Background We have previously reported that non-ischemic titrated cardiac injury caused by radiofrequency catheter ablation (RFCA) for atrial fibrillation (AF) mobilizes CD34+ bone marrow derived cells to the peripheral blood. It has been known that stromal cell derived factor (SDF)-1慣 plays an important role in mobilization of CD34+ cell after ischemic vascular injury. We investigated the pathway responsible for CD34+ cell mobilization in non-ischemic cardiac injury model. Methods and Results Forty-six patients (34 males, 54.9짹11.7 years old) with AF (paroxysmal AF (PAF): persistent AF (PeAF) = 26:20) who underwent RFCA were included. The percent changes in CD34+ cell (%��CD34+) were correlated with plasma levels of multiple chemotactic factors, at baseline, immediately after, 24 hours later, and 10 days after the RFCA. Results: 1. %��CD34+ cells increased significantly after RFCA (60.2짹87.3%, P<0.001). However, SDF-1慣 rather decreased 24 hours after RFCA (2.09짹0.69ng/mL vs. 1.60짹0.42ng/mL, p=NS) and had no correlation with %��CD34+ cells. 2. The plasma levels of GRO棺 increased after RFCA (0.28짹0.21ng/mL to 0.86짹0.60ng/mL, p<0.001), and had a correlation with 24 hour %��CD34+ cells (R=0.61, p<0.001). 3. Matrix metalloproteinase (MMP)-9 increased after RFCA (39.94짹26.40ng/mL vs. 119.65짹71.42ng/mL, p<0.0001), and had a correlation with post-ablation 24 hour %��CD34+ cells (R=0.44, p<0.01). 4. Angiopoietin-1 had a correlation with post- ablation 24 hour %��CD34+ (R=0.41, p<0.05). 5. Plasma levels of GRO棺 had good correlations with MMP-9 (R=0.62, p<0.01) as well as with angiopoietin-1 (R=0.75, p<0.0001). Conclusion Titrated cardiac injury from RFCA for AF mobilizes the bone marrow derived CD34+ cells to the peripheral blood through the pathway associated with Aniogiopoietin-1 - MMP-9 - GRO棺, not with SDF-1慣. Further studies will be required to differentiate cellular and molecular mechanisms for the mobilization of CD34+ cells between ischemic and non-ischemic vascular injury.