Main pathogenetic mechanisms
In pathophysiology, there are precisely three groups of factors that lead to a critical mismatch between myocardial oxygen demand and its delivery:
- Factors that decrease blood flow to the heart muscle via the coronary arteries.
- Factors that increase the consumption of oxygen and metabolic substrates by the myocardium itself.
- Factors that reduce the content of oxygen and/or metabolic substrates in the blood and myocardial cells.
Classification of causes
All causes responsible for this pathology are classified into two main categories:
- Coronogenic causes. These include any factors that decrease and/or completely stop blood flow through the coronary arteries.
- Non-coronogenic causes. This group includes factors that increase myocardial consumption of oxygen and/or metabolic substrates, as well as factors that reduce the levels of oxygen and/or substrates directly in the blood and myocardium.
Coronary artery disease
Organic vascular narrowing plays a key role. Coronary angiograms in patients reveal significant local narrowing (stenoses) of the lumen of at least one coronary artery. Such lesions are found in angina pectoris (including in young patients), systemic vasculitides, diabetes mellitus (DM), and systemic juvenile idiopathic arthritis.
Thrombus formation frequently occurs in the coronary arteries, predominantly consisting of erythrocytes and platelets. This process is promoted by the following factors:
- Atherosclerotic changes. Particularly dangerous in the presence of diabetes mellitus, arterial hypertension, and dyslipidemias.
- Polycythemia of various origins.
- Turbulent blood flow. Occurs in arterial disease with aneurysm and thrombus formation (most characteristic of Kawasaki disease).
- Hypercoagulation. Characterized by increased activity of coagulation factors and/or proaggregants released from damaged blood cells or the vascular wall (typical of systemic lupus erythematosus).
Complications of myocardial infarction
The pathology is accompanied by a number of life-threatening conditions. The most severe complications include:
- Acute heart failure (HF).
- Cardiogenic shock.
- Pulmonary edema.
- Cardiac rhythm disturbances (various arrhythmias).
- Thromboembolism.
- Heart valve insufficiency.
- Rupture of the heart walls, interventricular septum, or formed aneurysm.
Briefly: answers to topical questions
How does the pathogenesis of coronogenic infarction differ from non-coronogenic infarction?
The pathogenesis differs in the mechanism by which the mismatch between the demand for oxygen/metabolic substrates and their delivery arises.
| Sign | Coronogenic causes | Non-coronogenic causes |
|---|---|---|
| Primary mechanism | Reduction and/or cessation of blood flow to the myocardium via the coronary arteries | Increased myocardial consumption of oxygen and/or metabolic substrates, or a decrease in their levels in the blood and myocardium |
| Examples | Significant local narrowing of the lumen of at least one coronary artery; thrombus formation in the coronary arteries | Acute significant increase in BP (hypertensive crisis) or emotional stress: excess catecholamines increase cardiac workload and oxygen demand |
| Pathogenesis | Coronary artery disease impairs blood delivery to the myocardium | The demand for oxygen and metabolic substrates exceeds their actual delivery level; acute myocardial ischemia and infarction may develop |
Which biochemical markers of necrosis are used to diagnose myocardial infarction?
Cardiac troponins are used to diagnose myocardial infarction.
- Troponin T
- Troponin I
Assay methods must be high- or ultrasensitive. The coefficient of variation for 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 signs of the various stages of myocardial infarction?
For Q-wave myocardial infarction, 4 ECG stages are distinguished: hyperacute, acute, subacute, and cicatricial.
- Hyperacute stage — the first hours from the onset of the anginal attack: formation of a monophasic curve; prominent ST-segment elevation merging with an increased/giant positive T wave into a single dome.
- Acute stage — from day 1 to 2–3 weeks: the pattern of necrosis develops.
- Subacute stage — up to 6–8 weeks.
- Cicatricial stage — months and years; the pattern stabilizes, showing signs of a prior myocardial infarction.
Dynamic changes characteristic of Q-wave myocardial infarction include: decreased R-wave amplitude, appearance of a wide and deep pathological Q wave, domed ST elevation convex upward; subsequently, the ST segment shifts downward and a negative T wave is formed. 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 (closely related to reflex shock associated with the response to a pain attack).
- Arrhythmic variant — the development of hemodynamic disorders against the background of severe tachy- and bradyarrhythmias.
The three groups of factors causing myocardial hypoxia are easy to remember by the vector of the problem: DELIVERY is reduced (coronary blood flow is decreased), DEMAND is increased (myocardium consumes more oxygen), QUALITY has dropped (oxygen and substrate content in the blood is reduced).
Class and exam questions
Which diagnostic methods demonstrate organic vascular narrowing in myocardial infarction?
The main imaging method is coronaroangiography. On coronary angiograms, physicians can clearly identify significant local narrowing, i.e., 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 the development of post-infarction cardiosclerosis.
How do systemic lupus erythematosus and Kawasaki disease contribute to thrombosis?
In Kawasaki disease, arteries are affected with aneurysm formation, which creates turbulent blood flow. In systemic lupus erythematosus, hypercoagulation occurs due to increased activity of clotting factors and proaggregants from damaged cells.
Which mechanical injuries of heart structures are classified as life-threatening complications?
Extremely dangerous mechanical complications include cardiac wall rupture, interventricular septum rupture, as well as aneurysm rupture and acute heart valve insufficiency.
What else to study on this topic
- 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 lesions.
- Role of polycythemia and erythrocyte-platelet thrombi in coronary artery lesions.
- Hemodynamic disorders in turbulent blood flow and aneurysm formation.
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