Aims: During ageing, after infarction, in cardiomyopathies and other cardiac diseases, the percentage of fibrotic (connective) tissue may increase from 6% up to 10-35%. The presence of increased amounts of connective tissue is strongly correlated with the occurrence of arrhythmias and sudden cardiac death.
Methods and results: In this article, we investigate the role of diffuse fibrosis on wave propagation, arrhythmogenesis, and arrhythmia mechanism in human ventricular tissue using computer modelling. We show that diffuse fibrosis slows down wave propagation and increases tissue vulnerability to wave break and spiral wave formation. We also demonstrate that diffuse fibrosis increases the period of re-entrant arrhythmias and can suppress the restitution-induced transition from tachycardia to fibrillation.
Conclusion: The latter suggests that mechanisms different from restitution-induced spiral break-up might be more likely to account for the onset of fibrillation in the presence of large amounts of diffuse fibrotic tissue.