetes mellitus, arterial hypertension, and dyslipidemias.
Polycythemia of various origins.
Turbulent blood flow. Occurs in vascular lesions accompanied by aneurysm formation and thrombosis (most characteristic of Kawasaki disease).
Hypercoagulability. Characterized by increased activity of clotting factors and/or pro-aggregants released from damaged blood cells or the vascular wall (typical of systemic lupus erythematosus).

Complications of Myocardial Infarction

The pathology is accompanied by a range of life-threatening conditions. Severe complications include:

Acute heart failure (HF).
Cardiogenic shock.
Pulmonary edema.
Cardiac rhythm disturbances (various arrhythmias).
Thromboembolism.
Valvular heart insufficiency.
Rupture of the cardiac walls, interventricular septum, or a formed aneurysm.

Mnemonic

The three groups of myocardial hypoxia factors can be easily remembered by the vector of the problem: SUPPLY is down (reduced inflow via coronary arteries), DEMAND is up (myocardium consumes more oxygen), QUALITY is dropped (reduced oxygen and substrate content in the blood).

Frequently asked questions

How does the pathogenesis of coronary infarction differ from non-coronary infarction?

Pathogenesis differs in the mechanism causing the mismatch between myocardial demand for oxygen/metabolic substrates and their supply.

Feature	Coronary Causes	Non-Coronary Causes
Primary Mechanism	Reduction and/or cessation of blood flow to the myocardium via the coronary arteries	Increased myocardial consumption of oxygen and/or substrates, or decreased their levels in blood and myocardium
Examples	Significant focal stenoses of at least one coronary artery lumen; thrombus formation in coronary arteries	Acute significant BP elevation (hypertensive crisis) or emotional stress: excess catecholamines increase cardiac work and blood supply demand
Pathogenesis	Coronary artery disease impairs blood delivery to the myocardium	Demand for oxygen and substrates exceeds actual delivery; acute myocardial ischemia and infarction may develop

Which biochemical necrosis markers are used to diagnose myocardial infarction?

Cardiac troponins are used to diagnose myocardial infarction:

Troponin T
Troponin I

Assay methods must be high- or ultra-high-sensitivity. The coefficient of variation at the 99th percentile of the upper reference limit must not exceed 20% (ideally no more than 10%). The basis of diagnosis is the release of intracellular enzymes and proteins into the bloodstream from damaged cardiomyocytes.

What are the ECG features of the various stages of myocardial infarction?

For Q-wave myocardial infarction, 4 ECG stages are distinguished: hyperacute, acute, subacute, and scarred.

Hyperacute stage — first hours from the onset of anginal pain: formation of a monophasic curve; pronounced ST-segment elevation merging with an enlarged/giant positive T wave into a single dome.
Acute stage — from 24 hours to 2–3 weeks: picture of necrosis develops.
Subacute stage — up to 6–8 weeks.
Scarred stage — months and years; picture stabilizes, signs of prior infarction are present.

Dynamic features of Q-wave infarction include: decreased R wave amplitude, appearance of a wide and deep pathological Q wave, convex-upward ST segment elevation; later, ST shifts downward and a negative T wave forms. Non-Q-wave infarction is characterized by ST and T changes without the formation of a QS necrosis complex or pathological Q wave.

What pathogenetic mechanisms underlie cardiogenic shock in myocardial infarction?

There are three main pathogenetic mechanisms for the development of cardiogenic shock:

True cardiogenic shock — associated with decreased left ventricular contractility.
Shock due to hypovolemia — caused by relative or absolute hypovolemia (similar to reflex shock associated with pain response).
Arrhythmic variant — development of hemodynamic disturbances against the background of severe tachy- and bradyarrhythmias.

Which imaging methods reveal organic vascular narrowing in myocardial infarction?

The primary imaging modality is coronary angiography. Coronary angiograms clearly demonstrate significant focal stenoses of the lumen of at least one coronary artery.

What happens to the affected area of the heart if the patient survives?

The necrotic area of the heart muscle is replaced by connective tissue. This process ultimately leads to post-infarction cardiosclerosis.

How do systemic lupus erythematosus and Kawasaki disease promote thrombosis?

In Kawasaki disease, arteries are damaged with the formation of aneurysms, which creates turbulent blood flow. In systemic lupus erythematosus, hypercoagulability occurs due to increased activity of clotting factors and pro-aggregants released from damaged cells.

What mechanical injuries to cardiac structures are considered life-threatening complications?

Extremely dangerous mechanical complications include cardiac wall rupture, rupture of the interventricular septum, aneurysm rupture, and acute valvular heart insufficiency.

Go deeper

Pathogenesis of cardiogenic shock and pulmonary edema in acute heart failure.
Mechanisms of post-infarction cardiosclerosis formation from connective tissue.
Impact of arterial hypertension, dyslipidemias, and diabetes mellitus on atherosclerotic changes.
Role of polycythemia and erythrocyte-platelet thrombi in coronary artery disease.
Hemodynamic disturbances in turbulent blood flow and aneurysm formation.