Ultrastructural changes in ischemia
At the ultrastructural level, hypoxic damage to cardiomyocytes affects the most important intracellular structures. Electron microscopy records:
- Damage to the sarcolemma and plasma membrane.
- Destruction of mitochondria and breakdown of their cristae.
- Swelling of the sarcoplasmic reticulum and sarcoplasmic edema.
- Widening of intercalated discs.
At the light microscopy level, myofibril changes affecting Z-discs are visible.
Stages of pathogenesis and the role of collaterals
The pathogenesis of infarctus myocardii develops dynamically and includes three key stages:
- Ischemic (prenecrotic) stage — metabolic disorders increase, energy deficiency forms, compensatory mechanisms are activated, and the fate of the peri-infarct zone is determined.
- Necrotic stage — irreversible death of cardiomyocytes.
- Organization stage — replacement of the dead area with connective tissue (scarring).
The fate of the damage zone largely depends on collateral circulation. If collateral blood flow is sufficient, ischemic damage in the peri-infarct zone can be reversible. With insufficient blood supply, dystrophic changes progress to necrosis, increasing the size of the lesion.
Changes in the intact myocardium and the "vicious circle"
The preserved (intact) myocardium takes on an increased load due to the cessation of function of the ischemic area. This leads to a number of interconnected shifts:
- Energy deficiency arises, as the standard number of mitochondria meets needs only within the normal range.
- In response to increased work, hyperplasia of intracellular structures is triggered — primarily mitochondria.
- Due to mitochondrial hyperfunction, the breakdown of their cristae increases, incoming oxygen is not fully utilized, and tissue hypoxia develops.
The degree of hypoxia increases along with the destruction of organelles, creating the threat of a "vicious circle". The process of mitochondrial recombinational changes helps prevent this. In an optimal scenario, the body eliminates the energy deficiency, the patient survives the ischemic phase, after which infarction organization and reparative hypertrophy ensue.
Briefly: answers to topical questions
What macroscopic signs are characteristic of the necrotic stage of myocardial infarction?
In the necrotic stage of myocardial infarction, a dull ischemic focus with a reddish border is macroscopically revealed. Progressive disintegration of cells and tissues occurs, as well as a color change in the necrotic area of the heart muscle.
What microscopic signs are characteristic of the necrotic stage of myocardial infarction?
In the necrotic stage, cardiomyocytes lack nuclei and show signs of necrobiosis, such as karyolysis, cytoplasmic eosinophilia, and loss of cross-striation. Coagulation necrosis of the muscle tissue develops. On the second day, a clearly visible demarcation inflammatory wall with leukocytic infiltration forms around the focus, and on days 3–7, disintegration of the dead myofibrils and their resorption by macrophages begin.
What early complications can develop in the necrotic stage of myocardial infarction?
In the early period of myocardial infarction, severe rhythm and conduction disorders, acute heart failure in the form of cardiac asthma and pulmonary edema, as well as cardiogenic shock can develop. Dangerous morphological complications include myocardial rupture, acute cardiac aneurysm formation, detachment of a necrotic papillary muscle, interventricular septum perforation, and thromboembolic syndrome originating from fresh thrombotic masses on the endocardium.
What changes occur at the light microscopy level in the ischemic stage of myocardial infarction?
Light microscopy in the ischemic stage reveals myofibril changes at the Z-disc level, as well as swelling and fragmentation of cardiomyocytes. Disappearance of glycogen from the cell sarcoplasm is noted.
How does the organization stage of myocardial infarction proceed at the tissue level?
The organization stage begins with the resorption of necrotic masses by segmented neutrophils and macrophages. On days 7–10, granulation tissue grows from the demarcation zone into the damage zone, gradually replacing the necrotic area. Subsequently, maturation of granulations occurs, transforming them into mature connective tissue and forming post-infarction large-focal cardiosclerosis.
What compensatory mechanisms are triggered in the ischemic stage of myocardial infarction?
In response to a sharp energy deficiency in the intact myocardium, hyperplasia of intracellular structures is triggered, primarily mitochondria. To prevent deepening tissue hypoxia, mitochondrial recombinational changes are activated.
The three pillars of MI pathogenesis: Ischemia (reversible stage with the struggle for the peri-infarct zone) $\rightarrow$ Necrosis (tissue death) $\rightarrow$ Organization (scar).
Class and exam questions
What are the main stages of myocardial infarction pathogenesis?
Three stages are distinguished: ischemic (prenecrotic), necrotic, and organization (scarring) stages.
Why does the intact myocardium suffer during an infarction?
The preserved myocardium takes on an increased load due to the exclusion of the ischemic area. This causes energy deficiency, mitochondrial hyperfunction, destruction of their cristae, and the development of tissue hypoxia.
What is the role of collateral circulation?
With sufficient collateral blood flow, ischemic changes in the peri-infarct zone are reversible. Inadequate blood supply leads to the transition of dystrophy into necrosis and an increase in the lesion size.
What else to study on this topic
- Morphological changes in ventricular fibrillation
- Detailed mechanisms of mitochondrial recombinational changes
- Features of sudden cardiac death
- Dynamics of in-hospital mortality rates in the first 2–8 days
- Mechanisms of myocardial reparative hypertrophy
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