Pathogenesis of atherosclerosis complications
The development of ischemic catastrophes is directly linked to changes in the structure of atherosclerotic lesions—atheromas and fibroatheromas. Plaque modification triggers a cascade of destructive reactions in the vascular wall. Key processes include the deposition of calcium salts, crack formation, and deep ulceration of the fibroatheroma cap.
Thrombi immediately begin to form on the damaged endothelial surface. They can be of various types: mural, intramural, completely occluding the lumen (obstructive), or becoming a source of detached emboli. An additional factor of instability is the rupture of newly formed microcapillary walls at the periphery of the atheroma, leading to massive hemorrhages directly into the arterial wall.
The consequences of these processes are pronounced clinical complications:
- Internal organ infarctions (brain, heart, lungs, kidneys).
- Internal hemorrhages and bleeding.
- Tissue ischemia, including coronary artery disease (CAD), ischemic strokes, and bowel and limb ischemia.
- Formation of aneurysms and dangerous dissection of the walls of the aorta and large arteries.
The mechanism of ischemic focus formation is always combined. It consists of a physical barrier to blood flow (atheroma, thrombus, or embolus) and pronounced vascular spasm. The spasm is caused by the contraction of arteriolar smooth muscle cells under the influence of locally released vasoconstrictors: endothelin, leukotrienes, thromboxane $A_2$, and vasoconstrictor prostaglandins.
Acute myocardial infarction and ACS
Myocardial infarction (MI) is an acute focal ischemic necrosis of the heart muscle. This condition is a logical outcome of absolute or relative coronary insufficiency, when oxygen delivery fails to meet the vital demands of the myocardium. Irreversible death of cardiomyocytes occurs if transient ischemia continues for over 60–120 minutes.
In the overall morbidity structure, acute MI accounts for 7–27%, while chronic forms of CAD account for 20–68%. CAD itself is based on two types of disorders:
- Organic (irreversible) — persistent narrowing of the lumen due to coronary atherosclerosis.
- Functional (transient) — intravascular thrombosis and acute spasm.
In modern clinical practice, acute coronary syndrome (ACS) is distinguished, uniting conditions from unstable angina to full-blown infarction. The isolation of ACS is dictated by the fact that the first day of the disease is a critical period claiming the lives of 70–80% of deceased patients. Pathogenetic processes in the first hours change rapidly, which is why rescue tactics require strictly phased therapeutic measures.
Morphology of ischemic injury using the spleen as an example
Organ infarctions have characteristic morphological features depending on the affected vascular bed. A classic example demonstrating the role of the level of occlusion is splenic infarction.
| Characteristic | White (ischemic) infarction | Red (venous) infarction |
|---|---|---|
| Status | Typical, most frequent | Rare variant |
| Pathogenesis | Obstruction of arterial inflow (thrombosis or embolism of arterial branches) | Thrombosis or occlusion of the splenic vein |
| Morphology | Dense white-yellowish wedge-shaped focus, base facing the capsule | Necrosis zone impregnated with blood, color ranging from dark red to black |
| Demarcation | Clearly defined leukocyte zone | Not prominent, occupies a small area |
In addition to classification by mechanism (arterial anemia versus congestive-hemorrhagic variant), foci are classified by prevalence into single and multiple. By size, small subcapsular areas and extensive lesions are distinguished, up to total necrosis of the organ. It is the volume of the lesion that determines the risk of severe complications, such as rupture of the splenic capsule or purulent fusion (abscess formation).
To memorize the main mediators causing vascular spasm during ischemia (Endothelin, Leukotrienes, Thromboxane, Prostaglandins), use the phrase: Endothelin Locally Triggers Problems.
Class and exam questions
What is acute coronary syndrome and why is this diagnosis so important?
This is a collective term encompassing a spectrum of conditions from unstable angina to infarction. It is singled out for emergency risk assessment, as 70–80% of fatalities occur in the first 24 hours, and therapy must immediately adapt to the stage of pathogenesis.
How soon does myocardial ischemia lead to necrosis?
Irreversible death of a myocardial area (infarction) occurs if transient ischemia and acute blood flow insufficiency last longer than 60–120 minutes.
How does a white splenic infarction visually differ from a red one?
White infarction appears as a dense yellowish wedge with a clear leukocyte border, arising from an arterial block. Red infarction is the consequence of venous thrombosis, where the necrosis zone lacks clear borders and acquires a dark red or black color due to blood imbibition.
Which substances cause vascular spasm in the ischemic zone?
Contraction of smooth muscle cells is triggered by vasoconstrictors locally released by cells: endothelin, thromboxane $A_2$, leukotrienes, and vasoconstrictor prostaglandins.
What else to study on this topic
- Stages of atherosclerotic plaque modification: from cracks to calcification
- Organic and functional changes in coronary artery disease
- Types of intravascular thrombi: mural, intramural, occlusive
- Complications of splenic infarction: abscess formation and capsule rupture
- Pathogenesis of aneurysm formation and arterial wall dissection
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