Etiology and inflammatory factor
The disease predominantly affects men. Risk factors are completely identical to those identified for other forms of coronary artery disease.
The morphological basis is severe stenosing coronary atherosclerosis, which is critically exacerbated by coronary spasm. Notably, classical coronary artery thrombosis is rarely detected in this condition.
The key initiating factor is the rupture of an unstable atherosclerotic plaque. This process is closely linked to local inflammation, a diagnostic and prognostic marker of which is an elevated serum level of C-reactive protein (CRP). Its mechanism of action is as follows: CRP stimulates protein I expression in endothelial cells, which triggers monocyte chemotaxis and their active migration through the endothelium into the vessel intima.
Ischemic cascade and electrical instability
Arterial spasm causes acute ischemia, triggering a destructive biochemical cascade. As early as 5–10 minutes after the onset of oxygen deprivation, degradation of cardiomyocyte cell membranes begins with the formation of fatty acids and lysophosphoglycerides.
The mechanism of electrical instability development includes the following stages:
- Lysophosphoglycerides accumulate in the tissues.
- Excessive cAMP production occurs.
- The influx of Ca²⁺ ions into cardiomyocytes increases sharply.
- Glycogenolysis and lipolysis processes are activated.
Concurrently, vascular spasm causes activation of the sympathoadrenal system, leading to hypercatecholaminemia. A sharp increase in adrenaline concentration can provoke ventricular fibrillation. Free radical lipid peroxidation products that are formed possess an additional arrhythmogenic effect.
Reperfusion paradox and differences from infarction
Paradoxically, the main trigger of ventricular fibrillation is reperfusion (blood recirculation). The critical period for this phenomenon is 40–60 minutes after the onset of ischemia.
The mechanism is that restored blood flow (or residual blood flow) washes out the accumulated arrhythmogenic substances from the ischemic focus. These toxic products damage the membranes of the surrounding, normally functioning myocardium, causing electrical instability and fibrillation.
This lies the main difference from classical myocardial infarction without blood flow restoration. In infarction, arrhythmogenic substances remain "walled off" inside the coagulation necrosis zone and do not enter the systemic circulation. Therefore, fibrillation occurs less frequently in infarction and is associated with pathological processes in the peri-infarction zone rather than the necrosis focus itself.
Morphological changes
Since death occurs rapidly, full-blown signs of necrosis do not have time to develop.
- Macroscopic appearance: The heart becomes flabby, and the left ventricular cavity is dilated.
- Microscopic appearance: The most characteristic histological sign is fragmentation of muscle fibers. It occurs as a consequence of excessive cardiomyocyte contraction leading to physical ruptures of myofibrils.
Briefly: answers to topical questions
What ultrastructural changes occur in cardiomyocytes during acute ischemia?
During acute ischemia, ultrastructural damage to the sarcolemma, mitochondria, and sarcoplasmic reticulum is detected in cardiomyocytes.
- Sarcolemmal damage.
- Mitochondrial destruction — characterized by their swelling, matrix washout, and destruction of cristae.
- Changes in the sarcoplasmic reticulum — its swelling.
- Sarcoplasmic edema.
- Widening of intercalated discs.
Also, after 5–15 minutes, uneven hypercontraction and relaxation of myofibrils, vacuolar and fatty dystrophy are noted.
What macroscopic histochemical tests are used at autopsy to detect early myocardial ischemia?
Special oxidation-reduction enzyme tests are used for the macroscopic detection of early myocardial ischemia areas.
- Potassium tellurite test: in the presence of oxygen, potassium tellurite is reduced to tellurium, so viable tissue acquires a dark color; ischemic areas have a pale appearance. Potassium tellurite makes it possible to detect the disappearance of enzymatic activity in the pre-necrotic stage.
- Nitro-BT reaction: the principle is similar to the tellurite test; viable myocardium stains dark purple.
The 4Rs rule for pathogenesis: Rupture (of the plaque) → Breakdown (of membranes into lysophosphoglycerides) → Reperfusion (washout of toxins) → Rupture (of myofibrils during fragmentation).
Class and exam questions
Why is a thrombus rarely found in sudden coronary death?
Unlike infarction, the main cause is not complete vessel occlusion by a thrombus, but severe stenosing coronary atherosclerosis combined with pronounced arterial spasm and rupture of an unstable plaque.
What role does reperfusion play in the development of fibrillation?
Restoration of blood flow (especially after 40–60 minutes) washes out the accumulated arrhythmogenic substances from the ischemic zone. They damage the membranes of healthy myocardium, provoking fatal electrical instability.
Why does ventricular fibrillation occur less frequently in myocardial infarction?
In infarction without blood flow restoration, toxic breakdown products remain "walled off" in the coagulation necrosis zone and do not enter the systemic circulation, unlike the situation with reperfusion.
Which microscopic feature is most characteristic of this pathology?
The main marker is the fragmentation of muscle fibers. It occurs due to excessive cardiomyocyte contraction, which leads to physical ruptures of myofibrils.
What else to study on this topic
- Mechanisms of formation and rupture of an unstable atherosclerotic plaque
- The role of C-reactive protein and protein I in endothelial dysfunction
- Biochemistry of the ischemic cascade: cAMP and calcium ion metabolism
- The effect of hypercatecholaminemia on myocardial electrical stability
- Morphological differences between the coagulation necrosis zone and the peri-infarction zone
Master the entire topic in the "Pathological Anatomy" course
This is a summary. The course covers everything tested in classes and exams.
- Complete study guide on "Sudden coronary death" and 4,414 more pages of the subject
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 153 video lessons on the subject
Other topics in the section "Pathology of the Cardiovascular System"
Free video lessons: pathological anatomyShort lessons with study notes — no registration required.
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.