Fibrosis in Chagas disease disrupts myocardial microarchitecture, creating structural inhomogeneity that promotes re-entrant circuits and malignant arrhythmias.
Identifies fibrosis as key driver of reentrant arrhythmias in Chagas; leaves open whether antifibrotic strategies improve outcomes.
Histopathological evidence of extensive fibrosis may produce myocardial areas where fibrous tissue separates the muscle fibers from each other. The dismally connected fibers in infected myocardial tissue with continuous fibro-degenerative modification may induce anomalous electrophysiological characteristics. Electrical coupling between adjacent fibers is difficult to occur when fibrosis surrounds groups of myocytes The microarchitecture and anisotropic characteristics may play an important role in re-entry by causing inhomogeneous and discontinuous propagation of the impulse. This non-uniform anisotropic property causes an irregular and fractionated propagation of the depolarization wave in the transverse direction Structural inhomogeneity or the common distinction in electrophysiological or ultra-structural properties plays a major role in the induction of re-entrant circuits and malignant arrhythmias due to the elevated probability of unidirectional block of the premature impulse and conduction delay
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Centurión et al. (2017) studied this question.
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