Key result
Ventricular false chordae tendineae in DCM show fibrosis and Cx43 remodeling, potentially contributing to reentrant arrhythmias.
Fibrous tissue proliferation and Cx43 remodeling in the ventricular false chordae tendineae of DCM patients may provide a pathological basis for reentrant arrhythmias and electrical heterogeneity.
Should not yet change DCM arrhythmia management; hypothesis-generating for reentrant substrate and requires validation before adoption.
In DCM patients, the gross morphology of ventricular false chordae tendineae showed no significant changes; however, marked proliferation of fibrous connective tissue was frequently observed, separating cardiomyocytes or Purkinje fibers into bundles or completely replacing the cellular components. This may contribute to the pathological basis of reentrant arrhythmias. Furthermore, the remodeling of Cx43 from an end-to-end to a lateral-lateral distribution may underlie electrical heterogeneity.
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Xu et al. (2026) studied this question. Ventricular false chordae tendineae in dilated cardiomyopathy patients exhibit marked fibrous tissue proliferation and Cx43 remodeling, potentially contributing to reentrant arrhythmias.
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