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Effects of Inflammatory Cell Death Caused by Catheter Ablation on Atrial Fibrillation
Dishiwen Liu1,2,3, Yajia Li1,2,3, Qingyan Zhao1,2,3
1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, People's Republic of China.
Insights
Catheter ablation for atrial fibrillation (AF) can cause inflammation, impacting long-term success. Pulsed-field ablation shows promise for reduced inflammation and improved outcomes in AF treatment.
Area of Science:
- Cardiology
- Electrophysiology
- Cell Biology
Background:
- Atrial fibrillation (AF) presents a significant healthcare challenge due to high morbidity and complications like thrombosis and heart failure.
- Catheter ablation aims to cure AF by creating linear lesions for electrical isolation, but long-term success rates remain suboptimal.
- Inflammation and fibrosis are recognized as key drivers in AF progression, with ablation-induced cell death potentially influencing outcomes.
Purpose of the Study:
- To review the inflammatory responses (apoptosis, necrosis, necroptosis, pyroptosis, ferroptosis) associated with catheter ablation and their link to arrhythmia.
- To compare the cell death mechanisms induced by different ablation modalities: radiofrequency, cryoballoon, and pulsed-field ablation.
- To discuss the impact of inflammation-induced structural and electrical remodeling on AF recurrence post-ablation.
Main Methods:
- Literature review focusing on inflammatory cell death pathways in AF.
- Comparative analysis of cell death profiles across radiofrequency, cryoballoon, and pulsed-field ablation techniques.
- Discussion of remodeling and recurrence based on current scientific consensus.
Main Results:
- Catheter ablation triggers various inflammatory cell death pathways, influencing cardiac remodeling and arrhythmia.
- Different ablation modalities induce distinct patterns of cell death, with varying inflammatory consequences.
- Pulsed-field ablation demonstrates potential for greater tissue selectivity and a reduced inflammatory response, primarily through apoptosis-dominated cell death.
Conclusions:
- Inflammation and associated cell death mechanisms play a critical role in the efficacy and recurrence of AF after catheter ablation.
- Pulsed-field ablation represents a potentially revolutionary approach, offering improved safety, selectivity, and a less inflammatory profile compared to traditional methods.
- Further research into ablation-induced inflammation is crucial for optimizing AF management and improving long-term patient outcomes.
Abstract:
Atrial fibrillation (AF) poses a serious healthcare burden on society due to its high morbidity and the resulting serious complications such as thrombosis and heart failure. The principle of catheter ablation is to achieve electrical isolation by linear destruction of cardiac tissue, which makes AF a curable disease. Currently, catheter ablation does not have a high long-term success rate. The current academic consensus is that inflammation and fibrosis are central mechanisms in the progression of AF. However, artificially caused inflammatory cell death by catheter ablation may have a significant impact on structural and electrical remodeling, which may affect the long-term prognosis. This review first focused on the inflammatory response induced by apoptosis, necrosis, necroptosis, pyroptosis, ferroptosis and their interaction with arrhythmia. Then, we compared the differences in cell death induced by radiofrequency ablation, cryoballoon ablation and pulsed-field ablation. Finally, we discussed the structural and electrical remodeling caused by inflammation and the association between inflammation and the recurrence of AF after catheter ablation. Collectively, pulsed-field ablation will be a revolutionary innovation with faster, safer, better tissue selectivity and less inflammatory response induced by apoptosis-dominated cell death.
