From Ischemic Injury to Arrhythmogenic Substrate: Molecular and Histopathological Insights into Post-Infarction Sudden Cardiac Death

Figures

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  Figure 1. Integrated pathophysiological pathways linking myocardial infarction to ventricular arrhythmias and sudden cardiac death. The figure also illustrates the integrative approach adopted throughout this review, emphasizing the progressive interaction between histopathological, molecular, microvascular, and electrophysiological mechanisms leading to ventricular arrhythmias and sudden cardiac death.

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  Figure 2. Histological features of acute myocardial infarction. (A) Hematoxylin and eosin (H&E) staining, ×10 original magnification, showing the characteristic “wavy fibers” in the ischemic myocardium. (B) Higher magnification (H&E, ×20) highlighting the undulating appearance of injured cardiomyocytes, an early morphological hallmark of ischemic injury resulting from traction exerted by the surrounding viable myocardium.

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  Figure 3. Histological features of acute myocardial infarction. (A) H&E staining, ×20 original magnification, showing coagulative necrosis in the acute phase, characterized by cytoplasmic hypereosinophilia, loss of transverse striations, and nuclear disappearance (karyolysis). (B) H&E staining, ×20 original magnification, highlighting contraction band necrosis, a characteristic feature observed in the subsequent hours and particularly associated with reperfusion injury and intracellular calcium overload.

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  Figure 4. Histological features of inflammatory response following myocardial infarction. H&E staining, ×10 original magnification (A) and ×20 original magnification (B), demonstrating a mixed inflammatory cell infiltrate with cardiomyocyte necrosis.

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  Figure 5. Histological features of the transition zone following myocardial infarction. H&E staining, ×5 original magnification, showing the transition between necrotic and preserved myocardium.

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  Figure 6. Histological features of post-infarction fibrotic scar formation. (A) H&E staining, ×10 original magnification, showing replacement of necrotic myocardium by fibrous scar tissue. (B) Masson’s trichrome staining, ×20 original magnification, highlighting collagen deposition within the fibrotic scar.

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  Figure 7. Electrophysiological mechanisms underlying post-infarction ventricular arrhythmogenesis. Myocardial fibrosis and infarct border-zone remodeling promote slow and anisotropic conduction, leading to unidirectional conduction block and the formation of reentrant circuits. Together with triggered activity and electrical remodeling, these mechanisms facilitate ventricular tachycardia, which may degenerate into ventricular fibrillation and ultimately result in sudden cardiac death.