Systemic inflammatory changes after pulmonary vein radiofrequency ablation do not alter stem cell mobilization

Area of Science:

• Cardiology
• Regenerative Medicine
• Inflammation Biology

Background:

• Atrial fibrillation (AF) is a common arrhythmia.
• Pulmonary vein (PV) isolation using radiofrequency (RF) ablation is a standard treatment for paroxysmal AF.
• RF ablation induces localized myocardial necrosis, potentially triggering inflammatory responses and progenitor cell mobilization for tissue repair.

Purpose of the Study:

• To investigate changes in circulating progenitor cells, inflammatory mediators, and myocardial necrosis markers after RF ablation for paroxysmal AF.
• To determine if myocardial necrosis and inflammation following PV isolation enhance progenitor cell mobilization.

Main Methods:

• Blood samples were collected from patients with paroxysmal AF before and after PV isolation.
• Measured inflammatory mediators (IL-6, IL-1beta, TNF-alpha, etc.) and stromal derived factor (SDF)-1 using immunoassay.
• Analyzed circulating progenitor cells (CD34+CD133+, CD117+, EPCs) via flow cytometry and culture assays.
• Assessed myocardial necrosis using creatine kinase and troponin T levels.

Main Results:

• PV isolation induced myocardial necrosis and a significant increase in leukocyte counts, C-reactive protein, and IL-6 levels.
• Increased IL-6 correlated with myocardial necrosis and inflammatory response (P = 0.007).
• SDF-1 levels decreased post-ablation (P = 0.004), while other measured cytokines showed no significant change. Circulating progenitor cells (CD34+CD133+, CD117+) remained unchanged, with a trend towards decreased EPCs.

Conclusions:

• RF ablation for paroxysmal AF triggers a systemic inflammatory response and myocardial necrosis.
• Despite inflammation and necrosis, circulating progenitor cell numbers did not increase.
• Isolated myocardial necrosis following PV isolation may not be sufficient to mobilize progenitor cells.