Non-ischaemic titrated cardiac injury caused by radiofrequency catheter ablation of atrial fibrillation mobilizes CD34-positive mononuclear cells by non-stromal cell-derived factor-1α mechanism

AimsIt has been known that myocardial ischaemia mobilizes CD34+ bone marrow-derived cells by the stromal cell-derived factor (SDF)-1α pathway. We hypothesized that non-ischaemic titrated cardiac injury caused by radiofrequency catheter ablation (RFCA) of atrial fibrillation (AF) recruits CD34+ cells by an alternative mechanism.Methods and resultsFifty-six patients (39 males, 53.0 ± 13.5 years old) who underwent electrophysiology study (EPS; n = 10) or RFCA of AF (n = 46) were included. Peripheral blood CD34+ cell count and multiple serologic markers were evaluated before, immediately after, at 24 h, and 10 days after the procedure. The results are as follows: (i) the per cent increase in CD34+ cells (ΔCD34+) was significant after RFCA compared with after EPS (P < 0.01), and correlated with RF duration and troponin I, respectively. (ii) In contrast, SDF-1α decreased after RFCA and had no correlation with ΔCD34+ cells while matrix metalloproteinase (MMP)-9 (P < 0.0001) and GROβ (P < 0.001) increased after RFCA and had correlations with 24 h ΔCD34+ cells.ConclusionNon-ischaemic titrated cardiac injury caused by AF ablation mobilizes CD34+ cells to the peripheral blood through a non-SDF-1α pathway associated with MMP-9 and GROβ.