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Influence of diffuse fibrosis on wave propagation in human ventricular tissue
Kirsten H W J Ten Tusscher1, Alexander V Panfilov
1Department of Theoretical Biology, Utrecht University, Padualaan 8, 3584 CH Utrecht, The Netherlands. khwjtuss@hotmail.com
Insights
Diffuse fibrosis in the heart significantly impacts electrical activity, increasing arrhythmia risk. Computer modeling reveals it slows wave propagation and promotes spiral wave formation, suggesting new mechanisms for cardiac fibrillation.
Area of Science:
- Cardiology
- Biophysics
- Computational Biology
Background:
- Cardiac fibrosis, the increase of connective tissue, is prevalent in aging and heart disease.
- Elevated fibrosis levels (10-35%) correlate strongly with arrhythmias and sudden cardiac death.
Purpose of the Study:
- To investigate the impact of diffuse fibrosis on cardiac electrical wave propagation.
- To explore the role of fibrosis in arrhythmogenesis and arrhythmia mechanisms within human ventricular tissue.
Main Methods:
- Utilized advanced computer modeling techniques.
- Simulated wave propagation in human ventricular tissue with varying degrees of diffuse fibrosis.
Main Results:
- Diffuse fibrosis was shown to significantly slow down cardiac electrical wave propagation.
- Increased vulnerability to wave break and spiral wave formation was observed due to fibrosis.
- Fibrosis prolonged re-entrant arrhythmias and suppressed restitution-induced tachycardia-to-fibrillation transitions.
Conclusions:
- The findings suggest that mechanisms beyond restitution-induced spiral breakup are critical for fibrillation onset in fibrotic hearts.
- Alternative mechanisms must be considered for understanding and treating arrhythmias in conditions with significant diffuse fibrosis.
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.
