Etiology and Inflammatory Factors
The condition predominantly affects males. Risk factors are entirely analogous to those identified for other forms of coronary artery disease.
The morphological basis is severe stenosing coronary atherosclerosis, critically exacerbated by coronary vasospasm. Notably, classic coronary artery thrombosis is rarely identified in this condition.
The key triggering event is the rupture of an unstable atherosclerotic plaque. This process is closely linked to local inflammation, for which elevated serum levels of C-reactive protein (CRP) serve as a diagnostic and prognostic marker. Its mechanism of action involves CRP stimulating 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 triggers acute ischemia, initiating a destructive biochemical cascade. As early as 5–10 minutes after the onset of oxygen deprivation, degradation of cardiomyocyte cell membranes begins, yielding free fatty acids and lysophosphoglycerides.
The mechanism of electrical instability involves the following stages:
- Accumulation of lysophosphoglycerides in tissues.
- Excessive production of cAMP.
- A sharp influx of Ca²⁺ ions into cardiomyocytes.
- Activation of glycogenolysis and lipolysis.
Simultaneously, vascular spasm activates the sympathoadrenal system, resulting in hypercatecholaminemia. A sharp increase in epinephrine concentration can provoke ventricular fibrillation. Lipid peroxidation-derived free radicals exert an additional arrhythmogenic effect.
The Reperfusion Paradox and Differences from Infarction
Paradoxically, the primary trigger for ventricular fibrillation is reperfusion (blood recirculation). The critical window 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 accumulated arrhythmogenic substances from the ischemic focus. These toxic products damage the membranes of the surrounding, normally functioning myocardium, inducing electrical instability and fibrillation.
This represents the main distinction from classic myocardial infarction without restoration of blood flow. In infarction, arrhythmogenic substances remain "trapped" within the zone of coagulative necrosis and do not enter the systemic circulation. Therefore, fibrillation occurs less frequently in infarction and is associated with pathological processes in the peri-infarct zone rather than the necrotic core itself.
Morphological Changes
Because death occurs rapidly, fully developed features of necrosis do not have time to form.
- Macroscopic appearance: The heart becomes flabby, and the left ventricular cavity is dilated.
- Microscopic appearance: The most characteristic histological feature is muscle fiber fragmentation. It occurs as a consequence of excessive cardiomyocyte contraction, leading to physical ruptures of the myofibrils.